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by Charles Daney in Science and Reason
Galaxies are made of stars, and stars are made of... gas. So a large part of understanding how galaxies evolve and grow is understanding how much "gas" (literally, not "gasoline") is present in galaxies – but has not yet been incorporated in stars – at different periods in the history of the universe.What periods of the universe are most interesting in this regard? The answer is: periods somewhat less than the first half of the universe's existence since the time of the big bang, roughly the first 5.5 billion years, 40% of the total. That's because astronomers have good reason to believe that is the time when star formation, and hence galaxy growth, occurred most vigorously. Assuming the best current estimate, that is has been about 13.7 billion years since the big bang, this means we're interested in observing the universe as it was more than 8.2 billion years ago. That's quite a long time ago, and until fairly recently observation of objects that far back in time has been infeasible. Technology is only now becoming available to study the details of such a remote time.Astronomers find it convenient to represent distance (in either space or time) in terms of redshift. Because it takes light a finite amount of time to travel, any observable object is seen not as it looks "today", 13.7 billion years after the big bang, but instead as it looked a some time T<13.7, and so we see the object as it looked 13.7-T billion years ago. The light from such an object has taken 13.7-T billion years to reach us.Due to the expansion of the universe, the wavelength of any photon of light has been increased by a factor of (z+1), where z is the observed redshift – z=0 corresponding to nearby objects for which the shift is negligible. z increases as a complicated function of the distance of the object, but it increases in a regular way as the distance increases. For objects at an age T=5.5 billion years, corresponding to a distance of 8.2 billion light years, the redshift would be about 1.1.Astronomers have now done surveys of galaxies around z≈1.1. It's not easy, but there is plenty of data, even though only very large, bright galaxies can be observed in detail at that distance. It's even more difficult, though still feasible, to survey galaxies that are even more remote, say at z≈2.3, which corresponds to T≈2.9 billion years.For the research under discussion here, the investigators relied on existing surveys to sample from, because of the difficulty of doing new surveys from scratch. There was a trade-off to be made. In order to be able to study a selected sample of galaxies in sufficient detail, it's desirable to pick the largest, brightest galaxies. On the other hand, it's also important to study galaxies that are representative of "typical" mature galaxies today, such as our Milky Way. Unfortunately, the most luminous objects at large z tend to be atypical things like quasars and merging galaxies. Those are "freaks", quite unlike typical nearby galaxies, and whatever we might learn about them might not tell us much about the typical case. So the investigators had to select galaxies for study that were as large and bright as possible, but still "normal". In this case, they included only galaxies of estimated stellar mass (excluding dark matter) of ≥ 3×1010 M⊙. (1 M⊙ is our Sun's mass.) Since we are inside the Milky Way and can't see all of it (because of thick dusty regions), it's hard to be sure of our galaxy's total stellar mass, but it's estimated to be about 5×1010 M⊙. (Ref: here.)An important objective of the research was to get a better understanding of galaxies in which new stars are actively being formed – unlike the Milky Way and other nearby large spirals, which are currently forming stars at the rate of about 5 M⊙ per year. Star formation rate is something else that's easier to determine from outside the galaxy, by measuring light flux in various parts of the spectrum (especially infrared and ultraviolet). For the present research, only galaxies with a star formation rate ≥ 40 M⊙ per year were selected.For reasons we're coming to, the required observations are difficult and time-consuming, so for this kind of preliminary study it was necessary to work with small numbers. The net result is that the study was done with 11 galaxies selected from one survey, with z≈1.2, and 12 galaxies selected from another survey with z≈2.3.Remember that the ultimate objective of the research is to determine how much gas is available for star formation in typical galaxies at the given values of z. That's what is so difficult that it had not been done before (for such distant galaxies).It's relatively straightforward to determine how much of a galaxy's mass is in the form of stars. This "stellar mass" is proportional to the intrinsic luminosity of the galaxy (which is known since the galaxy distance is known), because most galaxies consist of stars with a predictable distribution of stars of given mass and luminosity ("initial mass function").However, the total mass of a galaxy also includes non-baryonic dark matter, whose mass in the universe as a whole is known to be about 5 times as large as the mass of "ordinary" baryonic matter. The total mass of a galaxy can sometimes be inferred from measuring galaxy rotation curves. The baryonic matter of a galaxy consists of stars, gas, and (perhaps) massive nonluminous objects such as black holes. Even if one knew reliably the total mass of a galaxy, including dark matter, and one could neglect the contribution of nonluminous objects, one still could not estimate the mass of gas as the difference between the mass of a galaxy's stars and the roughly 17% of total mass that baryonic matter represents in the universe as a whole. That's because there's no a priori reason to expect that a 1:5 ratio of baryonic matter to non-baryonic matter is present in any particular galaxy – it might well be either more or less. So there needs to be some way to measure fairly directly the amount of matter a galaxy contains in the form of gas that could form stars.It is known that stars form only out of gas that's rather cold – with temperature less than 100 K. This is simply because hotter gas has a higher internal pressure that prevents the gravitational collapse that's necessary to form a star. Gas that cold is very hard to detect. Black body radiation at 100 K peaks at 29 μm, in the far infrared, and cooler gas emits at even longer wavelengths. Redshift stretches the wavelengths even more (by factors of 2 or 3 for z=1 or 2). Most of the radiation at such wavelengths is blocked by our atmosphere, so is observable only from space – and the necessary instruments don't exist yet.Fortunately, black body radiation is not the only type of electromagnetic emission from cold gas. Vibrations and rotations of gas molecules also radiate at certain frequencies. Now, most of a galaxy's cold gas is in the form of atomic helium and molecular hydrogen. It would be convenient if hydrogen molecules, especially, had emissions at convenient wavelengths for ground-based observation, but no such luck. It turns out, however, that there is one molecule present in small amounts in interstellar gas which does have a convenient emission: CO (carbon monoxide). CO has a rotational emission at 870 μm (346 GHz). At the values of z of interest here (1.2 and 2.3) these fall into the 2 mm and 3 mm bands – which can be observed.In a nutshell, then, what the research under discussion did was to measure the total flux from the selected galaxies at the appropriate wavelengths. This indicates that amount of cold CO gas present in the galaxies. Studies of nearby galaxies show that this accurately indicates the total amount of cold gas present. From this, and the estimated mass in the form of stars, one has fraction of total mass (stars + gas) represented by the cold gas available to form stars.For the galaxies in the sample, this fraction was found to be 34% at z≈1.2 and 44% at z≈2.3. By contrast, contemporary large spiral galaxies have fractions in the 3% to 12% range – quite a difference.For a summary of the results, here's the abstract:High molecular gas fractions in normal massive star-forming galaxies in the young UniverseStars form from cold molecular interstellar gas. As this is relatively rare in the local Universe, galaxies like the Milky Way form only a few new stars per year. Typical massive galaxies in the distant Universe formed stars an order of magnitude more rapidly. Unless star formation was significantly more efficient, this difference suggests that young galaxies were much more molecular-gas rich. Molecular gas observations in the distant Universe have so far largely been restricted to very luminous, rare objects, including mergers and quasars, and accordingly we do not yet have a clear idea about the g... Read more »
Tacconi, L., Genzel, R., Neri, R., Cox, P., Cooper, M., Shapiro, K., Bolatto, A., Bouché, N., Bournaud, F., Burkert, A.... (2010) High molecular gas fractions in normal massive star-forming galaxies in the young Universe. Nature, 463(7282), 781-784. DOI: 10.1038/nature08773
by Charles Daney in Science and Reason
We discussed supernovae a bit in this recent post on gamma-ray bursts. There is now interesting new information on the connection between supernovae and gamma-ray bursts from two recently-described supernovae with atypical properties.Let's first review a little. Gamma-ray bursts (GRBs) are identified by detection of relatively brief (usually less than a few minutes) but highly energetic emissions of gamma rays. Although there's a great deal of diversity, most events fall into one of two categories: "short", emitting strongly for less than two seconds, and "long", having strong gamma-ray emissions for more than a few seconds and higher total energy.Short GRBs are less well understood, but they are commonly thought to result from the merger of two stellar-weight black holes or neutron stars. Short GRBs are not relevant for the present discussion.Long GRBs are thought, with fairly general consensus, to result from certain types of supernovae (the "core-collapse" kind). One reason for this consensus is that the total energy output of a long GRB appears to be in the same neighborhood as that of a core-collapse supernova: around 1051 ergs (1044 joules, if you prefer). Also, if a GRB occurs sufficiently nearby, we can optically identify it with a bright supernova event, and there have been several instances of this.Supernovae also come in several different kinds, which differ in their internal mechanisms. The main types are Type I, which have no evidence of hydrogen in their spectra, and Type II, which do have hydrogen lines in the spectrum.There are further subdivisions of the Type I case: Type Ia supernovae are thought to be associated with progenitors that are white dwarfs. These are the end stage reached by most stars, which have less than about ten times the mass of the Sun (10 M⊙). Such stars lose most of their mass when they pass through an earlier red giant stage. After they have burned (via fusion) all of their hydrogen they shrink down to become white dwarfs with a mass less than about 1 M⊙. Eventually such a star can no longer produce energy even by fusing heavier elements. The star produces energy only by gravitational contraction. Contraction stops only when degeneracy pressure (due to the Pauli exclusion principle) prevents further collapse. Degeneracy pressure, however, can support a stellar mass only if it's less than 1.38 M⊙ – the Chandrasekhar limit. If a star reaches this stage with a mass of more than 1.38 M⊙, it will collapse further into a neutron star or black hole. If this doesn't happen, yet the star later accretes mass from an external source – such as a companion in a multiple star system – the star may wind up with enough additional matter to sustain an explosive fusion reaction – and then you get a Type Ia supernova. There's some controversy now whether this is more likely to happen due to the merger of two white dwarfs or gradual accretion from a companion, but that's irrelevant for the present discussion, because Type Ia supernovae are not associated with GRBs.The problem with Type Ia supernovae is that there's no conceivable mechanism to create one particular hallmark of a GRB – namely, jets of matter ejected from the explosion in opposite directions at speeds near the speed of light. It takes a particular mechanism called a "central engine" to accelerate matter that dramatically. This mechanism is thought to be a rapidly spinning neutron star or black hole that is surrounded by a gaseous accretion disk. The matter is sucked in by the central object, but because it has such a large amount of angular momentum it is expelled outwards in jets along the axis of rotation, instead of falling into or onto the central object.A "core collapse" supernova is required in order to produce the right conditions for a central engine of this sort to form. (And even in this case, only a small percentage of events seem to have just the right conditions.) To have a core collapse supernova, it's necessary for the progenitor star to have a mass more than about 10 M⊙. In this case, which is pretty rare, after a certain point, even though fusion of heavy elements may still be going on, the energy available from fusion becomes insufficient to support the entire mass of the star, and the whole thing then collapses very rapidly to a black hole or neutron star. If there is still some hydrogen remaining in the outer shell of the star immediately before collapse, you get a Type II supernova. Otherwise you get a Type Ib supernova, if there's still some helium remaining, or else a Type Ic (no helium).If the progenitor star had a mass between about 10 M⊙ and 20 M⊙, the end result is a neutron star. Above 20 M⊙ the result is a black hole. However, as noted, it's not known what conditions are required in order to have a central engine capable of producing a GRB. From the relative frequency of observed GRBs compared to Type Ib/c or Type II supernovae, the right conditions seem to occur only 1 or 2% of the time.The new wrinkle that two recently described supernova events exhibit is that it is possible to have relativistic jets of matter from a supernova without detectable gamma ray activity. Just how fast are we talking about in terms of the ejected matter? Well, in an "ordinary" supernova matter is ejected at speeds, at most, only 2 or 3% of the speed of light (which is still plenty fast). Yet in the recent examples, the matter is accelerated to more than 50% of the speed of light.How is the speed actually measured? Well, the interesting thing is that it's easy to measure at radio frequencies, using radio telescopes. Let's consider the case of the supernova known as SN 2009bb, to be specific, which was first observed on March 21, 2009. This one showed up in a galaxy called NGC 3278, which is about 130 light-years away.Astronomers didn't even have to act especially quickly to do the measurement – in fact it's best to do it several weeks after the event. Using radio interferometry it's straightforward to observe the size of the expanding sphere of radio emissions. Divide the radius of the sphere by the time since the initial event and you have (roughly) the rate of expansion.Actually, it's slightly more complicated than that, because relativistic speeds are involved. It's necessary to apply equations of special relativity. Suppose R is the apparent radius of the sphere, and the time interval is Δt. Then the apparent velocity of expansion is R/Δt. It is even possible for this apparent velocity to exceed c (the speed of light). However, this apparent velocity is not actually the rate at which the ejected matter is moving. Suppose that rate is denoted by v. Let β=v/c, the ratio of the actual speed to the speed of light. Define the quantity (Lorentz factor) γ=1/√(1-β2). Then what's actually true is that γβc=R/Δt. In the case of SN 2009bb the apparent velocity that was measured was ~0.85c. Solving for β you get β~0.65. That is, ejected matter was moving at about 65% of the speed of light. This matter was just lightweight electrons, but it still takes one honking explosion to move even electrons that fast – perhaps 30 times as fast as what one gets in an "ordinary" supernova.Here's the research abstract:A relativistic type Ibc supernova without a detected γ-ray burstLong duration γ-ray bursts (GRBs) mark the explosive death of some massive stars and are a rare sub-class of type Ibc supernovae. They are distinguished by the production of an energetic and collimated relativistic outflow powered by a central engine (an accreting black hole or neutron star). Observationally, this outflow is manifested in the pulse of γ-rays and a long-lived radio afterglow. Until now, central-engine-driven supernovae have been discovered exclusively through their γ-ray emission, yet it is expected that a larger population goes undetected because of limited satellite sensitivity or beaming of the coll... Read more »
Soderberg, A., Chakraborti, S., Pignata, G., Chevalier, R., Chandra, P., Ray, A., Wieringa, M., Copete, A., Chaplin, V., Connaughton, V.... (2010) A relativistic type Ibc supernova without a detected γ-ray burst. Nature, 463(7280), 513-515. DOI: 10.1038/nature08714
Paragi, Z., Taylor, G., Kouveliotou, C., Granot, J., Ramirez-Ruiz, E., Bietenholz, M., van der Horst, A., Pidopryhora, Y., van Langevelde, H., Garrett, M.... (2010) A mildly relativistic radio jet from the otherwise normal type Ic supernova 2007gr. Nature, 463(7280), 516-518. DOI: 10.1038/nature08713
by Charles Daney in Science and Reason
Everybody knows what a spiral galaxy looks like. Here's a typical nearby example (M74):Among the largest and brightest galaxies close to our own, about 72% are of this spiral type, like M74. There is a classification system for galaxy shapes, and the remaining 28% of large, bright, nearby galaxies fall into classes called "elliptical", "lenticular", or simply "peculiar". (For simplicity and for other reasons that will become apparent, we're ignoring smaller, dimmer galaxies – such as the Magellanic Clouds – which may be very small and difficult to detect. Such galaxies tend to have more irregular shapes.) Actually, two types of spiral galaxies are normally recognized: "ordinary" spirals, such as M74, above. In these the spiral arms reach all the way in to the center of the galaxy. However, in the variant known as a "barred" spiral the arms originate at either end of a "bar" through the center of the galaxy. The figure to the right shows how the Milky Way is thought to appear if viewed from outside.Our own galaxy, the Milky Way, has been placed in this category. Although we can't see it as it looks from a distance, the classification is based on detailed surveys of star frequencies in varying directions and distances. The Milky Way's bar is fairly small. Here's another, more dramatic, barred spiral, NGC 1300:The classification system for galaxy shapes was developed by Edwin Hubble, and so it's called the Hubble sequence. In addition to the two types of spirals, it includes elliptical galaxies and lenticular galaxies. A final type that Hubble recognized is the irregular galaxy, which is anything that doesn't fit in another classification.Elliptical galaxies are classified as such based on their 2-dimensional appearance being elliptical. The actual 3-dimensional shape is generally ellipsoidal, in which the three principal axes may be of different lengths. A purely spherical galaxy would be a special case. Elliptical galaxies lack any distinct internal features besides smoothly increasing brightness towards the center. A lenticular galaxy is a transition type between elliptical and spiral. It has a central bulge that is ellipsoidal in shape, but also a flattened disk outside the bulge, like the disk of a spiral galaxy, except that there are no distinct spiral arms.The Hubble classification scheme recognizes distinctions within each type, based on the degree of elongation (for an ellipse) or how tightly wound the spiral arms are. For our purposes here, it's enough just to consider just main types: ellipticals, lenticulars, spirals, and everything else (irregulars).Hubble constructed his classification based on nearby galaxies, whose structure was easily observable at the time (1936). There is no compelling reason to think that a very similar sequence could be used to classify galaxies in existence at some very different age of the universe, whose present age is ~13.7 billion years. So, now that our instruments are capable of studying galaxies at much greater distances, and hence at earlier times, a very interesting question is how much different would a useful classification system be for a very different time period. Would there be entirely different types? Or would the types be much the same, but perhaps in different proportions relative to each other?Astronomers have been wondering about this for some time, and reaching out to greater distances as their equipment allows. Now there is some recent research that covers a substantial number of selected galaxies (143) at redshifts around z~.65, which are about 6 billion light-years distant, and hence observed as they were 6 billion years ago, about 7.7 billion years after the big bang. We have no way to know how old any particular galaxy is, but most must have been little more than 7 billion years old. For comparison, an appropriate sample of 116 local galaxies was selected, to determine the relative proportion of each type at the present time. All galaxies sampled, both local and distant, were required to have at least a certain minimum intrinsic brightness.In a nutshell, what the research found is that the types observed are just the same as today. There are no obviously distinct new types such as (say) circular rings with little in the center. However, the percentages of spiral and irregular galaxies are dramatically different, though the percentages of ellipticals and lenticulars are almost the same as in the present-day universe. The research deliberately included only intrinsically bright, massive galaxies in both samples – because, in the distant group, dimmer, less massive galaxies would mostly not be sufficiently bright to reveal useful details of their shape, if they were even detectable at all. But on top of that, even today the less massive galaxies tend to have more irregular shapes that don't fit in the Hubble classification.In the resulting sample, fully 72% of local galaxies were spirals, but only 31% of distant ones were. On the other hand, irregular galaxies made up only 10% of the local sample but 52% of the distant one. Yet there was hardly any difference in the percentages for ellipticals and lenticulars, being 3% and 15% (respectively) in the local case and 4% and 12% in the distant case.Stated differently, on a percentage basis spirals are 2.3 times as abundant now as they were 6 billion years ago. Yet irregulars are now 5.2 times less abundant.Here's the research abstract:How was the Hubble sequence 6 Gyr ago?The way galaxies assemble their mass to form the well-defined Hubble sequence is amongst the most debated topic in modern cosmology. One difficulty is to link distant galaxies, which emitted their light several Gyr ago, to those at present epoch. Such a link is affected by the evolution or the transformation of galaxies, as well as by numerous selection and observational biases. We aim to describe the galaxies of the Hubble sequence, 6 Gyr ago. We intend to derive a past Hubble sequence that can be causally linked to the present-day one.... We found that our single criterion is particularly appropriate to relating distant and nearby galaxies, either if gas is transformed to stars in relatively isolated galaxies or, alternatively, if they accrete significant amounts of gas from the intergalactic medium. Subsequent mergers during the elapsed 6 Gyr, as well as evolution of the stellar populations, are found to marginally affect the link between the past and the present Hubble sequence.... We do find an absence of number evolution for elliptical and lenticular galaxies, which strikingly contrasts with the strong evolution of spiral and peculiar galaxies. Spiral galaxies were 2.3 times less abundant in the past, which is compensated exactly by the strong decrease by a factor 5 of peculiar galaxies. It strongly suggests that more than half of the present-day spirals had peculiar morphologies, 6 Gyr ago, and this has to be taken into account by any scenario of galactic disk evolution and formation. The past Hubble sequence can be used to test these scenarios and to test evolution of fundamental planes for spirals and bulges.One obvious concern with this kind of analysis is to eliminate as much as possible the chance that the results might be biased by selection effects. This is why the primary criterion from including galaxies in either the local or distant sample is that they all have more than a minimum intrinsic brightness. It goes a long way to ensure that enough detail is present in images of the remote galaxies that accurate classification is possible. There is additional analysis to show that effects such as very recent mergers of galaxies and overall aging of stellar populations should not make substantial differences.Further, the criteria used to classify galaxies are the same for both samples, and simple enough that they can be applied just as accurately to the distant galaxies as the nearby ones. Consequently, it should not be the case that so many irregular (or "peculiar", in the terminology of the paper) types are found in the distant sample simply because the level of detail is inadequate.Here are some of the characteristics necessary for a galaxy to be... Read more »
Delgado-Serrano, R., Hammer, F., Yang, Y., Puech, M., Flores, H., & Rodrigues, M. (2010) How was the Hubble sequence 6 Gyr ago?. Astronomy and Astrophysics. DOI: 10.1051/0004-6361/200912704
by Charles Daney in Science and Reason
Astronomers have long known that there is a rather close relationship between the intrinsic luminosity of a spiral galaxy and the rotational velocity of stars (around the galactic center) in the outer portions of the galaxy. This relationship even has a name: the Tully-Fisher relation.It has also been known that small, nearby dwarf galaxies, which are irregular in shape, are not nearly as bright as they "should" be, according to the Tully-Fisher relation, given the measured average velocities of their stars. Recent research shows that, nevertheless, the Tully-Fisher relation can actually be extended, with slight modification, to very large structures: entire clusters of galaxies. In that case, the intrinsic brightness of a cluster is mostly in the X-ray part of the spectrum (because it's due to very hot intergalactic gas), yet the correlation of cluster brightness to the average velocities of galaxies in the cluster is still quite good.There's actually a very good explanation for the correlation, in that intrinsic brightness and average velocity of constituents are both closely tied to the total mass of the object.And this is where things get very interesting. One has to consider the mass of ordinary "baryonic" matter separately from the mass of non-luminous dark matter. Many different kinds of independent observations point to the existence of almost 5 times as much mass of the universe in the form of dark matter as there is in the form of ordinary matter. Stated differently, ordinary matter makes up only 17% (a bit more than 1 part in 6) of the total mass of matter in the universe.As long as the intrinsic luminosity of an object is proportional to its total mass, then mass can be taken as a proxy for luminosity, and a relationship between total mass and average constituent velocity is to be expected. This relationship is in fact predicted even by Newtonian mechanics – total mass should be proportional to the 4th power of velocity (M ∝ V4).If one could further assume that the ratio of mass in the form of ordinary matter to mass in the form of dark matter in a galaxy or cluster is the same as the ratio in the universe as a whole (1 : 5), then the Tully-Fisher relation makes perfect sense. And this is so even though luminosity is entirely produced by ordinary matter, not the invisible dark matter. Indeed, this holds up very well – for spiral galaxies.Surprisingly, there is also a fairly good relationship between luminosity and average velocity even in galaxy clusters – but there's a slight difference in the exponent: M ∝ V3. Again, this holds regardless of whether one considers total mass (including dark matter), or just visible ordinary matter. (The mass of a large cluster can be determined independently by techniques such as gravitational lensing.)It's customary to plot mass vs. velocity (on vertical and horizontal axes, respectively) with logarithmic scales on both axes. When this is done, one gets straight lines that have slopes of approximately 4 (for spiral galaxies) and 3 (for galaxy clusters).However, when plotting visible mass vs. velocity, the relationship breaks down almost completely for nearby dwarf galaxies. The smallest and dimmest dwarf galaxies are far below the curve. Their visible mass and luminosity – not counting dark matter – is far too small. On a log-log plot, such galaxies fall, with quite a large scatter, around a straight line having a slope of 5 or more.There's a simple way to restate this observation: dwarf galaxies have far less visible ordinary matter than predicted by a traditional Tully-Fisher relation, and even much less than that if the ratio of ordinary matter to dark matter in the dwarf galaxies were close to what it is in the universe as a whole. In most dwarf galaxies, the ratio is less than 1% of what it "should" be.In other words, there's an awful lot of ordinary matter missing and unaccounted for in dwarf galaxies. Hence the question (since ordinary matter is mostly hydrogen (protons)): where have all the protons gone?Observations of nearby dwarf galaxies are pretty reliable – these are our closest neighbors. Assuming Newtonian gravity, we know the masses of these objects very reliably from the velocities of the stars (which we can see individually) within them. There's no hot hydrogen in these galaxies, as there is in distant galaxy clusters, since we see no signal of it in any part of the spectrum down to the infrared. Astronomers are also pretty certain that there's not a lot of cold hydrogen, which should emit strongly at radio frequencies – the famous HI 21-centimeter line.So where are all the protons? Quite possibly they've been blown outside of the dwarf galaxy entirely, by supernova winds. Escape velocity from a dwarf galaxy is a lot less than what it is for a typical spiral, yet supernovae have just as much bang as they do anywhere else. Very recent detailed simulations have supported this idea, as I discussed here.An alternative, and rather more radical, possibility is that Newtonian gravity is wrong – the protons still aren't there (why?) but neither is any "dark matter". Instead, the total mass of visible stars – as surprisingly small as it seems to be – is still enough to account for observed stellar velocities, using some form of "modified Newtonian dynamics" (MOND).Unfortunately, for believers in MOND, the theory was concocted as an alternative to dark matter for explaining rotational velocities in spiral galaxies. MOND theories are typically adjusted carefully to fit the spiral galaxy data. They would need to work differently in dwarf galaxies. And they are already known not to work right for large galaxy clusters either.Lots of intriguing questions here...Original abstract:The Baryon Content of Cosmic StructuresWe make an inventory of the baryonic and gravitating mass in structures ranging from the smallest galaxies to rich clusters of galaxies. We find that the fraction of baryons converted to stars reaches a maximum between M500 = 1012 and 1013 M⊙, suggesting that star formation is most efficient in bright galaxies in groups. The fraction of baryons detected in all forms deviates monotonically from the cosmic baryon fraction as a function of mass. On the largest scales of clusters, most of the expected baryons are detected, while in the smallest dwarf galaxies, fewer than 1% are detected. Where these missing baryons reside is unclear.McGaugh, S., Schombert, J., de Blok, W., & Zagursky, M. (2010). THE BARYON CONTENT OF COSMIC STRUCTURES The Astrophysical Journal, 708 (1) DOI: 10.1088/2041-8205/708/1/L14Further reading:The Baryon Content of Cosmic Structures – preprint at arXivTeam Shines Cosmic Light on Missing Ordinary Matter (1/7/10)Dark Matter and Dark Energy Update (1/9/10)... Read more »
McGaugh, S., Schombert, J., de Blok, W., & Zagursky, M. (2010) THE BARYON CONTENT OF COSMIC STRUCTURES. The Astrophysical Journal, 708(1). DOI: 10.1088/2041-8205/708/1/L14
by Charles Daney in Science and Reason
Cosmology has, for a decade, had its "standard model", which largely explains most of the cosmological phenomena that astronomers are able to observe. Except for a relatively small number of things that don't seem to make sense in the model. Prominent among the latter are dwarf galaxies – by one definition, galaxies having less than 10% of the total mass of the Milky Way.The standard model of cosmology is known officially as the Λ-cold-dark-matter model – ΛCDM. (This theory has no particular relation to the Standard Model of particle physics.) Cold dark matter (CDM) refers to the hypothesis that a large part of the detectable mass content of the universe consists of particles that are not accounted for by the Standard Model of particle physics. The dark matter is said to be "cold", because it appears to consist mostly of "non-relativistic" particles, meaning particles moving at speeds not close to the speed of light. That excludes, for example, neutrinos.As weird as the idea of dark matter might seem, there is abundant evidence for it, which can't easily be better explained in other possible ways. (Although, many other possibilities have been proposed.) I haven't written a lot about this recently, since the evidence for CDM just keeps piling up, but here's one important study. Dark matter is "observed" indirectly through its gravitational effects on ordinary visible matter. For instance, the motions of stars in the Milky Way have recently been analyzed closely enough to show that the dark matter in which the Milky Way is embedded has the shape of a squashed beach ball. (See here, here, here.)Λ is the conventional symbol used for the "cosmological constant", which is a concept from Einstein's general theory of relativity. It is supposed to account for the observed phenomenon of "dark energy". This too is controversial, but there is much evidence for it, from a variety of different studies that are not all based on the same kinds of observations. I last wrote at length on the evidence here. I need to write a lot more about recent evidence for dark energy, but I'll be very brief about it here. There is very recent evidence involving the motion of galaxies quite near our own (see here). Other than that, the evidence for dark energy is based on observations of distant Type Ia supernovae (about which there's a lot of recent news), "weak lensing" (see here), and "baryon acoustic oscillations" (a large topic).In spite of all this evidence, ΛCDM isn't without its problems. As already suggested, one set of problems involves dwarf galaxies. There are at least two (somewhat related) parts to this problem. The larger part of the problem is simply that not enough very small dwarf galaxies (masses less than a percent of the Milky Way's) have been detected. This is often known as the "missing satellite problem". Dwarf galaxies, being very small, are also intrinsically dim, and thus difficult to observe at all unless they're very nearby. However, only about 11 dwarf galaxies are known to be satellites of the Milky Way – and such satellites should be the easiest of dwarf galaxies to detect. This is a serious problem, since simluations of expected galaxies sizes based on the way that dark matter should be expected to clump together predict as many as 500 dwarf satellites of the Milky Way.The other problem is known as the cuspy halo problem. "Halo" refers to the cloud of cold dark matter in which all visible galaxies are expected to be embedded. Simulations indicate that the dark matter should be concentrated in the center of the halo instead of being evenly distributed throughout. This is intuitively reasonable – after all, most of the ordinary matter in our solar system is concentrated right in the middle, in the Sun itself.This problem exists somewhat even for large galaxies like the Milky Way, but it is much more severe for dwarf galaxies. In fact, it seems as though the smaller the galaxy is, the greater the tendency for the dark matter (as indicated by orbital motion of stars within the galaxy) to be distributed fairly smoothly, with little or no density cusp in the center. Related to this is a recent finding (see here) that smaller galaxies seem to have a smaller proportion of ordinary baryonic matter to dark matter than does the universe as a whole. And, in fact, the smaller the galaxy, the smaller the proportion of ordinary matter. In the universe as a whole, there is much evidence, based on detected abundances of light elements and observations of the cosmic microwave background, that there should be about 5 times as much mass in the form of dark matter as there is of ordinary matter. One might expect this proportion to be about the same in galaxies. Yet instead, in the smallest galaxies, astronomers can detect less than 1% as much ordinary matter (in the form of visible stars) as one would expect to find.This would suggest that an important reason we can't detect very many small galaxies is that they simply have too few stars and are too dim to see. But it still doesn't explain why this should be the case.In fact, I wrote 2½ years ago about a study that reported finding many small galaxies consisting of 99% or more of dark matter (here). The authors of the study even speculated that the reason such galaxies were mostly composed of dark matter was that "the fierce ultraviolet radiation given off by the first stars, which formed just a few hundred million years after the Big Bang, may have blown all of the hydrogen gas out of the dwarf galaxies forming at that time." And they added, "The loss of gas prevented the galaxies from creating new stars, leaving them very faint, or in many cases completely dark. When this effect is included in theoretical models, the numbers of expected and observed dwarf galaxies agree."Kind of makes sense, doesn't it? In fact, even for galaxies that began to form later, a large number of supernovae early in the life of a galaxy might be enough to blow away most of the hydrogen from which additional stars could form. And indeed, a recent much more detailed simulation of galaxy formation supports precisely this idea.Why is it that previous simulations had not caught this? The reason is very simple: detailed simulations of galaxy formation and evolution are exceedingly demanding of computer resources. In order to make such simulations even possible – up until now – astrophysicists considered only the effect of gravitational collapse of a mixture of ordinary and dark matter. The effects resulting from star formation and subsequent supernovae were omitted entirely. Duh.Actually, this simplification is pretty understandable. The simulation that is the subject of the research under discussion here, that did take into account stellar formation processes, consumed an almost incredible amount of computing time. According to one report, "The simulation was carried out using about 250 processors running for about two months." That's more than 40 processor-years.And that's just for one simulation, involving a single set of initial conditions.Here's the abstract:Bulgeless dwarf galaxies and dark matter cores from supernova-driven outflowsFor almost two decades the properties of ‘dwarf’ galaxies have challenged the cold dark matter (CDM) model of galaxy formation. Most observed dwarf galaxies consist of a rotating stellar disk embedded in a massive dark-matter halo with a near-constant-density core. Models based on the dominance of CDM, however, invariably form galaxies with dense spheroidal stellar bulges and steep central dark-matter profiles, because low-angular-momentum baryons and d... Read more »
Governato, F., Brook, C., Mayer, L., Brooks, A., Rhee, G., Wadsley, J., Jonsson, P., Willman, B., Stinson, G., Quinn, T.... (2010) Bulgeless dwarf galaxies and dark matter cores from supernova-driven outflows. Nature, 463(7278), 203-206. DOI: 10.1038/nature08640
by Charles Daney in Science and Reason
If you're interested in something out of the ordinary, astronomically speaking, the best place to look for the exotic may be as far away (in both space and time) as possible.Perhaps that's why I like to consider really far out stuff, like the most distant gamma-ray burst seen yet. Or maybe I just like to get away from the depressing chaos and confusion of "modern" life.In any case, there's always something new, just beyond the farthest thing we've seen yet. That far-out gamma-ray burst (GRB 090423) discussed in the post just linked – which resides at z~8.2, about 13 billion light-years away – has already been superseded in remoteness by 3 galaxies around z~10, 13.2 billion light-years away. z~10 objects are seen as they were only about 480 million years after the big bang. (See here for a refresher on how redshift works.)How are high-z objects actually detected? It's surprisingly easy, in principle, even though astronomers are working at the outer limits of their instruments. The term of art for the technique used is "Lyman-break" detection, which we've discussed in detail here.Here's the short summary of that technique. We assume that the objects of interest are galaxies composed of stars, instead of something really strange. (GRBs can be ruled out, since they appearance is very brief, and gamma-rays are far outside the range of emissions produced by stars, even given substantial redshifts.) The thing is that even the hottest stars produce relatively little output (such as x-rays) on the high-energy side of the part of the ultraviolet spectrum known as the "Lyman limit", which has a wavelength of 91.1 nm. And almost all higher energy photons will be absorbed by the interstellar medium anyhow.At z=10, the shift factor (z+1) is 11, yielding a wavelength of 1002 nm – i. e. about 1 micron, which is in the infrared. So an object that's really at z~10 will not have any observable light to the blue side (shorter wavelength) of 1002 nm.The main instrument used in the recently refurbished Hubble telescope to detect the high-redshift galaxies is known as the Wide Field Camera 3 (WFC3). It was installed in May 2009, and in August it did the infrared imaging on which the research described here is based. As noted, the research team identified 3 objects at z~10, using WFC3. Two of those objects were also captured in an image of the same area, using Hubble's Near Infrared Camera and Multi-Object Spectrometer (NICMOS).WFC3 has three filters covering near-infrared wavelengths. The light from a galaxy at z~10 will be visible through the filter that passes only longer infrared photons, but not through the other two filters that pass only shorter (bluer) photons. So z~10 galaxies will stand out on account of their absence from images made using the shorter-wave filters.The neat thing about this technique is that it does not require collecting a somewhat complete spectrum, which is a much more difficult feat. In principle, all sufficiently luminous z~10 galaxies should be caught. The problem is false positives – things that aren't really z~10 galaxies, such as dim reddish galaxies that are actually much closer (zThe research that reports on this has used careful statistical tests to rule out false positives. The analysis in fact suggests that a slightly earlier study that claimed to find 20 z~10 galaxies could be all false positives.This is the study we're discussing now:Constraints on the First Galaxies: z~10 Galaxy Candidates from HST WFC3/IRThe first galaxies likely formed a few hundred million years after the Big Bang. Until recently, it has not been possible to detect galaxies earlier than ~750 million years after the Big Bang. The new HST WFC3/IR camera changed this when the deepest-ever, near-IR image of the universe was obtained with the HUDF09 program. Here we use this image to identify three redshift z~10 galaxy candidates in the heart of the reionization epoch when the universe was just 500 million years old. These would be the highest redshift galaxies yet detected, higher than the recent detection of a GRB at z~8.2. The HUDF09 data previously revealed galaxies at z~7 and z~8. Galaxy stellar population models predict substantial star formation at z9-10. Verification by direct observation of the existence of galaxies at z~10 is the next step. ... Our z~10 sample suggests that the luminosity function and star formation rate density evolution found at lower redshifts continues to z~10, and pushes back the timescale for early galaxy buildup to z10, increasing the likely role of galaxies in providing the UV flux needed to reionize the universe.There was a more serious purpose behind this effort than simply bagging a few more objects at record-breaking distances. The ultimate goal is to understand the sequence of events when the earliest stars and galaxies formed in the early universe, and what characteristics those first stars and galaxies had.As we discussed here, at the time of "recombination", about 380,000 years after the big bang, most of the hydrogen and helium gas in the universe was in the form of neutral (un-ionized) atoms. Much later (relatively speaking), in what is known as the "reionization" period, this gas became ionized again by the intense light from young, very hot stars and galaxies. This probably happened over a period of several hundred million years and was essentially complete by 900 million years after the big bang. What is not so clear is when the reionization (and hence the first stars) began, or how rapidly it proceeded. The best way to understand this process is to determine the numbers of galaxies per unit volume of space throughout this period, and the intrinsic brightness of these galaxies.Astronomers have gradually been able to make reliable counts of the number of bright galaxies for zWe can see more galaxies at smaller values of z not only because the necessary intrinsic brightness decreases with z, but also because there are actually increasing numbers of galaxies having any given intrinsic brightness as the universe grows older – up to a point. This is simply because galaxies themselves became larger and brighter over time as new stars formed.Another way to view the accumulated data is in terms of the rate of star formation. The more rapidly stars are forming, the more rapidly galaxies grow to reach any particular intrinsic brightness. When read in this way, the data show that the number of stars being formed per year increased monotonically from as far back as we can tell up to a peak with z between 2 and 3, and that the rate of star formation drops after z~2, 3.3 billion years after the big bang.However, the actual data, so far, become very sparse for z6. If stars were forming at z~10 at the same rate as they do at z~6, astronomers should find 20±5 galaxies at z~10. Or, using z~7 as a baseline, there should be 9±3 galaxies at z~10. Instead, there were only 3. (Keep in mind this is all for a patch of sky of the same size.)What this means is that for z7, stars were forming at even slower rates. And in fact, if one extrapolates the function for the number of observable galaxies back to z~10, 2 or 3 fits very nicely. Further, if that is the case, then the energy emitted by galaxies at z~10 is only about 13% of what would be needed to completely ionize the interstellar gas. Which means, finally, that the largest part of reionization occurred more than 500 million years after the big bang.Astronomers would, however, like to know much more than that. Ideally one would like more precisely the rates of star formation during the whole time period beginning with the first stars, perhaps 200 or 300 million years after the big bang. As well as other things, such as the distribution of shapes and sizes of galaxies in that period.Such information isn't important just for its own sake, either. It will also help astronomers answer other questions, such as: What were the characteristics of the very first stars and galaxies, and how did they form? How was dark matter distributed at that time, and how did that affect the formation of stars and galaxies? What role did black holes pl... Read more »
R. J. Bouwens, G. D. Illingworth, I. Labbe, P. A. Oesch, M. Carollo, M. Trenti, P. G. van Dokkum, M. Franx, M. Stiavelli, V. Gonzalez.... (2009) Constraints on the First Galaxies: z~10 Galaxy Candidates from HST WFC3/IR. Nature. arXiv: 0912.4263v2
by Charles Daney in Science and Reason
Gamma-ray bursts (GRBs) are the most dramatic short-lived violent events observed in the universe. They are often described as releasing a quantity of energy, in less than a minute, that is at least as much as a star like the Sun releases in its entire 10 billion year lifetime. Since the first detection of a gamma-ray burst in 1967, the central question has been to determine the nature of the process or processes that can release so much energy so quickly.We've discussed gamma-ray burst several times before, such as here, here, and here.The defining characteristic property of a GRB is a rapid, highly energetic burst of gamma rays, lasting only a few seconds. Most of the GRB energy is released in that event. But beyond that, GRBs exhibit a bewildering diversity of characteristics – reflecting a diversity in the conditions that can produce a GRB.The most noticeable difference observed in GRBs is that some events are over very quickly – within 1 or 2 seconds – while others include an "afterglow" of radiation less energetic than gamma rays, lasting as long as minutes in some cases. In a few instances there are events that have some properties of both "short" and "long" types of GRB.Gamma rays cannot penetrate the Earth's atmosphere, so the initial phase of any GRB is detectable only from a satellite-based instrument. This is rather limiting in terms of the types of observations that can be made. For example, satellites lacked instruments that could record a spectrum of a GRB event in lower-energy electromagnetic radiation. Without a spectrum, astronomers cannot measure redshift, and hence the distance of the event. The development and deployment within the last 10 years of systems that could use satellite detection of GRBs to activate automated ground-based telescopes have dramatically improved this situation. It's now possible to collect much more detailed data, so that astronomers have been able to learn a lot more about GRBs – in many cases.Even so, many short GRB events are over in just a few seconds, and therefore much less is yet known about short GRBs. The best current guess is that such events are caused by the merger of a pair of binary neutron stars. The research to be described here, therefore, concerns long GRBs, where it is relatively easy to study the characteristics of the lower-energy electromagnetic radiation, which makes up the afterglow for several minutes or even tens of minutes after the initial burst.A general consensus has emerged that gamma-ray burst progenitors are certain types of supernovae. Not just any type, either, because the progenitor must be capable of releasing the amount of energy actually observed in a GRB. This rules out Type Ia supernovae, which result from a thermonuclear explosion of matter that has accreted onto the surface of a white dwarf star. Type Ia supernovae are important in cosmology, because they all have roughly the same intrinsic brightness. This makes it possible to determine the approximate distance of a Type Ia supernova event, just from the observed brightness. By comparing this distance with the redshift of the supernova it is possible to determine how rapidly the universe has expanded in the past. This, in turn, is what made it possible to conclude, in 1997, that the expansion of the universe is accelerating. However, the energy released by a Type Ia supernova is far too small to account for a GRB. Instead, a different supernova mechanism, known as "core collapse" is needed. Classification of supernovae is a little confusing, since it was originally done on the basis of spectral characteristics. Type II supernovae have a particular line in their spectrum due to hydrogen, while Type I supernovae do not. Type II supernovae result from the collapse of very massive stars at the end of their lives, when they can no longer support their own weight by the pressure of fusion occuring in their constituent matter. But it turns out that some supernovae lacking the hydrogen spectral line are too energetic to result from the same mechanism as that of Type Ia supernovae. These types are known as Type Ib and Type Ic, and they also result from core collapses of massive stars (that have already burned off all their hydrogen).So there are significant differences even among core collapse supernovae, resulting from such factors as the total mass of the progenitor star and the original composition of the star, among other things. Such differences can account for some of the differences observed if such supernovae are responsible for GRBs.But by no means all core collapse supernovae produce a GRB. Theoretical considerations dictate that several other factors must also be present. For one thing, the supernova must result in the formation of a black hole that is massive enough to support a large accretion disk of matter orbiting around it. A neutron star, which is the alternative remnant of a supernova, just isn't massive enough. To get a sufficiently massive black hole, the progenitor star must be at least 40 Solar masses.High mass alone, however, is not enough. The progenitor star must also be rotating rapidly enough that the angular momentum of the system is large enough to cause most of the matter and energy from the supernova explosion to be focused into a jet of angular width at most about 20 degrees. This concentrates most of the energy of the explosion into a narrow beam, so that the energy emitted in our direction matches what we actually observe. If the beam were not so narrow, the energy would not appear to be the magnitude that we observe.There are additional factors that affect the varying characteristics of GRBs that we observe. In particular, the distribution of matter in the interstellar medium surrounding the supernova is important. It is the collision between the jets and this matter that determines the intensity and duration of the afterglow we observe for some time after the original burst.And there's more. The jets of matter and energy from a GRB event may well be powered by the energy of the original explosion. But that's not the only possibility. Suppose there are strong magnetic fields surrounding the progenitor star. Then there will also be a considerable amount of energy in the magnetic flux, and this can also supply power to the jets.Strong magnetic fields would have another consequence as well. The jets consist partly of electrons moving at relativistic speeds (very close to the speed of light). These electrons will follow a spiral path around lines of magnetic flux. This creates a type of electromagnetic radiation known as synchrotron radiation. If present, this radiation would make up part of the afterglow we can observe.How would we know if synchrotron radiation, and hence magnetic fields, are present? That's simple – the radiation would be partly polarized, provided that the magnetic fields are orderly and not all tangled up.And this is precisely what recent research has observed in the case of one particular GRB event (GRB 090102), which was detected January 2, 2009. Specifically, a polarization of 10±1% was observed at optical wavelengths. This degree of polarization is quite rare in astrophysical events, and it strongly suggests the presence of large-scale magnetic fields associated with GRB 090102. These fields should contribute substantially to the observable energy of the GRB.Abstract: Ten per cent polarized optical emission from GRB 090102The nature of the jets and the role of magnetic fields in gamma-ray bursts (GRBs) remains unclear. In a baryon-dominated jet only weak, tangled fields generated in situ through shocks would be present. In an alternative model, jets are threaded with large-scale magnetic fields that originate at the central engine and that accelerate and collimate the material. To distinguish between the models the degree of polarization in early-time emission must be measured; however, previous claims of gamma-ray polarization have been controversial. Here we report that the early optical emission from GRB 090102 was polarized at 10 ± 1 per cent, indicating the presence of large-scale fields originating in the expanding fireball. If the degree of polarization and its position angle were variable on timescales shorter than o... Read more »
Steele, I., Mundell, C., Smith, R., Kobayashi, S., & Guidorzi, C. (2009) Ten per cent polarized optical emission from GRB 090102. Nature, 462(7274), 767-769. DOI: 10.1038/nature08590
by Charles Daney in Science and Reason
It would take you a lot longer to hike a significant distance over very hilly terrain than it would over a completely flat plain. For much the same reason, it would take light longer to cover the same distance depending whether the space through which it moves does or doesn't have large "hills".But what does it mean for space to contain "hills"? And how large do "hills" need to be to make a difference?Consider the second question first. There's no natural place on Earth that is perfectly flat, of course. So if you look closely enough, there are always "hills" of some size to cross when you're on a hike. But if the height of those hills is a lot less than the length of your stride, they will make little difference. In the same way, if the irregularities in the texture of space are much smaller than the wavelength of light, they won't make much difference either.Physicists aren't even sure that space does contain "irregularities" at very short distances. No measurement yet made has given any evidence of irregularities. But all theories of quantum gravity – none of which is yet considered satisfactory – predict that irregularities must exist at a sufficiently small scale.No attempted quantum theories of gravity are satisfactory yet, because physicists have not been able, with a mathematically consistent theory, to reconcile general relativity and quantum mechanics at very small scales. Nature, however, is somehow able to do the trick. So it seems quite plausible that space does have irregularities at sufficiently small scales. The only real question is "how small?"Recent research now says, "smaller than can presently be detected."And how would one go about detecting the smallest irregularities? With light whose wavelength is about the same size, of course. Which would mean photons with the highest energy one can find. So far, photons with the highest energy physicists know of are not indicating any quantum irregularities in space.We're talking about photons with energies far higher than can be produced in laboratories. The most energetic photons correspond to the part of the electromagnetic spectrum known as gamma rays. By convention, physicists regard gamma rays as electromagnetic radiation with a wavelength of less than 10-11 m (10 picometers). That corresponds to an energy of 105 eV (eV = electron-volt). (Recall that photon energy is related to frequency by the relation E=ℎ&nu, where ℎ is Planck's constant and ν is the photon frequency. Since wavelength λ is inversely related to ν so is energy; i. e. E &prop 1/λ.)Gamma rays are produced naturally in some types of atomic decay, and such gamma rays have energies up to 107 eV. That's not terribly energetic in the great scheme of things. The Large Hadron Collider will be able to accelerate protons up to energies around 1013 eV. Since photons have no electric charge, unlike protons, they can't be accelerated the way protons can. Much more energetic gamma rays can be produced in particle-antiparticle annihilations, but such high-energy photons are rather rare, even in cosmic events like gamma-ray bursts, which may produce gamma-rays with energies of 3×1010 eV or more (3.34×1010 eV is the largest yet observed). That's 3×105 times as energetic as the least energetic gamma rays and so corresponds to wavelengths ~.3×10-16 m.Fortunately, even with gamma rays in this energy range, much smaller irregularities in space can be detected if the gamma ray photons travel a very large distance. Suppose, for instance, that a gamma-ray photon were detectably slowed down only by 1 part in a million, a factor of 10-6, over a distance of 100,000 light-years, about the diameter of a large spiral galaxy. But really cosmic distances at which we can observe gamma-ray bursts are about 1010 light-years, or 105 times the diameter of a galaxy. Since a light-year is about 1016 m, we're talking scales like 1026 m. On that scale, the possible slow-down of a gamma-ray photon could be very noticeable – roughly 1 part in 10.The result is that if we can detect how much a gamma-ray photon is slowed down over a distances around 1010 light-years, we could be able to probe energies much higher than those possessed by a gamma-ray photon itself, and therefore distance scales much smaller than a very energetic gamma-ray photon wavelength of about 10-17 m. Detecting small differences in the velocities of photons of different wavelengths is made much easier when both photons travel 1010 light-years over a time of (naturally) 1010 years. Gamma-ray bursts, fortunately, produce gamma rays over a range of energies that differ by several times 105 from smallest to largest. To be more concrete, suppose you have a gamma-ray burst at a redshift of z~.9. That corresponds to a distance of ~7×109 light-years and a travel time of ~7×109 years. The wavelength of photons traveling that distance is stretched by a factor of 1.9 (i. e. 1+z), but there's still a factor of several times 105 between the wavelenghts of the most and least energetic gamma-ray photons, so they are readily distinguishable. If the difference in arrival time of gamma-ray photons is 1 second, that is only one part in 2×1017 (i. e. 7×109 years times about 3×107 seconds/year ≅ 2×1017 seconds).It's reasonable to suppose that the slowdown of the least energetic gamma-ray photons due to irregularities in space is negligible. Suppose we could relate the slow-down of the most energetic photons to the actual size of spatial irregularities. For instance, suppose a spatial irregularity of 1 part in 1017 of the photon's wavelength caused a slow-down that was also 1 part in 1017 of the photon's velocity. That would cause a 2 second delay in photon arrival times – which is very readily detectable.Recall that energetic gamma-ray photons from gamma-ray bursts have wavelengths of .3×10-16 m or less. Thus we might expect to be able to detect spatial irregularities as small as ~.3×10-33 m = 3×10-34 m = 3×10-32 cm.In fact, it is now possible to measure arrival times of photons from gamma-ray bursts to within mere hundredths of a second. So we can probe length scales around 10-33 cm. Interestingly enough, this is very close to the Planck length scale lPlanck ≈ 1.62×10-33 cm.That's just a back-of-the-envelope calculation based on hypothetical data. But we don't need to be hypothetical, because photons from the gamma-ray burst GRB 090510, which was observed on May 10, 2009, were measured very precisely. The most energetic photon observed had an energy of ~3.1×1010 eV (31 GeV), and it showed up precisely .829 seconds after the very first photons from the burst were detected. Further, spectroscopic observations of the afterglow from this burst showed a redshift of z very close to .9, as in our hypothetical example.Since we don't have a reliable quantum gravity theory, we don't know exactly how much of a slowdown very high-energy, short-wavelength photons should experience. However, several theories predict that, to first order approximation, if vph is the effective average velocity of the photon, then its ratio to c, the speed of light, should satisfy |vph/c - 1| ≈ Eph/(MQGc2). One can think of MQG as the "mass" that the photon would have in the quantum gravity theory so that the photon energy is c2 times the mass.Given that notation, then if you have two photons that differ in energy by ΔE, the difference in arrival times should be Δt ≈ (|ΔE|/(MQGc2))D/c, where D is the distance traveled. In this relationship, all quantities except for MQG are directly measured, which implies a value of MQG.The most sensible unit in which to measure MQG is in terms of the Planck mass, MPlanck ≅ 2.17644×10-5 g, which is quite a lot for small things, being about the m... Read more »
Abdo, A., Ackermann, M., Ajello, M., Asano, K., Atwood, W., Axelsson, M., Baldini, L., Ballet, J., Barbiellini, G., Baring, M.... (2009) A limit on the variation of the speed of light arising from quantum gravity effects. Nature, 462(7271), 331-334. DOI: 10.1038/nature08574
by Charles Daney in Science and Reason
On April 23 of this year the Swift Gamma-Ray Burst Telescope detected, just as it was designed to do, a gamma-ray burst (GRB). Within less than a day two of the most powerful Earth-based telescopes had begun studying the quickly fading light of the object, known as GRB 090423. (There were other observatories investigating it as well.)Because the light from GRBs fades so rapidly, most such objects are detected from space-based instruments that are especially designed for the purpose, like Swift. On average about 1 GRB is detected every 2 or 3 days. But GRB 090423 turned out to be, perhaps, the most interesting one yet observed.I've written about GRBs a couple of times before, such as here and here.You can refer to those articles for more details, but the most widely accepted hypothesis concerning the nature of GRBs is that they result from either the core collapse supernova explosion of a massive star or the merger of neutron stars in a binary system. Both processes most likely occur. In the former case, the emission of light lasts somewhat longer than in the latter, so the corresponding types of GRBs are called either "long" or "short". The long type lasts for more than 2 seconds and tends to be brighter than the short type (whose emissions last less than 2 seconds). Since short GRBs typically appear in locations where new star formation is not occurring, they must result from some cause other than the explosion of a very massive star, which is necessarily quite young. In both cases, there is a prolonged, but much dimmer "afterglow", which is the only part of the event that can be observed except from satellites such as Swift. Not just any supernova or neutron star collision will result in a detectable GRB. Most of the energy from the event must also be directed in two very narrow and oppositely directed beams, and the Earth must be in the path of one of those. It is because the energy is so narrowly concentrated that a GRB can appear to be far brighter than an entire galaxy or quasar. For such narrowly focused beams to be produced, the progenitor star (or binary system) must have a great deal of angular momentum, due to rapid rotation.The afterglow is thought to result from the interaction between the matter and energy contained in the beam and the interstellar medium at the location of the GRB. Although it's a secondary effect, there is a wealth of information that can be deduced from this afterglow. However, the information concerns more than just details about the nature of GRBs – events that occur much closer to us are much more useful for that. There are two other things of far greater interest about which we can learn from very distant GRBs, such as 090423 and subsequent examples we are likely to observe.Since this event had a redshift of z ≈ 8.2 it actually occurred very long ago, a comparatively short time after the big bang. About 630 million years after, to be more exact. GRB 090423 is farther and earlier than any other object or event we've actually observed, except for the cosmic microwave background (CMB). It is more distant in time and space than even any galaxy or quasar we've ever seen. (See here if you want to review how redshift works.) GRBs, directly or indirectly, tell us about the nature of the largest stars at that time, which is one thing that's presently very difficult to study with other observations. There's simply no way to observe individual stars 13 billion light-years away. The other thing astronomers are very curious about regarding that time period is the nature of the intergalactic medium (IGM) then.Let's start with the second of these things. 630 million years after the big bang is somewhere in the middle of what astronomers call the "cosmic dark ages". Precisely where it falls is what we don't know. I wrote about that subject here, last March. We do know pretty closely when the "dark ages" began – about 380 thousand years after the big bang. That's when the CMB appeared. The time is equivalent to a redshift of z ≈ 1100. The CMB was, and still is, "blackbody" radiation, so wavelengths are distributed around a peak. At the peak of the distribution now, CMB photons have a wavelength of 1.9 mm, in the short microwave part of the spectrum. (That's a lot shorter, so more energetic, than in your microwave oven, where microwaves are about 12 cm.) But when the CMB actually appeared, its photons had a wavelength 1100 times shorter, around 2200 nm – in the infrared part of the spectrum. That's still much cooler and "darker" than human eyes can see.Effectively, then, there wasn't much light in the universe, certainly not human-visible light, until the first stars showed up. So the time after the CMB appeared but before the first stars is known as the "dark ages". However, we don't know very closely when those first stars appeared – they're far too faint to observe, and even the first galaxies and quasars are too dim to be detected by our present instruments. GRBs seem to be our best observational hope, and GRB 090423 is the earliest we've seen yet. Since existing GRB models presuppose an origin that involves massive stars, at least indirectly, we now know there were such stars 630 million years after the big bang. There is evidence in the GRB 090423 observations that the progenitor of this object was not one of the first population of stars to form. (Astronomers call such stars "Population III".) Also, GRB 090423 doesn't seem to have been one of the most powerful GRBs ever, so astronomers now figure that with current technology we may be able to find GRBs back to z ≈ 20. That would correspond to 250 million years after the big bang. Theoretical models suggest that the first stars may have appeared even earlier than that, at perhaps 150 million years after the big bang. When they formed, these first stars did not contain elements heavier than helium, as such elements were created (in other than trace quantities) only in the first generation of stars. (See here for a discussion of the earliest stars.)The observations of GRB 090423 give some evidence that the galaxy in which it occurred did have small amounts of elements heavier than helium. Further, the afterglow that occurs following the peak brightness of any GRB is generally similar between both GRB 090423 and much closer GRBs. These facts are hints that the progenitor of GRB wasn't one of the Population III stars.How does a GRB give us information about the intergalactic medium at z ≈ 8.2? That turns out to be closely related to the way that the redshift was estimated in the first place. Normally this is done by identifying known emission or absorption lines in a spectrum and simply calculating the amount of shift directly. However, GRB 090423 is so faint, and declined in brightness so quickly, that it wasn't possible in the time available to obtain a detailed spectrum.Instead, an important feature of the IGM at that time comes to the rescue. The feature is that there is at that time a substantial, though not precisely known, quantity of un-ionized hydrogen atoms in the IGM. This hydrogen is left over from the period of "recombination" in which the CMB appeared. CMB photons are far too weak to "scatter" from hydrogen atoms, because quantum mechanics requires that a photon must have a certain minimal amount of energy to raise an electron bound in a hydrogen atom out of its "ground state" of lowest energy.The minimum amount of energy required is that possessed by a 10.2 eV photon of wavelength 121.6 nm, which is in the ultraviolet part of the spectrum. This spectral point is known as "Lyman-α". (We covered this concept in detail here.) Ordinary stars like the Sun in the universe at present emit little light at this wavelength, but much larger, hotter, and brighter stars emit quite a bit of this ultraviolet light.Consequently, as soon as such hot stars began to shine, the atomic hydrogen in the IGM began to reionize. There was a price to be paid for this, of course: all the photons with enough energy lost some of their energy in the process of reionizing the hydrogen. And so, most of the light whose photons had enough energy was absorbed or "scattered" in this reionization period.Eventua... Read more »
Tanvir, N., Fox, D., Levan, A., Berger, E., Wiersema, K., Fynbo, J., Cucchiara, A., Krühler, T., Gehrels, N., Bloom, J.... (2009) A γ-ray burst at a redshift of z ≈ 8.2. Nature, 461(7268), 1254-1257. DOI: 10.1038/nature08459
Salvaterra, R., Valle, M., Campana, S., Chincarini, G., Covino, S., D’Avanzo, P., Fernández-Soto, A., Guidorzi, C., Mannucci, F., Margutti, R.... (2009) GRB 090423 at a redshift of z ≈ 8.1. Nature, 461(7268), 1258-1260. DOI: 10.1038/nature08445
by Charles Daney in Science and Reason
Astronomers are beginning to learn significant details of the structure of galaxies in the early universe. And what they're learning is rather surprising: at least some early galaxies are almost as massive as otherwise similar galaxies in the present universe, yet they are much smaller in linear size, by a factor of five, thus much more compact.What time period are we talking about here? It's not actually the time that the earliest galaxies formed, which was less than a billion years after the big bang. Instead, the time in question was around 3 billion years after the big bang. Although that's roughly 10.7 billion years ago, many galaxies at that time were actually fairly mature, even old. This is because they had been around for more than 2 billion years, which is more than time enough for all their massive, hot, bright stars to have burned out long before. If these galaxies had depleted most of their star-forming material, not many new, hot, young stars could form. The rate of star formation might be as small as it is now in the Milky Way, only two to four solar masses worth per year, compared to thousands per year at the peak.Young stars include proportionately more massive stars, because it's the massive ones that burn out quickly. Stars that are more than 2 billion years old have to be smaller. Smaller stars are also dimmer, cooler, and redder in color. (Recall the Hertzsprung–Russell diagram, which displays the relationship between luminosity and color.) Consequently, older galaxies that are no longer forming many new stars are also redder, and that's how astronomers estimate roughly galaxy age, or at least the length of time since rapid star formation ceased.Certain events, such as collisions and mergers between galaxies can fire up rapid star formation again. So the correlation between color and age is not at all exact, but it's still there.Another fact about galactic appearance is that the central part of any galaxy, even a spiral, is much brighter than the outer reaches, like the spiral arms (if any), simply because the central part of a galaxy contains most of the stars. So at the distances we're concerned with here – over 10 billion light-years – all we can really observe with existing optical telescopes is the central part of a galaxy. To a first approximation, then, very distant galaxies look ellipsoidal in shape, even if they're really spirals.For the time period we're interested in, 3 billion years after the big bang, the redshift of light we see from objects at that time (denoted by z) is about 2.2. (See here for a fuller explanation.) The definition of redshift means that the wavelength of light emitted at z~2.2 is stretched by a factor of z+1~3.2. So visible light, with a wavelength of about 400 to 700 nanometers is shifted to 1.3 to 2.2 microns, in the near infrared. Although this kind of infrared light can be studied by ground-based spectroscopy, the best optical imagery has to be done from space-based instruments, which makes the job a lot harder.With all that as background, the newly published result we're concerned with is really pretty simple. It has confirmed that a certain galaxy, named 1255-0, at z=2.186 is about a third as massive (~2×1011M⊙) as the Milky Way and similar galaxies in our neighborhood at the present time, even though its central region is much smaller, with a radius of about 2500 light years. Consequently, stars in the central region of 1255-0 are packed much more closely together. This observation raises two distinct problems: First, most existing models of galaxy formation do not predict that typical galaxies of that age will be so compact. Second, no galaxies of that sort seem to exist in our general neighborhood, so at least some of them presumably evolved from galaxies like 1255-0 – and it's not clear how that could happen.Here's the research abstract:A high stellar velocity dispersion for a compact massive galaxy at redshift z = 2.186Recent studies have found that the oldest and most luminous galaxies in the early Universe are surprisingly compact, having stellar masses similar to present-day elliptical galaxies but much smaller sizes. This finding has attracted considerable attention, as it suggests that massive galaxies have grown in size by a factor of about five over the past ten billion years (10 Gyr). A key test of these results is a determination of the stellar kinematics of one of the compact galaxies: if the sizes of these objects are as extreme as has been claimed, their stars are expected to have much higher velocities than those in present-day galaxies of the same mass. Here we report a measurement of the stellar velocity dispersion of a massive compact galaxy at redshift z = 2.186, corresponding to a look-back time of 10.7 Gyr.Note that the research isn't the first to identify very massive but compact galaxies at z~2. Rather, it's new in that it has confirmed the estimate of mass by a new method, and that's what's significant.You see, there are basically two different ways, at present, to estimate the mass of a very distant galaxy. One method relies on a plausible assumption, that stars less than 2 billion years old, except for the very youngest, have fairly well-known distributions of mass and luminosity. And so, from the total luminosity of the galaxy that we can observe, we can form a good estimate of the total mass of stars. This is sometimes called the "photometric" mass. This sort of measurement is what has been used to infer that a number of galaxies at z~2 may have been very massive in spite of being small in extent. As suggested above, this observation raises at least two problems, so astronomers would like to measure mass in a different way, just to be sure. Besides, perhaps the assumptions about the mass and luminosity distributions of the stars in such galaxies could be wrong.Fortunately, there is another type of observation that can lead to good mass estimates, but it is much more difficult to make. This involves measuring the "dispersion" of velocities of stars in the galaxy. That is related to the distribution of stellar velocities. But since we can't distinguish individual stars at that distance we certainly can't measure their velocities (by very slight differences in stellar redshifts from the redshift of the galaxy as a whole).Even though the measurement is difficult to make in practice, it's simple to describe. One simply looks at the width of a few absorption lines in the galaxy's spectrum. If the lines are wide, it means that individual stars have substantially different velocities, including a certain proportion which are quite large. This is, basically, the meaning of "dispersion".From the relative number stars with high velocities one can infer the total mass. This yields what is called the "dynamical" mass of the galaxy. What the present research found is simply that the dynamical mass of 1255-0 is pretty close to the known photometric mass.Why is it that lots of high-velocity stars indicates a substantial mass? Just fairly basic physics, based on two of Newton's laws. (If you're a physicist, you learned this a long time ago, so it's "obvious".) The first is Newton's law of gravitation, which is F=G×M×m/r2. This describes the gravitational force (F) between two objects having masses M and m separated by a distance r. G is a certain constant called, of course, the gravitational constant. This can be applied to a galaxy with mass M and one of its stars, with mass m, where r is the distance from the star to the center of mass of the galaxy.The other law is Newton's second law of motion, which says F=ma. F is, again, the gravitational force of the galaxy, m is the mass of a particular star, and a is the acceleration of the star due to the force. (F and a are actually "vector" quantities, of couse, meaning they have a direction in 3-space.) You can think of the acceleration of an object as a way of measuring the force acting on it.Putting the two laws together, we find that for any particular star its accleration will satisfy a = G×M/r2, so the star's mass doesn't matter at all, only the mass of the galaxy. Just as in our own galaxy, almost all stars are in orbit around the center of mass of the galaxy, so a star's velocity, as seen from far away, varies periodically in a predictable way, deducible from acceleration (which is the rate of change of velocity).From calculations that are routine (at least for a physicist) one thus obtains a good estimate of the mass of a galaxy from the distribution of velocities of its stars, which in turn is deducible from the dispersion of spectral lines.There is one additional complication: matter in any form other than what makes up stars, most especially dark matter. But the present research shows that the mass as estimated photometrically (where any nonluminous ... Read more »
van Dokkum, P., Kriek, M., & Franx, M. (2009) A high stellar velocity dispersion for a compact massive galaxy at redshift z . Nature, 460(7256), 717-719. DOI: 10.1038/nature08220
by Charles Daney in Science and Reason
Now that research into telomeres and telomerase has (finally) garnered a Nobel Prize, it's a good time to write about recent research on the subject.Seminal work on telomeres by Elizabeth Blackburn, one of the Nobel winners, was published way back in 1978, and active studies have been going on ever since. So perhaps it's not surprising that the rate of new findings is not so rapid as occurs in newer areas – such as stem cells.But fascinating new results on telomeres and telomerase do still appear, and one of them connects with more recent research areas – such as Wnt signaling and... stem cells.Here's the press release:Discovery pinpoints new connection between cancer cells, stem cells (7/1/09)A molecule called telomerase, best known for enabling unlimited cell division of stem cells and cancer cells, has a surprising additional role in the expression of genes in an important stem cell regulatory pathway, say researchers at the Stanford University School of Medicine. The unexpected finding may lead to new anticancer therapies and a greater understanding of how adult and embryonic stem cells divide and specialize.Don't bother getting excited about the "new anticancer therapies" bit. That's just boilerplate that about 77.3% of all press releases dealing with cell biology contain, presumably to impress the rubes. If you need something to get excited about, you might recall that telomerase is also being investigated intensively in connection with issues of aging and longevity, independently from cancer. However, while it's possible that something of medical significance may come from this research, that's probably way down the road.Before discussing the new research, let's review some of the background on telomeres, telomerase, and Wnt signaling.To begin with, a telomere is a series of short repeated segments of DNA found at the ends of chromosomes in all eukaryotic cells. In cells of vertebrate animals the repeated segment is TTAGGG (where the letters represent nucleobases: T=thymine, A=adenine, G=guanine).The total number of nucleotides in these repeated segments varies a great deal from species to species, but in humans it is (initially) about 10,000 nucleotides (or ~1700 complete segments). I say "initially", because part of the telomere is lost every time a cell divides – perhaps 50 to 200 nucleotides per division. Obviously, this means that an adult cell newly derived from a stem cell can divide at most 50-200 times before the telomere is all gone. In practice, the number is a lot less than the maximum, perhaps 40 to 60 times, which is called the Hayflick limit. Cells are programmed to stop dividing on reaching this limit, since otherwise useful DNA would be lost or damaged upon further division.Why does this loss occur? It seems to be somewhat of an accident of the nitty-gritty details of how DNA replication occurs during cell division. I won't go into that, since it's best explained with some diagrams; you can read about it at Wikipedia. In fact, in the early days of molecular biology (around 1972), what happens at the end of chromosomes during DNA replication was rather puzzling, and the puzzle was called the "end replication problem". Now it's pretty well understood, though somewhat messy.In any case, the loss of DNA from the telomeres during cell division is a fact, and it conveniently explains the existence of the Hayflick limit, which had been recognized since 1965. What happens when the teleomere is all used up and the limit is reached? Cells that have reached the limit don't necessarily die (though they might), but they do stop dividing, and they enter a static phase of cell like known as senescence.If you think about it, senescence can be a problem, especially in certain tissues that need to continually replenish their cells, such as skin and the lining of the intestines, as well as hair, fingernails, etc. How is senescence circumvented in such tissues? The answer is (adult) stem cells. It turns out that stem cells are not subject to the Hayflick limit. It's not clear whether they are subject to limits at all.Like any other cell type, stem cells also divide (by the process technically known as mitosis). But there is one difference from the way "ordinary" cells divide. Stem cells can divide asymmetrically, where one daughter cell is another stem cell, but the other daughter is a "progenitor cell", which is close to a normal, fully-differentiated adult cell of a fixed tissue type. Progenitor cells differentiate further into the final form when they divide, and they are able to divide only a limited number of times.So how is it that stem cells are able to escape the Hayflick limit, dividing an indefinite number of times, even though they are also subject to the same loss of telomere nucleotides with each division? The answer is the enzyme telomerase, which is able to rebuild shortened teleomeres. It's fortunate for the longevity of complex organisms that telomerase exists, otherwise stem cells would not be able to divide often enough to allow tissues exposed to harsh conditions (such as skin and intestinal lining) to be replenished.In order to explain the results of the research to be described here we need to say more about telomerase, but first let's summarize the function of telomeres. At first it may seem that all they do is compensate for the sloppy way that DNA replication works, by providing long stretches of expendable DNA at the ends of chromosomes. But there is one other notable function: teleomeres are a useful "cap" at the end of a chromosome that is recognizable to cellular mechanisms responsible for detecting DNA damage. If it weren't for the telomeres, the ends of chromosomes would be indistinguishable from DNA damage, which can result from errors in the replication process, as well as damage due to external agents such as ionizing radiation or harmful chemicals. Cells have various mechanisms for repairing many kinds of damage, but even if repair isn't possible, other mechanisms exist that recognize the damage and prevent further cell division or cause programmed cell death (apoptosis). Not all DNA damage can be repaired or compensated for by apoptosis or cessation of cell division. Unrepaired DNA damage (however it occurs) is the main cause of cancer (though not the only one). So the existence of the Hayflick limit as a result of teleomere shortening acts as one defense against cancer. Cancer can be defined as the uncontrolled proliferation of cells as a result of DNA damage (affecting existing mechanisms that normally control proliferation) or other causes. So fixed limits on the number of times a cell can divide is one of a number of mechanisms organisms have to guard against cancer.Before moving on, here's a quick summary of the functions served by telomeres: (1) compensate for the chromosome "end replication problem"; (2) make it possible for cells to distinguish chromosome ends from damaged chromosomes; (3) provide natural limits to the number of times ordinary cells can divide, as protection against cancer.As noted above, the third of these functions is a problem for stem cells that do need the ability to divide an indefinite number of times. Repair of tissues exposed to harsh conditions is not the only circumstance this ability is needed. Another very important case is that of embryonic development. Multicellular, sexually-reproducing organisms start from a single cell (zygote). Yet there are close to 1014 cells in an adult human.It is true that a single cell that underwent 47 cycles of cell division could theoretically produce that many cells. But that's really pushing the limits, since some cell types are needed in much larger numbers than others. The bottom line is that embryonic development is the other main circumstance when limits on cell division need to be overcome.Telomerase is what makes this overcoming of telomere limits possible. And it does it in a pretty straightforward way. Telomerase is a complex molecule with three distinct parts. Two of these are proteins: Telomerase Reverse Transcriptase (TERT) and dyskernin, which are coded for by distinct genes. TERT does most of the work. The other part is a short piece of RNA, called the telomerase RNA component (TERC), which ... Read more »
Park, J., Venteicher, A., Hong, J., Choi, J., Jun, S., Shkreli, M., Chang, W., Meng, Z., Cheung, P., Ji, H.... (2009) Telomerase modulates Wnt signalling by association with target gene chromatin. Nature, 460(7251), 66-72. DOI: 10.1038/nature08137
by Charles Daney in Science and Reason
Just under three years ago, in October 2006, some important stem cell research was announced by a Japanese scientific team led by Shinya Yamanaka. The team showed how ordinary mouse skin cells could be transformed into cells that turned out to be pluripotent, just like embryonic stem cells (ESCs). The new cells were called induced pluripotent stem cells (iPSCs). Although "ground-breaking" is an over-used term, this research genuinely deserved the description.Aside from the fact that it could be done at all, the surprising thing was that the transformation could be effected by adding transcribable genes for just four transcription factors to the skin cell DNA. Those genes were Oct4, Sox2, c-Myc, and Klf4. And now very recent research shows that, under the right conditions, just the addition of Oct4 alone can accomplish the same feat.We discussed some of the early research here, with additional reports here, here, and here.In the three years since the original announcement, research has extended and improved the process in a number of ways. The ultimate goal is to be able to produce pluripotent human stem cells that are in all important respects equivalent to embryonic stem cells, by a process that meets several important criteria:Cells to be reprogrammed into a pluripotent state should be readily obtainable from human subjects (unlike embryonic cells or rare types of adult stem cells).No permanent changes to cellular DNA should be made, only changes to gene expression.The process should be relatively quick and efficient, so that reasonable number of pluripotent cells can be obtained for routine therapeutic or experimental uses.Reprogramming of other cell types into pluripotent cells is important not just as a technical feat to prove it can be done. There are two other important objectives. The first is to develop human cell lines that model many types of pathology (cancer, Parkinson's disease, or whatever) to facilitate research into therapeutics for these diseases. The best way to develop such lines is first to obtain pluripotent cells with the appropriate pathology, derived from human subjects with the disease, which can't generally be done from embryonic sources. From there, several techniques can be used to produce appropriate cell cultures with the desired model pathology.The second objective is longer-range but even more important: to manufacture cells, for patients with certain diseases, that can be used as therapeutic replacements for the patient's own malfunctioning tissue. This would be accomplished by obtaining pluripotent cells derived from the patient, correcting genetic problems in those cells, and then inducing the cells to differentiate into the required tissue type. Diseases that should be treatable in this way include Parkinson's disease, Type 1 diabetes, and heart disease. Starting with cells from the actual patient eliminates the problem of tissue incompatibility.The criteria listed above that are imposed on the process are important for meeting both of these objectives.In the three years since the original work was announced, dozens of research groups have set about testing improvements to the original procedures in order to progress towards the ultimate objectives. The improvements that have been made include:adapting the procedures to work in species other than mice – including pigs and fruit flies, as well as humansreducing the number of transcription factors that need to be introduced, or finding other suitable transcription factorsfinding other cell types besides skin cells to start with, generally various types of non-pluripotent stem cells – which makes other improvements in the process easier to accomplishchanging the way that the transcription factors are introduced into the target cells, in order to avoid alteration of the original DNA (since such alterations may introduce risks of cancer or other cellular malfunction)finding other proteins or small molecule compounds that can be added to enhance the efficiency and speed of the processQuite a few important improvements have been announced within the past several months, along with other related news. The most interesting related news is a demonstration that iPSCs really are not only equivalent to ESCs in terms of gene expression, but are in fact equally pluripotent. This latter fact was convincingly demonstrated by cloning several generations of live, healthy mice from iPSCs. (We'll discuss that in a separate article, but here's an overview.)What I want to discuss here is how the list of transcription factors (or their genes) that need to be added to a non-pluripotent cell has been reduced to just one: Oct4. The work was done by a mostly German team led by Hans Schöler of the Max Planck Institute for Molecular Biomedicine.So how was this accomplished? Well, the trick is, you have to start with the right kind of cells. In this case the researchers used human fetal neural stem cells (HFNSCs). While such cells aren't pluripotent, they are "multipotent", which means they can normally differentiate into various other cell types.Back in February the researchers in this study reported that reprogramming with just Oct4 could be done in mouse neural stem cells (see here, here, or here). But would this also work with human cells?Yes. The latest report shows that HFNSCs can be reprogrammed to a pluripotent state using only Oct4 and Klf4, and (generally) even with Oct4 alone. How is this possible? It is known that mouse neural stem cells already express Sox2, c-Myc, and Klf4. As for the human case, the paper says, cautiously, that "The feasibility to reprogram directly NSCs by OCT4 alone might reflect their higher similarity in transcriptional profiles to ES cells than to other stem cells like haematopoietic stem cells or than to their differentiated counterparts."And the main indication of this is that the process works: "One-factor human NiPS cells resemble human embryonic stem cells in global gene expression profiles, epigenetic status, as well as pluripotency in vitro and in vivo. These findings demonstrate that the transcription factor OCT4 is sufficient to reprogram human neural stem cells to pluripotency."What this is saying is that there are several criteria for similarity to embryonic stem cells that the reprogrammed HFNSCs meet. At a molecular level the reprogrammed cells express the same genes and have the same epigenetic markers as ESCs. In addition, they can differentiate into many adult cell types both in vitro and in vivo (in the latter case, by forming teratomas (mixed masses of cell types) when implanted in mice).There are still several drawbacks to this method for practical purposes, even of research. For one thing, human fetal neural stem cells are not exactly easily obtainable. And in addition, retroviruses were used (as in the original Yamanaka work) to introduce Oct4 into the cells. For therapeutic applications it would be absolutely necessary to use one of the other methods that have been explored and that do not disrupt the existing cell DNA or leave exogenous DNA in derived cells – since either alternative means the derived cells might revert to a more undifferentiated state. On top of all that, the process is still inefficient and slow.Reprogramming methods that have been explored in other research include the introduction of genetic material in forms other than retroviruses, as well as direct delivery of the transcription factor proteins. The researchers in this study intend to investigate such possibilities, as well as use of other initial cell types: "Future studies will show if direct reprogramming is possible with small molecules or OCT4 recombinant protein alone. ... It will be interesting to extend this study to human NSCs derived from other sources, such as dental pulp, as well as to other stem-cell types."... Read more »
Kim, J., Greber, B., Araúzo-Bravo, M., Meyer, J., Park, K., Zaehres, H., & Schöler, H. (2009) Direct reprogramming of human neural stem cells by OCT4. Nature. DOI: 10.1038/nature08436
by Charles Daney in Science and Reason
I suppose that just about everyone knows of the important role the p53 protein plays in protecting cells from becoming cancerous. The protein was identified 30 years ago and its gene (TP53) cloned soon thereafter. What's not so widely known is just how complex the operation of p53 in protecting against cancer really is. And very recent research shows the complexity is even more than previously thought. However, the complexity is to be expected, because evolution doesn't "design" cellular mechanisms to work in a straightforward way. The mechanisms are simply the result of about a billion years of trial and error. Being pretty and elegant was not a criterion for success. Nature is "hairy", knowing nothing of Occam's Razor, and caring even less. Simplicity is for wimps.But one thing is clear: p53 plays a large role in preventing, or at least suppressing, the development of cancer. In many types of cancer, p53 is found to have mutations more than 50% of the time. Even if p53 isn't mutated, cancer cells generally have other p53 abnormalities, such as low levels of the protein or the presence of various factors that interfere with its activity.Until the latest research, there have been two principal ways known in which p53 works against cancer, and several additional minor ways. The two main ways p53 has been known to act are binding to DNA as a transcription factor, and binding directly to certain proteins. And each of these mechanisms can lead to either of two main types of tumor suppression: apoptosis (cell death) and temporary or permanent suspension of the cell cycle, which is the process a cell goes through in order to divide and proliferate.P53 is primarily a transcription factor. In this role it is found in a cell nucleus and binds to various specific DNA gene promoter regions, in order to direct transcription of the associated gene – the first step in production of proteins from a gene.The proteins that are expressed as a result of this p53 activity can play a part in either apopotosis or cell cycle control (as well as other functions not directly related to cancer – see here, here, here). Which function is invoked depends on the type of signal that activates the p53. Among the possible conditions that may be signaled are detection of correctable or uncorrectable damage to DNA and detection of chromosome telomeres that are too short.In addition to binding to DNA as a transcription factor, p53 is also capable of binding directly to other proteins in order to control their behavior. Mainly these proteins are involved with apoptosis, such as members of the Bcl2 family. P53 itself is actually a family of proteins – there are at least 9 different RNA transcripts that can be derived from the TP53 gene. But one thing that each of these family members have in common is a segment, called the DNA binding domain. It is this part of the p53 that is capable of binding to either DNA or other proteins. (In general, a protein domain is a more-or-less self-sufficient component of a protein. Often the same domain appears in different members of a family of proteins.)One indication of the importance of this p53 domain is the fact that point mutations (errors involving only a single nucleotide pair) in the part of TP53 that code for the binding domain are the only type of point mutations of p53 that are commonly found in tumors. Errors that affect portions of p53 outside of the binding domain are not associated with cancer.There's one more thing to note about p53's role as a transcription factor. Namely, the RNA that is transcribed under the direction of p53 is not always messenger RNA (mRNA) that will eventually code for the production of a protein. P53 can also initiate the transcription of genes that code for microRNA (miRNA), which is a single-stranded RNA molecule that's normally only 21 to 23 nucleotides in length. Over 500 different types of miRNA have been found in human cells.MicroRNA is never translated into a protein. Instead, miRNA molecules regulate the translation of messenger RNA for many different proteins (by binding with the mRNA to prevent translation). It has been known for some time that p53 acts as a transcription factor for the miRNA family known as miR-34. It has also been learned that among the proteins regulated by miR-34 are some found in pathways that lead to apoptosis or cell cycle arrest. The net effect is that miR-34 has tumor-suppressing properties, so this is another way that p53, as a transcription factor, helps suppress tumors.Many other miRNA molecules, on the other hand, are found at high levels in cancer cells. Such miRNAs most likely inhibit expression of tumor suppressing genes, whose proteins might otherwise control cell proliferation or migration. We've discussed a number of miRNAs associated with cancer, mostly of the sort that promote cancer, here and here.Nevertheless, there are miRNAs besides miR-34 that have anti-cancer effects. Three in particular are miR-16-1, miR-143, and miR-145. It has been observed that these miRNAs, and several others, are found at higher levels in cells where p53 has been activated as a result of DNA damage. (Normally, p53 formed in non-cancer cells is either quickly degraded or else inhibited by certain proteins, especially MDM2, so as not to unnecessarily promote apoptosis or cell cycle arrest. The presence of DNA damage results in the removal of these inhibitions on p53.)It therefore appears that p53 is doing something to help produce a number of miRNAs, some of which are tumor suppressors. The curious thing, though, is that it can be shown that p53 is not a transcription factor for the genes that encode these miRNAs.So what is it that p53 is doing instead to help produce these miRNAs? New research published in the July 23, 2009 issue of Nature answers this question – and it uncovers an entirely new mechanism through which p53 (and its binding domain, in particular) acts as a tumor suppressor. Here's the research abstract:Modulation of microRNA processing by p53MicroRNAs (miRNAs) have emerged as key post-transcriptional regulators of gene expression, involved in diverse physiological and pathological processes. Although miRNAs can function as both tumour suppressors and oncogenes in tumour development, a widespread downregulation of miRNAs is commonly observed in human cancers and promotes cellular transformation and tumorigenesis. This indicates an inherent significance of small RNAs in tumour suppression. However, the connection between tumour suppressor networks and miRNA biogenesis machineries has not been investigated in depth. Here we show that a central tumour suppressor, p53, enhances the post-transcriptional maturation of several miRNAs with growth-suppressive function, including miR-16-1, miR-143 and miR-145, in response to DNA damage. ... These findings suggest that transcription-independent modulation of miRNA biogenesis is intrinsically embedded in a tumour suppressive program governed by p53. Our study reveals a previously unrecognized function of p53 in miRNA processing, which may underlie key aspects of cancer biology.To understand what's going on, it's necessary to explain a few things about how miRNAs are produced. It's not a simple 1-step process of transcribing an miRNA gene into the final short piece of RNA.There are, instead, three steps. The first step is transcription, done just as is done for any other gene. The RNA produced in this step is many nucleotides long, and is called the "primary transcript" or pri-miRNA. This pri-miRNA is then cut into smaller pieces having a hairpin shape, called pre-miRNA. The pre-miRNA, in turn, is further processed to produce the final "mature" miRNA.The intermediate step that converts pri-miRNA to pre-miRNA is performed by a protein complex known as the "microprocessor complex" (having nothing to do with computers, of course). One of the key proteins in this complex is an enzyme called Drosha. The final step, which is performed by another enzyme called Dicer, sp... Read more »
Suzuki, H., Yamagata, K., Sugimoto, K., Iwamoto, T., Kato, S., & Miyazono, K. (2009) Modulation of microRNA processing by p53. Nature, 460(7254), 529-533. DOI: 10.1038/nature08199
by Charles Daney in Science and Reason
If there's just one single point worth making about the biology of cancer, it would have to be "it's complicated".Cells in general, and animal cells in particular, are extremely intricate Rube-Goldberg-like mechanisms. Their correct functioning depends on the integrity of 20,000 or so genes (in the case of humans), and at least 5 times as many proteins whose form is specified by the genes. Damage to even one of a few thousand important genes can put a cell on the road to becoming cancerous. So the first fact about cancer isn't really all that hard to understand: cancer (in all of its many forms) is a disease that begins with damage to the DNA of one or more genes.This damage, which is necessary but not sufficient, can occur in many ways. Sometimes it happens because of the action of external agents, like carcinogenic chemicals or high-energy radiation (including ultraviolet light). Other times it happens simply because of occasional errors made in copying DNA during the process of cell division. These are just a few of many ways in which DNA can suffer damage. It's estimated that from 10,000 to a million DNA mutations can occur in a single human cell per day.Fortunately, only a few percent of the 3 billion fundamental units (base pairs) of DNA actually occur within genes – everything else is "noncoding DNA". Although much of this noncoding DNA serves some useful purpose, we have little idea at present what that might be. However, it's certainly less critical to cell function than the DNA of actual genes. Even so, 10,000 or so genes in every cell could suffer mutations every day.Of course, complex multicellular life couldn't exist unless nature had evolved some means for coping with all this random genetic damage. And so, there are a large number of ways that cells have of detecting and repairing the damage that does occur. Then in the relatively small number of cases where damage cannot be repaired, cells have additional fail-safe mechanisms to avoid malfunctions which lead to unlimited proliferation – i. e. cancer. One such mechanism is for a cell to enter a state of "senescence", where it ceases to be able to divide at all. A more drastic, but common, mechanism is for the cell to undergo "apoptosis" – orderly cell death.A necessary condition, therefore, for a cell to become cancerous, even after DNA damage remains unrepaired (perhaps because of damage to part of the repair mechanism), is that the damage occurs in a gene that codes for proteins needed for one of the various fail-safe mechanisms. Consequently, in almost every case of cancer where a tumor has begun to form, one finds problems in some part of the cell's anti-proliferation machinery.We'll look at a recent piece of research that identifies one particular way this can happen, and it's interesting for the variety of different cell processes that become involved.Many of the known "causes" of cancer are fairly easy to understand. Certainly, the cancer risk from DNA-damaging carcinogenic chemicals is obvious enough. And once one understands how important a key protein known as p53 is in crucial cellular processes such as detection of unrepaired DNA damage and invocation of apoptosis if necessary, it's not hard to understand why more than 50% of human tumors have mutated genes for p53.But there are other factors which have been found, in epidemiological studies, to be statistically associated with cancer development. One of these is inflammation, which is a very normal part of the body's immunological defenses against infection. Inflammation itself is a highly complex process – too complex to outline here. Chronic infections by various agents can cause a state of persistent inflammation. An example is the result of H. pylori bacterial infections. In addition to being responsible for stomach ulcers, such infections are also found in cases of stomach cancer. Obesity is also known as an epidemiological factor in various cancers, and the reason is now thought to be the state of chronic inflammation that obesity often causes.What is not clear is exactly what mechanism connects inflammation with cancer. There's undoubtedly a variety of mechanisms, given how complicated cellular processes turn out to be when you get down to the finer details. The recent research mentioned above illustrated one such mechanism, in one single type of cancer.Anti-inflammatory drugs may defeat a treatment-resistant type of cancer (6/24/09)The research focused on a type of non-Hodgkin lymphoma called diffuse large B-cell lymphoma. In some patients with the disease, chemotherapy works well. In a recent study of 40 patients more than 75 percent of patients with one form of this type of lymphoma survived five years or longer.But that study also identified a group of patients whose cancer proved difficult to treat. Their tumors failed to respond to chemotherapy, and only 16 percent of patients with this form of lymphoma survived more than five years after they were diagnosed.Several molecular flags mark this treatment-resistant lymphoma, but the links between them were unknown until now. The new paper reports that tumor cells isolated from these patients have depressed levels of a protein called SHIP1, which was known to suppress tumors. In fact, patients with the lowest levels of SHIP1 are the least likely to survive. SHIP1 is a phosphatase enzyme. That means it removes phosphate groups from proteins. So a phosphatase has the opposite effect of enzymes known as kinases, which attach phosphate groups to proteins. Having a phosphate group attached at the right place on a protein is what enables the protein to take part in a signaling pathway, which is the basic communication mechanism in a cell responsible for making things happen. Therefore, phosphatases disrupt pathways, and stop things from happening. This can be beneficial, for example, if what's happening is the excessive cell division that occurs in cancer. Accordingly, SHIP1 has been found to be a tumor suppressing protein.In the case of diffuse large B-cell lymphoma (DLBCL), it is found that SHIP1 levels are abnormally low. It's not that the SHIP1 is defective; there's just not enough of it. So the question is why. Is there some other defective gene that's responsible?Apparently, there is not. Instead, it's the presence of inflammation that's responsible, and in an interesting way. Inflammation is a perfectly normal product of the body's immune system, and it exists to counteract harmful agents such as bacteria. The immune system initiates and regulates the process of inflammation by means of signaling molecules called cytokines. One of the more common and important of these cytokines is TNFα.Now, TNFα normally goes about its business without causing cancer or other lasting ill effects. In fact, under the right conditions it can induce apoptosis or inhibit tumor formation in other ways. But for some reason, in DLBCL, TNFα suppresses SHIP1, and thus promotes cancer. The research in question also discovered the mechanism of SHIP1 suppression. It turns out that the real culprit here is a small piece of microRNA called miR-155. This little bugger was already known to be involved with leukemia in mice, and with other cancers. (See references in here.)The resistant type of lymphoma cells also have elevated levels of miR-155, a specific example of a type of genetic material called microRNA, the team found. They demonstrated that miR-155 suppresses SHIP1 by sticking to the template for the protein, preventing its manufacture. ...The final clue came from earlier reports that an inflammatory molecule called TNFα could boost levels of miR-155. Additional laboratory work confirmed the observation for this type of lymphoma cell. Some anti-inflammatory drugs, used for diseases such as arthritis and inflammatory bowel disease, where inflammation gets out of hand, work by suppressing TNFα. So it was hypothesized that such a drug might be beneficial in treating DLBCL. And voilà:The anti-inflammatory drugs etanercept and infliximab, which are currently used to treat arthritis and inflammatory bowel disease, work by suppressing TNFα, suggesting a new way to curb the malignancy of this type of lymphoma.The team tested the idea in mice that had been injected with aggressive lymphoma cells and found that nascent tumors shrank in six days. However, mice are not humans, so the drugs need to be tested in human DLBCL patients. Patients are already being recruited for clinical studies.Now, there... Read more »
Pedersen, I., Otero, D., Kao, E., Miletic, A., Hother, C., Ralfkiaer, E., Rickert, R., Gronbaek, K., & David, M. (2009) Onco-miR-155 targets SHIP1 to promote TNFα-dependent growth of B cell lymphomas. EMBO Molecular Medicine, 1(5), 288-295. DOI: 10.1002/emmm.200900028
by Charles Daney in Science and Reason
Will a pill containing the immunosuppressant drug rapamycin someday extend human lifespan a few years? In spite of the hopeful research announcements that appeared a few days ago, I wouldn't recommend getting one's hopes up just yet.This is a topic I've discussed before: Calorie restriction, TOR signaling, and aging. And for related stuff on mTOR: here.The executive summary is that inhibition of mTOR signaling has been shown to extend lifespan in yeast, roundworms, and fruit flies. Mice can now be added to this list, in experiments that included rapamycin in their diet.Here's the press release: Easter Island Compound Extends Lifespan Of Old Mice: 28 To 38 Percent Longer Life (7/8/09)On July 8, in the journal Nature, The University of Texas Health Science Center at San Antonio and two collaborating centers reported that the Easter Island compound – called "rapamycin" after the island's Polynesian name, Rapa Nui – extended the expected lifespan of middle-aged mice by 28 percent to 38 percent. In human terms, this would be greater than the predicted increase in extra years of life if cancer and heart disease were both cured and prevented.Although rapamycin and some related compounds have been investigated as anti-cancer therapies, the hypothesized lifespan-extending benefits are thought to be related to the by now well-documented benefits of calorie restricted diets. (For very recent news on that front, see here, for example.)Aging researchers currently acknowledge only two life-extending interventions in mammals: calorie restriction and genetic manipulation. Rapamycin appears to partially shut down the same molecular pathway as restricting food intake or reducing growth factors.It does so through a cellular protein called mTOR (mammalian target of rapamycin), which controls many processes in cell metabolism and responses to stress.A decade ago, Dr. [Dave] Sharp proposed to his colleagues that mTOR might be involved in calorie restriction. "It seemed like an off-the-wall idea at that time," Dr. Richardson said.Experiments were performed in parallel at three separate research centers and consisted of feeding hundreds of mice, starting at an age of 20 months, a diet containing a special formulation of rapamycin designed to evade breakdown in the digestive system. It was found that the age at which 90% of mice had died rose from 1,078 days to 1,179 days in male mice, compared to controls, and from 1,094 days to 1,245 days in females. The total lifespan extension, on average, was therefore 9.4% in males and 13.8% in females. Note that some accounts of the research claim lifespan extensions of 28% to 38%, but this is misleading, since those figures represent the extension of the "old age" period of mouse life beginning at 20 months. They do not mean that the mice lived up to almost 40% longer in total. (Some pretty shoddy reporting going on here....) And there was no particular evidence to indicate that extensions of such size would have occurred if the special diet began at an earlier age. However, in experiments still going on, there is evidence for some extension when addition of rapamycin to the diet begins for mice 270 days old.Of course, even an extension of human lifespan in the 10% range – 7 or 8 years – would be quite an accomplishment, provided quality of life in the final years remained about where it is today. (Which is a big if.)But there are various reasons to suspect that even a 10% extension in humans is rather optimistic. Some reasons:Rapamycin is an immunosuppressant, currently used therapeutically to prevent organ transplant rejection. The experimental mice were maintained under conditions that carefully protected them from infection – conditions that would not be realistic for humans.Although mice and humans are both mammals, their genetics are not all that similar. The complete sequence of the mouse genome was recently announced (see here), and it turns out that about 20% of mouse genes are different from human analogs, or not found in humans at all. (It's been 90 million years since the last common ancestor of mice and humans.)Rapamycin is known to inhibit an important protein kinase called mTOR (mammalian target of rapamycin). mTOR plays a key role in regulating cell growth, proliferation, and survival, so it's not all that surprising that rapamycin might affect cell biology relevant to aging and longevity. This same property of rapamycin makes it interesting as an anti-cancer agent. Rapamycin and similar compounds that inhibit mTOR have in fact been found to have anti-cancer properties in animal models. Several analogs of rapamycin have been investigated as anti-cancer therapies, and one has even been approved for human use (Torisel). But even in the anti-cancer setting, mTOR inhibitors haven't yet been slam-dunk successes.It is not clear that rapamycin in these experiments was working the same way as calorie restriction. None of the rapamycin-fed mice lost body weight, and calorie restriction usually works best when started relatively early in life.Experimental mice that received rapamycin got a dose of 2.24 mg per kg of body weight. That's quite a lot – about 30 to 60 times (per kg) what would be given to a 60 kg human for immunosuppression.The unfortunate truth is that cell signaling pathways that affect cell growth, proliferation, and survival are rather complicated, and any interventions in such pathways are very likely to not have the expected effects and/or to have various unexpected side-effects. Here's a diagram of just some of the important pathways mTOR is involved in. Imagine that were an electrical circuit and you made ad hoc changes to important components of the circuit.... Perhaps you can see how trying to affect mTOR in order either to control cancer or enhance longevity might be a dicey proposition.In spite of all the reservations, there are still promising signs for the role of mTOR inhibition in lifespan extension. The mechanism of action need not be the same as calorie restriction, even though that hasn't been ruled out either. For example, TOR is known from yeast and nematode studies to promote protein production in ribosomes and to inhibit protein degradation via autophagy. Invertebrate studies have shown that reversal of these TOR effects can increase lifespan. And TOR signaling is also known to influence cell growth, cell-cycle progression, mitochondrial metabolism, and insulin-analog signaling. Remember what we said about the diversity of effects of mTOR signaling? That's definitely a sword that can cut both ways – it's powerful, but hard to predict and control. We need to understand a lot more of the biological details – otherwise we're just swinging the sword in the dark.Harrison, D., Strong, R., Sharp, Z., Nelson, J., Astle, C., Flurkey, K., Nadon, N., Wilkinson, J., Frenkel, K., Carter, C., Pahor, M., Javors, M., Fernandez, E., & Miller, R. (2009). Rapamycin fed late in life extends lifespan in genetically heterogeneous mice Nature DOI: 10.1038/nature08221Further reading: Tests raise life extension hopes (7/8/09) – BBC news storyImmune drug boosts lifespan (7/8/09) – TheScientist.com... Read more »
Harrison, D., Strong, R., Sharp, Z., Nelson, J., Astle, C., Flurkey, K., Nadon, N., Wilkinson, J., Frenkel, K., Carter, C.... (2009) Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. Nature. DOI: 10.1038/nature08221
by Charles Daney in Science and Reason
We've discussed the mystery of amino acid chirality – the fact that all biological amino acids on Earth seem to be left-handed. Alternative chiral forms of molecules are called enantiomers. Previous discussion and background is here.In that earlier discussion we considered a hypothesis that was described last year. It is known that amino acids can be formed in interstellar space. The hypothesis suggests that the first amino acids on Earth were carried here by meteorites. Further, there was some excess of left-handed over right-handed amino acids that arrived this way (but not necessarily entirely the left-handed kind). The last detail is to explain how the imbalance of one handedness over the other occurred in space. That could be explained by the fact that light that is strongly polarized could selectively destroy one chiral form of amino acid. Such light is emitted by rapidly spinning neutron stars. But, as we'll see, there are other possibilities.This hypothesis was expounded by Ronald Breslow of Colombia University. He has conducted experiments that showed a small initial imbalance could be amplified by successive evaporations of solutions containing phenylalanine, a process that could easily have occurred on Earth. [2] [3]Although experiments were done to verify the plausibility of the various mechanisms required, there's no direct evidence that the supposed sequence of events is actually responsible for the observed chirality. However, ten years ago analyses of the Murchison meteorite by Sandra Pizzarello and John Cronin did find a preponderance of left-handed amino acids. There was a possibility that this finding could have resulted from some process occurring after the meteorite hit the ground. But last year Pizzarello and others analyzed another meteorite that fell in Antarctica and seemed especially pristine. The researchers reported that there was a similar chiral imbalance in that sample as well, and not only in amino acids but also in precursor aldehydes. [1]Now there is still more evidence for chiral imbalances – in the Orgueil meteorite, which fell almost 150 years ago:Clues To A Secret Of Life Found In Meteorite Dust (3/17/09)Over the last four years, the team carefully analyzed samples of meteorites with an abundance of carbon, called carbonaceous chondrites. The researchers looked for the amino acid isovaline and discovered that three types of carbonaceous meteorites had more of the left-handed version than the right-handed variety – as much as a record 18 percent more in the often-studied Murchison meteorite. "Finding more left-handed isovaline in a variety of meteorites supports the theory that amino acids brought to the early Earth by asteroids and comets contributed to the origin of only left-handed based protein life on Earth," said [Dr. Daniel] Glavin.There's also evidence about how the imbalance may have occurred:The team also found a pattern to the excess. Different types of meteorites had different amounts of water, as determined by the clays and water-bearing minerals found in the meteorites. The team discovered meteorites with more water also had greater amounts of left-handed isovaline. "This gives us a hint that the creation of extra left-handed amino acids had something to do with alteration by water," said [Dr. Jason] Dworkin.The researchers focused on the amino acid isovaline, because it can "preserve its handedness for billions of years, and it is extremely rarely used by life, so its presence in meteorites is unlikely to be from contamination by terrestrial life."Here's the abstract of the research paper:Enrichment of the amino acid l-isovaline by aqueous alteration on CI and CM meteorite parent bodiesA large l-enantiomeric excess (ee) of the α-methyl amino acid isovaline was found in the CM meteorite Murchison (lee = 18.5 ± 2.6%) and the CI meteorite Orgueil (lee = 15.2 ± 4.0%). The measured value for Murchison is the largest enantiomeric excess in any meteorite reported to date, and the Orgueil measurement of an isovaline excess has not been reported previously for this or any CI meteorite. The l-isovaline enrichments in these two carbonaceous meteorites cannot be the result of interference from other C5 amino acid isomers present in the samples, analytical biases, or terrestrial amino acid contamination. We observed no l-isovaline enrichment for the most primitive unaltered Antarctic CR meteorites EET 92042 and QUE 99177. These results are inconsistent with UV circularly polarized light as the primary mechanism for l-isovaline enrichment and indicate that amplification of a small initial isovaline asymmetry in Murchison and Orgueil occurred during an extended aqueous alteration phase on the meteorite parent bodies. The large asymmetry in isovaline and other α-dialkyl amino acids found in altered CI and CM meteorites suggests that amino acids delivered by asteroids, comets, and their fragments would have biased the Earth's prebiotic organic inventory with left-handed molecules before the origin of life.Note that evidence in the samples analyzed was not consistent with circularly polarized light as a cause of the imbalance, and a process involving water seems more likely.Other accounts of this research: [6], [7]There's other relatively recent research that demonstrates another way enantiomeric excesses of one form of amino acid could be produced. When inorganic materials are irradiated with high-energy photons (e. g. X-rays), they may emit electrons whose spins are polarized in a specific direction by a magnetic field. Experiments showed that this could affect the chirality of organic molecules adsorbed on the surface of a magnetic material:Electrons put a new spin on chirality (11/5/08)Researchers in the US have shown that the presence of spin-polarized electrons can make a chemical reaction involving “right-handed” molecules occur faster than the same reaction involving “left-handed” molecules. The discovery could help scientists understand why nature favours a certain handedness in many biological molecules.Although the organic molecule used in this experiment was butanol (not an amino acid), the researchers plan to perform a similar experiment with the amino acid alanine. While this research doesn't show this is the mechanism actually responsible for left-handedness of amino acids found on meteorites, it's a least a possibility.Press release on this research: [4]Glavin, D., & Dworkin, J. (2009). Enrichment of the amino acid L-isovaline by aqueous alteration on CI and CM meteorite parent bodies Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0811618106References and further reading:[1] Key To Life Before Its Origin On Earth May Have Been Discovered (2/28/08)[2] Amplification of enantiomeric concentrations under credible prebiotic conditions – July 2006 research paper by Ronald Breslow and Mindy S. Levine [3] Radiation-induced racemization and amplification of chirality: implications for comets and meteorites – February 2007 research paper[4] Possible Mechanism For Creating 'Handedness' In Biological Molecules (12/2/08)[5] Rock Offers Mirror-Image Clues to Life's Origins (10/5/08) – good overview article in the Washington Post[6] Did lefty molecules seed life? (3/16/09) – The Scientist[7] Southpaw Solar System (3/16/09) – ScienceNOWTags: amino acid chirality... Read more »
Glavin, D., & Dworkin, J. (2009) Enrichment of the amino acid L-isovaline by aqueous alteration on CI and CM meteorite parent bodies. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.0811618106
by Charles Daney in Science and Reason
I just wrote about this at some length, here.It's funny, sometimes, how there are a bunch of results released in a short time period on the same topic. Usually it's because there's a big meeting that covers the topic, or else the editor of some journal wants several papers on the topic.I've just come across three more papers on the topic and can't recall such a flurry of activity related to it. The papers were all published in different journals, and there doesn't appear to have just been a meeting on the topic, but it's understandably an active area of research.The issue is whether or not variants of genes for DNA repair proteins make good biomarkers for cancer risk. As I discussed before, the recent meta-analysis suggests that in general this isn't as great a place to look for biomarkers as one might expect.Compared to the most common allele of a DNA repair gene, less common alleles may correlate with either increased or decreased cancer risk, depending on the type of cancer and type of DNA repair involved. In neither case can one automatically conclude that the common allele yields protection against cancer. By repairing DNA, the repair enzyme might actually help cancerous cells survive, offsetting any benefit from preventing further genome damage.As a result, if one finds that a specific allele reduces cancer risk, it could be because the allele is actually less effective at repairing DNA. Conversely, if another allele increases cancer risk, it could be because the allele is too effective at repairing DNA.Just looking at the situation from an anticancer perspective, when DNA damage is detected, the smart thing to do is to sacrifice the cell via apoptosis. But that's not the way nature looks at things. The type of damage involved may be so common that it's smarter to try to fix it, and then hope for the best cancer-wise. After all, most cancer depends on the presence of other, unrelated and probably very uncommon, kinds of genomic damage.Research studies in this area really need to try to suss out what is actually happening, and that could be rather difficult. Basically, this is an evolutionary problem, with the outcome depending on what happens, statistically, in millions or billions of cells over a period of time. Which alleles will ultimately win out? The ones trying to fix DNA damage, or the others trying to exploit the damage? All the "players" in this game have different interests at stake.Progress here may require some heavy-duty computer simulations trying to sort it all out. Cancer research could turn out to be a lot like climate modeling.What would better understanding mean therapeutically? It could be possible to discover biomarkers – alleles that indicate significant cancer risk. Where serious risk is indicated to exist, then standard interventions like surgery or chemotherapy may be appropriate.On the other hand, developing drugs that attempt to silence an allele which is found to predict significant cancer risk may not be very rewarding, for all the usual reasons that drugs may fail (e. g. side effects). That's what clinical trials are for – and trials are very expensive.The first study we'll look at here involves fairly unique circumstances. It does not address many of the issues we'd like to know about, in particular concerning a direct mechanistic relationship between DNA repair and cancer.But let's look at what it does say, with a view towards where further research could go. The study, first, determines that a specific type of DNA repair ("nucleotide excision repair") rises and falls substantially with the circadian clock. Second, it finds that levels of a specific repair-related protein (xeroderma pigmentosum A, or XPA) also rises and falls with the clock. Third, it shows levels of XPA are directly related to DNA repair activity.Now, it's well known that certain types of chemotherapy have a circadian dependency. Quoting from the paper, there exists "empirical observation that circadian time of delivery of chemotherapeutic drugs such as cisplatin, whose major DNA lesions are cisplatin-d(GpG) and cisplatin-d(GpXpG) diadducts (6, 7), may be a significant contributing factor to the efficacy of the drug and the severity of its side effects (4, 5)." Thus it's at least plausible that circadian variability of the levels of repair-related proteins could account for this.However, that hypothesis remains to be checked directly. It will be interesting to see how this develops.Here's a press release:Chemotherapy Most Effective At Time Of Day When Particular Enzyme At Lowest Level (1/13/09)For years, research has hinted that the time of day that cancer patients receive chemotherapy can impact their chances of survival. But the lack of a clear scientific explanation for this finding has kept clinicians from considering timing as a factor in treatment.Now, a new study from the University of North Carolina at Chapel Hill has suggested that treatment is most effective at certain times of day because that is when a particular enzyme system – one that can reverse the actions of chemotherapeutic drugs – is at its lowest levels in the body. ...The study, published in the Proceedings of the National Academy of Sciences, provides the first solid evidence that the daily oscillations of the cell's repair machinery can affect the potency of cancer drugs.Meta-observation: It's apparently difficult to pin down specific mechanisms at work here, so a fair amount of indirect inference is needed to draw conclusions. We'll see the same thing in two other recent studies (below).Research paper:Circadian oscillation of nucleotide excision repair in mammalian brainT.-H. Kang, J. T. Reardon, M. Kemp, A. Sancar (2009). Circadian oscillation of nucleotide excision repair in mammalian brain Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0812638106Next up is a a case-control study that looked at nine single-nucleotide polymorphisms (SNPs) of seven DNA repair genes. The researchers were looking for correlations with the occurrence of pancreatic cancer. They studied 734 pancreatic cancer patients and 780 individuals without cancer. The strongest association was with a variant allele of one gene (LIG3), where individuals with the allele were 77% less likely than carriers of the normal gene to have cancer. The next strongest association was with a variant allele of another gene (ATM), carriers of which were in excess of 100% more likely to have cancer. (ATM also figures prominently in the third study, discussed below.)Further investigation considered other cancer risk factors, such as smoking, heavy alcohol consumption, excess body weight, or diabetes – factors which might be responsible for excess DNA damage. The most significant factor turned out to be diabetes. In individuals with diabetes, carriers of an ATM allele were more than 200% likelier to have cancer, while carriers of a LIG4 allele were more than 100% likelier to have cancer.So here's a study that successfully found several biomarkers, but involving only a few of the DNA genes studied.Press release:Abnormal DNA Repair Genes May Predict Pancreatic Cancer Risk (1/15/09)Abnormalities in genes that repair mistakes in DNA replication may help identify people who are at high risk of developing pancreatic cancer, a research team from The University of Texas M. D. Anderson Cancer Center reports in the Jan. 15 issue of Clinical Cancer Research.Defects in these critical DNA repair genes may act alone or in combination with traditional risk factors known to increase an individual's likelihood of being diagnosed with this very aggressive type of cancer. ...With this in mind, [lead author Donghui] Li and her colleagues set out to identify DNA repair genes that could act as susceptibility markers to predict pancreatic cancer risk. In a case-control study of 734 patients with pancreatic cancer and 780 healthy individuals, they examined nine variants of seven DNA repair genes. The repair genes under investigation were: LIG3, LIG4, OGG1, ATM, POLB, RAD54L and RECQL.The researchers looked for direct effects of the gene variants (also called single nucleotide polymorphisms) on pancreatic cancer risk as well as potential interactions between the gene variants and known risk factors for the disease, including family history of cancer, diabetes, heavy smoking, heavy alcohol consumption and being overweight.Research abstract:DNA Repair Gene Polymorphisms and Risk of Pancreatic CancerThese observations suggest that genetic variations in DNA repair may act alone or in concert with other risk factors on modifying a patient's risk for pancreatic cancer.The last study we'll consider here is a little more tangential to the issue of DNA repair genes and cancer. It's primarily about how defects in DNA repair genes may be responsible for two related neurological diseases – ataxia telangiectasia-like disease (ATLD) and Nijmegen breakage syndrome (NBS).The two diseases result from defects in the proteins Mre11 and Nbs1 (respectively), which are part of a protein complex called MRN (Mre11-Rad50-Nbs1). MRN is a part of a mechanism that repairs double-stranded DNA breaks.The research used mouse models. Mice engineered to have an ATLD-like disease had defective genes for Mre11, while those with the NBS-like disease had defective genes for Nbs1. In both cases, DNA-damage stress was induced either by radiation or by knocking out another DNA repair enzyme. The idea was to trigger disease effects due to inadequate damage repair by MRN.A further relevant fact is that part of the MRN damage-repair process invokes a protein kinase called ATM. Part of the role of ATM is to trigger apoptosis if the damaged DNA cannot be repaired.For our purposes here, the relevant finding was that neurons of the ATLD mice were resistant to apoptosis, and consequently DNA-damaged neurons survived longer than they should, in view of their defects. The disease pathology results from the persistence of damaged neurons that cannot perform as required. However, neurons of the NBS mice were not unusually resistant to apoptosis, so the neurons died more rapidly, and pathology results from the excessive cell death.How Defective DNA Repair Triggers Two Neurological Diseases (1/14/09)To explore the differences between ATLD and NBS, the researchers used mice engineered to have defects in the causative genes, which produce two proteins that help form a critical component of the DNA repair machinery, called the MRN complex. The MRN complex zeroes in on broken DNA segments and attaches to them. It then recruits another important DNA repair protein, called ATM, to launch the repair process. However, if the damage is too severe, ATM may also trigger programmed cell death called apoptosis."It happens that defects in ATM also lead to a disease similar to ATLD, highlighting the connections between diseases resulting from defects in this DNA repair pathway," [senior author Peter] McKinnon said.The mice engineered to mimic ATLD, like their human counterparts, had defective genes that produce a protein called Mre11; while NBS mice were engineered to have defects in the gene for the protein called Nbs1.The key point may be this: when Mre11 is defective and ATM is then activated, it does not always trigger apoptosis when it should. But when Nbs1 is defective, ATM is able to do its job properly. In any event, when either Mre11 or Nbs1 is defective, MRN does not repair DNA damage as well as it should (in cells other than neurons). This may raise the risk of cancer due to randomly damaged DNA."There is a suspicion that people who carry these mutations may be predisposed to cancer and also more susceptible to chemotherapy agents or even to standard X-rays," McKinnon said. "Those agents induce the type of DNA damage that requires the MRN complex and ATM for repair. More generally, studies of the MRN complex and ATM are fundamental to understanding how to prevent changes to DNA that lead to cancer."Understanding more about how these proteins signal and interact, and how different cells in the body transduce the DNA damage signal, is of fundamental biological importance," McKinnon said. "This knowledge is necessary not only for understanding DNA repair diseases but for understanding the broader implications of maintaining of the stability of DNA."Tags: cancer, DNA damage, DNA repair... Read more »
T.-H. Kang, J. T. Reardon, M. Kemp, & A. Sancar. (2009) Circadian oscillation of nucleotide excision repair in mammalian brain. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.0812638106
by Charles Daney in Science and Reason
There's a fascinating interrelationship among the things mentioned in the title – and it takes us through equally fascinating topics in molecular cell biology and neurobiology.No, Chinese food has not been found to cause the listed maladies – although with the additives that the People's Republic of China seems to be allowing in many of its food products these days (e. g. melamine), who knows for sure?So what's the connection? Try monosodium glutamate (MSG). That, of course, is the sodium salt of glutamic acid (which itself is often referred to as "glutamate"). MSG is a rather well known food additive which at one time was very commonly used in Chinese food for its ability to "enhance" flavor. Technically, the form of glutamate responsible for flavor is the ionic form rather than the sodium salt – the former being what is found in aqueous solution rather than the latter dry crystalline form.MSG became notorious some time ago when Chinese food became popular in western countries, because it was at first unfamiliar and also tended to cause headaches or at least a peculiar lightheaded sensation after eating food to which it had been added. Consequently, most Chinese restaurants, at least in the U. S., now carefully inform customers that their food "contains no MSG".Nevertheless, it's impossible to escape glutamate, because glutamic acid is one of the 20 amino acids that make up all proteins. It's essential to life as we know it, and so in fact it can't be avoided. It also happens to be one of the most important neurotransmitters, and in that role is absolutely essential to the function of animal nervous systems. This role of glutamate is the key part of the story here.As a flavor, glutamate is responsible for the much hyped "fifth taste" known in Japanese as umami. The first four basic tastes are sweetness, bitterness, sourness, and saltiness. Each of these is detected by specialized receptors on human tongues. Like the others, umami is also detected by its own receptor, but what's actually being detected is the amino acid glutamate present in all protein-containing foods, especially meats, cheese, and soy products.Although the flavor is enjoyable, it's as a neurotransmitter that glutamate is important for the present story. As a neurotransmitter, glutamate is excitatory. In fact, it's the most abundant excitatory neurotransmmitter in mammalian nervous system. An electrical impulse traveling down a neuron's axon triggers the release of glutamate at the presynaptic side of glutamate synapses. When this glutamate is picked up by receptors at the other side (the postsynaptic side) of the synapse it contributes to possible excitation of the postsynaptic neuron. This is the basic mechanism by which signals are transmitted through an animal's nerves. (But there are other neurotransmitters besides glutamate that may be involved.)However, this excitatory behavior can get out of hand, and when it does glutamate can have a toxic effect, called excitotoxicity. This can kill neurons and cause disease conditions such as autism, schizophrenia, and epilepsy.Since glutamate is both essential but also (in excessive amounts) potentially toxic, an elaborate negative feedback system has evolved to keep glutamate production and release under careful control. It is when this feedback system fails somehow that neurological diseases develop. A typical cause of failure is mutation of genes that produce proteins essential to the feedback system.So what are some of these genes/proteins? The first of these is the metabatropic glutamate receptor, mGluR for short. This is a receptor found on the surface of an axon, close to a glutamate synapse. When glutamate outside the neuron binds to such a receptor, it acts to tamp down the exited state of the neuron that led to release of glutamate in the first place. This process is called autocrine signaling, meaning that it involves a cell releasing a signaling molecule that can trigger a receptor on the same cell to modify cell behavior. This is the start of the negative feedback loop.One source of failure is in mutation of mGluR itself, if this mutation causes further steps in the feedback loop to fail. What are some of these further steps? The first and possibly most important involves a protein enzyme with the charming name of PI3K. That's short for "Phosphoinositide 3-kinase", and we should be grateful for not having to write it out in full every time.PI3K is a kinase, which means its enzymatic action is to cause phosphorylation of other proteins. A sequence of phosphorylating kinsaes constitutes a signal cascade or "pathway". PI3K is the start of a pathway that plays a huge role in cell survival and proliferation – among other things. Clearly, it's an important protein. The next step in the pathway is another kinsase called AKT. It's actually, in humans, a small family of proteins, Akt1, Akt2, and Akt3. Akt1 is the main player. One of its main jobs is cell survival, as an inhibitor of apoptosis. There are many reasons, both good and bad, for a cell to die by apoptosis. Akt1 is there to prevent the bad reasons for being responsible for too much cell death. However, in cells that have become cancerous, one or another member of the AKT family typically functions only too well, resulting in the uncontrolled proliferation of cells that is the hallmark of cancer. In fact, an AKT kinase is hyperactive in the majority of human cancers. These molecules have been called perhaps the most frequently activated type of oncoprotein. (Reference: here.) Not only is AKT, in one form or another, involved in a majority of cancers, in many types of cancer, some form of AKT is a key factor. For instance, in melanoma, the interaction of Akt3 and another important cancer-related protein, c-Raf, is involved in 60-70% of melanoma-related tumors. (Reference: here.)Not too long ago we discussed several other kinases (mTOR and MAP kinases), as well as PI3K and AKT, that play a role in cancer.Its significant involvement in cancer is far from the only reason AKT is interesting, though. It is a versatile kinase involved in multiple pathways. In particular, it also participates in the negative feedback loop for glutamate because it deactivates a FoxO transcription factor. (For many details on that topic, see here.)Now we're really getting into the heart of the story on the negative glutamate feedback loop. Recent research on fruit fly motor neurons, which we're about to refer to, suggests (among other things) that an AKT kinase inhibits a FoxO transcription factor that otherwise would stimulate glutamate release.In a nutshell, the autocrine stimulation of the mGluR glutamate receptor activates PI3K, which activates an AKT kinase, which then inhibits a transcription factor, thereby inhibiting further glutamate release. This negative feedback loop keeps motor neurons from becoming overactive. Here's a picture of what's going on:Any mutation of the signaling kinases involved in this feedback loop would, of course, destabilize the control mechanism, but would likely cause other pathology as well, because of the involvment of PI3K, AKT, and FoxO in many other important cellular processes. However, if it was the mGluR glutamate receptor that was affected by a mutation, the main consequence would be some neurological pathology such as epilepsy. A further reasonable speculation would be that mutations affecting mGluR in other types of neurons could cause other neurological problems, such as autism or schizophrenia. The present research does not actually deal with this more general case. However, other research has implicated PI3K and mGluRs in epilepsy, neurofibromatosis (a type of non-cancerous tumor), autism, schizophrenia, and other neurological disorders in humans.Here's the research and its abstract:A PI3-Kinase–Mediated Negative Feedback Regulates Neuronal ExcitabilityUse-dependent downregulation of neuronal activity (negative feedback) can act as a homeostatic mechanism to maintain neuronal activity at a particular specified value. Disruption of this negative feedback might lead to neurological pathologies, such as epilepsy, but the precise mechanisms by which this feedback can occur remain incompletely understood. At one glutamatergic synapse, the Drosophila neuromuscular junction, a mutation in the group II metabotropic glutamate receptor gene (DmGluRA) increased motor neuron excitability by disrupting an autocrine, glutamate-mediated negative feedback. We show that DmGluRA mutations increase neuronal excitability by preventing PI3 kinase (PI3K) activation and consequently hyperactivating the transcription factor Foxo. Furthermore, glutamate application increases levels of phospho-Akt, a product of PI3K signaling, within motor nerve terminals in a DmGluRA-dependent manner. Finally, we show that PI3K increases both axon diameter and synapse number via the Tor/S6 kinase pathway, but not Foxo. In humans, PI3K and group II mGluRs are implicated in epilepsy, neurofibromatosis, autism, schizophrenia, and other neurological disorders; however, neither the link between group II mGluRs and PI3K, nor the role of PI3K-dependent regulation of Foxo in the control of neuronal excitability, had been previously reported. Our work suggests that some of the deficits in these neurological disorders might result from disruption of glutamate-mediated homeostasis of neuronal excitability.Further reading:Possible Clues To Root Of Epilepsy, Autism, Schizophrenia (12/9/08) – press releaseEric Howlett, Curtis Chun-Jen Lin, William Lavery, Michael Stern (2008). A PI3-Kinase–Mediated Negative Feedback Regulates Neuronal Excitability PLoS Genetics, 4 (11) DOI: 10.1371/journal.pgen.1000277Tags: autism, schizophrenia, epilepsy... Read more »
Eric Howlett, Curtis Chun-Jen Lin, William Lavery, & Michael Stern. (2008) A PI3-Kinase–Mediated Negative Feedback Regulates Neuronal Excitability. PLoS Genetics, 4(11). DOI: 10.1371/journal.pgen.1000277
by Charles Daney in Science and Reason
One of the key questions about galaxies concerns the process in which they form. Galaxies are made up of stars, but in general stars do not form in isolation – except for the very first stars in the universe, which we discussed here.More normally, stars form simultaneously in close proximity to each other as part of the larger process of galaxy formation. But galaxy formation can happen in one of at least two different ways. In the first case, the baryonic matter that will eventually form stars gradually contracts under gravitational force along with the larger mass of dark matter in which it is "trapped". This is a gradual process in which the entire galaxy is formed as the baryonic matter eventually collapses to a state that is dense enough for individual stars to form, much as stars form even today, albeit quite slowly, as in the Milky Way of the present time. (The present rate is only 2 or 3 per year on average.)Alternatively, in the second case, relatively small groups of stars form within irregular protogalaxies, which then over long periods of time (billions of years) merge with each other to form galaxies as we are familiar with them today.The first scenario is typically called "monolithic collapse" or formation by "gas accretion". The second is called the "hierarchical" or "merger" scenario.Of course, both processes can occur. Conceivably some of the large galaxies we can see today were built up from the merger of many smaller galaxies, while others formed more or less in isolation. But the interesting question is whether one or the other of these scenarios was more common in the early days of the universe. (Since at the present time most matter available to feed galaxy growth is already part of a galaxy, most galaxy growth now is by merger.)In the very early universe, that is for the first 2 or 3 billion years after the big bang (which was about 13.7 billion years ago), there would have been less opportunity for galaxy mergers, so one might expect that more of the galaxies back then formed in isolation rather than in a hierarchical process of mergers.As explained in this article on redshift, galaxies that formed within the first 3 billion years after the big bang all have redshifts of about 2.2 or more.Unfortunately, at such redshifts, the objects are at distances of 10.7 billion to more than 13 billion light-years, so it's nearly impossible to make out any details, even with the most powerful existing telescopes, and even using sophisticated technology like adaptive optics. Therefore, there's very little reliable information about the actual morphology of early galaxies, making it impossible at present to obtain enough evidence to decide between the two scenarios.In particular, it's certainly not possible to discern the overall shape of such a distant galaxy, to determine whether it's an ordinary spiral, a more shapeless elliptical galaxy, or something else, such as a pair of merging galaxies. Morphological information is what one needs in order to discriminate between nice orderly spiral galaxies and galaxies that are distorted due to mergers.Even though situating a telescope in space, such as the HST, or on the Moon solves the problem of atmospheric distortions, the only way to get better resolution is by using a larger mirror. Telescopes with larger optics are being planned, but fortunately nature itself provides some help even today, albeit in very rare circumstances, as we'll explain in a moment.Although we can't easily determine the properties of such early galaxies, at least it's possible to find them relatively easily in surveys, without even having to study them spectroscopically. We just discussed the technique for finding these early galaxies by the Lyman break techniques.It turns out that even though we cannot see the structure of these Lyman-break galaxies directly, we can do spectroscopic measurements that tell us a surprising amount of information about these galaxies. This information can tell us about galaxy rotation, whether there are strong outflows of gas (due to stellar winds or supernova ejecta), and even the approximate rate of star formation in the galaxy.One thing that spectroscopic data allows astronomers to do is to map "velocity fields" in different parts of a galaxy. That is, we can determine how fast specific parts of the galaxy are moving relative to the galaxy as a whole. For example, in a rotating spiral galaxy, we should detect that the half of the galaxy rotating away from us has an additional redshift beyond the overall redshift of the galaxy, while the other half has a slightly lower redshift. If this pattern varies in a regular way from one end of the galaxy to the other, we can be fairly sure the galaxy is a spiral. On the other hand, if the relative velocities of different parts of the galaxy are irregular or "chaotic", we probably have a galaxy without much regular structure.However, even this velocity field information we have is at a rather low resolution compared to the size of the galaxy. For historical reasons, astronomers customarily use a length scale called a parsec, or "parallax arcsecond", which is about 3.26 light-years. The resolution, for spectroscopic purposes, of an object at redshift z≳2.2 is about 1300 pc (parsecs), or 4000 light-years, and this is more than half the size of the visible part of a typical Lyman-break galaxy. (Our Milky Way is a lot larger, roughly 100,000 light-years in diameter.)What can be done about this? Not a whole lot, actually, until we have telescopes with much better resolution – except in certain very special circumstances. Those circumstances exist when another large galaxy or galaxy cluster lies directly in the line of sight between us and the very distant galaxy we're interested in. Then we have what is called a gravitational lens. This works pretty much like an ordinary optical lens, because according to general relativity massive objects are capable of bending light.A group of astronomers have now examined one example of exactly this circumstance. The distant galaxy in question is named J2135-0102 (a catalog number). It lies at z=3.075. So we see it as it was 2.13 billion years after the big bang. We know that there were already galaxies much less than a billion years after the big bang, so this one isn't that unusual.Because of this gravitational lens, it has been possible to map the velocity field of J2135-0102 with a resolution of ~120 pc, about 5 times better than possible without the gravitational lens. The abstract of the research paper reveals what can be learned from this:The formation and assembly of a typical star-forming galaxy at redshift z ≈ 3Recent studies of galaxies ~2–3 Gyr after the Big Bang have revealed large, rotating disks, similar to those of galaxies today. The existence of well-ordered rotation in galaxies during this peak epoch of cosmic star formation indicates that gas accretion is likely to be the dominant mode by which galaxies grow, because major mergers of galaxies would completely disrupt the observed velocity fields. But poor spatial resolution and sensitivity have hampered this interpretation; such studies have been limited to the largest and most luminous galaxies, which may have fundamentally different modes of assembly from those of more typical galaxies (which are thought to grow into the spheroidal components at the centres of galaxies similar to the Milky Way). Here we report observations of a typical star-forming galaxy at z = 3.07, with a linear resolution of ~100 parsecs. We find a well-ordered compact source in which molecular gas is being converted efficiently into stars, likely to be assembling a spheroidal bulge similar to those seen in spiral galaxies at the present day. The presence of undisrupted rotation may indicate that galaxies such as the Milky Way gain much of their mass by accretion rather than major mergers.So, the researchers have concluded that in the case of this small, but typical, Lyman-break galaxy, a fairly regular structure is present, and it is more likely due to gas accretion rather than hierarchical assembly.That's the big news, but the researchers were able to deduce a few other things as well.For example, from the rotation curve, J2135-0102 appears to have a mass of ~2×109 M⊙ (solar masses) within a radius of 1800 pc. (The Milky Way, by comparison, is about 5.8×1011 M⊙.) The galaxy's rate of star formation has also been estimated at 40±5 M⊙ per year – much higher (per unit volume) than the Milky Way's rate of only 2 or 3 M⊙ per year. This high rate, however, does seem to be typical of the rate in other Lyman-break galaxies that have been studied.Further reading:Cosmic Eye Sheds Light On Early Galaxy Formation, Just Two Billion Years After Big Bang (10/8/08) – press releaseCosmic eye telescope used to spot distant galaxy (10/8/08) - news article in the Telegraph (UK)Daniel P. Stark, A. Mark Swinbank, Richard S. Ellis, Simon Dye, Ian R. Smail, Johan Richard (2008). The formation and assembly of a typical star-forming galaxy at redshift z ≈ 3 Nature, 455 (7214), 775-777 DOI: 10.1038/nature07294Tags: galaxies... Read more »
Daniel P. Stark, A. Mark Swinbank, Richard S. Ellis, Simon Dye, Ian R. Smail, & Johan Richard. (2008) The formation and assembly of a typical star-forming galaxy at redshift z ≈ 3. Nature, 455(7214), 775-777. DOI: 10.1038/nature07294
by Charles Daney in Science and Reason
Perhaps interest in politics has dropped off a lot now that the U. S. elections are over (for this year). But there's still some interesting political science that came up before the big event.Even though political scientists, year in and year out, are as busy publishing as any other kind, quite a number of research announcements were noted recently outside of traditional professional venues. That has tapered off now, but there were a number of items that seem to call for some comment here. So I'll do some of that despite what is bound to be a declining interest in the subject.A perennial favorite of election-oriented political research centers around questions of how the appearance of a candidate affects electoral success. That's no different this year. Here's a fairly typical example:A Pretty Face Can Make A Difference In Whom You Vote For (10/30/08)According to new Northwestern University research, it is not at all surprising that everyone also is talking about the great looks of vice presidential hopeful Palin.Whether or not you believe the McCain campaign's $150,000 expenditure for Palin's wardrobe and the much-talked-about salary of her makeup artist are over the top, the decision to play up the looks of the former beauty queen is a winning strategy.Even in 2008, a perception of competence -- a strong predictor of whether people will vote for political candidates -- is not enough to give women the winning edge in political contests, according to the new Northwestern psychology study.For both men and women, female political candidates needed to be seen as attractive as well as competent to get their votes. ...While gender bias related to a female candidate's attractiveness was consistent across both male and female voters, good looks was almost all that mattered in predicting men's votes for female candidates. And, true to prevailing stereotypes, competence was almost all that mattered in predicting men's votes for male candidates.The idea that good looks positively affects electoral success has been researched many times – as well as being often suspected by a lot of people who aren't professional – in all kinds of elections from student councils on up. I discussed one study on this in a post here almost 2 years ago.The new research I want to examine here was not entirely, or even primarily, about the importance of attractiveness in winning elections. Instead, experimental participants were first asked to rate candidates independently, based on their photos, on four different attributes: "competence", "dominance", and "approachability", as well as "attractiveness".The politicians in question were actually candidates in 2006 U. S. Congressional elections. The politicians' photos were then presented in pairs actually competing with each other. Experiment participants were asked to chose which of each pair they would vote for if the office were actually the U. S. presidency.The resulting data were analyzed in various ways. First, in comparison of participants' voting choice to how they had rated the candidates on each of the four attributes. Second, in comparison of candidates' gender and facial appearance to actual Congressional election outcomes. And third, in comparison between how the candidates won or lost in the simulated presidential election and in the actual Congressional election. Since I want to focus just on the attractiveness issue, I won't attempt to summarize all the results here. You can find the summary in the research paper itself (citation below). I'll mention only two specific observations: (1) "Female candidates were more likely to win votes if they were more attractive." (2) "Male voters were significantly more likely to vote for candidates that appeared attractive." (I presume these statements represent correlations between opinions of attractiveness and voting behavior of each experimental participant.)Now, it may be true as the research asserts, that attractiveness matters more for female candidates, while a perceptions of "competence" is relatively more important for male candidates. However, the attractiveness of male candidates (especially in contests exclusively between two males) is a still a net positive. There's another possibility that should be considered even when voters seem to make their voting choices based on judgment of "competence" of male (or female, for that matter) candidates. Namely, that "attractiveness" (perhaps in a form not consciously associated with the term) might bias this judgment. One has to wonder exactly what visual characteristics might signify "competence" to voters, and whether certain factors – such as a "strong jawbone" (for a male) – don't contribute simultaneously to judgments of both attractiveness and competence.Humans are fairly sophisticated in making judgments about traits like "competence", since evaluations of other people's character and ability are important in deciding whom to trust. The ability to do this reliably has a lot of evolutionary importance. This doesn't mean people are infallible about such judgments – clearly they aren't. But people probably can do better than chance in making such judgments, at least when not faced with situations where the person being judged is skilled at faking appearances. Perhaps it's more a case of detecting lack of competence, as might be signaled by poorly managed facial expressions (e. g. simply looking perplexed or "stupid").But judgments about good looks and attractiveness are even more natural. We make them all the time, hardly giving any thought to the matter. Research has shown that people tend to make judgments about facial attractiveness very quickly. (See here.) This suggests people tend to use simple heuristics that may well be hard-wired.Research apparently shows that even babies prefer to stare at beautiful faces. Note, too, how illustrated children's literature (and now movies) usually portrays virtuous or heroic characters as beautiful or handsome, while evil or villainous characters are ugly, often very ugly, and much to be feared. So there may be an element of social conditioning here, at least for children beyond infancy.An interesting observation in the report of the research just mentioned, about the quickness of making judgments, is that "It seems that pretty faces 'prime' our minds to make us more likely to associate the pretty face with a positive emotion." ("Priming" is a hot topic in current psychological research.) So, comparatively speaking, a face that isn't "pretty" would be associated with less positive emotions. That alone would be enough to influence voting choices, if "everything else" is assumed to be equal.There are different possible factors that may enter into such a judgment. So let's consider further what factors and heuristics might be used in judging facial attractiveness. It would be quite interesting to know how the various factors about to be mentioned perhaps have different effects on political choice.A small number of factors are often suggested. One of the oldest is that the property of "youthfulness" is associated with attractiveness. That makes plenty of evolutionary sense, as fertility, reproductive capacity, and ability to nurture children all decline with age after the beginning of adulthood. It should be noted that youthfulness should be especially salient in the judgment of young people – such as the experimental subjects (college students, average age 19.5) in the research under discussion A more recent suggestion is that "symmetry" is important, as that would tend to indicate general healthiness. (Recent research here.) That makes sense, too, but does it have any reasonably apparent relevance to voting decisions?"Symmetry" is probably a looser criterion than in an older and fairly well-known theory of attractiveness, often called simply the "averageness" hypothesis. This holds that average phenotypes in a population are judged more attractive than phenotypes with notably atypical features. An average value on a particular facial metric (such as width of nose or chin) is considered to be what is "normal", yet for most features all to be close to average might be fairly unusual.So "averageness" is used in a somewhat special sense here – literally, as having size and proportion of most important facial features being close to the overall average. Probably faces that have "averageness" in this sense are fairly rare, which might add to the quality of "attractiveness". So "averageness" as a descriptor of faces is not the same as "common" or "ordinary" or "typical".Since averages of many faces will wipe out most asymmetry (e. g. some part being off center), an averaged face will be symmetrical. So facial symmetry is a more common characteristic than averageness. A symmetrical face could still have features that are far from average values in size or position.Since facial symmetry will be more common in a population than faces that have the property of averageness (in the special sense used here), averageness is a more stringent criterion for attractivness. Consequently, a voter who perceives one candidate's face as more attractive than the candidate's opponent is making a more significant discrimination, which could have higher weight in the final choice. Indeed, two candidates might have equally symmetrical faces, or at least faces that are difficult to distinguish in terms of symmetry, yet differ considerably in averageness and hence (perhaps) in attractiveness. And so, to the extent that people actually judge attractiveness based on averageness rather than symmetry, it will be more likely that judgment affects a voting decision. In other words, we would expect on these general considerations that attractiveness is more likely to affect voting decisions if the criterion is actually "averageness".There is some amount of research supporting the idea that averageness is the important criterion for attractiveness, such as findings that images created by averaging photographs of many individuals tend to receive higher ratings for attractiveness. So at least for the sake of discussion, let's assume there's some validity to this notion.Deviations from averageness do not imply deviations from symmetry, so they would not be expected to have the stronger negative implications for overall health and (hence) fertility that asymmetry does, so there would be a smaller indication of "riskiness". It would therefore be harder to understand the evolutionary importance of judging the riskiness of another person based on attractiveness if averageness is the underlying consideration. Is it possible that averageness is important in judging riskiness for other evolutionary reasons – reasons that apply to evaluating others in more general contexts than the context of mate selection?Yes, I think so. As I wrote in my previous post, "people who are considered attractive within a population are those who are most 'typical' or 'average'. Or inversely, least atypical, least different from the largest number of people in the population. People who are considered less attractive have facial features that vary a lot from the norm, such as lips that are too thin or too thick (compared to the average), eyes too far apart or too close together, eyebrows that are too sparse or too bushy."The evolutionary rationale at work here is that people who appear too "different" from the norm are more likely to belong to a different, more genetically distant tribe. Such people are probably less likely to deserve trust, and might even be "dangerous".I think this matter of perceived trustworthiness vs. potential "danger" in the eyes of voters could be rather important, especially if it is unconsciously inferred from perceptions of a candidate's attractiveness. I've written more on that here, not too long ago, so I won't repeat it now.More generally, I see conscious and unconscious issues of fear and perceived danger as especially important factors in a voter's attitudes towards, and relationship with, government. This is because, as a matter of both philosophy and sociology, one of the primary reasons for the existence of governments is to "protect" citizens from a variety of potential evils, whether they be dishonest businesspeople, common criminals, foreign and domestic terrorists, or whatever. I've written a lot more about that here.The question, then, is whether the research now under discussion supports the idea of a connection between fear and voting behavior, or is even relevant to it. To be honest, the relevance is somewhat tentative, since it relies on the idea that there is a negative correlation between the attractiveness of a political candidate and whether a voter feels fear associated with the candidate at some level. It would be very interesting to see more research that addresses this issue more directly.Regarding the present research itself, I have a few reservations as well. For example, the experimental participants were university students of average age 19.5 years. Quite possibly many of the participants had never even voted in a governmental election, and they certainly did not have a few decades of adult experience – with politicians, elections, and actual government performance – that could shape and inform their voting decisions. It's not surprising that individuals with little adult experience would base decisions on appearance factors.Aside from that, there's also the question of whether the socioeconomic demographics of university students would skew the results from what would be found in the electorate as a whole. And then there's the whole other issue of possibly relevant cultural differences between the U. S. and other democratic countries.So there's reason to suspect that typical, experienced voters, even in the U. S., might produce rather different results in a similar sort of experiment. Here's the research paper, with some of the abstract:The Political Gender Gap: Gender Bias in Facial Inferences that Predict Voting BehaviorContrary to the notion that people use deliberate, rational strategies when deciding whom to vote for in major political elections, research indicates that people use shallow decision heuristics, such as impressions of competence solely from a candidate's facial appearance, when deciding whom to vote for. Because gender has previously been shown to affect a number of inferences made from the face, here we investigated the hypothesis that gender of both voter and candidate affects the kinds of facial impressions that predict voting behavior.Joan Y. Chiao, Nicholas E. Bowman, Harleen Gill (2008). The Political Gender Gap: Gender Bias in Facial Inferences that Predict Voting Behavior PLoS ONE, 3 (10) DOI: 10.1371/journal.pone.0003666Update on 11/24/08: I have extensively reworked the discussion about "attractiveness" and its relationship to "symmetry" and "averageness". One would like to see more experimental evidence to sort out these factors in general and specifically as to how they affect voting choice.Tags: political science, political psychology, voting... Read more »
Joan Y. Chiao, Nicholas E. Bowman, & Harleen Gill. (2008) The Political Gender Gap: Gender Bias in Facial Inferences that Predict Voting Behavior. PLoS ONE, 3(10). DOI: 10.1371/journal.pone.0003666
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