The great autism research spotlight continues to focus its gazerbeam on the very earliest days of being for any clues governing why some children might go on to develop autism. I've kinda lost count of how many times I've talked about maternal exposure for this or that having been linked to an elevated risk of offspring autism; ranging from maternal inflammation to parental occupational exposure to the possibility that maternal medication history during pregnancy might singularly or cumulatively exert some potential effect on risk.Baby @ Wikipedia Indeed this last factor on medication during pregnancy has once again been the source of some speculation following the publication of a paper by Bromley and colleagues* suggesting an increased risk of offspring autism in cases of exposure to various antiepileptic drugs in-utero.A quick search of PubMed reveals that Dr Bromley has some history in looking at foetal antiepileptic exposure on developmental outcomes as per papers like this one and this one (open-access). There were a few clues in these papers that autism and other developmental disorders might well have been next on the list for investigation for this research group.Press attention for the current study? Er, yes, it goes without saying particularly in light of headlines like: Epilepsy drug linked to tenfold increase in autism (complete with picture of pregnant mums holding their tummy) and Epilepsy drug link to brain damage in 17,500 babies. Aside from thinking that there is probably lots of money to be made in stock photos of pregnant women and their bumps, if I were a pregnant mum with epilepsy taking such meds, I would probably be straight on the phone to my doctor/midwife to ask about these findings.So what did Bromley et al actually find and report:Based on an analysis of children born to 528 pregnant mums based here in Blighty, physical and cognitive abilities were assessed at various point during early infancy and childhood.Of the total cohort, data across various testing points were available for 415 children; of which 19 had been diagnosed with a "neurodevelopmental disorder" by the age of 6 years.Some of these neurodevelopmental disorders included autism (n=12); others had diagnoses of conditions like ADHD and dyspraxia (developmental coordination disorder, DCD).Looking through the kind of meds being taken by mum's during pregnancy, the authors reported a connection between greater offspring neurodevelopmental issues in those mothers who were taking anti-epileptic medication compared to those who weren't (7.4% vs. 1.8% respectively) as per the rate of epilepsy in mums-to-be (243/528; 46%).Sodium valproate was in particular singled out as part of the study as per the text: "children exposed to valproate alone in the womb were six times more likely to be diagnosed with a neurodevelopmental disorder". Indeed an even greater risk if a cocktail of other meds were also used during pregnancy.As one would expect, the authors have cautioned that pregnant women with epilepsy taking these medications does not automatically translate into offspring autism and on no account should pregnant women just stop taking the drug without appropriate medical advice. Risk, as I have discussed before, is risk not certainty and epilepsy can be a life-threatening condition.Valproate has already some history with regards to its possible effects on the developing infant as per the description of foetal valproate syndrome** (open-access) highlighting its potential teratogenicity. With autism in mind, this is also not the first time that valproate has appeared in the research texts. I note for example papers like this one from Bristot Silvestrin and colleagues*** which talked about an "animal model of autism induced by prenatal exposure to valproate", also bringing in words like 'glutamate' which has also seen its fair share of scientific inquiry in recent times (see this post). There are several other papers I could cite with a valproate-autism connection but I don't want to bore you.Valproate is also a compound I've become quite interested in recently as a result of being part of some very brief forays into the science writing domain and in particular on the topic of epigenetics (see here but now for PJ members only). Since doing a little bit of research in that area I've for example, read quite a bit on how valproate is now considered to be quite a potent HDAC inhibitor**** (open-access) with some potentially useful effects in cancer therapy. This HDAC inhibition quality - leading on to histone hyperacetylation - has also been questioned as a possible route towards some of the autism-like findings. To quote from the paper by Kataoka and colleagues***** "findings suggest that VPA-induced histone hyperacetylation plays a key role in cortical pathology and abnormal autism-like behaviours in mice". Bearing in mind mice are mice and not humans.The Bromley paper is an interesting paper and certainly invites a lot more study into how prenatal valproate exposure *might* show some connection to offspring risk of autism and other developmental conditions. Not trying to be anti-medication or anything, the study also highlights how little we actually know about the medicines we take and in particular their potential for things like trans-generational effects...----------* Bromley RL. et al. The prevalence of neurodevelopmental disorders in children prenatally exposed to antiepileptic drugs. J Neurol Neurosurg Psychiatry. January 2013.** Kini U. Fetal valproate syndrome: a review. Pediatric & Perinatal Drug Therapy. 2006; 7: 123-130.*** Bristot Silvestrin R. et al. Animal model of autism induced by prenatal exposure to valproate: Altered glutamate metabolism in the hippocampus. Brain Res. 2013; 1495: 52-60.**** Göttlicher M. et al. Valproic acid defines a novel class of HDAC inhibitors inducing differentiation of transformed cells. EMBO J. 2001;20:6969–6978.***** Kataoka S. et al. Autism-like behaviours with transient histone hyperacetylation in mice treated prenatally with valproic acid. Int J Neuropsychopharmacol. 2013; 16: 91-103.----------... Read more »
Bromley, R., Mawer, G., Briggs, M., Cheyne, C., Clayton-Smith, J., Garcia-Finana, M., Kneen, R., Lucas, S., Shallcross, R., Baker, G.... (2013) The prevalence of neurodevelopmental disorders in children prenatally exposed to antiepileptic drugs. Journal of Neurology, Neurosurgery . DOI: 10.1136/jnnp-2012-304270
No doubt alongside quite a few others, I was interested to read the latest paper from Richard Frye and colleagues* (open-access) discussing the potential links between an animal model of autism spectrum disorder (ASD) and real-world ASD in a particular cohort of participants.This is not the first time that I've talked about (a) the work of Dr Frye - as per my [don't panic] post on folate receptor autoantibodies in cases of autism (see here) and (b) some of the difficulties attached to translating rat/mouse model findings in autism research into 'real-world' findings (see here). Indeed this last point might also tie into my recent musings on the use of LPS in autism research (see here).Daddy o' microbiology @ Wikipedia My interest in the latest Frye paper was further piqued upon realising that Derrick MacFabe was also part of the authorship team given his insightful work on how administration of propionic acid - a short chain fatty acid - to rodents might provide some interesting perspectives overlapping with various findings noted in cases of autism (see my previous post here).The Frye paper is open-access and available to all but here are a few points worth mentioning:Based on the animal model work looking at propionic acid (PPA) infusions and some of the collected effects (presentation of autism-type behaviours**, mitochondrial issues***, abnormal measures of glutathione, etc.), the aim of the current study was to map out whether some of the observations in the PPA rodent model were also present in real-life autism.Based on a clinic-based sample of children with autism (N=326), acyl-carnitine panels were conducted on about two-thirds of participants (n=213).Acyl-carnitines, as their name suggests, are related to carnitine which has previously been tied back to autism (see here) and represent a number of different compounds - complexes of carnitine and various fatty acids - involved in the transport of fatty acids into the mitochondrial matrix.The previous PPA rodent model indicated some disturbance in the amount of various acyl-carnitines, particularly with regards to short- and long-chain fatty acids (not so much in the medium-chain fatty acids) reflective of some mitochondrial dysfunction.So the authors looked at short-, medium- and long-chain acyl-carnitines in their autism cohort to see if there were any overlaps compared with the PPA treated animals.Results: 35% of the autism cohort showed "an increase in three or more acyl-carnitines when initially measured". When further testing were conducted on some of these participants showing elevation, this figure was revised to 17% of the cohort who "demonstrated consistent elevations in short-chain and long-chain, but not medium-chain, acyl-carnitines". You'll note the similarity with PPA animal model in terms of the short- and long-chain acyl-carnitines.Furthermore, four participants were also examined with regards to glutathione and oxidative stress markers. As per the quite consistent literature on things like total- and free-reduced glutathione (see this post), compared with controls, there were some familiar trends emerging.And relax.There is a lot to take in from this paper both in the protocol and testing undertaken and the possible interpretation of findings. A quote best sums up the results: "This study has demonstrated that ~17% of children with ASD manifest biomarkers of abnormal mitochondrial fatty-acid metabolism that parallel similar biomarkers in the PPA rodent model of ASD".As perhaps expected, there has been some press attention following the publication of this paper. The headline: Researchers discover link between certain types of autism and gut bacteria has been a common one, reflective of the fact that when it comes to the production of PPA outside of injecting the stuff directly into the rodent brain, the gut and in particular, certain types of gut bacteria, have been suggested as a route to PPA production in cases of autism. Indeed, I'm taken back to the findings by Wang and colleagues from Oz (see this post) on levels of fecal short chain fatty acids (SCFAs) in their cohort of children with autism which included propionic acid (propionate). I'm also reliably informed that there is 'more to come' from the Australian research group in the coming months.There are a few final aspects to the Frye study which I should have mentioned earlier. This includes the notion that "it is very likely that MD [mitochondrial dysfunction] is acquired" given that in the most part, both nuclear and mitochondrial DNA examinations in their cohort were negative for anything that might genetically account for the results. I'll be coming to DNA and mitochondrial issues in a subsequent 'training' post scheduled quite soon but one can perhaps see how this might strengthen any argument of disruptions to gut bacteria/microflora facilitating the production of elevated PPA onwards to disrupting acyl-carnitine chemistry. Additionally there is the implication based on the PPA rodent model that affecting PPA production could be a potential therapeutic route for some cases of autism at some point. I don't really want to go too far into the hows and whys of this suggestion at the current time given the current lack of evidence for any effect. Aside that is, from drawing your attention to a related field of inquiry into how disrupting PPA-producing gut bacteria might have some important implications for those suffering from conditions like propionic acidaemia****.I'm not going to get too carried away with the Frye results as they stand. As per my previous post on PPA, there is still a bit of a stretch from injecting rodent brains with PPA and recording outcomes to suggesting that gut bacteria will be able to produce enough PPA so as to exert a similar effect in humans. At least one group is asking the same question***** (open-access). That being said, I am still interested in the details of this study and how the authors have at least tried to model animal findings into real-life autism. Indeed how we really should be putting a lot more research effort into looking at mitochondria and autism as we potentially also should gut bacteria and autism.A song to finish... something mellow yet catchy.... Lovefool by the Cardigans.----------* Frye RE. et al. Unique acyl-carnitine profiles are potential biomarkers for acquired mitochondrial disease in autism spectrum disorder. Translational Psychiatry. 2013; 3: e220.** MacFabe DF. et al. Effects of the enteric bacterial metabolic product propionic acid on object-directed behavior, social behavior, cognition, and neuroinflammation in adolescent rats: Relevance to autism spectrum disorder. Behav Brain Res. 2011; 217: 47-54.*** Thomas RH. et al. Altered brain phospholipid and acylcarnitine profiles in propionic acid infused rodents: further development of a potential model of autism spectrum disorders. J Neurochem. 2010; 113: 515-529.**** Mellon AF. et al. Effect of oral antibiotics on intestinal production of propionic acid. Arch Dis Child 2000; 82: 169-172.***** El-Ansary AK. et al. C... Read more »
Frye RE, Melnyk S, & Macfabe DF. (2013) Unique acyl-carnitine profiles are potential biomarkers for acquired mitochondrial disease in autism spectrum disorder. Translational psychiatry. PMID: 23340503
Today in LabLulz, I’m going to walk through a recent preparation I did in my chemistry lab: increasing and measuring the concentration of hydrogen peroxide. WARNING: This procedure involves heat and the end product is a powerful oxidizer. Don’t get burned and don’t get it on yourself – wear gloves, splash-resistant goggles, and an apron. […]... Read more »
Easton, M., Mitchell, A., & Wynne-Jones, W. (1952) The behaviour of mixtures of hydrogen peroxide and water. Part 1.?Determination of the densities of mixtures of hydrogen peroxide and water. Transactions of the Faraday Society, 796. DOI: 10.1039/TF9524800796
Since 2007 when terahertz pulsed imaging (TPI) was first developed to non-destructively measure the coating thickness of pharmaceutical tablets there has been intense research in the PSSRC into how this technique can help improve the quality of pharmaceutical coatings and thus make controlled release technology based on coatings of single dosage forms attractive to industry.... Read more »
Zeitler, J., Shen, Y., Baker, C., Taday, P., Pepper, M., & Rades, T. (2007) Analysis of coating structures and interfaces in solid oral dosage forms by three dimensional terahertz pulsed imaging. Journal of Pharmaceutical Sciences, 96(2), 330-340. DOI: 10.1002/jps.20789
Brock, D., Zeitler, J., Funke, A., Knop, K., & Kleinebudde, P. (2012) A comparison of quality control methods for active coating processes. International Journal of Pharmaceutics, 439(1-2), 289-295. DOI: 10.1016/j.ijpharm.2012.09.021
The seafloor has no shortage of spiky wildlife or hairy mysteries. One such mystery is logistical: where do the animals that live around deep-sea vents and cold seeps come from?
On the black and generally barren bottom of the ocean, food is scarce. Hydrothermal vents and cold seeps—places where methane, sulfides and other chemical goodies leak out of the seafloor—are like desert oases. Whole communities of weird creatures that live on these chemicals rather than the sun cluster around them.
Researchers think big pieces of organic junk that fall to the bottom of the ocean, such as sunken ships and deceased whales (called "whale falls"), may act as stepping stones for these communities. Species might disperse from one seafloor chimney to the next via a visit to a wrecked ship.
"Wood is a foreign substance in the deep sea," says Christina Bienhold of the Max Planck Institute. To find out whether resourceful ocean critters can easily make use of wood that falls into the ocean, she and other researchers dropped some in. They rigged together small heaps of Douglas fir logs, weighted them with cement, and carried them a mile down into the Mediterranean.
The researchers used four wood piles, each two meters long. They were at various distances from a known cold seep. The closest log was 70 meters away—so if any animals scooted over from that community, it would be a bit of a trek.
One of the wood heaps was sampled just one day later. (It looked the same.) The other three rested on the ocean floor for a year before robotic vehicles returned to collect wood samples and scoop up the animals that had moved in.
And did they ever move in. Bienhold was surprised to find that her logs, after only a year on the seafloor, held thriving colonies of wildlife.
The logs' most abundant tenants were wood-boring bivalves called Xylophaga, or "shipworms." Built like a worm with a shell on one end, these mollusks burrow into wood while symbiotic bacteria help them digest it. All around the logs were evidence of their work: the researchers observed a layer of "fine wood chips and fecal matter" two to four centimeters thick.
The shipworms seemed to have attracted other animals interested in feeding on the mollusks themselves or on the waste piles they left everywhere. As these creatures ate and respired, they used up oxygen in the water and allowed oxygen-hating bacteria to move in. These bacteria created pockets of sulfides—food for the kinds of animals that live at cold seeps or hydrothermal vents. (Normally, they would find this food coming straight out of the ground.)
Like very unattractive doves out of a hat, those animals began to materialize out of the blackness of the ocean. Clustered around the logs were sea urchins, fish, and deep-sea mussels and crabs. There were small crustaceans that couldn't be identified, and several types of worms, including two brand-new species.
All three wood piles had similar animal communities living on and around (and, in the case of the crabs, hiding underneath) them. Their bacterial communities were more diverse. But they all included bacteria that could break down the cellulose in wood, as well as bacteria that consume sulfate instead of oxygen.
Bienhold says her results show how wood that falls to the seafloor can create hotspots of ocean life. Hunks of organic trash like her log piles, even though they're few and far between on the bottom of the ocean, could help rare deep-sea species to spread. The key player in her set of experiments was the little wood-boring bivalve that moved in first and made the logs into a habitat that other wildlife could use.
"It remains enigmatic," Bienhold says, how the wood-borers (or any of the other organisms) found this new habitat in the first place. The researchers observed a greater density of sea urchins as they got closer to the wood piles; they seemed to be attracted to the wood by some chemical signal. Sea urchins and other animals may sniff out chemical cues from afar that help them find organic matter. For now, though, the secret remains sealed in their lipless bodies.
Bienhold C, Pop Ristova P, Wenzhöfer F, Dittmar T, & Boetius A (2013). How deep-sea wood falls sustain chemosynthetic life. PloS one, 8 (1) PMID: 23301092
Image: Sea urchins, courtesy of New Zealand-American Submarine Ring of Fire 2005 Exploration, NOAA Vents Program.
... Read more »
Bienhold C, Pop Ristova P, Wenzhöfer F, Dittmar T, & Boetius A. (2013) How deep-sea wood falls sustain chemosynthetic life. PloS one, 8(1). PMID: 23301092
Scientists have reassured that the proton is 4% smaller than the previous research findings.
This research has been published online in the journal Science.
Although the new research has decreased the weight of the proton but the same new research has increased the chances of finding the new particles and/or forces.
Before 2010, there were only two methods for measuring the size of the proton. One was firing the electron beams at protons and measuring the deflection, and the other method was studying the behavior of electrons in hydrogen atoms. Both the methods showed that the radius of proton is nearly 0.88 femtometers, or 0.88 quadrillionths of a meter.
In 2010, scientists developed a new technique to check the proton size in which the muons, instead of electrons, were studied in hydrogen atoms. Muons are the elementary particles with 200 times the mass of the electron. After using this new technique, physicist Aldo Antognini at ETH Zurich and his team published a paper in Nature in which they reported that the proton’s radius is 0.84 femtometers i.e. about 4% less than previous measurements.
Now after more than two years, scientists used the technique and re-examined the size of proton that eliminates the possibility of certain systematic errors and decreases the measurement’s uncertainty by 40%.
“This shows that our experiment is consistent and that there were no mistakes,” Antognini said in a statement.
Antognini, A., Nez, F., Schuhmann, K., Amaro, F., Biraben, F., Cardoso, J., Covita, D., Dax, A., Dhawan, S., Diepold, M., Fernandes, L., Giesen, A., Gouvea, A., Graf, T., Hansch, T., Indelicato, P., Julien, L., Kao, C., Knowles, P., Kottmann, F., Le Bigot, E., Liu, Y., Lopes, J., Ludhova, L., Monteiro, C., Mulhauser, F., Nebel, T., Rabinowitz, P., dos Santos, J., Schaller, L., Schwob, C., Taqqu, D., Veloso, J., Vogelsang, J., & Pohl, R. (2013). Proton Structure from the Measurement of 2S-2P Transition Frequencies of Muonic Hydrogen Science, 339 (6118), 417-420 DOI: 10.1126/science.1230016... Read more »
Antognini, A., Nez, F., Schuhmann, K., Amaro, F., Biraben, F., Cardoso, J., Covita, D., Dax, A., Dhawan, S., Diepold, M.... (2013) Proton Structure from the Measurement of 2S-2P Transition Frequencies of Muonic Hydrogen. Science, 339(6118), 417-420. DOI: 10.1126/science.1230016
And now, the final step in how to build your computational model of a neuron: Add Synaptic Channels. All the steps in this series can be found here.Synapses connect neurons (source)So you already have a neuron, and you've added intrinsic channels to it. The next thing you want to do is add synaptic channels so you can hook this neuron up to other cells.The main synaptic channels you want to add are the excitatory channels: NMDA and AMPA and the inhibitory channel GABA. These channels don't have the same kind of activation and inactivation curves and the intrinsic channels do because they aren't activated by voltage, they are activated by a neurotransmitter. AMPA and NMDA receptors are activated primarily by glutamate, and cause an influx of sodium and calcium ions. Since both sodium and calcium ions are positively charged, this depolarizes the cell membrane and brings it closer to firing an action potential.AMPA receptors (source)GABA receptors, on the other hand are primarily activated by GABA, and cause and influx of chloride ions into the cell. Because chloride ions are negatively charged, this hyperpolarizes the cell membrane and brings it further away from firing an action potential.So if you want to have a realistic model of a neuron, you need to add an approximation of these channels. This is easier than adding intrinsic channels, because it is an on/off style (binary) rather than an analogue activation. So basically you just put in the parameters you want like how fast does the channel open and close, how much current does it allow through when activated, and where are they on the neuron.Of course deciding these parameters is not always easy. A paper out this year in PLoS Computational Biology describes 4 different ways the NMDA receptor can be configured and analyzes the consequences during different stimulation patterns. Evans et al., (2012) Figure 3The 4 NMDA configurations (based on the 4 different GluN2 subunits) vary in their sensitivity to a magnesium block, how fast they decay, and their maximal current. Above are their responses to the same stimulation patterns (an STDP protocol). Even though they were all receiving the same input pattern, they each show a very different response.So when considering adding synaptic channels to your model neuron, take the time to find out what the configuration of the receptors should actually be in the type of neuron you are building. © TheCellularScaleIf you are good at following clues, you will realize that I am very, very familiar with this paper. Evans RC, Morera-Herreras T, Cui Y, Du K, Sheehan T, Kotaleski JH, Venance L, & Blackwell KT (2012). The effects of NMDA subunit composition on calcium influx and spike timing-dependent plasticity in striatal medium spiny neurons. PLoS computational biology, 8 (4) PMID: 22536151... Read more »
Evans RC, Morera-Herreras T, Cui Y, Du K, Sheehan T, Kotaleski JH, Venance L, & Blackwell KT. (2012) The effects of NMDA subunit composition on calcium influx and spike timing-dependent plasticity in striatal medium spiny neurons. PLoS computational biology, 8(4). PMID: 22536151
One of the most important take home messages of this work is that we need get rid of the common “oxidants are bad guys and antioxidants are good guys” myth. Oxidants can be harmful in some context, but they can also serve as important regenerative signals. Indiscriminate use of antioxidants can actually impair these important endogenous signals. Instead of consuming large quantities of non-specific antioxidants, we need to use antioxidants in a very targeted, context-specific and perhaps time-limited manner so that they only prevent oxidative damage without affecting beneficial oxidant signaling.... Read more »
Love, N., Chen, Y., Ishibashi, S., Kritsiligkou, P., Lea, R., Koh, Y., Gallop, J., Dorey, K., & Amaya, E. (2013) Amputation-induced reactive oxygen species are required for successful Xenopus tadpole tail regeneration. Nature Cell Biology. DOI: 10.1038/ncb2659
Before I moved to my current position in Maastricht, I had the great pleasure to work with Prof. Roland Grafström (check his pathway bioinformatics done with his then PhD Rebecca) and Prof. Bengt Fadeel at the Karolinska Institutet. During this year I part-time worked on ToxBank and part-time on nano-QSAR, and worked on semantics, predictive toxicology, and Open Data. This blog post is about the ToxBank work.
I promised firework, and the first rockets are heading upwards: a key ToxBank paper has now been published in Molecular Informatics. Pekka Kohonen wrote up a nice overview of the ToxBank project, the current platform (based on RDF, REST, ISATab, and OpenTox (my archives)), and the test compounds that the SEURAT-1 cluster identified. Various bioinformatics approaches were used to visualize the diversity of the selected compounds. The idea is that the all EU FP7 projects in the SEURAT-1 cluster (consisting of six consortia) will test at least these compounds, creating a rich data set of toxicology-related data for these compounds.
As a temporary, quick solution I proposed the Semantic MediaWiki to create a semantic knowledge base, which was extensively and very productively continued by David from Leadscope. This way, we could easily list all compounds, by doing a search, rather than manually adding them:
Each compound has extensive information on the mode of action, physicochemical properties and more (such as here for acetaminophen):
All this information is available as semantic data. For example, check this link. Network and Gene Ontology analyses on these compounds have been performed, and presented in the paper, further confirming the diversity of the compound set. This leads to possible integration of their work with WikPathways and PathVisio, and I will do my best to get the right people talking to each other.
The ToxBank project further develops Open Source software for an online data warehouse for hosting experimental data on these compounds. A mix of approaches is used here to base their warehouse on, including OpenTox (RDF and REST(-like)-based), ISATab, and various ontologies.
In designing their software, they use a pretty unique approach for EU projects, based on formal requirement analyses protocols, resulting in a user-oriented platform. Now, there is much to say about who the user is, and in fact, there are multiple user types, called personas, and ToxBank takes that idea into account.
Therefore, in many ways, ToxBank is, in my humble but somewhat biased opinion, a project that leads the (predictive) toxicology community into a new era. Congratulations to the full ToxBank consortium! It was great being part of it!
Kohonen, P., Benfenati, E., Bower, D., Ceder, R., Crump, M., Cross, K., Grafström, R., Healy, L., Helma, C., Jeliazkova, N., Jeliazkov, V., Maggioni, S., Miller, S., Myatt, G., Rautenberg, M., Stacey, G., Willighagen, E., Wiseman, J., & Hardy, B. (2013). The ToxBank Data Warehouse: Supporting the Replacement of In Vivo Repeated Dose Systemic Toxicity Testing Molecular Informatics DOI: 10.1002/minf.201200114... Read more »
Kohonen, P., Benfenati, E., Bower, D., Ceder, R., Crump, M., Cross, K., Grafström, R., Healy, L., Helma, C., Jeliazkova, N.... (2013) The ToxBank Data Warehouse: Supporting the Replacement of In Vivo Repeated Dose Systemic Toxicity Testing. Molecular Informatics. DOI: 10.1002/minf.201200114
A while ago I wrote about how bacteria make their way into clouds, where they act as seeds around which …Continue reading »... Read more »
Vaitilingom, M., Deguillaume, L., Vinatier, V., Sancelme, M., Amato, P., Chaumerliac, N., & Delort, A. (2012) Potential impact of microbial activity on the oxidant capacity and organic carbon budget in clouds. Proceedings of the National Academy of Sciences, 110(2), 559-564. DOI: 10.1073/pnas.1205743110
In 1953, Cambridge researchers Watson and Crick published a paper describing the interweaving ‘double helix’ DNA structure – the chemical code for all life.
Now, in the year of that scientific landmark’s 60thAnniversary, Cambridge researchers have published a paper proving that four-stranded ‘quadruple helix’ DNA structures – known as G-quadruplexes – also exist within the human genome. They form in regions of DNA that are rich in the building block guanine, usually abbreviated to ‘G’.... Read more »
Fred Lewsey. (2013) Four-stranded ‘quadruple helix’ DNA structure proven to exist in human cells. University of Cambridge. info:/
The enormously diverse complexity seen amongst individual species within the animal kingdom evolved from a surprisingly small gene pool. For example, mice effectively serve as medical research models because humans and mice share 80-percent of the same protein-coding genes. The key to morphological and behavioral complexity, a growing body of scientific evidence suggests, is the regulation of gene expression by a family of DNA-binding proteins called “transcription factors.” Now, a team of researchers with the U.S. Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) and the University of California (UC) Berkeley has discovered the secret behind how one these critical transcription factors is able to perform – a split personality.... Read more »
Lynn Yarris. (2013) New Key to Organism Complexity Identified. Berkeley Lab News Center. info:/
Rice University’s latest nanotechnology breakthrough was more than 10 years in the making, but it still came with a shock. Scientists from Rice, the Dutch firm Teijin Aramid, the U.S. Air Force and Israel’s Technion Institute this week unveiled a new carbon nanotube (CNT) fiber that looks and acts like textile thread and conducts electricity and heat like a metal wire. In this week’s issue of Science, the researchers describe an industrially scalable process for making the threadlike fibers, which outperform commercially available high-performance materials in a number of ways.... Read more »
Jade Boyd. (2013) New nanotech fiber: Robust handling, shocking performance. Rice University News. info:/
Again it is time for me to answer some questions. As always, these are real true 'search terms' that have resulted in some one finding The Cellular Scale. While some questions (like 'how do you build a model of a neuron') are answered by this blog, the ones I answer is these LMAYQ posts are almost certainly not. All the questions and answers in this series can be found in the Let Me Answer Your Questions index.Drawing by Grave Unicorn1. "Why do I like ketamine so much?"This is actually a pretty interesting question. Ketamine is a psychoactive drug known to cause hallucinations and feelings of dissociation, but it's not thought to be super-addictive in the same way that heroin or cocaine are thought to be. So why do you like it? First let me get a 'safety warning' out of the way. Even though research is currently being conducted to investigate ketamine as an acute anti-depressant and to investigate its possible role in neurogenesis, it is not all considered a safe drug. It can seriously damage your urinary system for one thing, and probably damages your brain. Don't take it. Ketamine (source)Having said that, ketamine might give you a 'good feeling' because it is a partial agonist (meaning helps activate) the dopamine D2 receptor and the serotonin 5-HT2 receptor. In 2002, Kapur and Seeman published a paper showing that ketamine (and PCP) affects the dopamine and serotonin system by binding to these specific receptors. However dopamine is a confusing molecule and the idea that ketamine activates the D2 dopamine receptors does not necessarily mean 'pleasure.'A classic test of 'wanting something' in rats is the self-administration paradigm, where rats can press a lever and get a dose of some drug or an electrical stimulation directly into the brain. A recent paper by De Luca and Badiani (2011) shows that rats will self administer ketamine when given the chance. Interestingly, they found that the amount of self-administration was much higher when they took the rat out of its cage and put it somewhere new for the self-administration session. When the rat was allowed to self-administer ketamine in its home cage it just didn't give itself as much.So your 'liking' of ketamine might have to do with where you are when you do it.Kapur S, & Seeman P (2002). NMDA receptor antagonists ketamine and PCP have direct effects on the dopamine D(2) and serotonin 5-HT(2)receptors-implications for models of schizophrenia. Molecular psychiatry, 7 (8), 837-44 PMID: 12232776De Luca MT, & Badiani A (2011). Ketamine self-administration in the rat: evidence for a critical role of setting. Psychopharmacology, 214 (2), 549-56 PMID: 210695152. "What do neurons like?"This question cracks me up because it reminds me of two personal anecdotes. First it reminds me of one of my professors who just can't stand when people say "the neurons behaved this way or that way." The idea being that behavior is a thing animals do, not a thing that neurons do. I basically agree that neurons don't behave per se, but I also don't really care if someone wants to 'be cute' by anthropomorphizing a cell.Second, thinking about neurons 'liking' things or being happy reminds me of a yoga class when during the final relaxation segment, the teacher started saying things like 'You are happy. Your cells are happy, they are all smiling at each other.' It was hard for me to relax and let my cells smile at each other when all my willpower was being engaged preventing me from bursting into laughter. Regardless, I will do my best to answer this question. I suppose, neurons 'like' glucose, which gives them energy. Other than that I don't think it's meaningful to talk about neurons liking things.3. "Why do men like big women?" This is one of a long string of questions that resulted from me having the words 'small', 'men', 'like', 'big', and 'women' all in the title of a post. As you might imagine, this is far from the worst 'search term' that has dropped people onto that page.And believe it or not, this question has a scientific answer.A paper this year by Swami and Tovee (2012) investigates the influence of stress in men's judgement of women's bodies. They found that men who were stressed for just 15 minutes (by being forced to give a speech explaining how suitable they are for a job) found 'bigger' women more attractive than the men who were not stressed did. Poor guy, if only he had a nice motherly type to cook him a pie. (source)The 'explanation' could be (though this is speculation, of course) that bigger women represent more 'security.'"The Environmental Security Hypothesis –... Read more »
Kapur S, & Seeman P. (2002) NMDA receptor antagonists ketamine and PCP have direct effects on the dopamine D(2) and serotonin 5-HT(2)receptors-implications for models of schizophrenia. Molecular psychiatry, 7(8), 837-44. PMID: 12232776
De Luca MT, & Badiani A. (2011) Ketamine self-administration in the rat: evidence for a critical role of setting. Psychopharmacology, 214(2), 549-56. PMID: 21069515
Swami V, & Tovée MJ. (2012) The impact of psychological stress on men's judgements of female body size. PloS one, 7(8). PMID: 22905153
Researchers still have much to learn about the volcanism that shaped our planet’s early history. New evidence from a team led by Carnegie’s Frances Jenner demonstrates that some of the tectonic processes driving volcanic activity, such as those taking place today, were occurring as early as 3.8 billion years ago. Their work is published in Geology [...]... Read more »
Jenner, F., Bennett, V., Yaxley, G., Friend, C., & Nebel, O. (2013) Eoarchean within-plate basalts from southwest Greenland. Geology. DOI: 10.1130/G33787.1
Sometimes the most amazing discoveries are those that occur completely by accident. Which is very much the case of a new energy source that has been discovered by a team from MIT in the form of a polymer film. How could a polymer film generate electricity? That’s about where the unexpected part begins.... Read more »
Ma, M., Guo, L., Anderson, D., & Langer, R. (2013) Bio-Inspired Polymer Composite Actuator and Generator Driven by Water Gradients. Science, 339(6116), 186-189. DOI: 10.1126/science.1230262
Don't trust your weighing scale too much, it might nog be that accurate anymore.... Read more »
Cumpson, P., & Sano, N. (2013) Stability of reference masses V: UV/ozone treatment of gold and platinum surfaces. Metrologia, 50(1), 27-36. DOI: 10.1088/0026-1394/50/1/27
The protoplanet Vesta has been witness to an eventful past: images taken by the framing camera onboard NASA’s space probe Dawn show two enormous craters in the southern hemisphere. The images were obtained during Dawn’s year-long visit to Vesta that ended in September 2012. These huge impacts not only altered Vesta’s shape, but also its surface composition. Scientists under the lead of the Max Planck Institute for Solar System Research in Katlenburg-Lindau in Germany have shown that impacting small asteroids delivered dark, carbonaceous material to the protoplanet. In the early days of our solar system, similar events may have provided the inner planets such as Earth with carbon, an essential building block for organic molecules.... Read more »
Max Planck Institute. (2013) Carbon in Vesta's craters. Max Planck Institute Astronomy News. info:/
The U.S. Department of Energy’s (DOE) National Renewable Energy Laboratory (NREL) will help develop microbes that convert methane found in natural gas into liquid diesel fuel, a novel approach that if successful could reduce greenhouse gas emissions and lower dependence on foreign oil.... Read more »
NREL Public Relations. (2013) NREL to Help Convert Methane to Liquid Diesel. NREL Newsroom. info:/
As promised, here are my favorite posts from each month.January: The Human Neuron" not so special after all?Butti C, Santos M, Uppal N, & Hof PR (2011). Von Economo neurons: Clinical and evolutionary perspectives. Cortex; a journal devoted to the study of the nervous system and behavior PMID: 22130090February: If you give a mouse a placebo...Wise RA, Wang B, & You ZB (2008). Cocaine serves as a peripheral interoceptive conditioned stimulus for central glutamate and dopamine release. PloS one, 3 (8) PMID: 18682722 March: Plant neurons: Sensation and Action in the Venus FlytrapBenolken RM, & Jacobson SL (1970). Response properties of a sensory hair excised from Venus's flytrap. The Journal of general physiology, 56 (1), 64-82 PMID: 5514161Volkov AG, Adesina T, & Jovanov E (2007). Closing of venus flytrap by electrical stimulation of motor cells. Plant signaling & behavior, 2 (3), 139-45 PMID: 19516982 Forterre Y, Skotheim JM, Dumais J, & Mahadevan L (2005). How the Venus flytrap snaps. Nature, 433 (7024), 421-5 PMID: 15674293... Read more »
Butti C, Santos M, Uppal N, & Hof PR. (2011) Von Economo neurons: Clinical and evolutionary perspectives. Cortex; a journal devoted to the study of the nervous system and behavior. PMID: 22130090
Benolken RM, & Jacobson SL. (1970) Response properties of a sensory hair excised from Venus's flytrap. The Journal of general physiology, 56(1), 64-82. PMID: 5514161
Volkov AG, Adesina T, & Jovanov E. (2007) Closing of venus flytrap by electrical stimulation of motor cells. Plant signaling , 2(3), 139-45. PMID: 19516982
Kindt M, Soeter M, & Vervliet B. (2009) Beyond extinction: erasing human fear responses and preventing the return of fear. Nature neuroscience, 12(3), 256-8. PMID: 19219038
Kim IJ, Zhang Y, Yamagata M, Meister M, & Sanes JR. (2008) Molecular identification of a retinal cell type that responds to upward motion. Nature, 452(7186), 478-82. PMID: 18368118
Kay JN, De la Huerta I, Kim IJ, Zhang Y, Yamagata M, Chu MW, Meister M, & Sanes JR. (2011) Retinal ganglion cells with distinct directional preferences differ in molecular identity, structure, and central projections. The Journal of neuroscience : the official journal of the Society for Neuroscience, 31(21), 7753-62. PMID: 21613488
Kraskov A, Dancause N, Quallo MM, Shepherd S, & Lemon RN. (2009) Corticospinal neurons in macaque ventral premotor cortex with mirror properties: a potential mechanism for action suppression?. Neuron, 64(6), 922-30. PMID: 20064397
Blackiston DJ, Silva Casey E, & Weiss MR. (2008) Retention of memory through metamorphosis: can a moth remember what it learned as a caterpillar?. PloS one, 3(3). PMID: 18320055
Marx M, Günter RH, Hucko W, Radnikow G, & Feldmeyer D. (2012) Improved biocytin labeling and neuronal 3D reconstruction. Nature protocols, 7(2), 394-407. PMID: 22301777
Triana-Del Rio R, Montero-Domínguez F, Cibrian-Llanderal T, Tecamachaltzi-Silvaran MB, Garcia LI, Manzo J, Hernandez ME, & Coria-Avila GA. (2011) Same-sex cohabitation under the effects of quinpirole induces a conditioned socio-sexual partner preference in males, but not in female rats. Pharmacology, biochemistry, and behavior, 99(4), 604-13. PMID: 21704064
Labour MN, Banc A, Tourrette A, Cunin F, Verdier JM, Devoisselle JM, Marcilhac A, & Belamie E. (2012) Thick collagen-based 3D matrices including growth factors to induce neurite outgrowth. Acta biomaterialia, 8(9), 3302-12. PMID: 22617741
Fu M, Yu X, Lu J, & Zuo Y. (2012) Repetitive motor learning induces coordinated formation of clustered dendritic spines in vivo. Nature, 483(7387), 92-5. PMID: 22343892
Do you write about peer-reviewed research in your blog? Use ResearchBlogging.org to make it easy for your readers — and others from around the world — to find your serious posts about academic research.
If you don't have a blog, you can still use our site to learn about fascinating developments in cutting-edge research from around the world.
Research Blogging is powered by SMG Technology.
To learn more, visit seedmediagroup.com.