Migrants to ancient Rome, more advanced Mesolithic Swedish communities, delayed transatlantic flights, expanding bird populations, and greener deserts thanks to climate change. Here are five of the latest scientific studies published open-access this week.... Read more »
Killgrove, K., & Montgomery, J. (2016) All Roads Lead to Rome: Exploring Human Migration to the Eternal City through Biochemistry of Skeletons from Two Imperial-Era Cemeteries (1st-3rd c AD). PLOS ONE, 11(2). DOI: 10.1371/journal.pone.0147585
Stidham, T., & Eberle, J. (2016) The palaeobiology of high latitude birds from the early Eocene greenhouse of Ellesmere Island, Arctic Canada. Scientific Reports, 20912. DOI: 10.1038/srep20912
Boethius, A. (2016) Something rotten in Scandinavia: The world's earliest evidence of fermentation. Journal of Archaeological Science, 169-180. DOI: 10.1016/j.jas.2016.01.008
Lu, X., Wang, L., & McCabe, M. (2016) Elevated CO2 as a driver of global dryland greening. Scientific Reports, 20716. DOI: 10.1038/srep20716
There’s something missing from all the coverage of Zika virus, the mosquito-spread flavivirus that’s spread across 26 countries in the Americas since May 2015. While Zika usually doesn’t cause symptoms in adults, the outbreak coincided with a 20- to 40-fold … Continue reading →... Read more »
Tetro JA. (2016) Zika and microcephaly: causation, correlation, or coincidence?. Microbes and infection / Institut Pasteur. PMID: 26774330
I think that the day after Valentine’s Day is actually the best. After all, chocolate is 50 percent off. However, using the holiday as an excuse to delve into the myriad of studies that attempt to explain the complexity of human attraction and relationships is pretty fun. Last year I examined moves, specifically some fly dance moves and rather cheesy pick-up lines. Today, I think I’ll explore gift giving.In the field of animal behavior, gift giving (or nuptial gifts) is practically its own subdiscipline, particularly in insects. These gifts are typically food items (but sometimes are inedible tokens) presented from the male to the female during courtship. They may be to show the female that he is worth her time, show how healthy the he is, how good a provider he can be, or simply to keep her distracted from eating him during the actual mating (except in those cases of specialized body parts or “suicidal food transfers”…now that is the ultimate sacrifice for your bae!). The gift giving behavior, especially if it involves an extreme sacrifice on the part of the male, can only arise if the giver has some net fitness benefit. He must be able to increase his paternity share (particularly in polyandrous mating systems) and/or boost the female’s fecundity, thereby increasing the number of offspring.Humans are not insects. Obviously. But gift giving, and many of its underlying behavioral mechanisms, is still very important to our mating system. I’ve already mentioned chocolate that, while offering little nutritive value, sure does make us ladies happy. As you know, these are not the only gifts given on Valentine’s Day. An interesting paper by Rugimbana et al., published in the Journal of Consumer Behavior in 2003, examines the role of gift giving on Valentine’s Day. The authors point out right up front that if you think about this “holiday,” you might notice that it is rather small in scale compared to the high rollers (i.e., Christmas). However, it is unique in that it has become almost ritualistic in its symbolic gift giving. So much so that it has become over-commercialized and now causes increased anxiety and pressure to those who involve themselves in it. The study looks at the role of social power exchanges as the basis for gift giving on Valentine’s Day, specifically in young men. To assess this, they interviewed male participants aged 18-25, asking about their attitudes towards Valentine’s Day, perceptions of female expectations and various types of gifts, and the appropriateness of various types of gifts to the length of a relationship.This study found that for young men “the overwhelming motive for [giving] gifts on Valentine’s Day was obligation.” The men thought that gift giving was necessary when in a relationship simply because their significant other was expecting it. How romantic. This obligatory gift giving was thought essential early on in a relationship, especially if they wanted to avoid a conflict. The phrases “all hell would break loose” and “I hope…I’d still have a girlfriend” were used. However, only 25 percent of men replied that they expected something in return for the Valentine’s Day present. That sounds a bit harsh. But not so fast. When the researchers broke things down by their altruistic value, or lack of, some interesting patterns emerged. For example, when men were asked “if you were to buy lingerie for your partner, would it be for you, or for her?,” 90 percent said that it would be for themselves. Shocker on that one, I know. That isn’t to say that altruistic answers weren’t given (e.g., “you don’t need a day to say I love you”), just that it is difficult to separate from self-interest (e.g., “if you do it right, you’ll be glad”).The authors were able to boil Valentine’s Day gift giving down to three motives: 1) obligation, 2) self-interest, and 3) altruism. Importantly, these motives existed in combination and a “social power exchange” was present. In other words, giving rewards the giver. All of this sounds rather callous and almost Machiavellian. Ladies, we sound rather demanding…I mean, “all hell will break loose” over one day and one gift? Wow. And guys, while turning an obligation into a reward is rather cunning and evolutionarily arguable, it is also sort of cliché at this point. Perhaps both sexes should consider the gift giving rules of other holidays like Christmas. Just a thought.Rugimbana, R., Donahay, B., Neal, C., & Polonsky, M. (2003). The role of social power relations in gift giving on Valentine's Day Journal of Consumer Behaviour, 3 (1), 63-73 DOI: 10.1002/cb.122(image via Valentines Day Pictures)... Read more »
Rugimbana, R., Donahay, B., Neal, C., & Polonsky, M. (2003) The role of social power relations in gift giving on Valentine's Day. Journal of Consumer Behaviour, 3(1), 63-73. DOI: 10.1002/cb.122
Humans, like all social animals, have a fundamental need for contact with others. This deeply ingrained instinct helps us to survive; it’s much easier to find food, shelter, and other necessities with a group than alone. Deprived of human contact, most people become lonely and emotionally distressed.
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Matthews GA, Nieh EH, Vander Weele CM, Halbert SA, Pradhan RV, Yosafat AS, Glober GF, Izadmehr EM, Thomas RE, Lacy GD.... (2016) Dorsal Raphe Dopamine Neurons Represent the Experience of Social Isolation. Cell, 164(4), 617-631. PMID: 26871628
A new paper in PNAS raises the interesting suggestion that our brain function goes through yearly cycles. According to authors Christelle Meyer and colleagues, their findings reveal new evidence of seasonal effects in human cognitive brain function "that could contribute to cognitive changes at specific times of year."
However in my view, the study is too small to be conclusive.
Meyer et al. used fMRI to scan 28 young participants. Each of the volunteers spent 4 1/2 days in a laborator... Read more »
The detection of gravitational waves produced by the collision of two black holes over 1 billion light years away confirms Einstein's vision of our Universe.... Read more »
Abbott, B., Abbott, R., Abbott, T., Abernathy, M., Acernese, F., Ackley, K., Adams, C., Adams, T., Addesso, P., Adhikari, R.... (2016) Observation of Gravitational Waves from a Binary Black Hole Merger. Physical Review Letters, 116(6). DOI: 10.1103/PhysRevLett.116.061102
I won't keep you too long today as I bring the paper by Adam Young and colleagues  (open-access available here) to your attention and some discussions around the concept of inflammation and autism. To quote: "An emerging focus of research into the aetiology of ASC [autism spectrum condition] has suggested neuroinflammation as one candidate underlying [the] biological model."Including one Simon Baron-Cohen on the authorship list, I have to say that I was impressed to see this quite comprehensive review of the peer-reviewed literature covering "the mechanisms that may underlie neuroinflammation and the evidence at genetic and protein levels for each of these mechanisms." The authors concluded that whilst there are some important gaps to be filled in the research literature in this area - "the greatest area of weakness in the field is that in general, the findings tend to be from individual studies and rarely are these replicated" - to mention 'inflammation' and 'autism' in the same sentence is no longer 'crazy talk'.I've discussed quite a bit about inflammation and autism on this blog down the years. Personally, I've seen and read enough (peer-reviewed) papers on the topic to form an opinion that for at least some on the autism spectrum ('autisms' people, autisms) there is an overwhelming case for much more detailed investigation in this area. If you don't believe me, well, take a look at some of the science and form your own opinion (see here and see here for example). And when I say that some of the genetics of 'some' autism might also implicate inflammation and inflammatory processes too (see here), there appears to be something for everyone in the field.One area that I would like to see more study on (aside from what science can potentially do when inflammation runs amok) is inspection of the interplay between genetic and biological factors pertinent to inflammation/inflammatory processes and behaviour and psychology. We've already had some hints down the years about how inflammation might 'affect' things like social cognitive processing (see here) including mention of a concept not unfamiliar to Prof. Baron-Cohen - Theory of Mind (ToM) - and potentially pertinent to autism. I'd like to see much more investigation on whether for example, cyclical patterns of inflammation might correspond to some of the cyclical patterns of behaviour noted in some on the spectrum. This set against the idea that some of the contents of the medicine cabinet already applied to some cases of autism might have some relevant actions on facets of immune function overlapping with inflammation and inflammatory processes (see here). Much more research is indicated.Oh, and since we are on the topic of neuroinflammation and autism, I'd also suggest you having a look at the recent review from Janet Kern and colleagues  (open-access) too. They've also included some important mention of anti-NMDA-receptor encephalitis and autism (see here) which I'm particularly interested in...Music: Me First and the Gimme Gimmes - My Heart Will Go On. Please, give the song a chance...---------- Young AM. et al. From molecules to neural morphology: understanding neuroinflammation in autism spectrum condition. Mol Autism. 2016 Jan 20;7:9. Kern J. et al. Relevance of Neuroinflammation and Encephalitis in Autism. Front Cell Neurosci. 2016 Jan 19;9:519.----------Young AM, Chakrabarti B, Roberts D, Lai MC, Suckling J, & Baron-Cohen S (2016). From molecules to neural morphology: understanding neuroinflammation in autism spectrum condition. Molecular autism, 7 PMID: 26793298... Read more »
Young AM, Chakrabarti B, Roberts D, Lai MC, Suckling J, & Baron-Cohen S. (2016) From molecules to neural morphology: understanding neuroinflammation in autism spectrum condition. Molecular autism, 9. PMID: 26793298
Whatever the ins and outs behind the tragic shootings at Planned Parenthood clinic in Colorado, it seems safe to assume that the heated and inflammatory rhetoric that has characterised the debate around abortion in the USA has played a major role. A couple of weeks ago, Planned Parenthood innocently asked Twitter users for one word [Read More...]... Read more »
Ritter, R., Preston, J., Salomon, E., & Relihan-Johnson, D. (2015) Imagine no religion: Heretical disgust, anger and the symbolic purity of mind. Cognition and Emotion, 1-19. DOI: 10.1080/02699931.2015.1030334
Scientists at the UCLA Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research and Center for Duchenne Muscular Dystrophy at UCLA have developed a new approach that could eventually be used to treat Duchenne muscular dystrophy. The stem cell gene therapy could be applicable for 60 percent of people with Duchenne, which affects approximately 1 in 5,000 boys in the U.S. and is the most common fatal childhood genetic disease.
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Young, C., Hicks, M., Ermolova, N., Nakano, H., Jan, M., Younesi, S., Karumbayaram, S., Kumagai-Cresse, C., Wang, D., Zack, J.... (2016) A Single CRISPR-Cas9 Deletion Strategy that Targets the Majority of DMD Patients Restores Dystrophin Function in hiPSC-Derived Muscle Cells. Cell Stem Cell. DOI: 10.1016/j.stem.2016.01.021
People are still talking about the Ebola virus and its deadly outbreak in West Africa, and now a new virus is making the headlines: mostly innocuous and fairly unknown until a few weeks ago, the Zika virus is suddenly dominating the news for its putative link with a congenital birth defect that causes babies to be born with abnormally small heads and undeveloped brains. But what is the Zika virus, and how can it be harmless to most people yet cause such harm to an unborn fetus? To answer this question we have to take a step back and understand how viruses work and why some are endemic in the population, while others seem to come and go in waves. The Zika virus was first isolated in 1947 from a rhesus monkey and from a pool of mosquitos from the Zika forest, in Uganda. It belongs to the same family of viruses as dengue, yellow fever, and West Nile virus. However, unlike its close relatives, Zika was thought to be relatively harmless: most infected people will experience no symptoms and a few just a rash and mild fever. Originally confined to Africa, it started spreading to Asia in 2007. Since then the spread of the virus has been exponential.Viruses like Zika and Ebola replicate in animal reservoirs, i.e. populations where they are endemic. Ebola, for example, is usually found in bats and jumps to humans through consumption of meat from infected animals. Zika is found in monkeys and both monkeys and humans contract it through bites from mosquito carriers. In order to evade the host’s immune system, viruses evolve continuously: as organisms build immunity to fight them off, viruses accumulate genetic changes that enable them to escape the newly made defenses. Contrary to Ebola, Zika is a less spectacular virus in many ways. It’s much smaller, and most of the people who contract it don’t even realize they’ve been infected except for a pesky mosquito bite. But that pesky mosquito bite is exactly the virus’s added strength: it becomes an invisible enemy, one that hides and migrates through a tiny insect. You can stay away from infected people when you see them sniffing and sneezing, but how do you avoid a symptomless agent that spreads through a flying bug?You don’t. In areas where these mosquitos are endemic, children get infected early in life, build immunity against the virus, and don’t worry about it ever again. Why is Zika posing a threat now, then? The problem arises when the virus moves to a new geographical area and encounters a population that has never been infected before. Pregnant women are particularly at risk: unless they’ve been infected earlier in life, in which case their immune system can clear the infection before it reaches the fetus, any disease agent that has the ability to cross the placenta is a potential threat. Even a virus with normally mild symptoms like Zika, when it reaches the completely naïve immune system of a fetus in the early stages of pregnancy, can potentially cause permanent damage. Currently, the connection between microcephaly and Zika is still putative and has yet to be confirmed. The danger, however, is real. As Los Alamos National Laboratory scientist Brian Foley explains, over the last two decades, vector-borne viruses like Zika and yellow fever have spread globally at increased rate. That human behavior is once again responsible for this new spread comes as no surprise. Increased traveling between continents, an exponentially growing population and, least but not last, a rise in temperatures have created the perfect haven for mosquitos—and hence the diseases they may carry—to spread virtually unstopped. Densely populated areas that are humid and riddled with stagnant water become the ideal habitat for these bugs. The race for a vaccine has started, and several companies have already announced a time schedule to begin human trials in the near future. Zika is not a very diverse virus like HIV, for which the making of a vaccine has turned out much more challenging than originally anticipated. However, making any vaccine is regulated by strict government safety rules that require years of testing. “Under normal circumstances, it takes 10-20 years to make a vaccine,” Foley explains. “In an emergency situation, they could push it to 2-4 years. That’s still a long time in the event of an outbreak.”And it’s even longer if you think that Zika may only be the tip of the iceberg of a phenomenon we are bound to see over and over again in the near future. “The distribution, transmission, and abundance of vectors that bear and transmit diseases are being enhanced by global warming,” Foley and colleagues state in a recent publication . “The mean global temperature increased approximately by 1° centigrade during the last several hundred years. However, during the next 20 years it is anticipated to increase by 2–3° centigrade.”Geographic areas that used to be too cold for mosquito-borne diseases are now seeing an increase in encephalitic viruses, dengue, and West Nile. Zimbabwe and Ethiopia are experiencing an increase in typhoid and cholera due to the same reason: combine poor hygiene with stagnant water and climate change, and you have the recipe for disaster. So yes, a vaccine can provide a solution. But if this is only the beginning, we need to think globally. It’s not just one virus we’re fighting but a global change that’s happening too fast for the natural world to adapt on its own.  Paul Shapshak , Charurut Somboonwit, Brian T. Foley, Sally F. Alrabaa, Todd Wills, John T. Sinnott (2015). Zika Virus. Global Virology I - Identifying and Investigating Viral Diseases Springer-Verlag... Read more »
Paul Shapshak , Charurut Somboonwit, Brian T. Foley, Sally F. Alrabaa, Todd Wills, John T. Sinnott. (2015) Zika Virus. Global Virology I - Identifying and Investigating Viral Diseases. Springer-Verlag. info:/
Let's talk about hearts and how they get broken. Literally, with drugs. When we swallow a pill, it's often to help address a problem we're experiencing with a particular body part. An aching head or a sore throat, for example. The pill breaks down in our guts and we absorb the drug into our bloodstream. It travels around our body and eventually ends up at the hurting locale where it works to fix the problem. Unfortunately, sometimes the drug will end up somewhere else and act there to cause an unwanted side effect. So while you can ingest a gel capsule filled with ibuprofen in order to have it travel to your head and relieve a headache, if you take any of about a zillion other drugs to fix a non-head-related issue you risk the drug causing a headache as a side effect. No body part is safe from the collateral damage inflicted by medicines. A particularly weird example I can think of is Cipro and other fluoroquinolones (used to treat bacterial infections), which on rare occasions can cause your Achilles tendon to tear in half.Some drugs have cardiotoxic (heart-hurting) side effects. Obviously this is a big deal, since a properly functioning heart is somewhat essential to carrying on being alive. Using drugs known to be toxic to the heart is an exercise in risk assessment. If the side effect is super rare or the drug is super necessary for treating a life-threatening disease, it's likely to be deemed to be worth taking. I mean, penicillin and Tylenol will, on incredibly rare occasions, cause your skin to melt off (Google yourself some Stevens-Johnson syndrome if you dare), but they remain in widespread use. Sometimes a heart-wreaking side effect doesn't make itself apparent until after the drug reaches the market, at which point a swift withdrawal tends to take place.Let's take a brief closer look at some heartbreakers.Anthracyclines are a group of drugs used to treat cancers of the blood and various other tissues. They bind to an enzyme called topoisomerase-II in cancer cells, disrupting the transcription and replication of DNA, and thus preventing cells from multiplying. They also bind directly to DNA to accomplish the same task. The big problem with using anthracyclines is while they are great at killing cancer cells, they also damage non-cancerous heart cells (by inhibiting their topoisomerase-II, which appears to be particularly susceptible to the drugs). This eventually brings about ventricular dysfunction and heart failure, which sucks. The risk of heart failure is directly dependent on how much of the drug a person is given over the course of their chemotherapy, so oncologists watch things very carefully. The first of the anthracyclines to be discovered was daunorubicin, isolated from Streptomyces peucetius, a ruby red bacterium growing in soil near a 13th-century castle in southeast Italy. After this drug proved to be unreasonably toxic to people's hearts, researchers intentionally mutated S. peucetius and managed to coax it into producing a similar, slightly less cardiotoxic compound they named doxorubicin. Derivatives of the first two anthracyclines include epirubicin and mitoxantrone. Even with these engineered drugs, heart damage remains a concern.A huge number of drugs are capable of breaking your heart by disrupting its electrical conduction system, which coordinates the sequential contraction of the four heart chambers to ensure maximum blood-moving efficiency. Shorting out the heart, so to speak, can result in torsades de pointes, an abnormal heartbeat that can sometimes lead to sudden death. Drugs known to mess with the heart's wiring include certain antiarrhythmics (e.g. amiodarone), antimicrobials (e.g. erythromycin), antipsychotics, and antihistamines.A couple of drugs once used to promote weight loss (e.g. fenfluramine) or treat migraines (e.g. methysergide) can cause valvular heart disease. They accomplish their beneficial tasks by acting on serotonin receptors in the brain. However, they also appear to be able to affect receptors found in the valves of the heart, bringing about the development of structural abnormalities. The abnormal valves can leak (regurgitation), lowering the overall effectiveness of the heart. Symptoms of drug-induced valve disease can resemble those associated with heart murmurs or heart failure.Finally, some drugs just straight up increase your risk of having a heart attack (also known as a myocardial infarction). These include oral contraceptives (aka "the pill") and certain non-steroidal anti-inflammatory drugs designed to specifically inhibit an inflammation-driving enzyme called COX-2 (e.g celecoxib).ReferencesRoden DM. 2008. Cellular basis of drug-induced torsades de pointes. British Journal of Pharmacology 154(7):1502-1507. [Full text]Wu AH. 2008. Cardiotoxic drugs: Clinical monitoring and decision making. Heart 94(11):1503-1509. [Snippet]Zhang S, Liu X, Bawa-Khalfe T, Lu LS, Lyu YL, Liu LF, Yeh ET. 2012. Identification of the molecular basis of doxorubicin-induced cardiotoxicity. Nature Medicine 18(11):1639-1642.... Read more »
Wu A. (2008) Cardiotoxic drugs: Clinical monitoring and decision making. Heart, 94(11), 1503-1509. DOI: 10.1136/hrt.2007.133876
The world is full of ideas. How does science decide which ideas are good and which are bad...?... Read more »
Renal cell carcinomas (RCCs) can be life-threatening and although mostly sporadic, approximately 5% are associated with genetic conditions such as BHD. Early identification of families carrying cancer-predisposing mutations enables access to regular screening and earlier treatment. However, it can be difficult to distinguish between sporadic and inherited RCC based on standard immunohistological analysis. New research from Kato et al. (2016) assessed whether variability in the chromosomal status of chromosomes 17, 2, and 6 could be used to identify BHD-associated RCC.... Read more »
Kato, I., Iribe, Y., Nagashima, Y., Kuroda, N., Tanaka, R., Nakatani, Y., Hasumi, H., Yao, M., & Furuya, M. (2016) Fluorescent and Chromogenic in situ Hybridization of CEN17q as a Potent Useful Diagnostic Marker for Birt-Hogg-Dubé Syndrome-associated Chromophobe Renal Cell Carcinomas. Human Pathology. DOI: 10.1016/j.humpath.2016.01.004
I'll admit to being pretty fascinated by the Branched Chain α-Keto acid Dehydrogenase Kinase (BCKDK) gene. As per previous blog entries about this gene (see here and see here) and the important biological step it plays in the metabolism of the branched-chain amino acids (BCAAs), at least one 'form' of autism might be particularly sensitive to issues with it . I take it you've heard of the idea that the autisms (plural) might be a better description of autism? If you haven't, here is a peer-reviewed take on it ...I'm happy to report that science continues to study this gene; its biology and it's associations with "a novel dietary-treatable form of autism" as per the findings reported by Oyarzabal and colleagues . The focus of the Oyarzabal paper was to study the "mitochondrial response to the BCKDK-deficiency" potentially brought about for example, when there are issues with the BCKDK gene given its links to the mitochondria matrix. This work also takes on particular relevance given the idea that mitochondrial issues - mitochondria: the powerhouse of cells - might not be something entirely new to at least some autism (see here for example).Anyhow, fibroblasts were the starting material and the measurement of "bioenergetics, ultra-structural and dynamics parameters" of fibroblasts from those who had BCKDK-deficiency. Although not totally au-fait with all the science included in the paper, the authors report results on: "a general bioenergetics depletion that could affect the mitochondrial dynamics and cell fate." They even reported complementary findings following a: "Knockdown of BCKDK gene in control fibroblasts" and mention of some findings relevant to maple syrup urine disease (MSUD) in light of the involvement of the BCAAs there. In short: "All these data gives us a clue to understand the positive dietary response to an overload of branched-chain amino acids."This is an exciting area of autism research pertinent to the idea that (a) there may be various types of autism characterised by various different genetic and biological factors being involved, and (b) the possibility that at least some autism might stem from one or more inborn errors of metabolism is gaining ground (see here) and hence might be potentially 'treatable'. For that last point I'm minded to take you back to a recent post on phenylketonuria and autism (see here) and some more recent [peer-reviewed] research talking about 'Succinic Semialdehyde Dehydrogenase Deficiency Presenting as Autism Spectrum Disorder' . Dare I even present the idea of carnitine issues falling into this area?Screening for such inborn errors of metabolism seems to be the important conclusion; screening not assuming nor guessing nor making grand generalisations. Just screening.Music: the glorious music accompanying the film Interstellar has to be the one for today in light of new discoveries in recent days...---------- Novarino G. et al. Mutations in BCKD-kinase lead to a potentially treatable form of autism with epilepsy. Science. 2012 Oct 19;338(6105):394-7. Poot M. Towards identification of individual etiologies by resolving genomic and biological conundrums in patients with autism spectrum disorders. Mol Syndromol. 2013 Jun;4(5):213-26. Oyarzabal A. et al. Mitochondrial response to the BCKDK-deficiency: Some clues to understand the positive dietary response in this form of autism. Biochim Biophys Acta. 2016 Jan 22. pii: S0925-4439(16)30003-5. Gogou M. et al. Succinic Semialdehyde Dehydrogenase Deficiency Presenting as Autism Spectrum Disorder. Indian J Pediatr. 2016 Jan 25.----------Oyarzabal A, Bravo-Alonso I, Sánchez-Aragó M, Rejas MT, Merinero B, García-Cazorla A, Artuch R, Ugarte M, & Rodríguez-Pombo P (2016). Mitochondrial response to the BCKDK-deficiency: Some clues to understand the positive dietary response in this form of autism. Biochimica et biophysica acta PMID: 26809120... Read more »
Oyarzabal A, Bravo-Alonso I, Sánchez-Aragó M, Rejas MT, Merinero B, García-Cazorla A, Artuch R, Ugarte M, & Rodríguez-Pombo P. (2016) Mitochondrial response to the BCKDK-deficiency: Some clues to understand the positive dietary response in this form of autism. Biochimica et biophysica acta. PMID: 26809120
Compared with Whites, Black Americans have high levels of an important stress hormone called cortisol circulating in their bloodstream. No-one really knows why this is, but the differences remain even after you take into account social and psychological factors. It seems likely that simply being black exposes you to a cumulative effect of increased lifetime [Read More...]... Read more »
Assari, S., Moghani Lankarani, M., Malekahmadi, M., Caldwell, C., & Zimmerman, M. (2015) Baseline Religion Involvement Predicts Subsequent Salivary Cortisol Levels Among Male But not Female Black Youth. International Journal of Endocrinology and Metabolism, 13(4). DOI: 10.5812/ijem.31790
Biosensors are powerful tools in synthetic biology for engineering metabolic pathways or controlling synthetic and native genetic circuits in bacteria. Scientists have had difficulty developing a method to engineer "designer" biosensor proteins that can precisely sense and report the presence of specific molecules, which has so far limited the number and variety of biosensor designs able to precisely regulate cell metabolism, cell biology, and synthetic gene circuits.
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Taylor, N., Garruss, A., Moretti, R., Chan, S., Arbing, M., Cascio, D., Rogers, J., Isaacs, F., Kosuri, S., Baker, D.... (2015) Engineering an allosteric transcription factor to respond to new ligands. Nature Methods, 13(2), 177-183. DOI: 10.1038/nmeth.3696
Scientists may be in agreement on the causes of climate change, but the US public is not. We can blame biased news sources all we want for this disconnect, but a new study suggests yet another explanation: our science teachers. Although most are teaching about global warming, many simply aren’t doing it right.... Read more »
Eric Plutzer, Mark McCaffrey, A. Lee Hannah, Joshua Rosenau, Minda Berbeco, & Ann H. Reid. (2016) Climate confusion among U.S. teachers. Science, 351(6274). info:/10.1126/science.aab3907
A new agent of the tick-borne illness known as Lyme disease has emerged in the upper Midwest. The bacterium is genetically related to Borrelia burgdorferi, until now believed to be the only cause of Lyme disease in the United States. The name proposed for the bacterium is Borrelia mayonii because the work was conducted at the Mayo Clinic. B. mayonii has not been detected in patients outside of the Midwest (so far). The findings are described in The Lancet Infectious Diseases.The new species was discovered at the Mayo Clinic during routine testing of specimens (blood, cerebral spinal fluid, and joint fluid) received from all regions of the U.S. Over 100,000 specimens collected from 2003 through 2014 were tested by real-time PCR for Lyme disease bacteria. The PCR probes were designed to detect the oppA1 gene from Borrelia species belonging to the Lyme disease group, known in the scientific literature as "B. burgdorferi sensu lato." The Lyme disease group comprises 18 species that fall into the same genetic cluster within the genus Borrelia. They include species known or suspected to cause Lyme disease (B. burgdorferi, B. garinii, B. afzelii, B. spielmanii, B. valaisiana, B bissettii, B. bavariensis, and B. lusitaniae) and another ten species that do not cause illness. The PCR probes do not react with DNA from species belonging to the other cluster of Borrelia, the relapsing fever group.The key to the discovery of the new species was the melting temperature analysis routinely programmed onto the end of real-time PCR runs. The oppA1 PCR products amplified from B. burgdorferi strains have melting temperatures of 63.6 through 64.9°C. For other Lyme disease species, the melting temperature ranges from 52.3°C (B. valaisiana) to 59.2°C (B. californiensis). Therefore, the melting temperature of the oppA1 PCR product was used to distinguish B. burgdorferi from other Lyme disease Borrelia.Over 9,000 specimens were collected from the states of Minnesota, Wisconsin, and North Dakota from January 2012 through September 2014. 102 were PCR positive, and most of the PCR products had the melting temperature profile of B. burgdorferi. However, six had melting temperatures ranging from 60.4°C to 61.2°C, too low to be B. burgdorferi but too high to be any other member of the Lyme disease group. The novel spirochetes were cultured from the blood of two of the patients. The DNA sequence of several "housekeeping" genes of the new isolates differed enough from those of other Borrelia species to signify that a new Borrelia species has been found. The investigators named the new spirochete Borrelia mayonii. No specimen collected from other regions of the U.S. exhibited the atypical melting temperatures, and neither did any collected earlier than 2012 from the Midwest. These findings led the authors to conclude that B. mayonii has recently emerged in the upper Midwest and that the six patients are the first known cases of Lyme disease to be caused by the new species.The investigators also collected Ixodes scapularis ticks in Wisconsin. PCR and melting temperature analysis showed that 19 of 658 ticks (2.9%) were positive for B. mayonii, 195 (29.6%) positive for B. burgdorferi, and two positive for both.One striking feature of B. mayonii infections is the larger number of spirochetes circulating within the patients. The densities ranged from 420,000 to 6,400,000 bacterial cells per milliliter, at least a hundred times higher than observed in the blood of patients with B. burgdorferi infections. The numbers were high enough that spirochetes could be seen in blood collected from one of the patients.Fig. 1b from Pritt et al., 2016The six patients had many of the typical Lyme disease symptoms: headache, neck pain, muscle aches, joint pain, and fatigue. Although mild fever is also common in Lyme disease, two of the six patients had severe fevers with temperature readings approaching 40°C (104°F). Four had nausea or were vomiting, which are also uncommon Lyme disease symptoms. Two patients were hospitalized because of the severity of their illness. Lyme disease may be missed in those infected with B. mayonii because of the unusual symptoms.The standard two-tier antibody test, which uses B. burgdorferi antigens to detect reactive antibody, may help with the diagnosis. Blood from five of the six patients were tested. Four patients either tested positive or, if negative initially, tested positive with blood drawn weeks later. The one patient who tested negative had blood drawn only on the first day of illness, so it's likely that the antibody response hadn't kicked in fully. The test appears to help with the diagnosis of Lyme disease caused by B. mayonii, but the number of patients tested was too small to draw firm conclusions.The authors conclude:In view of the differing clinical manifestations for patients infected with the novel B burgdorferi sensu lato genospecies, it is likely that Lyme borreliosis is not being considered—and therefore not diagnosed—in some patients with this infection. The clinical range of illness must be better defined in additional patients to ensure that physicians can recognise the infection and distinguish it from other tick-borne infections. Many tick-borne pathogens have global distribution, therefore studies are needed to establish the geographic distribution of human beings and ticks infected with the novel B. burgdorferi sensu lato genopecies. Finally, clinicians should be aware of the potential role of oppA1 PCR for diagnosing infection with this novel pathogen.ReferencePritt BS, Mead PS, Johnson DK, Neitzel DF, Respicio-Kingry LB, Davis JP, Schiffman E, Sloan LM, Schriefer ME, Replogle AJ, Paskewitz SM, Ray JA, Bjork J, Steward CR, Deedon A, Lee X, Kingry LC, Miller TK, Feist MA, Theel ES, Patel R, Irish CL, & Petersen JM (2016). Identification of a novel pathogenic Borrelia species causing Lyme borreliosis with unusually high spirochaetaemia: a descriptive study. The Lancet. Infectious diseases. PMID: 26856777... Read more »
Pritt BS, Mead PS, Johnson DK, Neitzel DF, Respicio-Kingry LB, Davis JP, Schiffman E, Sloan LM, Schriefer ME, Replogle AJ.... (2016) Identification of a novel pathogenic Borrelia species causing Lyme borreliosis with unusually high spirochaetaemia: a descriptive study. The Lancet. Infectious diseases. PMID: 26856777
Home of tumbleweeds and roadrunners, it’s no surprise that the Southwest is the driest region of the United States. And yet, new research confirms that which many have predicted: it’s getting even dryer. Not only are droughts more common, but they are more intense and longer-lasting too.... Read more »
Prein, A., Holland, G., Rasmussen, R., Clark, M., & Tye, M. (2016) Running dry: The U.S. Southwest's drift into a drier climate state. Geophysical Research Letters. DOI: 10.1002/2015GL066727
Way, way up in northwestern Canada (on the lower east side of Cape Bathurst, Northwest Territories), where the mainland meets the Arctic Ocean, a 30 km stretch of seacoast has been smoldering away for hundreds if not thousands of years.The Smoking Hills, named by the explorer John Franklin during one of his early 19th century expeditions to the Canadian Arctic, consist of shale bedrock covered by several meters worth of soil and loose rocks deposited by ancient glaciers and rivers. The land falls away at the coast (we're talking a 100 m high escarpment carved out by waves), exposing the otherwise buried shale to the atmosphere.The Smoking Hills, as captured in 2010 (top) (Source) and prior to 1857 (bottom) (Source)Now, this shale is notable for containing bitumen (an extremely gooey form of crude oil) as well as very fine grains of sulfide minerals such as pyrite. Both contain lots of electrons and are thus susceptible to reacting with electron-craving substances such as oxygen gas. This doesn't tend to happen while they are buried in the ground, but at the cliffs they encounter our oxygen-filled atmosphere.Uncovered by erosion of the cliff, sulfide in the shale gives up its electrons to oxygen and is converted to sulfate. This reaction generates heat, which can build up to the point at which bitumen in the shale will catch fire (in other words, start reacting violently with oxygen). It then burns into the cliff until the oxygen supply drops too low and the fire is extinguished.-The Smoking Hills area is tundra with a smattering of small (<1 ha) shallow (<1 m) ponds. Given their polar locale, the ponds are free of ice only a couple of months of the year. The soil in the area is calcareous, a fancy way of saying it's mostly calcium carbonate (marl, to be exact). Consequently, the ponds and surrounding soils tend to be alkaline (pH 8-10), contain lots of calcium, and are well-buffered (they can absorb the addition of a lot of acid before their pH drops by a lot).However, the soils and ponds closest to the burning cliffs are acidic (pH ~2-4). They've been impacted by the large amounts of sulfur dioxide (which reacts with water to form sulfuric acid) released from the sulfur-rich shale as it burns. As a whole, the Smoking Hills pump out roughly 300 grams of sulfur dioxide every second. When the wind is right, visible plumes made up of sulfur dioxide, sulfuric acid mist, and smoke are carried dozens of kilometers inland from the cliffs, sowing the tundra with acid (any rain falling directly through the plume ends up with a pH as low as 2).Ponds near the Smoking Hills also have high concentrations of metals, which accumulate there after being leached from surrounding acidified soils or deposited via smoke from the burning shale. Their solubility increases as pH decreases, so although the acidic ponds appear clear and clean they actually are chock-full of dissolved metals. In this form, metals are easy to absorb and so are at their most toxic. The hidden metals are revealed when the pH of water collected from the ponds is raised to ~4, at which point the water turns cloudy and red-orange-brown as iron and aluminum (along with other less abundant metals) precipitate out of solution.-As you might expect, acidic and metal-rich ponds offer a very different sort of living space than ponds not being bombarded with plumes from the Smoking Hills. Given the detrimental effects of low pH and high concentrations of relatively toxic metals on living things, the diversity and abundance of organisms is lower in the acidic ponds:One paper I came across reported finding 90 species of algae in unimpacted ponds, but only 14 in acidic ponds.The average density of phytoplankton (any microscopic organism making its living via photosynthesis) in highly acidic ponds was observed by researchers to be only 1% of the density in unimpacted ponds.The acidic ponds have been reported to be devoid of larger crustaceans and any vascular aquatic plants.Interestingly, the algal residents of acidic ponds tend to also be found in acidic environments across the globe, while neighbouring unimpacted ponds are inhabited by algae typical to the Arctic. The low pH seems to have been too much for local algae to handle, so instead acid-tolerant species have somehow made their way there from afar (perhaps via migrating birds).Algae flourishing in the acidic ponds include Chlamydomonas acidophila (also found in a highly acidic volcanic lake in Japan and acidic streams in Britain) and Euglena mutabilis (occurs worldwide in acid mine drainage and volcanic lakes). They tend to grow at the bottom of the ponds, which may be due to the pH being slightly higher near the sediment surface.Euglena mutabilis: (A) a single cell (400x) (Source), (B) the bit of green in an acidic stream (Source) E. mutabilis is also noteworthy for being best friends with a yeast. Wherever this alga is found, so too is the yeast. It reminds me of a lichen, which is a fungus interwoven with an alga and/or cyanobacterium, although in this case the two buds are submerged in water and have a far looser association. The yeast appears to provide a local source of carbon dioxide to fuel photosynthesis by the alga, and receives a supply of food for its troubles. In the lab, the two grow better together than apart when the pH is low and the metal concentrations are high. This cooperative lifestyle appears to be key to their survival in highly acidic environments.-Another organism found in acidic ponds near the Smoking Hills is Chironomus riparius, a non-biting (woo!) midge somewhat reminiscent of a mosquito (here's a swarm of them). Its larvae are known as blood worms due to their vibrant red colour, the result of having lots of hemoglobin in their hemolymph. This enables them to store up oxygen and live underwater in places where there isn't much of the gas to be had. Large numbers of C. riparius have been observed at the bottom of acidic ponds, suggesting they're very good at dealing with acidity and metals.Chironomus riparius larvae (top) (Source) and a fishing lure based on it (bottom) (Source)A study comparing C. riparius larvae from acidic ponds near the Smoking Hills with larvae found in Sweden concluded the former tended to tolerate acidic water better than their Swedish relatives. The Canadians contained twice as much hemoglobin as the Swedes and their hemolymph had a relatively high buffering capacity. These features likely are adaptations to acidic pond life.-Plants growing in soils close to the Smoking Hills have to deal with not only highly acidic soil filled with toxic metals, but also direct exposure to harmful sulfur dioxide and acid rain.Nearest to the burning cliffs, the land is barren. The first plants, covering <5% of the land, appear 150-200 m from the cliff edge. They are Artemisia til... Read more »
Adams C, & Hutchinson T. (1984) A comparison of the ability of leaf surfaces of three species to neutralize acidic rain drops. New Phytologist, 97(3), 463-478. DOI: 10.1111/j.1469-8137.1984.tb03612.x
Sheath R, Havas M, Hellebust J, & Hutchinson T. (1982) Effects of long-term natural acidification on the algal communities of tundra ponds at the Smoking Hills, N.W.T., Canada. Canadian Journal of Botany, 60(1), 58-72. DOI: 10.1139/b82-008
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