Post List

  • April 20, 2014
  • 03:34 PM

420: How Marijuana Messes With the Brain

by Alexis Delanoir in How to Paint Your Panda

Cannabis use has previously been associated with cognitive impairment, and Smith et al. (2013) showed that heavy marijuana use was associated with poor working memory and brain abnormalities. Now, Gilman et al. (2014) propose that even casual use of marijuana is associated with such negative effects. Is this an issue of correlation/causation, of funding bias, or are the world's weed smokers really in neurological danger? In this post, in celebration of 4/20, I provide context for the recent study associating casual marijuana use with brain abnormalities and pose these questions.... Read more »

Meier, M., Caspi, A., Ambler, A., Harrington, H., Houts, R., Keefe, R., McDonald, K., Ward, A., Poulton, R., & Moffitt, T. (2012) Persistent cannabis users show neuropsychological decline from childhood to midlife. Proceedings of the National Academy of Sciences, 109(40). DOI: 10.1073/pnas.1206820109  

  • April 20, 2014
  • 09:31 AM

Was Lamarck right after all? A look at epigenetic inheritance

by EE Giorgi in CHIMERAS

Myths © EEGFrom the Wikipedia definition of epigenetics: "In biology, and specifically genetics, epigenetics is the study of heritable changes in gene activity that are not caused by changes in the DNA sequence."Wait a minute... how can we inherit anything that's not encoded in the DNA? All the information we inherit from our parents is coded in the DNA ... Right?That's correct. However, there's something very important that goes hand in hand with the information contained in the genes: how and when to use those genes. Not all genes are expressed in all cells at all times: different cells express different genes, depending on the tissue and function they need to fulfill. Epigenetics studies the changes inside the nucleus that determine which genes are expressed and which are, instead, silenced. It turns out, these changes happen throughout our life. And even though they are not "written" in our DNA, in some instances these acquired changed can indeed be passed on to future generations. This should be surprising. A mouse that loses its tail can still have offsprings with tails because the loss of the tail has not altered the DNA inside the mouse's cells. Yet, studies have altered in a similar way the eye color in fruit flies and the coat color in mice and shown that the changes were preserved in the next generation. In humans, there have been studies indicating that changes established not only through the mother's diet, but even through the father's diet could possibly affect the health of the embryo and be carried down to future generations."Animal models have also revealed that these diet-induced epigenetic changes are not limited to one generation, but can ripple down to descendants. Females with an increased disposition to metabolic problems during pregnancy can transfer this to their offspring [3]."Why is this relevant? Because some of these changes can increase the risk of diseases like cancer.For years we've been looking at associations between genetic variants and disease risks. Yet for most of the observed heritable diseases and cancers no responsible genes or alleles have been found. Could this be because the majority of heritable diseases are caused not by genetic mutations, but by epigenetic ones?As Heard and Martienssen state in a recent review Cell [1]:"Since the human genome was sequenced, the term epigenetics is increasingly being associated with the hope that we are more than just the sum of our genes [1]."Epigenetics makes you rethink genetics. Back in school we studied that Darwin was right and Lamarck was wrong: Lamarck's view of evolution was that phenotypes developed out of necessity to survive to the environment. For example, according to Lamarck, giraffes developed a long neck because they kept reaching for higher branches when feeding, and then this acquired trait was passed on to the next generations. Darwin, on the other hand, pointed out that the longer neck was just a random trait that appeared at some point during the evolution of giraffes. Giraffes with longer necks experienced an advantage over the ones with shorter necks because they could reach for better food. The long-neck giraffes had an advantage and had more and stronger offsprings than short-neck giraffes, and were therefore selected for. This view has led to two common misconceptions:Misconception #1: All genes we have today have been selected for. This is absolutely not true. Many of the mutations we see in the human genome today are due to random drift, basically the "reshuffling" of genes that happens from one generation to the next.Misconception #2: The environment cannot change our genome and therefore environmental exposures on one generation bear no effect on the following generation. Though this is what Darwin taught us, today we know that Lamarck was not completely wrong after all: while the environment cannot change our genes, it can indeed alter the way the genes work, and these changes can indeed be passed on to future generation. This has been the most surprising lesson epigenetics has taught us in the past few decades. Jean-Baptiste Lamarck was wrong because acquired traits cannot be inherited -- they need to be encoded in the genome in order to be passed on to the next generation. If you cut the tail of a mouse, the offsprings will still have tails. The theory that giraffes elongated their necks by stretching it farther to higher branches and that by doing so, their offsprings would naturally acquire a longer neck is wrong. However, it's interesting to note that Lamarck was a botanist and plants do employ epigenetics to pass acquired traits on to the next generation, a phenomenon called "epigenetic inheritance." The key point is this: the environment cannot change our genome, but it can indeed change the way our genes work (the "epigenome"). Epigenetics studies how these changes can be inherited across generations without being encoded in the genome. The paradox is the following: we, as individuals, constantly adapt to the environment around us. The best example is certainly the immune system, which, throughout our lifetime, learns to recognize pathogens and kill them. So, what pathogens we are exposed to can induce epigenetic changes. Stress and diet can also affect our metabolism through, again, epigenetic changes. These environment-induced changes affect different cells in our body. Yet, when an offspring is conceived, the very first cells during embryonic development have to be completely reset as they are the cells that will make all different organs in the new organism. It's like completely erasing your hard drive so you can start over. Mother nature does that through a mechanism called "epigenetic reprogramming:" all the lifelong acquired information from the parents is erased in the germline (cells that originate oocytes and spermcytes) and erased again during the first phases of embryonic development. Epigenetic changes not only take place during embryonic development, but also throughout the lifetime of an organism. The same mechanisms—notably DNA methylation and histone modification—have a role in the acquisition and maintenance of epigenetic changes induced by dietary or other environmental factors. [...] For a long time, scientists assumed that these environmentally induced changes lasted, at most, for the lifetime of the individual organism, but did not influence its offspring because gametogenesis would ‘wipe the slate clean' and the offspring would inherit a completely unadulterated set of genes. However, the specific mechanisms that cause the epigenetic modification of gene expression are now known to be involved in non-Mendelian—i.e. non-genetic—inheritance [3].Though the mechanism of "epigenetic inheritance" is not yet fully understood, scientists hypothesize that it could happen during this reprogramming when some markers are not completely erased. Another theory is that the intestinal flora could be transmitting information across generations. And finally, the information could be carried on to the next generation through modifications in the RNA.[1] Heard E, & Martienssen RA (2014). Transgenerational Epigenetic Inheritance: Myths and Mechanisms. Cell, 157 (1), 95-109 PMID: 24679529[2] Lim JP, & Brunet A (2013). Bridging the transgenerational gap with epigenetic memory. Trends in genetics : TIG, 29 (3), 176-86 PMID: ... Read more »

  • April 20, 2014
  • 06:03 AM

The Mystery of “Quantum Resonance Spectroscopy”

by Neuroskeptic in Neuroskeptic_Discover

Can quantum physics help to diagnose schizophrenia and depression? A paper just published in the Journal of Nervous and Mental Disease claims that a technique called ‘quantum resonance spectroscopy’ (QRS) can accurately diagnose various mental health problems. But is it quantum wizardry or magic quackery? According to the authors of the new paper, Zhang et […]The post The Mystery of “Quantum Resonance Spectroscopy” appeared first on Neuroskeptic.... Read more »

Zhang Y, Liu F, Shi J, Yue X, Zhang H, Du X, Sun L, & Yuan J. (2014) Exploratory quantum resonance spectrometer as a discriminator for psychiatric affective disorders. The Journal of nervous and mental disease, 202(4), 287-91. PMID: 24647211  

  • April 19, 2014
  • 02:19 PM

Introduction to Traditional Peer Review

by Hadas Shema in Information Culture

Peer review was introduced to scholarly publication in 1731 by the Royal Society of Edinburgh, which published a collection of peer-reviewed medical articles. Despite this early start, in many...

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Biagioli, M. (2002) From Book Censorship to Academic Peer Review. Emergences: Journal for the Study of Media , 12(1), 11-45. DOI: 10.1080/1045722022000003435  

Benos DJ, Bashari E, Chaves JM, Gaggar A, Kapoor N, LaFrance M, Mans R, Mayhew D, McGowan S, Polter A.... (2007) The ups and downs of peer review. Advances in physiology education, 31(2), 145-52. PMID: 17562902  

Bornman, L. (2008) Scientific Peer Review: An Analysis of the Peer Review Process from the Perspective of Sociology of Science Theories. Human Architecture: Journal of the Sociology of Self-Knowledge, 6(2). info:/

Brown, R. (2006) Double Anonymity and the Peer Review Process. The Scientific World JOURNAL, 1274-1277. DOI: 10.1100/tsw.2006.228  

Callaham ML, Baxt WG, Waeckerle JF, & Wears RL. (1998) Reliability of editors' subjective quality ratings of peer reviews of manuscripts. JAMA : the journal of the American Medical Association, 280(3), 229-31. PMID: 9676664  

Spier R. (2002) The history of the peer-review process. Trends in biotechnology, 20(8), 357-8. PMID: 12127284  

  • April 19, 2014
  • 12:51 PM

First female “penis” discovered in cave-dwelling insects

by beredim in Strange Animals

Image showing the female penis of N. auroraCredit: Current Biology, Yoshizawa et al.Kingdom: AnimaliaPhylum: ArthropodaClass: InsectaOrder: PsocopteraFamily: PrionoglarididaeGenus: NeotroglaSpecies: N. aurora, N. curvet and 2 otherThis Thursday, researchers announced that they have discovered several insect species that display the "world's first" known instance of gender-reversed genitalia. In simple words, they have found 4 insect species with female... "penises." and male "vaginae"!All four species live in dry Brazilian caves and feed on bat guano. They belong to the genus Neotrogla, of the Psocoptera order which is commonly known as booklice or barklice."Although sex-role reversal has been identified in several different animals, Neotrogla is the only example in which the intromittent organ is also reversed." said leading author, Kazunori Yoshizawa from the Hokkaido University in Japan.Prolonged and reversed matingThe researchers found that these insects mate for an impressive 40 to 70 hours, during which, the female inserts an elaborate, penis-like organ -called gynosome- into the male's vagina-like opening.According to co-author Rodrigo Ferreira, the females may forcibly hold on the males for such long periods of time to get as much of their sperm and seminal fluid as possible."One of the couples copulated for around 73 hours." said Ferreira.The spikes along the female penis anchors it to the male's "vagina" so strongly that when the researchers tried to separate one of the couples, they tore apart the male’s body without affecting the genital coupling.Female N. curvet (top) mates with a maleCredit: Yoshizawa KazunoriThe researchers speculate that the prolonged copulation and the genitalia reversal may be an evolutionary trait guided by the resource-poor cave environment in which these insects live. Males provide females with nutritious seminal fluids in addition to sperm, making it advantageous for the females to mate for prolonged periods.The findings on Neotrogla offer new opportunities to test ideas about sexual selection, conflict between the sexes, and the evolution of novelty, claim the researchers, who now plan to look into studies of behavior, physiology, and more. First on their list is to establish a healthy population of the insects in the lab."It will be important to unveil why, among many sex-role-reversed animals, only Neotrogla evolved the elaborated female penis." said Yoshitaka Kamimura from Keio University in Japan. It has a penis, so it should be a male, no?Contrary to what common sense may tell you, the presence or absence of certain genitalia isn't the determining factor to whether an individual is male or female. Gametes are.  By definition,male gametes are small, motile, and optimized to transport their genetic information over a distance, while female gametes are large, non-motile and contain the nutrients necessary for the early development of the young organism.It just happens that males usually have a penis and females a vagina. Usually..References- Yoshizawa, K., Ferreira, R., Kamimura, Y., & Lienhard, C. (2014). Female Penis, Male Vagina, and Their Correlated Evolution in a Cave Insect Current Biology DOI: 10.1016/j.cub.2014.03.022... Read more »

  • April 19, 2014
  • 07:34 AM

Typing Method for Cryptosporidium Meleagridis

by Christen Rune Stensvold in Christen Rune Stensvold

You can read about the development and use of a highly applicable typing method for C. meleagridis isolates in a newly published paper in Journal of Clinical Microbiology.... Read more »

  • April 19, 2014
  • 07:34 AM

Typing Method for Cryptosporidium Meleagridis

by Christen Rune Stensvold in Blastocystis Parasite Blog

You can read about the development and use of a highly applicable typing method for C. meleagridis isolates in a newly published paper in Journal of Clinical Microbiology.... Read more »

  • April 19, 2014
  • 05:34 AM

Dump fossil fuels for the health of our hearts

by Andy Extance in Simple Climate

Cleaning up air pollution will provide immediate health gains as well as longer-term climate benefits, highlights New York University's George Thurston... Read more »

Thurston, G. (2013) Mitigation policy: Health co-benefits. Nature Climate Change, 3(10), 863-864. DOI: 10.1038/nclimate2013  

Rice, M., Thurston, G., Balmes, J., & Pinkerton, K. (2014) Climate Change. A Global Threat to Cardiopulmonary Health. American Journal of Respiratory and Critical Care Medicine, 189(5), 512-519. DOI: 10.1164/rccm.201310-1924PP  

  • April 19, 2014
  • 05:32 AM

The nose knows: How to pick your friends

by Teodora Stoica in CuriousCortex

The importance of human odor in a social context. ... Read more »

  • April 19, 2014
  • 12:46 AM

Energy Expenditure (Calories Burned) in Anorexia Nervosa Patients

by Tetyana in Science of Eating Disorders

How many calories do patients with anorexia nervosa need to eat to gain a kilo (2.2 lbs)? It seems like a simple question and one that we should have figured out a long time ago, given the importance (err, necessity) of refeeding and weight restoration in recovery from anorexia nervosa.
Unfortunately, research in this area has often led to contradictory results (see Salisbury et al., 1995 and de Zwaan et al., 2002 for reviews). Fortunately, a paper by Stephan Zipfel and colleagues (2013, freely available here) sheds light on one potential cause of the discrepancies.
But first, some definitions:
TDEE stands for total daily energy expenditure. TDEE has three components: resting energy expenditure (REE), dietary-induced thermogenesis (DIT), and activity-induced thermogenesis (AIT). The gold standard for measuring TDEE is through something called the doubly labelled water technique. REE is usually measured through indirect calorimetry. (These techniques were used in this study as well.)
Generally, when people lose weight, their REE is also reduced as a result of decreased body weight and decreased lean mass, as well as metabolic adaptations. Since …

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Zipfel S, Mack I, Baur LA, Hebebrand J, Touyz S, Herzog W, Abraham S, Davies PS, & Russell J. (2013) Impact of exercise on energy metabolism in anorexia nervosa. Journal of Eating Disorders, 1(1), 37. PMID: 24499685  

  • April 18, 2014
  • 01:56 PM

Moving Beyond “Just-So Stories”: Young Children Can Be Taught Basic Natural Selection

by amikulak in Daily Observations

Spend more than a few hours with a child under the age of 10 and “why?” is a question you’re likely to hear a. Children are naturally curious explorers, and […]... Read more »

  • April 18, 2014
  • 01:07 PM

Overcomming Social Phobia with CBT and Pharmacotherapy

by Vivek Misra in Uber Notions

photo credit: ParadigmMalibu.comSocial phobia, a type of anxiety disorder, is characterized by persistent fear of one or more social or performance situations in which the person is exposed to unfamiliar people or to possible scrutiny by others (1). The individual fears that he or she will act in a way (or show anxiety symptoms) that will be embarrassing and humiliating.  Exposure to the feared situation almost invariably provokes anxiety, which may take the form of a situationally bound or situationally pre-disposed Panic Attack. The person recognizes that this fear is unreasonable or excessive. The feared situations are avoided or else are endured with intense anxiety and distress. The avoidance, anxious anticipation, or distress in the feared social or performance situation(s) interferes significantly with the person's normal routine, occupational (academic) functioning, or social activities or relationships, or there is marked distress about having the phobia. The mechanisms underlying the symptoms of social phobia are believed to be early negative life experiences along with maladaptive parenting styles leading to cognitive distortion, a shy and perfectionistic personality, in combination with genetic vulnerability, sympathetic hypersensitivity and autonomic dysregulation. Genetic factors in Social PhobiaSome genetic factors that have been linked to social phobia are the serotonin transported linked polymorphic region (5HTTLPR) genotype and polymorphisms in the Brain Derived Neurotrophic Factor (BDNF) gene. The fewer the number of high-risk alleles, the better the response of social anxiety symptoms to selective serotonin re-uptake inhibitors (SSRI) (2). Also, blushing propensity, which as an intermediate phenotype of social anxiety disorder is considered to be more precisely defined than the overall categorical disease phenotype and closer to the underlying genotype, has been linked to 5-HTTLPR/5-HTT rs25531 haplotypes that are associated with reduced function of the serotonin transporter and consequently, less serotonin at the synapse (3). The role of BDNF in social phobia is a focus of current research in Korea.  BDNF is the most abundant neurotrophin in the brain, acts on the hippocampus, basal forebrain, and frontal cortex, plays an important role in neuronal growth and differentiation during development and contributes to the survival, function, and plasticity of neurons in adulthood. Associations between a variety of psychiatric disorders and the BDNF Val66Met polymorphism have been found (4), including social phobia. (5) The Autonomic System in Social PhobiaProlonged social phobia is associated with an increase in QT dispersion. This association may result from prolonged anxiety and, in turn, a decrease in vagal modulation and/or increase in sympathetic modulation.  Electrocardiographic Data showed that in Patients with Social Phobia and Normal controls normal subjects had lesser QT Dispersion and corrected rate QT dispersion. RR and HR didn’t significantly vary, in patients with Social Phobia Generalized Type showed less QT Dispersion than the patients with Social Phobia of Non-Generalized Type. (6)Neuropsychological Study on SAD:Difference in the perception of six basic facial emotional expressions and neutral face using Ekman study analysis on 32 social phobia and 20 healthy controls and Children with social phobia had significantly poorer facial recognition skills than normal controls and reported greater anxiety upon completion of the recognition task. Social phobia patients exhibited increased timeout numbers, reaction and total time. The ability to correctly recognize facial expressions was decreased in social phobia patients compared to healthy subjects.The central effect of Oxytocin is said to play key role in social recognition, pair bonding, anxiety and maternal behaviours. Behaviour therapy and oxytocin stimulation has a positive feedback on Social Approach Behaviour, but the Social Anxiety governs it with a short leash. Another study shows that the administration of oxytocin improves mental representations of self, following exposure therapy. The increase rate of oxytocin was correlated with decrease rate of LSAS avoidance subscale score, however does not correlated with decrease rate of LSAS fear subscale score. No correlation between plasma oxytocin concentration and LSAS total score (or subscale scores). Low possibility as a state marker of SAD, Plasma oxytocin level was not associated with the scores of other scales for measuring anxiety (ASI, ST/IL HAM-A) or depression (MADRS) among the patients with SAD.Pharmacotherapy approach and their effect:Pharmacotherapy of social phobia includes Selective serotonin reuptake inhibitor (SSRI), Reversible inhibitor of MAO-A (RIMA), Benzodiazepines and Beta-adrenergic receptor blockers. Treatment duration is important factor that can significantly predict the response. When comparing treatment adherence between SSRIs and RIMA (moclobemide) in patients with social phobia,  the cumulative surviving proportions were significantly different between the SSRIs and moclobemide group at week 48 and week 96 (relatively late phase of treatment). When it comes to adherence the overall all-cause discontinuation rates were significantly lower with SSRIs than moclobemide (7). In conclusion, when the effect size of different modalities was compared, Combination therapy (SSRI+CBT) was most effective among three modalities, but there were no significant differences. 1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders-IV.1994.2. Stein MB, Seedat S, & Gelernter J (2006). Serotonin transporter gene promoter polymorphism predicts SSRI response in generalized social anxiety disorder. Psychopharmacology, 187 (1), 68-72 PMID: ... Read more »

Domschke K, Stevens S, Beck B, Baffa A, Hohoff C, Deckert J, & Gerlach AL. (2009) Blushing propensity in social anxiety disorder: influence of serotonin transporter gene variation. Journal of neural transmission (Vienna, Austria : 1996), 116(6), 663-6. PMID: 18629430  

Nahshoni E, Gur S, Marom S, Levin JB, Weizman A, & Hermesh H. (2004) QT dispersion in patients with social phobia. Journal of affective disorders, 78(1), 21-6. PMID: 14672793  

  • April 18, 2014
  • 11:04 AM

Danish Project to Make Polymer Solar Cells More Profitable

by dailyfusion in The Daily Fusion

Project Megawatt intends to make polymer solar cells profitable enough to allow power generation from polymer solar cells to compete on market terms with traditional coal-fired power plants.... Read more »

  • April 18, 2014
  • 09:09 AM

Corporate Culture Directly Affects Financial Performance

by Jeremiah Stanghini in Jeremiah Stanghini

The question as to whether corporate culture has an effect on financial performance has been asked before and it will likely be asked again. In a study published in the Cornell Hospitality Quarterly, research demonstrated a link between corporate culture and … Continue reading →... Read more »

  • April 18, 2014
  • 07:02 AM

Hey, trial lawyers! The FDA is watching you!

by Doug Keene in The Jury Room

And they want you to stop abusing their Adverse Event Reporting System (FAERS). We’ve worked a number of cases recently where FDA warnings were used as evidence at trial and were very interested to see this article in the American Journal of Gastroenterology. And the answer to the skeptic’s question is “no”. No, we don’t […]

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Racine A, Cuerq A, Bijon A, Ricordeau P, Weill A, Allemand H, Chosidow O, Boutron-Ruault MC, & Carbonnel F. (2014) Isotretinoin and risk of inflammatory bowel disease: a French nationwide study. The American Journal of Gastroenterology, 109(4), 563-9. PMID: 24535094  

  • April 17, 2014
  • 11:02 PM

Dear CNRS: That mouse study did not "confirm" the neurobiological origin of ADHD in humans

by in Neuroscientifically Challenged

Late last week the French National Centre for Scientific Research (CNRS - the acronym is based on the French translation) put out a press release describing a study conducted through a collaboration between several of its researchers and scientists from The University of Strasbourg. CNRS is a large (30,000+ employees), government-run research institution in France. It is the largest research organization in Europe, and is responsible for about 1/2 of the French scientific papers published annually. The study in question, conducted by Mathis et al., investigated the role of a brain region called the superior colliculus in disorders of attention. The superior colliculus, also known as the tectum, is part of the brainstem. It is strongly connected to the visual system and is thought to play an important role in redirecting attention to important stimuli in the environment. For example, imagine you are sitting in your favorite coffee shop quietly reading a book, when someone in a gorilla suit barges in and runs through the middle of the room. You would likely be surprised and you would, somewhat reflexively, direct your attention towards the spectacle. This rapid shift in attention would be associated with activity in your superior colliculus.It has been proposed that individuals who suffer from disorders like attention-deficit hyperactivity disorder (ADHD) may experience increased activity in the superior colliculus, which causes rapid, uncontrolled shifts of attention. Mathis et al. investigated the role of the tectum in attention using mice with a genetic abnormality that makes the superior colliculus hypersensitive.The researchers exposed mice with this defect to a series of behavioral tests. They found that the mice performed normally on tests of visual acuity, movement, and sensory processing. However, the mice seemed to be less wary than control mice of entering areas of bright light (usually something mice avoid as open spaces make them vulnerable to attacks from natural predators). Additionally, the mice performed worse on a task that required them to inhibit impulses. These abnormalities in behavior were associated with increased levels of the neurotransmitter norepinephrine in the superior colliculus.The authors of the study mention that their work supports the hypothesis that superior colliculus overstimulation is a contributing factor in ADHD. I have no qualms with the verbiage used in the paper, but CNRS's press release about the study is titled "Confirmation of the neurobiological origin of attention-deficit disorder" and they state in the article: "A study, carried out on mice, has just confirmed the neurobiologial origin of attention-deficit disorder (ADD)..."When it comes to psychiatric disorders without a clearly defined molecular mechanism (which is almost all of them), it is improbable that a finding in mice can confirm anything in humans. Our understanding ADHD in humans is limited. We have no objective diagnostic criteria; instead we base diagnosis on observable and self-reported symptoms. If our understanding of a disorder in humans is based primarily on symptomatology (as opposed to the underlying pathophysiology), then it makes the results of experiments that use animals to model the disorder more difficult to interpret. For, if we don't know what molecular changes we can expect to see as a correlate of the disease (e.g. senile plaques in Alzheimer's), then we are resigned to trying to match symptoms of mice with symptoms of men. In this type of situation where we don't know the true pathophysiology, we can never be sure that the symptoms we are seeing in mice and those we are seeing in men have an analogous biological origin. Thus, when it comes to psychiatric disorders, translating directly from animals to humans is difficult. In the case of ADHD, because the biological origins of the disorder are still mostly unknown, animal models can be used as a means to explore the neurobiology of a similar manifestation of symptoms in the animal. They can't, however, be used to "confirm" anything about the human disorder. In this case, CNRS drastically overstated the importance of the study. Of course, the wording used by CNRS in their initial press release was also found on dozens of other media outlets after they picked up the story.Do I doubt that ADHD has a neurobiological origin? No. But the study by Mathis et al. did not confirm that it does. CNRS, as an institution of science, should be more careful about the claims they make in their communications with the public. Mathis, C., Savier, E., Bott, J., Clesse, D., Bevins, N., Sage-Ciocca, D., Geiger, K., Gillet, A., Laux-Biehlmann, A., Goumon, Y., Lacaud, A., Lelièvre, V., Kelche, C., Cassel, J., Pfrieger, F., & Reber, M. (2014). Defective response inhibition and collicular noradrenaline enrichment in mice with duplicated retinotopic map in the superior colliculus Brain Structure and Function DOI: 10.1007/s00429-014-0745-5

... Read more »

  • April 17, 2014
  • 05:57 PM

Li-Sulfur Batteries Last Longer With Metal-Organic Frameworks

by dailyfusion in The Daily Fusion

Researchers at the PNNL added a kind of nanomaterial called a metal-organic framework, to the battery’s cathode to capture problematic polysulfides that usually cause lithium-sulfur batteries to fail after a few charges.... Read more »

  • April 17, 2014
  • 05:45 PM

X-Rays Help Understand High-Temperature Superconductivity

by dailyfusion in The Daily Fusion

A new study pins down a major factor behind the appearance of laser-induced high-temperature superconductivity in a promising copper-oxide material.... Read more »

  • April 17, 2014
  • 10:39 AM

Cheap, Abundant, Low-Toxic Photocatalyst Discovered

by dailyfusion in The Daily Fusion

A research group at Japan Science and Technology Agency (JST) led by the principal researcher Hideki Abe and the senior researcher Naoto Umezawa at the NIMS’s Environmental Remediation Materials Unit discovered a new photocatalyst, Sn3O4, that uses sunlight to produce hydrogen from water.... Read more »

Manikandan, M., Tanabe, T., Li, P., Ueda, S., Ramesh, G., Kodiyath, R., Wang, J., Hara, T., Dakshanamoorthy, A., Ishihara, S.... (2014) Photocatalytic Water Splitting under Visible Light by Mixed-Valence Sn O . ACS Applied Materials , 6(6), 3790-3793. DOI: 10.1021/am500157u  

  • April 17, 2014
  • 09:39 AM

What’s the Answer? (new Biostars interface)

by Mary in OpenHelix

BioStars is a site for asking, answering and discussing bioinformatics questions and issues. We are members of the community and find it very useful. Often questions and answers arise at BioStars that are germane to our readers (end users of genomics resources). Every Thursday we will be highlighting one of those items or discussions here […]... Read more »

Parnell Laurence D., Lindenbaum Pierre, Shameer Khader, Dall'Olio Giovanni Marco, Swan Daniel C., Jensen Lars Juhl, Cockell Simon J., Pedersen Brent S., Mangan Mary E., & Miller Christopher A. (2011) BioStar: An Online Question . PLoS Computational Biology, 7(10). DOI: 10.1371/journal.pcbi.1002216.g002  

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