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  • May 1, 2016
  • 03:01 AM
  • 18 views

The Truth About Cognitive Impairment in Retired NFL Players

by The Neurocritic in The Neurocritic

NINETY-TWO percent of retired National Football League players have decreased cognitive function, according to a new study:“In the NFL group, baseline neuropsychological assessments showed 92% of players had decreased general cognitive proficiency, 86% had decreased information processing speed, 83% had memory loss, 83% had attentional deficits, and 85% had executive function impairment.”The Truth?The study reported on a self-selected sample of 161 current and retired NFL players recruited via a blog (“The NFL concealed the danger of brain injuries!!”), the Los Angeles Chapter of the Retired NFL Players Association, The Summit (??), and possibly other sources. Perhaps these players were motivated to participate because they had cognitive complaints, or because they wanted an evaluation in advance of the $1 billion concussion settlement. The League's Baseline Assessment Program is a required part of the settlement.The quote above is the full extent of the report on the players' neuropsychological assessments. These were done using computerized test batteries (MicroCog or WebNeuro), which are largely unknown to most clinical neuropsychologists. Was there an adequately matched control population? What norms were used? They don't say.THE TRUTH IS, we don't know the extent of cognitive impairment in these football players, or the percentage of all players who are affected, or the severity of impairment in those who are. This new paper (by Daniel Amen, Bennet Omalu, and others) doesn't give us enough information, but it succeeds in sounding the alarm about the dangers of football and the inevitability of memory loss and attention deficits.Are blows to the head bad for your brain? Can repeated concussions cause cognitive impairment and chronic traumatic encephalopathy (CTE)? Yes, almost certainly, but we can't rely on biased samples, appeal to celebrity, and Frontline documentaries (“researchers have identified CTE in 96 percent of NFL players that they’ve examined”) as conclusive scientific evidence. What's needed are better sampling methods (in the short term) and longitudinal studies that follow a diverse cohort over time (in the long term).The Scans Caption for top figure: SPECT brain scans showing abnormal low blood flow in an NFL player compared to a normal healthy control subject.The new paper by Amen et al. (2016) was actually focused on SPECT scans, not surprisingly, since these are the backbone of his business at the Amen Clinics. The article claims “90% sensitivity, 86% specificity, and 94% accuracy” in discriminating NFL players from controls. I won't elaborate here, but check out This Neuroimaging Method Has 100% Diagnostic Accuracy (or your money back) and The Dark Side of Diagnosis by Brain Scan for detailed critiques of the methods used here. I will flag one tiny issue, however:“All NFL players were male, while 56% of the control group were women.”Why?? The authors have a database of 100,000 SPECT scans...ReferencesDaniel G. Amen, Kristen Willeumier, Bennet Omalu, Andrew Newberg, Cauligi Raghavendra, & Cyrus A. Raji (2016). Perfusion Neuroimaging Abnormalities Alone Distinguish National Football League Players from a Healthy Population Journal of Alzheimer's Disease : 10.3233/JAD-160207Caption (from press materials): SPECT brain scans showing improvement of abnormal low blood flow in an NFL player compared after 3.5 months on a customized brain rehabilitation program.

... Read more »

Daniel G. Amen, Kristen Willeumier, Bennet Omalu, Andrew Newberg, Cauligi Raghavendra, & Cyrus A. Raji. (2016) Perfusion Neuroimaging Abnormalities Alone Distinguish National Football League Players from a Healthy Population. Journal of Alzheimer's Disease. info:/10.3233/JAD-160207

  • April 30, 2016
  • 02:55 PM
  • 32 views

Salts in the brain control our sleep-wake cycle

by Dr. Jekyll in Lunatic Laboratories

Insomnia, fun fact those of us who have served or are serving in the military have a much higher incidence of sleep problems. So if you are like me and have ever been prescribed something to help you sleep, you know that there are some unwanted side effects. For instance the time I lost memory of a whole day of interacting with people to the ambien I had taken the night before, not fun. Thankfully Danish researchers found that the level of salts in the brain plays a critical role in whether we are asleep or awake.

... Read more »

  • April 30, 2016
  • 12:15 PM
  • 36 views

Words On The Brain: A Semantic Map of the Cortex

by Neuroskeptic in Neuroskeptic_Discover

In a new Nature paper, Berkely neuroscientists Alexander G. Huth and colleagues present a 'semantic atlas' of the human brain. Huth et al. have mapped which brain areas respond to words, according to the semantics (meanings) of each word. It turns out that these maps are highly similar across individuals - which could have implications for 'mind reading' technology.



Huth et al. recorded brain activity with fMRI while seven volunteers listened to over two hours of audio narrative (taken fr... Read more »

Huth AG, de Heer WA, Griffiths TL, Theunissen FE, & Gallant JL. (2016) Natural speech reveals the semantic maps that tile human cerebral cortex. Nature, 532(7600), 453-8. PMID: 27121839  

  • April 30, 2016
  • 02:45 AM
  • 41 views

The 'anti-neuroinflammatory activity' of oxytocin

by Paul Whiteley in Questioning Answers

Whilst the package inserts of the various drugs that modern medicine has at its disposal provides important information on potential mode of action, there is a growing realisation that drugs generally have quite a few more molecular targets than are perhaps listed. Take for example the quite commonly used (in some parts of the world anyway) compound called melatonin  that in some instances can provide almost miraculous relief when it comes to sleeping issues under certain circumstances. A derivative of the amino acid tryptophan, melatonin might however be quite the molecular handy-person when it comes to its biological targets including its actions on something called leaky gut for example...The paper by Lin Yuan and colleagues [1] similarly suggests that everyone's favourite 'cuddle hormone' (oxytocin) might also have a wider range of biological effects than has hitherto been fully appreciated.  Drawing on cell line results and intra-nasal administration of oxytocin (OT) to [artificially] immune-stimulated mice, authors reported that "OT possesses anti-neuroinflammatory activity and might serve as a potential therapeutic agent for treating neuroinflammatory diseases."One of the primary analytical targets of the Yuan study were microglia, those 'constant gardeners' according to one description, and how administration of OT might have some interesting effects on the activation of microglia under certain circumstances. "BV-2 cells and primary microglia were pre-treated with OT (0.1, 1, and 10 μM) for 2 h followed by LPS [lipopolysaccharides] treatment" we are told, and microglia activation and "pro-inflammatory mediators" subsequently monitored. The results tallied with those 'anti-neuroinflammatory' sentiments previously expressed as authors report on various possible reasons for such an effect: "OT suppressed the expression of TNF-α, IL-1β, COX-2, and iNOS at the mRNA and proteins levels and reduced the elevation of [Ca2+]i in LPS-stimulated microglia cells." If that wasn't enough, researchers also looked at what happened following OT pre-treatment when a certain strain of mouse was 'immune stimulated' again in terms of microglia activation and those pro-inflammatory mediators. We are similarly told that: "pre-treatment with OT showed marked attenuation of microglial activation and pro-inflammatory factor levels." So we have something of a match in the lab and in an animal model.These are interesting results. Yet again, one has to be a little cautious about the use of mouse models or indeed, cell lines (humans are so much more than a group of cells in a petri dish) and further, independent investigations are indicated. But: "These data suggested that OT would be a potential therapeutic agent for alleviating neuroinflammatory processes in neurodegenerative diseases."I was inclined to talk about the Yuan paper because of the various 'connections' that have been made between oxytocin and autism (see here). With a growing interest in the oxytocin-autism connection in the peer-reviewed literature, this nonapeptide (9 amino acids long) has attracted quite a few researchers to its cause [2] as a function of the idea that: "Oxytocin increases the salience of social stimuli and promotes parental nurturing and social bonds" [3]. As per my interpretation of the current state of the oxytocin-autism research base, there are some interesting results available but once again, universal 'effects' are nowhere to be seen - Autisms, people. Autisms. The Yuan and other results focusing on the 'anti-neuroinflammatory' activity of oxytocin perhaps add another dimension to the possible hows and whys of efficacy when it comes to a label like autism. That also a growing number of people are coming around to the idea that neuroinflammation might be a facet of 'some' autism (see here) and including some mention of microglia (see here) offers an additional correlate to add into the future research mix. Could those with autism who have more prominent signs of neuroinflammatory issues potentially be 'best responders' to oxytocin for example? I did also wonder whether the idea that inflammation or inflammatory issues might feature in complex behaviours like social cognitive processing (see here) could provide another explanation for some of the reported results observed following use of oxytocin in [some] autism?Much more research is indicated but again the message is... don't be too dogmatic when it comes to pharmacological targets and actions of medicines indicated for conditions such as autism. You might just end up being surprised...----------[1] Yuan L. et al. Oxytocin inhibits lipopolysaccharide-induced inflammation in microglial cells and attenuates microglial activation in lipopolysaccharide-treated mice. Journal of Neuroinflammation. 2016; 13:77.[2] Okamoto Y. et al. The Potential of Nasal Oxytocin Administration for Remediation of Autism Spectrum Disorders. CNS Neurol Disord Drug Targets. 2016 Apr 13.[3] Young LJ. & Barrett CE. Neuroscience. Can oxytocin treat autism? Science. 2015 Feb 20;347(6224):825-6.----------Yuan L, Liu S, Bai X, Gao Y, Liu G, Wang X, Liu D, Li T, Hao A, & Wang Z (2016). Oxytocin inhibits lipopolysaccharide-induced inflammation in microglial cells and attenuates microglial activation in lipopolysaccharide-treated mice. Journal of neuroinflammation, 13 (1) PMID: 27075756... Read more »

  • April 29, 2016
  • 04:10 PM
  • 45 views

Don’t retweet if you want to remember

by Dr. Jekyll in Lunatic Laboratories

The whole of human intelligence, right at your fingertips. Sure it might not make the layman an engineer or physicist, but if we want to learn about a particular topic the internet can give us that information. But you better hold on tight before you lose it. New research finds retweeting or otherwise sharing information creates a “cognitive overload” that interferes with learning and retaining what you’ve just seen.

... Read more »

  • April 29, 2016
  • 11:32 AM
  • 39 views

Cuckoldary is rare in humans!

by Farid Pazhoohi in Epistemophil

Human behavioral scientists argue that extra-pair copulation is adaptive in human females, as through extra-pair copulation, women can acquire good genes from other potential mates. This is suggested because it is found that women experience greater sexual attraction to particular extra-pair men, but not their own partners, during their highest peak of fertility (Gangestad & […]... Read more »

Gangestad, S., & Thornhill, R. (2008) Human oestrus. Proceedings of the Royal Society B: Biological Sciences, 275(1638), 991-1000. DOI: 10.1098/rspb.2007.1425  

Larmuseau MH, Matthijs K, & Wenseleers T. (2016) Cuckolded Fathers Rare in Human Populations. Trends in ecology , 31(5), 327-9. PMID: 27107336  

  • April 29, 2016
  • 11:02 AM
  • 47 views

Bringing ‘Dirty’ Mice Into Labs Opens A World Of Possibilities

by Rita dos Santos Silva in United Academics

Treating immune disorders might have gotten easier with a new mouse model.... Read more »

  • April 29, 2016
  • 09:38 AM
  • 46 views

Hunting For The Signatures of Cancer

by EE Giorgi in CHIMERAS

Signatures of Mutational Processes Extracted from the Mutational Catalogs of 21 Breast Cancer Genomes. Credit:http://dx.doi.org/10.1016/j.celrep.2012.12.008Cancer is the second leading cause of death worldwide, with approximately 14 million new cases and 8.2 million cancer related deaths each year (Source: WHO). A family history of cancer typically increases a person's risk of developing the disease, yet most cancer cases have no family history at all. This suggests that a combination of both genetics and environmental exposures contribute to the etiology of cancer. In this context, "genetics" means the genetic make-up we are born with and inherited from our parents. For example, women born with specific mutations in the BRCA1 and BRCA2 genes are known to have a much higher risk of developing breast cancer later in life.However, besides the genetic make-up we carry from birth, there are many geographical and environmental factors that contribute to the risk of cancer. For example, the incidence of breast cancer is over 4 times higher in North and West Europe compared to Asia and Africa (Source: WHO). Stomach cancer, on the other hand, is much more prevalent in Asia than the US. If you think that this may be linked to the genetic differences across ethnicities, think again. The National Cancer Institute published a summary of several studies that compared the incidence of first and second generation immigrants in the US with the local population. They found that:"cancer incidence patterns among first-generation immigrants were nearly identical to those of their native country, but through subsequent generations, these patterns evolved to resemble those found in the United States. This was true especially for cancers related to hormones, such as breast, prostate, and ovarian cancer and neoplasms of the uterine corpus and cancers attributable to westernized diets, such as colorectal malignancies."According to the World Health Organization (WHO), "around one third of cancer deaths are due to the 5 leading behavioral and dietary risks: high body mass index, low fruit and vegetable intake, lack of physical activity, tobacco use, alcohol use."Cancer is the result of a series of cellular mechanisms gone awry: every time a cell divides, somatic mutations accumulate in the cell's genome. These are not mutations we are born with, inherited from our parents. Rather, these are changes that accumulate in certain cells as we grow old and are not  the same across all cells in the body. Many environmental exposures contribute to this process and affect the rate at which these mutations accumulate. However, cells have various mechanisms that are normally able to repair harmful mutations or, when the damage is beyond repair, to trigger cell death. The immune system is also "trained" to recognize cancer cells and destroy them.When all these defense mechanisms fail, cancer cells start dividing uncontrollably.As a result, all cancer cells carry a number of somatic mutations that set them apart from healthy cells, and some tend to be the same across different cancer patients: for example, specific mutational patterns found in lung cancer have been attributed to tobacco exposure and were indeed reproduced in animal models. Another set of mutations has been attributed to UV exposure and has been found in skin cancers [1, 2].This prompts the ambitious question: can we find common mutations across individuals with the same cancer? And how many of these mutational patterns that are common across individuals can we attribute to particular exposures and/or biological processes? Distinguished postdoctoral researcher Ludmil Alexandrov, from the Los Alamos National Laboratory, has been working on this problem since his he was a PhD student at the Wellcome Trust Sanger Institute."It's like lifting fingerprints," Alexandrov explains. "The mutations are the fingerprints, but now we have to do the investigative work and find the 'perpetrator', i.e., the carcinogens that caused them." During his graduate studies, under the supervision of Mike Stratton of the Wellcome Trust Sanger Institute, Alexandrov developed a mathematical model that, given the cancer genomes from a number of patients, is able to pick the "common signals" across the patients -- i.e. mutation patterns that are common across the patients -- and classify them into "signatures." "When formulated mathematically," Alexandrov explains, "the question can be expressed as the classic 'cocktail party' problem, where multiple people in a room are speaking simultaneously while several microphones placed at different locations are recording the conversations. Each microphone captures a combination of all sounds and the problem is to identify the individual conversations from all the recordings." Taking from this analogy, each cancer genome is a "recording", and the task of the mathematical model is to reconstruct each conversation, in other words, the mutational patterns. These are sets of somatic mutations that are the observed across the cancer genomes and that characterize certain types of cancers.In 2013, Alexandrov and colleagues analyzed 4,938,362 mutations from 7,042 patients, spanning 30 different cancers, and extracted more than 20 distinct mutational signatures [2]. "Some patterns were expected, like the known ones caused by tobacco and UV light," Alexandrov says. "Others were completely new."Of the new signatures found, many are involved in defective DNA repair mechanisms, suggesting that drugs targeting these specific mechanisms may benefit cancers exhibiting these signatures [3]. But the most exciting part of this research will be finding the 'perpetrator' or, as Alexandrov explains, the mutations triggered by carcinogens like tobacco, UV radiation, obesity, and so on. The challenge will be to experimentally associate these mutational patterns to the exposures that caused them. In order to do this, the scientists will have to expose cultured cells and model organisms to known carcinogens and then analyze the genomes of the experimentally induced cancers.In the meantime, the signatures found so far are only the beginning: Alexandrov and colleagues have teamed up with the Los Alamos High Performance Computing Organization in order to analyze the genomes of almost 30,000 cancer patients. "The amount of data we will have to handle for this task is enormous, on the order of petabytes," Alexandrov says. "Few places in the world have the capability to handle this many data. Under normal circumstances, it takes months to answer a question on 10 petabytes of data. The supercomputing facility at Los Alamos can provide an answer within a day." Because of his research, in 2014 Alexandrov was listed by Forbes magazine as one of the “30 brightest stars under the age of 30” in the field of Science and Healthcare. In 2015 he was awardedthe AAAS Science & SciLifeLab Prize for Young Scientists in the category Genomics and Proteomics [2] and the Weintraub Award for Graduate Research. He is now the recipient of the prestigious Oppenheimer fellowship at Los Alamos National Laboratory.Disclaimer: Elena E. Giorgi is a computational biologist in the Theoretical Division of the Los Alamos National Laboratory. She does not represent her employer’s views. LA-UR-16-xxxx.ReferencesSiegel, R., Miller, K., & Jemal, A. (2015). Cancer statistics, 2015 ... Read more »

Siegel, R., Miller, K., & Jemal, A. (2015) Cancer statistics, 2015. CA: A Cancer Journal for Clinicians, 65(1), 5-29. DOI: 10.3322/caac.21254  

Alexandrov LB. (2015) Understanding the origins of human cancer. Science (New York, N.Y.), 350(6265), 1175. PMID: 26785464  

Alexandrov LB, Nik-Zainal S, Wedge DC, Aparicio SA, Behjati S, Biankin AV, Bignell GR, Bolli N, Borg A, Børresen-Dale AL.... (2013) Signatures of mutational processes in human cancer. Nature, 500(7463), 415-21. PMID: 23945592  

Alexandrov LB, Nik-Zainal S, Siu HC, Leung SY, & Stratton MR. (2015) A mutational signature in gastric cancer suggests therapeutic strategies. Nature communications, 8683. PMID: 26511885  

  • April 29, 2016
  • 07:02 AM
  • 47 views

Phubbing, more FOMO, blonde jokes, and what holds our  attention?

by Rita Handrich in The Jury Room

It’s time to run down some articles that are curious, but not substantial enough to justify a full blog post. Once again, we have kept a few pearls in our virtual filing cabinet, and have combined them here for your curiosity and possibly entertainment. This is one of those combination posts that will offer you […]

Related posts:
The Fear of Missing Out (FoMO) Scale
Red, redux: Men won’t pay attention to Tammy in red
Does this mean we need to pay no attention to 1 in  10 research findings?


... Read more »

  • April 29, 2016
  • 05:41 AM
  • 42 views

Review, Refine, Redesign

by AG McCluskey in Zongo's Cancer Diaries

Drug Discovery, Part III

How is a an Initial Hit optimised and turned into a Lead Compound?... Read more »

Hughes, J., Rees, S., Kalindjian, S., & Philpott, K. (2011) Principles of early drug discovery. British Journal of Pharmacology, 162(6), 1239-1249. DOI: 10.1111/j.1476-5381.2010.01127.x  

AG McCluskey. (2016) Review, Refine, Redesign. Zongo's Cancer Diaries. info:/

  • April 29, 2016
  • 04:34 AM
  • 58 views

Why organisations should encourage their staff to become friends

by BPS Research Digest in BPS Research Digest

They say you should never mix business and pleasure but in reality many of us find that we become friends with the people who we work with. No wonder, when you consider the hours spent together and the deep bonds formed through collaboration and sharing the highs and lows of the job.A new study in Personnel Psychology is among the first to examine the effects on job performance of having more "multiplex relationships" – colleagues you work with directly who are also your friends outside of work. The researchers say these relationships are "a mixed blessing", but on balance they found that the more of them people had, the better their work performance as judged by their supervisors. Jessica Methot and her colleagues first surveyed 301 staff at a large insurance company in southeastern United States. These staff, who had varied roles across the firm, provided a list of 10 colleagues they worked with closely in pursuit of their responsibilities and 10 staff who they considered to be friends and who they socialised with outside of work. The more overlap there was between a person's two lists, the more multiplex relationships they had. The participants also completed measures of emotional exhaustion and work-related positive emotions. Four weeks later, the participants' supervisors were contacted and rated the participants' job performance.The more multiplex relationships that participants had, the better their job performance. What's more, this was explained in part by the fact that such relationships were associated with experiencing more positive work-related emotions, like feeling excited and proud. In short, being friends with more of colleagues appeared to be good for staff and for their employer.However, the picture gets a little more complicated because the researchers dug deeper and found that multiplex relationships were also associated with more emotional exhaustion – presumably because of the effort involved in maintaining more complex relationships and of providing support to friends. In turn, emotional exhaustion was related to poorer work performance, hence the researchers describing workplace friendships as a mixed blessing. Overall though, the benefits to work performance outweighed the costs.The second study was similar but involved 182 workers at three shops and six restaurants. This time the participants also completed measures of the emotional support, trust, felt obligation, and "maintenance difficulty" (the effort of sustaining and juggling relationships) experienced in their work relationships. The results were similar, with more multiplex relationships again correlating with superior work performance – and this time the association was explained in part by feelings of greater trust towards colleagues who are also friends. But once more, although the overall association was positive, there were signs that these relationships can be a mixed blessing – the more multiplex relationships a person had, the more they tended to report having difficulties maintaining their relationships, which in turn was related to poorer job performance.We need to be aware these studies were correlational so they haven't demonstrated that work friendships causes better job performance, although that is certainly a plausible interpretation, especially in light of the mediating factors that the researchers identified. Given that having more friends at work appears to be beneficial overall, Methot and her colleagues recommended that "organisations should focus on practices that promote friendship among coworkers who can interact for work-related purposes" such as introducing friendly competition between staff, or implementing social intranet systems "that simultaneously allow employees to collaborate and share task information while getting to know each other on a social level"._________________________________ Methot, J., Lepine, J., Podsakoff, N., & Christian, J. (2016). Are Workplace Friendships a Mixed Blessing? Exploring Tradeoffs of Multiplex Relationships and their Associations with Job Performance Personnel Psychology, 69 (2), 311-355 DOI: 10.1111/peps.12109 Post written by Christian Jarrett (@psych_writer) for the BPS Research Digest.Our free weekly email will keep you up-to-date with all the psychology research we digest: Sign up!

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  • April 29, 2016
  • 02:33 AM
  • 49 views

Organophosphate exposure and ADHD?

by Paul Whiteley in Questioning Answers

"Children with higher urinary DMP [dimethylphosphate] concentrations may have a twofold to threefold increased risk of being diagnosed with ADHD [attention-deficit hyperactivity disorder]."So said the results presented in the paper by Yu and colleagues [1] who looking at "97 doctor-diagnosed ADHD cases and 110 non-ADHD controls who were 4-15 years of age" examined urine and blood samples for various factors including "biomarkers of OP [organophosphate] pesticide exposure." They concluded that, adjusting for creatinine, urine levels of DMP but not other dialkylphosphate (DAP) metabolites were higher in the ADHD group compared with the non-ADHD group. Further: "Organophosphate pesticide exposure may have deleterious effects on children's neurodevelopment, particularly the development of ADHD." At the same time, Yu et al also reported nothing very much to see when it came to blood lead levels (BLLs) between the groups.This is not the first time that examination of urinary metabolites of OPs have turned up something of a potential relationship with behavioural outcomes related to ADHD. The paper by Bouchard and colleagues [2] also reported a possible connection supporting a "hypothesis that organophosphate exposure, at levels common among US children, may contribute to ADHD prevalence." There too urine was the analytical medium and dialkylphosphate concentrations the target compounds. This and other research looking at this issue have led to statements [3] to the effect that: "Children's exposures to pesticides should be limited as much as possible." I don't think many people would disagree with that sentiment.I've talked about OPs quite a bit on this blog (see here and see here) and how various conditions/labels might be 'associated' with this class of compounds either when used as insecticides or as something rather more ominous. I've tried not to be too alarmist about the possibility of a connection with health because OPs do serve an important purpose (as an insecticide) and have probably saved quite a few lives as a result. But it is getting increasingly difficult to ignore the possibility that this and other classes of pesticides either alone or in combination with other factors, seem to be implicated in various conditions/labels and more needs to be done looking at the hows and whys. This can however be done without scaremongering.The Yu results whilst interesting are not however without some cautions. DAP metabolites as markers for OP exposure still requires further investigations [4], not least from which specific OP they are derived from. That other factors such as exposure to second-hand tobacco smoke might also link into the presentation of specific metabolites such as DMP [5] is another consideration. Continuing the theme that combinatorial exposures might also exert an effect [6] other research illustrates how difficult it might be to pin one specific type of exposure to specific behavioural outcomes. And then also we have the added layer of complexity that is the genetics of xenobiotic metabolism with specific focus on OPs. Relationships are likely to be pretty complicated as a result.Having said all that does not however mean that results like the ones from Yu et al can be just brushed under the carpet...Music to close, and having watched Guardians of the Galaxy for the Nth time last evening, all I can say is the film soundtrack is kinda cool...----------[1] Yu CJ. et al. Increased risk of attention-deficit/hyperactivity disorder associated with exposure to organophosphate pesticide in Taiwanese children. Andrology. 2016 Apr 12.[2] Bouchard MF. et al. Attention-deficit/hyperactivity disorder and urinary metabolites of organophosphate pesticides. Pediatrics. 2010 Jun;125(6):e1270-7.[3] Roberts JR. et al. Pesticide exposure in children. Pediatrics. 2012 Dec;130(6):e1765-88.[4] Sudakin DL. & Stone DL. Dialkyl phosphates as biomarkers of organophosphates: the current divide between epidemiology and clinical toxicology. Clin Toxicol (Phila). 2011 Nov;49(9):771-81.[5] Jain RB. Levels of dialkylphosphate metabolites in urine among general U.S. population. Environ Toxicol Pharmacol. 2016 Feb 26;43:74-82.[6] Osaka A. et al. Exposure characterization of three major insecticide lines in urine of young children in Japan-neonicotinoids, organophosphates, and pyrethroids. Environ Res. 2016 May;147:89-96.----------Yu CJ, Du JC, Chiou HC, Chung MY, Yang W, Chen YS, Fuh MR, Chien LC, Hwang B, & Chen ML (2016). Increased risk of attention-deficit/hyperactivity disorder associated with exposure to organophosphate pesticide in Taiwanese children. Andrology PMID: 27070915... Read more »

  • April 28, 2016
  • 05:33 PM
  • 50 views

MERS-CoV and antiviral singling: role of orf4b and M protein

by thelonevirologist in Virology Tidbits

Coronaviruses (CoV) are positive sense RNA viruses with a genome size of 29-32 kb with four genera (Alpha-, Beta-, Gamma- and Delta CoV) belonging to the family of the Coronaviridae within the order of Nidovirales, with the Betacoronaviruses further divided into four lineages (A-D).

Most CoV identified until now are causing severe disease only in animals including agricultural important animals such as chicken, cattle, and pigs. To date only six human CoV (HCoV) have been identified, namely HCoV-229E, HCoV-OC43, HCoV-NL63, HCoV-HKU1, Severe Respiratory Syndrome (SARS)-CoV and most recently Middle Eastern Respiratory Syndrome (MERS)-CoV, although a SARS-like CoV, WIV1-CoV, replicates in primary human epithelial cells at low levels as well as in mice expressing the human SARS-CoV receptor ACE2 albeit at lower levels compared to SARS-CoV.
Here recent advances concerning the inhibition of the antiviral response with a focus on the viral orf4b and M proteins derived from MERS-CoV are discussed. ... Read more »

Han, H., Wen, H., Zhou, C., Chen, F., Luo, L., Liu, J., & Yu, X. (2015) Bats as reservoirs of severe emerging infectious diseases. Virus Research, 1-6. DOI: 10.1016/j.virusres.2015.05.006  

Menachery VD, Yount BL Jr, Sims AC, Debbink K, Agnihothram SS, Gralinski LE, Graham RL, Scobey T, Plante JA, Royal SR.... (2016) SARS-like WIV1-CoV poised for human emergence. Proceedings of the National Academy of Sciences of the United States of America. PMID: 26976607  

Munster, V., Adney, D., van Doremalen, N., Brown, V., Miazgowicz, K., Milne-Price, S., Bushmaker, T., Rosenke, R., Scott, D., Hawkinson, A.... (2016) Replication and shedding of MERS-CoV in Jamaican fruit bats (Artibeus jamaicensis). Scientific Reports, 21878. DOI: 10.1038/srep21878  

Thornbrough JM, Jha BK, Yount B, Goldstein SA, Li Y, Elliott R, Sims AC, Baric RS, Silverman RH, & Weiss SR. (2016) Middle East Respiratory Syndrome Coronavirus NS4b Protein Inhibits Host RNase L Activation. mBio, 7(2). PMID: 27025250  

Li Y, Banerjee S, Wang Y, Goldstein SA, Dong B, Gaughan C, Silverman RH, & Weiss SR. (2016) Activation of RNase L is dependent on OAS3 expression during infection with diverse human viruses. Proceedings of the National Academy of Sciences of the United States of America, 113(8), 2241-6. PMID: 26858407  

Castelli, J., Wood, K., & Youle, R. (1998) The 2-5A system in viral infection and apoptosis. Biomedicine , 52(9), 386-390. DOI: 10.1016/S0753-3322(99)80006-7  

  • April 28, 2016
  • 11:30 AM
  • 72 views

Sophie Deneve and the efficient neural code

by neuroecology in Neuroecology

Neuroscientists have a schizophrenic view of how neurons. On the one hand, we say, neurons are ultra-efficient and are as precise as possible in their encoding of the world. On the other hand, neurons are pretty noisy, with the variability in … Continue reading →... Read more »

Denève, S., & Machens, C. (2016) Efficient codes and balanced networks. Nature Neuroscience, 19(3), 375-382. DOI: 10.1038/nn.4243  

  • April 28, 2016
  • 10:45 AM
  • 78 views

Phylo.io a new interactive way of visualising and comparing trees

by Christophe Dessimoz in Open Reading Frame

The paper introducing our new tree visualisation tool Phylo.io was just published in MBE.

Yet another tool to display trees, you might say, and indeed, so it is. But for all the tools that have been developed over the years, there are very few that scale to large trees, make it easy to compare trees side-by-side, and simply run in a browser on any computer or mobile device.

To fill this gap, we created Phylo.io.

Story behind the paper

The project started as a student summer internship project, with the aim of producing a tree visualiser that facilitates comparison of trees built on the same set of leaves. After reading the project description, Oscar Robinson, a brilliant student from the Computer Science department at UCL, decided to work on this project during a three month internship. He saw a chance to apply his experience in the development of web tools and to develop his knowledge in the field of data visualisation, one of his major interests.

Once Oscar started with the development of Phylo.io, he realised that only a few tools existed for visual comparison of two trees and either seemed to rely on old technology or were cumbersome to use. Especially this incentive lead him to develop our tool into a fully fledged online resource that is easy to use, platform independent and based on the newest javascript libraries (e.g. D3). Within three months, he managed to produce a prototype of the tool. However, due to the short length of the internship, some details still needed a bit of attention.

Luckily for me, I started my PostDoc in the Dessimoz Lab around that time. Being a novice in a computational lab, Christophe proposed to me to take over the project and bring it to completing as a way to kickstart my postdoc. Altough my computational background at that time did not include any experience in JavaScript programming, I anyway accepted the challenge and was eager to start learning the material. Especially my initial steep learning progress was facilitaed by the help of two other brilliant PhD students, Alex Vesztrocy and Clément Train. Once I acquired some basic understanding, I was able to resolve bugs and add some key missing functionalities such as automatic tree rerooting or persistent storage and sharing functionality.

What is phylo.io and what can it do?

Phylo.io is a web tool that works in any modern browser. All computations are performed client-side and the only restriction on performace is the machine it is running on. Trees can be input in Newick and Extended Newick format. Phylo.io offers many features that other tree viewers have. Branches can be swapped, the rooting can be changed, the thickness, font and other parameters are adaptable. Many of these operations can be performed directly by clicking on a branch or a node in the tree. Importantly, it features an automatic subtree collapsing function: this facilitates the visualisation of large trees and hence the analysis of splits that are deep in the tree.

Next to basic tree visualisation/manipulation it features a compare mode. This mode allows to compare two trees computed using different tools or different models. Similarities and differences are highlighted using a colour scheme directly on the individual branches, making it clear where the differences in two topologies actually are. Additionally, since the output of different tools provides trees with very different rootings and leaf order, Phylo.io has a function to root one of the trees according to the other one and adapt the order of the leaves according to a fixed tree.

How do you use phylo.io?

In order to save you some time below you find a screencast explaining the major features and usage of Phylo.io to visualise and compare trees.



 

Reference

Robinson, O., Dylus, D., & Dessimoz, C. (2016). Phyla.io: interactive viewing and comparison of large phylogenetic trees on the web
Molecular Biology and Evolution DOI: 10.1093/molbev/msw080
... Read more »

  • April 28, 2016
  • 09:33 AM
  • 75 views

Breathing Bordeaux is entirely different from drinking it!

by Rosin Cerate in Rosin Cerate

It was the summer of 1882, and grape farmers in the Médoc region of southwest France (north of Bordeaux, on the Atlantic coast) had a problem.Schoolchildren (or university students, or just anyone travelling the roads along which the grapevines grew, depending on what source you're reading) were pilfering their grapes. To try and ward them off, some farmers decided to dissolve some slaked lime and copper sulfate in water and spray it on their grapevines closest to the roads. The idea was... Read more »

  • April 28, 2016
  • 06:19 AM
  • 78 views

Portrait of a linguistic shirker

by Ingrid Piller in Language on the Move








I recently pointed out that the widespread belief that migrants refuse to learn the language of their new country does not stack up against the realities of adult language learning. I summarized the research that shows that adult language learning is complex and difficult and rarely an all-out success; to blame migrants for their failure to learn a new language (well) is adding insult to injury.
The German-language club (“Stammtisch”) in New York founded by Graf met until 2015 (Source: derstandard.at)
These well-established facts do not mean that individual migrants may not actively choose not to learn a new language. Unfortunately, we know surprisingly little about people who refuse to learn a new language. Partly, this is a problem of methods: how would one collect data about language refusal? While many non-migrants in Western societies believe themselves surrounded by language shirkers, it seems unlikely that advertising for research participants “who are refusing to learn the national language” would produce too many volunteers. Not only because, as I have shown, unadulterated language refusal is rare but also because migrants who actually might refuse to learn the language of their new society are, of course, in a double bind that would make it difficult to admit to language shirking.
Does that mean we are stuck between believing either those who see themselves surrounded by language shirkers or those who doubt their existence – depending on whether we are inclined to take a pessimistic or an optimistic view of our fellow humans? Not quite.
Let me introduce an unabashed language shirker, the German-language author Oskar Maria Graf, who spent almost half of his life in New York but was quite open about the fact that he had little interest in even trying to learn English.
Oskar Maria Graf (1894-1967) was a Bavarian “provincial author” (as he called himself) with an anarchist bent. As a committed socialist and pacifist, and an active participant in the socialist Munich revolution of 1919, which had established a short-lived Soviet republic in Bavaria, Graf fled Germany immediately after Hitler came to power in early 1933. He spent time in neighbouring Austria and Czechoslovakia but, as European countries of exile became increasingly precarious, Graf, like all German refugees, had to look for a safe haven further afield. In 1938 he and his wife were granted a US visa. They arrived in New York in September 1938 and continued to live there until their deaths.
Oskar Maria Graf, 1927, painting by Georg Schrimpf (Source: Wikipedia)
Back home, Graf had been a successful author during the interwar period. An autodidact (he left school when he was twelve years old and was apprenticed as a baker), Graf specialized in social realism with a focus on local Bavarian themes. After he had to leave his native country, the whole basis of his literary work – based as it was in the German language and the close observation of the mundane lives of Bavarian peasants – disappeared. He continued to write in German and his best-known book, Das Leben meiner Mutter (“The life of my mother”), was, in fact, written in exile but the success of his Munich years eluded him. Between 1933 and 1945, his opportunities to publish in German were severely limited; and he never returned to live in Germany even after the war despite the fact that his career was tied to German-language publishing.
Having been forced from home and wanting to retain the lost home are themes that, for Graf, are deeply connected to linguistic questions of maintaining the German language and not learning the English language. Let’s now examine what Graf’s language refusal looked like.
Graf almost celebrated the fact that he did not know how to speak English; it is a topic that comes up again and again in his later writing. A good example comes from his 1959 novel Die Flucht ins Mittelmäßige (“Taking refuge in mediocrity”), which is concerned with a group of German emigrants in New York. One of the main characters, Martin Ling, is commonly taken to be Graf’s alter ego, and Ling’s English language proficiency is introduced early in the novel as follows:













TranslationOriginal






Ling had been living in New York for almost twenty years and up to now understood little more than a few indispensable English phrases. He made no efforts to improve his language skills, either; he had adopted nothing ‘American’ apart from what seemed automatically and mechanically comfortable to him. As a result, of course, he had made no progress and never got anywhere.









Ling lebte schon fast zwanzig Jahre in New York und verstand bis jetzt immer noch kaum mehr als einige notwendige englische Redewendungen. Er gab sich auch gar keine Mühe, seine Sprachkenntnisse zu vervollständigen, und ausser demjenigen, was ihm gewissermaßen automatisch-mechanisch komfortabel erschien hatte er auch sonst noch nichts ‘Amerikanisches’ angenommen. Dadurch kam er natürlich nie vorwärts und weiter. (Flucht ins Mittelmäßige, p. 8)
















That his lack of English language proficiency was not only coy self-effacement has been confirmed by the observations of many others who knew him in New York. Lisa Hoffman, for instance, who was his lover in the 1950s, described in a 2010 newspaper interview how his English was j... Read more »

  • April 28, 2016
  • 03:46 AM
  • 71 views

The Neural Precursors of Spontaneous Thoughts

by Neuroskeptic in Neuroskeptic_Discover

Back in 2013, I wondered if we would ever discover the neural basis of spontaneous thoughts. Why, I asked, do certain ideas just "pop" into our minds at particular times? Now a new paper published in Neuroimage, Canadian neuroscientists Melissa Ellamil and colleagues reports on the neural basis of spontaneous thoughts.



Ellamil et al. recruited a group of 18 volunteers, all of whom were highly experienced practitioners of mindfulness meditation. These individuals were selected, the authors... Read more »

  • April 28, 2016
  • 02:55 AM
  • 81 views

What parents of children with autism expect from their child's therapists

by Paul Whiteley in Questioning Answers

"Parents ultimately wanted therapists to produce positive outcomes for their children and were willing to sacrifice other desired qualities, as long as the therapy program was effective."and"The SLPs [Speech-Language Pathologists] expressed strong support for evidence-based practice (EBP) and indicated that they thought parents expected their children would be provided with evidence-based interventions."Those quotes come from two papers recently published in the same journal; the first by Amelia Edwards and colleagues [1] attempting to identify "the qualities parents seek in therapists who work with their children with ASD [autism spectrum disorder]" and the second from David Trembath and colleagues [2] titled: 'What do speech-language pathologists think parents expect when treating their children with autism spectrum disorder?'Providing what is a quite fascinating (albeit small scale) insight into the expectations of therapists and parents who use therapists for their children when it comes to autism, these papers put some science to what many people might already have suspected. The Edwards paper also carried an important sentence in the paper title - "More than blowing bubbles" - implying how positive real world outcomes are always going to be the most important elements of any intervention program when it comes to autism or indeed, any other label. The idea that avenues towards those positive outcomes should be 'evidence-based' is perhaps a sentiment noted in the views and opinions of [many of] those professionals delivering intervention but might not necessarily be first and foremost for parents whose natural instinct is to want the best for 'their child'.The link between the concept of 'evidence-based' and autism is particularly interesting. A few years back I covered a paper by Gary Mesibov & Victoria Shea [3] (see here) carrying the idea that there may be both "benefits and limitations" when it came to the application of evidence-based policy and autism intervention. The sorts of variables that made evidence-based policy difficult when applied to autism ranged from the vast heterogeneity present under the label (or labels) to the idea that the gold-standard 'randomised controlled trial' (RCT) might not be all that suitable when assessing comprehensive intervention programs that for example, contain multiple elements. In subsequent years we've also learned that autism rarely appears in some sort of diagnostic vacuum (see here), something that might also impact on evidence-based policy with regards to intervention (see here). For scientific puritans, the Mesibov-Shea discussions could be construed as heresy. For me, there was some substance in their arguments and some lessons on how autism research in particular, needs to adapt and change away from the notion that 'autism' universally covers everyone with autism in terms of similar aetiology and pathology. Endophenotypes and 'snowflakes' people...It should of course be recognised that quite a lot of the 'not-knowing' when it comes to the autism spectrum has set the field of autism intervention up for a variety of 'unusual' proposals for interventions, many of which have not been suitably scientifically tested (see here). Some are even downright unsafe but are still pursued for one reason or another, probably pertinent to that opening sentence on 'effectiveness' and no doubt playing into other emotions as and when a child presents with autism [4]. Feelings run high on this topic as I once again refer you to the post by Tom Insel on the 'kingdoms of autism' (see here) with a suggestion that different views be respected but at the same time, safety should be paramount.Acknowledging that there is no 'one-size-fits-all- approach when it comes to autism intervention and that for some, mention of the words 'therapy' and 'intervention' are not necessarily high on their list of priorities, the Edwards and Trembath papers invite quite a bit more investigation. The possibility of a 'disconnect' between what parents want for their children and what therapists are currently able to deliver for their children represents something that could potentially impact on the delivery of intervention and the importance of the parent-professional relationship in this context. I'm also going to throw the paper by Paynter and colleagues [5] into this mix too...To close, I feel old. Jossy's Giants is 30 years old (although I'm more inclined to the Red and White)...----------[1] Edwards A. et al. "More than blowing bubbles": What parents want from therapists working with children with autism spectrum disorder. Int J Speech Lang Pathol. 2016 Apr 4:1-13.[2] Trembath D. et al. What do speech-language pathologists think parents expect when treating their children with autism spectrum disorder? Int J Speech Lang Pathol. 2016 Mar 10:1-9.[3] Mesibov GB. & Shea V. Evidence-based practices and autism. Autism. 2011 Jan;15(1):114-33.[4] Ooi KL. et al. A meta-synthesis on parenting a child with autism. Neuropsychiatric Disease and Treatment. 2016; 12: 745-762.[5] Paynter JM. et al. Utilisation of evidence-based practices by ASD early intervention service providers. Autism. 2016. April 18.----------Edwards, A., Brebner, C., Mccormack, P., & Macdougall, C. (2016). “More than blowing bubbles”: What parents want from therapists working with children with autism spectrum disorder International Journal of Speech-Language Pathology, 1-13 DOI: 10.3109/17549507.2015.1112835Trembath, D., Hawtree, R., Arciuli, J., & Caithness, T. (2016). What do speech-language p... Read more »

  • April 27, 2016
  • 04:55 PM
  • 159 views

Addiction, it’s in your genes… maybe

by Dr. Jekyll in Lunatic Laboratories

Why does one person who tries cocaine get addicted, while another might use it and then leave it alone? Why do some people who kick a drug habit manage to stay clean, while others relapse? And why do some families seem more prone to addiction than others? According to a new study, the road to answering these questions may have a lot to do with specific genetic factors that vary from individual to individual.

... Read more »

Flagel, S., Chaudhury, S., Waselus, M., Kelly, R., Sewani, S., Clinton, S., Thompson, R., Watson, S., & Akil, H. (2016) Genetic background and epigenetic modifications in the core of the nucleus accumbens predict addiction-like behavior in a rat model. Proceedings of the National Academy of Sciences, 201520491. DOI: 10.1073/pnas.1520491113  

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