Post List

  • May 3, 2016
  • 02:58 AM

Machine learning applied to autism screening going big time?

by Paul Whiteley in Questioning Answers

Machine learning, when machines, er.. learn, is of growing interest to the autism research field. The names Wall and Duda have filled quite a few posts on this blog (see here and see here for example) on this topic and their suggesting that applying machine learning algorithms to something like autism screening and detection could cut down on time taken and resources used.As per the publication of the paper by Daniel Bone and colleagues [1] it appears that others working in autism research are also waking up to the idea that this might be a useful area to investigate. So: "In this work, we fastidiously utilize ML [machine learning] to derive autism spectrum disorder (ASD) instrument algorithms in an attempt to improve upon widely used ASD screening and diagnostic tools." Fastidiously is such a lovely word (particularly in the context of science).The tools in question were the Autism Diagnostic Interview-Revised (ADI-R) and Social Responsiveness Scale (SRS) (both of which have already been machine learning 'applied') and their scores "for 1,264 verbal individuals with ASD [autism spectrum disorder] and 462 verbal individuals with non-ASD developmental or psychiatric disorders, split at age 10." And the results... well, let's just say that the authors were not disappointed - or at least less disappointed than on previous research occasions [2] - as they reported on created algorithms that "were more effective (higher performing) than the current algorithms, were tunable (sensitivity and specificity can be differentially weighted), and were more efficient (achieving near-peak performance with five or fewer codes)." Indeed: "We present a screener algorithm for below (above) age 10 that reached 89.2% (86.7%) sensitivity and 59.0% (53.4%) specificity with only five behavioral codes." Sensitivity and specificity are important concepts when it comes to something like screening instruments in terms of identifying 'all' those with a specific condition and making sure that no 'not-cases' aren't mistakenly identified as 'cases'. The nearly 90% sensitivity rate presented by Bone et al on the basis of 5 behavioural codes is not to be sniffed at.The addition of one Cathy Lord to the authorship of the Bone paper also adds an air of inevitability that applying machine learning to autism research (and practice) is going to continue and increase. Not only because of her historical connection to the ADI-R [3] (which is a hefty document in anyone's book) but also given her very prominent role in autism research history. Who knows, I might one day be blogging about more big autism research names talking about Wall/Duda things including autism screening triage by YouTube? The final question is: outside of just behavioural variables, who would be brave enough to talk genetics/epigenetics/biology machine learning as the next step in autism screening and/or assessment?----------[1] Bone D. et al. Use of machine learning to improve autism screening and diagnostic instruments: effectiveness, efficiency, and multi-instrument fusion. J Child Psychol Psychiatry. 2016 Apr 19.[2] Bone D. et al. Applying machine learning to facilitate autism diagnostics: pitfalls and promises. J Autism Dev Disord. 2015 May;45(5):1121-36.[3] Lord C. et al. Autism Diagnostic Interview-Revised: a revised version of a diagnostic interview for caregivers of individuals with possible pervasive developmental disorders. J Autism Dev Disord. 1994 Oct;24(5):659-85.----------Bone D, Bishop S, Black MP, Goodwin MS, Lord C, & Narayanan SS (2016). Use of machine learning to improve autism screening and diagnostic instruments: effectiveness, efficiency, and multi-instrument fusion. Journal of child psychology and psychiatry, and allied disciplines PMID: 27090613... Read more »

  • May 2, 2016
  • 02:45 PM

Origin of synaptic pruning process linked to learning, autism and schizophrenia identified

by Dr. Jekyll in Lunatic Laboratories

Vaccines don't cause autism, but because the brain is so complex, we still don't know how much of it works so figuring out the real causes (as in more than one) of autism has been slow going. Well, researchers have identified a brain receptor that appears to initiate adolescent synaptic pruning, a process believed necessary for learning, but in this case it is one that appears to go awry in both autism and schizophrenia.... Read more »

Sonia Afroz, Julie Parato, Hui Shen Sheryl, & Sue Smith. (2016) Synaptic pruning in the female hippocampus is triggered at puberty by extrasynaptic GABAA receptors on dendritic spines . eLife. info:/

  • May 2, 2016
  • 07:11 AM

"Neuroscience-Based Nomenclature" for Mental Health?

by Neuroskeptic in Neuroskeptic_Discover

Psychiatric drugs come in many kinds: there are antidepressants, antipsychotics, anti-anxiety medications, and more. But what all of these categories have in common is that they're anti- something. This is how we classify these drugs - by what they treat.

Except there's a problem - very few psychiatric drugs are only used to treat one thing. Take "antipsychotics". They're used in psychosis, but they're also a key tool in the treatment of mania, a different disorder entirely. Many of these dru... Read more »

Zohar J, Stahl S, Moller HJ, Blier P, Kupfer D, Yamawaki S, Uchida H, Spedding M, Goodwin GM, & Nutt D. (2015) A review of the current nomenclature for psychotropic agents and an introduction to the Neuroscience-based Nomenclature. European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology, 25(12), 2318-25. PMID: 26527055  

  • May 2, 2016
  • 04:30 AM

If the Helmet Don’t Fit, You May Have to Sit (Out Longer with a Concussion)

by Stephen Stache in Sports Medicine Research (SMR): In the Lab & In the Field

An athlete with a poorly fit helmet that sustains a concussion may have an increased risk of more severe symptoms and prolonged recovery.... Read more »

  • May 2, 2016
  • 03:50 AM

A statistical regression approach to estimate zooplankton mortality

by sceintists from the Marine group at CEES in Marine Science blog

It is notoriously difficult to estimate mortality rates for zooplankton populations in the open ocean. In a new paper, Kvile and colleagues demonstrate that mortality estimation can be improved using a statistical regression approach (SRA) that takes into account advection and spatiotemporal trends in recruitment. Using this method on
Calanus finmarchicus survey data from the Norwegian Sea–Barents Sea, they find indications of increased mortality for the oldest copepodite stage pair (CIV–CV), possibly reflecting higher predation pressure on larger copepodites.

... Read more »

  • May 2, 2016
  • 02:55 AM

On defining chronic fatigue syndrome / myalgic encephalomyelitis (CFS/ME)

by Paul Whiteley in Questioning Answers

Most people who know a little bit about chronic fatigue syndrome / myalgic encephalomyelitis (CFS/ME) will probably understand the potential importance of the findings reported by Leonard Jason and colleagues [1] (open-access available here). Suggesting that there may be "four groupings of patients" when it comes to how we "name and define the illnesses", this research group who surveyed over 500 people "in the United States, Great Britain, and Norway" report on one of the biggest challenges facing ME/CFS... how do we accurately define it?The problem of defining CFS/ME stems from the fact that there are currently several clinical presentations where CFS/ME might figure (or at least where patients fulfil ME/CFS criteria) and several different ways of clinically defining the condition(s) (see here and see here). That list of definitions may indeed also be growing (see here). With all that confusion about clinical overlap and what criteria are defining what patient group, it's little wonder that research is just starting to come to grips with some of the potential underlying biology of [some] CFS/ME (see here) after so many years in the scientific wilderness. Indeed, as with many conditions resting in that 'unexplained symptoms' category, not knowing can sometimes be fertile ground for various [unfounded] theorising...Jason et al (whose research has graced this blog before) set about categorising their participant group based on various case definitions and symptom presentations. They reported four groupings; by far the largest group of their participants (n=346) fell into a categorisation that "involves more specific criteria" defining CFS/ME including use of the relative new term SEID (Systemic Exertion Intolerance Disease). Further: "efforts have specified domains of substantial reductions of activity, post-exertional malaise, neurocognitive impairment, and sleep dysfunction" and "Patients with these characteristics were more functionally impaired than those meeting just chronic fatigue criteria." The term used by authors for this group was Neuroendocrineimmune Dysfunction Syndrome (NDS) following on from previous work [2]. Smaller numbers of people included on their study did meet criteria for chronic fatigue (greater than 6 months) with (n=47) or without (n=62) explanation "by medical or psychiatric conditions." Jason and colleagues also defined a smaller group who met the Ramsay ME criteria and who were described as an "even more impaired group." I wonder if this might include the 'housebound' group described in other research?The authors accept that there are 'limitations' to their research including issues around how they chose their sample(s) and some of the tools used relying on self-report; further work is indicated. But as a start trying to disentangle both the heterogeneity and issues with clinical classification when it comes to CFS/ME, their paper represents a good attempt to further focus minds on the spectrum of various overlapping fatigue conditions present and how we go about teasing apart phenotypes with a focus on core symptoms [2]. Minus the psychiatry focus, perhaps it is time to also looking at applying something like the principles of RDoC to the issue of ME/CFS?----------[1] Jason LA. et al. Case definitions integrating empiric and consensus perspectives. Fatigue. 2016;4(1):1-23.[2] Jason LA. et al. Factor Analysis of the DePaul Symptom Questionnaire: Identifying Core Domains. J Neurol Neurobiol. 2015 Sep;1(4).----------Jason LA, McManimen S, Sunnquist M, Brown A, Furst J, Newton JL, & Strand EB (2016). Case definitions integrating empiric and consensus perspectives. Fatigue : biomedicine, health & behavior, 4 (1), 1-23 PMID: 27088059... Read more »

Jason LA, McManimen S, Sunnquist M, Brown A, Furst J, Newton JL, & Strand EB. (2016) Case definitions integrating empiric and consensus perspectives. Fatigue : biomedicine, health , 4(1), 1-23. PMID: 27088059  

  • May 1, 2016
  • 02:17 PM

Influence of religion and predestination on evolution and scientific thinking

by Dr. Jekyll in Lunatic Laboratories

Generally seen as antithetical to one another, evolution and religion can hardly fit in a scientific discourse simultaneously. However, in a new article, a biology researcher delves into observations on the influences a few major religions have had on evolutionists and their scientific thinking over the centuries.

... Read more »

  • May 1, 2016
  • 11:00 AM

Being Explicit About Symmetry

by Joshua Fisher in Text Savvy

Working to orient oneself to the symmetries available in mathematical situations seems like one appropriate remedy to what I've called "left-to-rightism," or "cinemathematics"—a syndrome that makes us teach concepts like the equals sign (unwittingly) in a left-to-right way, such that students take away (unwittingly) the misconception that the equals sign indicates that some answer is to follow, rather than that two expressions are equal. Some recent research points to the benefits of thinking about symmetry when teaching negative numbers as well.... Read more »

  • May 1, 2016
  • 03:01 AM

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

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

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

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

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

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

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

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: 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

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

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

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

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 »

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