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  • April 15, 2016
  • 09:12 AM

Rewriting life: Adding letters to the ABC of DNA

by gdw in FictionalFieldwork

(Also appeared on United Academics.) The alphabet of life The grand tale of life is long and complicated. Storylines intertwine and many subplots twist and turn unexpectedly. Amazingly, this billion-year-spanning story is written in an alphabet that contains only four letters, the alphabet of DNA. A for adenine, C for cytosine, G for guanine, and […]... Read more »

Malyshev DA, Dhami K, Lavergne T, Chen T, Dai N, Foster JM, Corrêa IR Jr, & Romesberg FE. (2014) A semi-synthetic organism with an expanded genetic alphabet. Nature, 509(7500), 385-8. PMID: 24805238  

  • April 15, 2016
  • 05:01 AM

The transgenerational effects of prenatal immune activation?

by Paul Whiteley in Questioning Answers

The paper by Ulrike Weber-Stadlbauer and colleagues [1] provides some food for thought today with the suggestion that the concept of prenatal immune activation might have consequences further than just to exposed offspring.For those not familiar with the concept of prenatal immune activation, it refers to the process(es) that occur following "exposure to infectious or inflammatory insults" during the nine months that made us. As you'll probably be aware, our nine months of watery 'captivity' is an important time in making us who we are. It is also a time when we are unfortunately vulnerable to quite a few factors that can adversely affect our stay in the womb (see here and see here for examples) and indeed, that can have repercussions for our future development and wellbeing. Among the vast number of agents that can and do affect pregnancy, various infectious agents (such as viruses and bacteria) that have been with humankind since the year dot play a prominent role; either through their own actions or via what biochemical processes they initiate as a mother's body seeks to protect itself and its unborn child. In short, the maternal immune system might itself, at this crucial time of reprogrammed immune tolerance, exert a less than positive effect on the foetus as a result. The sorts of outcomes potentially linked to exposure to this prenatal immune activation are varied to say the least (see here).Weber-Stadbauer et al looking at a mouse model of prenatal immune activation - that's MOUSE model - took things one stage further by asking whether effects of such immune activation exposure might persist beyond just one generation of offspring. So: "Using an established mouse model of prenatal immune activation by the viral mimetic poly(I:C), we show that reduced sociability and increased cued fear expression are similarly present in the first- and second-generation offspring of immune-challenged ancestors." Further: "These transgenerational effects are mediated via the paternal lineage and are stable until the third generation, demonstrating transgenerational non-genetic inheritance of pathological traits following in-utero immune activation."When the authors suggest that their results "demonstrates for, we believe, the first time that prenatal immune activation can negatively affect brain and behavioral functions in multiple generations" they aren't kidding. Indeed, accompanied by the rise and rise of research talking about transgenerational inheritance not primarily mediated by more traditional structural genetics (as far as we know) the possibilities are truly endless if said processes are indeed transferable from mouse to humans.But just before we do get too carried away, let's be a little cautious. Aside from the fact that mice are mice and not humans (see here) and that complex behaviours like human sociability are probably not best served by looking solely at mice, these data need to be independently replicated. I note from other research by members of this authorship group [volumes of research it has to be said] the interest in how a label like 'schizophrenia' (or should that be schizophrenias?) might have a 'developmental neuroinflammation' element to it [2] implies that priming of the immune system should be something that is detectable (see here) and hence potentially amenable to change. Indeed, this may very well tie into the increasingly popular idea that immunopsychiatry is here to stay (see here). I would therefore, like to see a little more on how prenatal immune activation presents in immune system terms down the generations over and above "unique and overlapping genome-wide transcriptional changes in first- and second-generation offspring of immune-challenged ancestors." Does, for example, this imply that there is a potential biomarker set consisting of biochemical, epigenetic and transcriptional data that might characterise those at risk of such consequences? And indeed, are we all potentially the result of our grandmother's immune experiences as we might be her dietary patterns?To close, following the sad news that Gareth 'Blake's 7' Thomas has died, that theme tune...----------[1] Weber-Stadlbauer U. et al. Transgenerational transmission and modification of pathological traits induced by prenatal immune activation. Mol Psychiatry. 2016 Mar 29.[2] Meyer U. Developmental neuroinflammation and schizophrenia. Progress in Neuro-Psychopharmacology and Biological Psychiatry. 2013; 42: 20-34.----------Weber-Stadlbauer U, Richetto J, Labouesse MA, Bohacek J, Mansuy IM, & Meyer U (2016). Transgenerational transmission and modification of pathological traits induced by prenatal immune activation. Molecular psychiatry PMID: 27021823... Read more »

  • April 14, 2016
  • 03:45 PM

#Breadgate and nutritional psychiatry

by Paul Whiteley in Questioning Answers

The review paper by Paola Bressan & Peter Kramer [1] (open-access) titled: 'Bread and Other Edible Agents of Mental Disease' has been getting a few people a little hot under the collar recently. With it's own Twitter hashtag #breadgate it looks like the idea that certain foods might have something of a bearing on "human behaviour and mental health" has not been received particularly well. I might add that this not the first time that such ideas have been entertained (see here) but there was no such outcry on previous occasions...As anyone who drops by this blog might know, I'm quite interested in the idea that what we eat and how it's metabolised might have some important implications for SOME people in terms of not just their physical health but also other facets covering behaviour and cognition. I've also talked about it in the peer-reviewed domain quite a bit too using conditions such as phenylketonuria (PKU) as a template. In their latest paper, Bressan & Kramer discuss the quite long-running idea that [some] cereal grains, the starting material for foods like bread, might have some interesting physiological effects that could have a bearing on mental health and wellbeing.I should at this point mention that I was invited to peer-review the Bressan / Kramer article. I accepted (given my research in this area) and as well as providing a review also let the editor and authors know that my view whilst as unbiased as possible did come alongside a few conflicts of interest (COIs) such as the book that graces the edge of this blog. The journal editor accepted this fact and my comments alongside those of a far more notable researcher were included in the peer-review process.The Bressan / Kramer paper presents quite a thorough overview of the research looking at food and psychiatry. The language is quite stark in places as words like 'defect' and 'derangement' are included in the text (something that I queried during peer-review) and with a sub-heading titled 'Diet as a Cure' the authors are pretty forth-right in their interpretation of the available peer-reviewed evidence. I would be perhaps less strong in any claims made but ho-hum. I might add that this is not the first time that this authorship team have talked about big hypotheses...Without seeming like I am springing to the defence of the Bressan / Kramer paper I have decided to list a few previous blog entries that I've written about other relevant texts in the peer-reviewed domain that add something to the discussions in this area. I'm sure that Bressan / Kramer if they have heard about the 'discussions' around their paper are able to defend their writings and so I'm not doing this to somehow cover their backs. I do however think it is important to talk about this topic and this is as good an opportunity as any...So:Brain and gut in autism: a historical perspectiveFor many years now, diet and [some] autism has been discussed. The work of the late Curt Dohan was the leader in this emerging field and his suggestion that [some] schizophrenia might have a dietary component. Before you ask it, no, no-one has ever said that diets devoid of gluten and casein are some sort of cure-all for all autism... they're not. But that does not mean there might be 'best responders' to this type of intervention (see here) in terms of their effect on some behaviours linked to autism. The mechanism for any effect from diet could also be multi-fold (see here).Psychotic symptoms managed by a gluten-free diet?Yes. it's a case report, but there are quite a few of them in the peer-reviewed literature talking about dietary manipulations seemingly affecting often quite severe psychiatric presentation. There are more controlled trials too if you want to have a look...More gluten sensitivity and schizophreniaThe immune system seems to be in the ascendancy when it comes to psychiatry these days (see here also) and diet has been mentioned as an influencing variable on immune function...Gluten free diet adherence reduces depression in coeliac diseaseBuilding on the idea that coeliac disease - that archetypal autoimmune condition where gluten is the baddie - might have quite a few more 'presentations' than just the physical, there is some emerging peer-reviewed evidence to suggest that adherence to a gluten-free diet might have multiple benefits for certain groups.Just what is 'non-coeliac gluten sensitivity'?The idea that outside of coeliac disease there may be a spectrum of 'gluten-related ills' is not a new one. There are still gaps in the research literature and in particular, whether non-coeliac gluten sensitivity (NCGS) might intersect with certain behavioural and/or psychiatric labels but...Schizophrenia and milkWith the focus also on milk, or rather the casein protein that is also said to produce peptide metabolites that might not be a millions miles away from various opioid-like compounds like to gluten digestion (hence the name casomorphins), I've included reference to the David Niebuhr et al paper too titled: 'Association between bovine casein antibody and and new onset schizophrenia among US military personnel'. Correlation is not causation but this and other data are interesting.Intestinal permeability: an emerging scientific area (also with autism in mind)Gluten 'punching holes in the gut' is mentioned in some of the discussion about the Bressan / Kramer paper and with it the words 'leaky gut' make an appearance. As per my ramblings on some of the peer-reviewed science in this area, there is emerging evidence for this concept in relation to specific conditions including the fantastic paper by Laura de Magistris and colleagues [3] citing food as having a potentially modifying effect.These are just a selection of the entries that I've written on this blog covering the topic of nutritional psychiatry (see here) but there are more. Accepting that "mental disease" (authors term not mine) covers quite a lot of ground and even within the various labels we have a lot of heterogeneity (... Read more »

Bressan P, & Kramer P. (2016) Bread and Other Edible Agents of Mental Disease. Frontiers in human neuroscience, 130. PMID: 27065833  

  • April 14, 2016
  • 07:00 AM

Adding Letters To The ABC Of DNA

by Gunnar De Winter in United Academics

Researchers are working hard to expand the alphabet of life by adding new bases to DNA.... Read more »

Hirao I, & Kimoto M. (2012) Unnatural base pair systems toward the expansion of the genetic alphabet in the central dogma. Proceedings of the Japan Academy. Series B, Physical and biological sciences, 88(7), 345-67. PMID: 22850726  

Yang, Z., Chen, F., Alvarado, J., & Benner, S. (2011) Amplification, Mutation, and Sequencing of a Six-Letter Synthetic Genetic System. Journal of the American Chemical Society, 133(38), 15105-15112. DOI: 10.1021/ja204910n  

Malyshev, D., Dhami, K., Lavergne, T., Chen, T., Dai, N., Foster, J., Corrêa, I., & Romesberg, F. (2014) A semi-synthetic organism with an expanded genetic alphabet. Nature, 509(7500), 385-388. DOI: 10.1038/nature13314  

  • April 14, 2016
  • 02:51 AM

Risk of type 2 diabetes in autism

by Paul Whiteley in Questioning Answers

"Adolescents and young adults with ASD [autism spectrum disorder] were more likely to develop type 2 DM [type 2 diabetes mellitus] during the follow-up. In addition, those with ASD using atypical antipsychotics exhibited a high risk. Therefore, further research is necessary to investigate the common pathophysiology of ASD and type 2 DM."So said the findings reported by Mu-Hong Chen and colleagues [1] as, yet again, Taiwan and their very useful National Health Insurance Research Database (NHIRD) continues to give to autism and related research.Type 2 diabetes - the one where the pancreas don't produce enough insulin or the body's cells don't react to insulin - was the focus of NHIRD interrogation this time around, following in the scientific footsteps of previous research looking at both type 1 and type 2 diabetes in relation to autism (see here). Enrolling over 6,000 adolescents and young adults diagnosed with an autism spectrum disorder (ASD) and nearly 25,000 age and sex-matched controls "between 2002 and 2009", researchers followed participants until the end of 2011 watching for who and how many would be diagnosed with type 2 DM.Dividing groups into adolescents and young adults, researchers reported that those diagnosed with autism were at "higher risk of developing type 2 DM than those without ASD" after adjusting for various potential forms of bias including "atypical antipsychotics use, and medical comorbidities." Further: "Short-term... and long-term... use of atypical antipsychotics were associated with a higher likelihood of subsequent type 2 DM." Ergo, yet another important, growing and potentially life-changing comorbidity appears to be 'over-represented' when it comes to the label of autism.Accepting that it is not necessarily new news that certain pharmaceutical formulations can affect risk of type 2 diabetes [2], these are interesting and potentially important results. The focus on how maternal diabetes 'exposure' might modify risk of autism in offspring (see here) coupled to ideas about how autoimmunity inferred by type 1 diabetes history might link into some autism (see here) have tended to predominate in this area of the autism research landscape. The Chen results tap into a pretty under-appreciated idea that for one reason or another, a diagnosis of autism could potentially raise the risk of something like type 2 diabetes.There is additional research to do on this topic. So, in these days of greater appreciation that 'autism genes' might not necessarily just be 'genes for autism' (pleiotropy), one could reasonably ask the question of whether there are subtle genetic (or epigenetic) issues influencing risk of type 2 diabetes. As per my use of the word 'epigenetic' in that last sentence, I'm also minded to bring in the work from people like the late David Barker, and the idea that birth weight might also 'program' for a greater risk for type 2 diabetes and related health issues (see here) given what's known about this area with autism in mind (see here).That type 2 diabetes is not a wholly genetic issue is something else to bear in mind as issues such as weight and eating patterns come into the frame. Minus any sweeping generalisations, weight issues and particularly obesity are not uncommon research topics when it comes to autism (see here) and as for eating patterns and habits, well, let's just say there is some science there too (see here). Whether singularly or combined (and with potential added mention of exercise) one might already see how screening for type 2 diabetes should be added to the list of monitoring required when a diagnosis of autism is received. I might also mention some recent research chatter about leptin as being important to type 2 diabetes in kids and where that might go with regards to other autism research (see here). I'm sure there other factors too.And, if and when type 2 diabetes in diagnosed, there are a number of positive changes that can be made to lifestyle including the idea that 'reversal' is not something totally unheard of...So:  The Force Awakens and Dark Side of the Moon... synch or no synch?----------[1] Chen MH. et al. Risk of Developing Type 2 Diabetes in Adolescents and Young Adults With Autism Spectrum Disorder: A Nationwide Longitudinal Study. Diabetes Care. 2016 Mar 22. pii: dc151807.[2] Galling B. et al. Type 2 Diabetes Mellitus in Youth Exposed to Antipsychotics: A Systematic Review and Meta-analysis. JAMA Psychiatry. 2016 Mar 1;73(3):247-59.----------Chen, M., Lan, W., Hsu, J., Huang, K., Su, T., Li, C., Lin, W., Tsai, C., Tsai, S., Lee, Y., Chen, Y., Pan, T., Chang, W., Chen, T., & Bai, Y. (2016). Risk of Developing Type 2 Diabetes in Adolescents and Young Adults With Autism Spectrum Disorder: A Nationwide Longitudinal Study Diabetes Care DOI: 10.2337/dc15-1807... Read more »

  • April 14, 2016
  • 02:00 AM

Cancer metabolism and voluntary public goods games

by Robert Vander Velde in Evolutionary Games Group

When I first came to Tampa to do my Masters[1], my focus turned to explanations of the Warburg effect — especially a recent paper by Archetti (2014) — and the acid-mediated tumor invasion hypothesis (Gatenby, 1995; Basanta et al., 2008). In the course of our discussions about Archetti (2013,2014), Artem proposed the idea of combining two […]... Read more »

Hauert, C., De Monte, S., Hofbauer, J., & Sigmund, K. (2002) Replicator dynamics for optional public good games. Journal of Theoretical Biology, 218(2), 187-194. PMID: 12381291  

  • April 13, 2016
  • 06:35 PM

Zika Virus and induction of apoptosis: combination of IFN-β and downregulation of gene expression?

by thelonevirologist in Virology Tidbits

As described in a previous post, Zika virus (ZIKV) infection of primary human skin fibroblasts induces the upregulation of TLR3 mRNA as well as inducing the expression of MDA-5 and RIG-1, components of the antiviral response induced not only ZIKV but by RNA viruses in general. As a result of the activation of RIG-1 and MDA-5, the expression of both Interferon-α (IFN-α) and Interferon-β (IFN-β) is increased. In mouse models such as A129, AG129 or Ifnar1 -/- mice that are deficient for either the receptor for IFN-α or both for IFN-α and IFN-β, higher viral loads are established in a number of tissues compared to wt mice, suggesting that the induction of IFN-α and IFN-β by ZIKV limits viral replication. Here the induction of apoptosis by ZIKV in A549 is discussed.... Read more »

Ng CT, Sullivan BM, Teijaro JR, Lee AM, Welch M, Rice S, Sheehan KC, Schreiber RD, & Oldstone MB. (2015) Blockade of interferon Beta, but not interferon alpha, signaling controls persistent viral infection. Cell host , 17(5), 653-61. PMID: 25974304  

Tang H, Hammack C, Ogden SC, Wen Z, Qian X, Li Y, Yao B, Shin J, Zhang F, Lee EM.... (2016) Zika Virus Infects Human Cortical Neural Progenitors and Attenuates Their Growth. Cell stem cell. PMID: 26952870  

Faria NR, Azevedo RD, Kraemer MU, Souza R, Cunha MS, Hill SC, Thézé J, Bonsall MB, Bowden TA, Rissanen I.... (2016) Zika virus in the Americas: Early epidemiological and genetic findings. Science (New York, N.Y.). PMID: 27013429  

Hamel R, Dejarnac O, Wichit S, Ekchariyawat P, Neyret A, Luplertlop N, Perera-Lecoin M, Surasombatpattana P, Talignani L, Thomas F.... (2015) Biology of Zika Virus Infection in Human Skin Cells. Journal of virology, 89(17), 8880-96. PMID: 26085147  

Lazear, H., Govero, J., Smith, A., Platt, D., Fernandez, E., Miner, J., & Diamond, M. (2016) A Mouse Model of Zika Virus Pathogenesis. Cell Host . DOI: 10.1016/j.chom.2016.03.010  

Rossi SL, Tesh RB, Azar SR, Muruato AE, Hanley KA, Auguste AJ, Langsjoen RM, Paessler S, Vasilakis N, & Weaver SC. (2016) Characterization of a Novel Murine Model to Study Zika Virus. The American journal of tropical medicine and hygiene. PMID: 27022155  

Garcez PP, Loiola EC, Madeiro da Costa R, Higa LM, Trindade P, Delvecchio R, Nascimento JM, Brindeiro R, Tanuri A, & Rehen SK. (2016) Zika virus impairs growth in human neurospheres and brain organoids. Science (New York, N.Y.). PMID: 27064148  

Kumari J, Hussain M, De S, Chandra S, Modi P, Tikoo S, Singh A, Sagar C, Sepuri NB, & Sengupta S. (2016) Mitochondrial functions of RECQL4 are required for the prevention of aerobic glycolysis-dependent cell invasion. Journal of cell science, 129(7), 1312-8. PMID: 26906415  

Andersen J, VanScoy S, Cheng TF, Gomez D, & Reich NC. (2008) IRF-3-dependent and augmented target genes during viral infection. Genes and immunity, 9(2), 168-75. PMID: 18094709  

Aizawa S, Fujiwara Y, Contu VR, Hase K, Takahashi M, Kikuchi H, Kabuta C, Wada K, & Kabuta T. (2016) Lysosomal putative RNA transporter SIDT2 mediates direct uptake of RNA by lysosomes. Autophagy, 12(3), 565-78. PMID: 27046251  

Kimura T, Jain A, Choi SW, Mandell MA, Johansen T, & Deretic V. (2016) TRIM-Directed Selective Autophagy Regulates Immune Activation. Autophagy. PMID: 26983397  

Suthar, M., Aguirre, S., & Fernandez-Sesma, A. (2013) Innate Immune Sensing of Flaviviruses. PLoS Pathogens, 9(9). DOI: 10.1371/journal.ppat.1003541  

Han J, Back SH, Hur J, Lin YH, Gildersleeve R, Shan J, Yuan CL, Krokowski D, Wang S, Hatzoglou M.... (2013) ER-stress-induced transcriptional regulation increases protein synthesis leading to cell death. Nature cell biology, 15(5), 481-90. PMID: 23624402  

  • April 13, 2016
  • 11:30 AM

Hunting Bats Plan Two Bugs Ahead

by Elizabeth Preston in Inkfish

A flying insect that's suddenly swallowed by a bat probably doesn't have a lot of time to reflect on its fate. If it did, though, it might wonder how on Earth the swooping mammal managed to grab it with so little warning. The answer is that bats don't hunt just one bug at a time. While scanning the air with echoes, they manage to plan two victims ahead.

Bats aren't blind, despite what you may have read on Twitter. But bats that hunt at night rely on sound, not vision. They send out very h... Read more »

Fujioka, E., Aihara, I., Sumiya, M., Aihara, K., & Hiryu, S. (2016) Echolocating bats use future-target information for optimal foraging. Proceedings of the National Academy of Sciences, 201515091. DOI: 10.1073/pnas.1515091113  

  • April 13, 2016
  • 09:36 AM

Video Tip of the Week: Branch, a web-based tool offering decision trees for data analysis

by Mary in OpenHelix

Recently I highlighted a decision tree tool for experimental design. EDA, or Experimental Design Assistant, helps you to plan your experiment, choose the approrpiate groups and numbers you’ll need. Set some variables, etc. This week’s video also offers decision trees–but these help you to evaluate the data from your studies of interest instead. Branch is a […]... Read more »

  • April 13, 2016
  • 07:10 AM

Ivy League Climber

by Mark Lasbury in As Many Exceptions As Rules

English ivy doesn’t send out entwining tendrils, it doesn’t burrow into cracks as an anchor. It doesn’t have hooked thorns like a climbing rose – no, English ivy can grow up the side of Wrigley Field because its millions of adventitious roots secrete the strongest glue in the world. However, it doesn’t work like most glues – it works like a gecko’s feet. Oh, and it will help protect you from skin cancer too!... Read more »

  • April 13, 2016
  • 03:25 AM

Vitamin D deficiency and psychosis

by Paul Whiteley in Questioning Answers

In amongst my various ramblings about how vitamin D - the sunshine vitamin/hormone - might show more than a few connections to conditions/labels outside of just the English disease (see here), I've covered some science on a possible connection with psychosis (see here) and schizophrenia (see here). There are still gaps in terms of the hows and whys of vitamin D insufficiency and deficiency when it comes to this area of psychiatry, but I believe there is enough science in this area to initially warrant screening of vitamin D levels as and when a diagnosis is received. This similarly extends to other labels too (see here and see here).The paper by Lally and colleagues [1] (open-access) puts a little more scientific flesh on the bones about how vitamin D insufficiency/deficiency might manifest in cases of psychosis, with a particular focus on "increased cardiovascular disease risk factors and in particular metabolic syndrome [MetS]."With thanks to Brendon Stubbs (one of the authors of the paper) for bringing the findings to my attention, researchers set about looking at "the prevalence of vitamin D deficiency in a cohort of community patients with established psychotic illnesses" (N=324). Given my earlier mention of the 'English disease', the cohort were indeed all living in England and drawn from a larger study initiative. Vitamin D levels were assayed via a chemiluminescence immunoassay based on the examination of serum samples. Various other measures were also included for study around the issue of cardiovascular risk factors including body mass index (BMI), waist circumference, blood pressure, serum cholesterol levels and glucose levels. High sensitivity serum C-reactive protein (HS-CRP) was also included.Results: "Almost half of the sample (48.8 %, n = 158) were deficient in vitamin D while only 13.9 % (n = 45) had sufficient vitamin D." Ethnicity seemed to play a role in those determinations of deficiency/sufficiency with vitamin D levels generally lower in those who were black African or black Caribbean. Likewise the season of testing showed an effect. When it came to determining whether there was an association between vitamin D status and mental state, researchers reported nothing significant based on the use of the Positive And Negative Syndrome Scale (PANSS) and related measures.But... there might be quite a bit more to look at when taking into account those cardiovascular disease risk factors and vitamin D levels as the authors reported various significant correlations. So: "those with the highest levels of vitamin D have a lower prevalence of MetS (20.5 %), compared to those in the lowest (39.1 %), second (48.3 %) and third quartile (43.1 %) of vitamin D." Indeed, just about every measure of cardiovascular risk showed an association with measured serum vitamin D levels when controlling for "age, gender, ethnicity and season of 25-OHD blood sampling." The authors also add that: "Those engaging in low intensity physical activity over the week prior to sampling... had significantly lower 25-OHD levels... than those who engaged in moderate or high intensity physical activity."Teasing apart what might actually be doing what is a difficult task in such studies where various outcome measures might be implicated. The authors do speculate on how for example, their finding of "raised CRP and vitamin D deficiency in established psychosis" might tie into other research on inflammation or inflammatory processes with both variables in mind (see here and see here). Indeed, this might also tie in with calls for further integration of immunopsychiatry with psychotic disorders in mind [2]. But there remains more to do, including the intriguing question: "would the supplementation of vitamin D in psychosis prevent and/or ameliorate cardiovascular and metabolic risk?"I do have some small points to make about the study that might also require attention in follow-up work, not least the idea that immunoassay for determining functional vitamin D levels might not be the most accurate method [3]. Indeed, the authors make this point in their conclusions. One might also hope that comparisons with other patient groups might offer some further information about how specific the findings are to just psychosis or other psychiatric groupings. If found in a more general sense, the idea that vitamin D is related to variables affecting cardiovascular risk in such groups could make lots and lots of waves.For now however, this research extends the ideas that: (a) preferential screening for vitamin D might be indicated for this group/label, and (b) the focus on psychiatric presentation should not be made at the expense of somatic presentation. Parity of esteem and all that; or rather just making sure that health inequality does not follow from receipt of a psychiatric label...----------[1] Lally J. et al. Clinical correlates of vitamin D deficiency in established psychosis. BMC Psychiatry. 2016; 16: 76.[2] Leboyer M. et al. Is it time for immunopsychiatry in psychotic disorders? Psychopharmacology (Berl). 2016 Mar 18.[3] Yang Y. et al. High-throughput measurement of 25-hydroxyvitamin D by LC-MS/MS with separation of the C3-epimer interference for pediatric populations. Clin Chim Acta. 2016 Feb 15;454:102-6.----------Lally, J., Gardner-Sood, P., Firdosi, M., Iyegbe, C., Stubbs, B., Greenwood, K., Murray, R., Smith, S., Howes, O., & Gaughran, F. (2016). Clinical correlates of vitamin D deficiency in established psychosis BMC Psychiatry, 16 (1) DOI: 10.1186/s12888-016-0780-2... Read more »

Lally, J., Gardner-Sood, P., Firdosi, M., Iyegbe, C., Stubbs, B., Greenwood, K., Murray, R., Smith, S., Howes, O., & Gaughran, F. (2016) Clinical correlates of vitamin D deficiency in established psychosis. BMC Psychiatry, 16(1). DOI: 10.1186/s12888-016-0780-2  

  • April 12, 2016
  • 10:00 PM

Mating Oddities of the Southern Blue-Ringed Octopus

by Emily Makowski in Sextraordinary!

I discuss some unique characteristics of octopus mating and describe a recent article on the Southern blue-ringed octopus.... Read more »

  • April 12, 2016
  • 07:18 PM

The scientific brain: How the brain repurposes itself to learn scientific concepts

by Dr. Jekyll in Lunatic Laboratories

The human brain was initially used for basic survival tasks, such as staying safe and hunting and gathering. Yet, 200,000 years later, the same human brain is able to learn abstract concepts, like momentum, energy, and gravity, which have only been formally defined in the last few centuries. New research has now uncovered how the brain is able to acquire brand new types of ideas.
... Read more »

Robert A. Mason, & Marcel Adam Just. (2016) Neural Representations of Physics Concepts . Psychological Science. info:other/Pre-print

  • April 12, 2016
  • 11:53 AM

Bioterrorism: Lessons Learned From Anthrax

by Rita dos Santos Silva in United Academics

Anthrax attacks in 2001 were a wake-up call for the importance of preparedness.... Read more »

Riedel S. (2005) Anthrax: a continuing concern in the era of bioterrorism. Proceedings (Baylor University. Medical Center), 18(3), 234-43. PMID: 16200179  

Anderson, P. (2012) Bioterrorism: Toxins as Weapons. Journal of Pharmacy Practice, 25(2), 121-129. DOI: 10.1177/0897190012442351  

  • April 12, 2016
  • 09:47 AM

Return of the wild: How nature breaks down what we build up

by Rosin Cerate in Rosin Cerate

When I was a teenager, I read Stephen King's book The Stand. It begins with the near-obliteration of humankind by a lethal virus. This was weirdly alluring stuff for a angsty teenage daydreamer. What would you do if the world ended? What would be your fate? I figured I'd make it a couple of months on canned food before succumbing to some sort of brutal antibiotic-resistant bacterial infection.... Read more »

  • April 12, 2016
  • 02:51 AM

Evidence of blurring on the autism spectrum edges

by Paul Whiteley in Questioning Answers

A quote to begin: "multiple types of genetic risk for ASDs [autism spectrum disorders] influence a continuum of behavioral and developmental traits, the severe tail of which can result in diagnosis with an ASD or other neuropsychiatric disorder."That was the bottom line of the findings reported by Elise Robinson and colleagues [1] looking at data from "several large ASD consortium and population-based resources" (N~38,000) including the fabulous resource that is ALSPAC. Specifically analysing for various types of genetic 'risk' related to autism including inherited genetic issues and those so-called de novo variants (see here), researchers found that the genes thought to be influential in cases of autism also crossed over in to those who don't have autism in relation to skills such as social communication. To zoom in on some specific media interpretation of the findings: "The same genes involved in predisposing people to autism appear to influence social skills in the wider population, suggesting that the autism spectrum has no clear cut-off point, scientists have discovered."Personally, I'm not so surprised that these findings have turned out the way they have. As I was told many, many years ago when it comes to the presentation of [early] autism, the [core] behaviour(s) associated with autism in many respects, mirror that seen during various stages of child development. It is the intensity, duration and effect on daily life that merit the diagnosis. If one assumes that genes play a significant role in the presentation of certain facets of autism (or even certain types of autism [2]), the Robinson findings fit rather well into the whole autism as a "continuum model." I say this bearing in mind that common genetic variations have been previously discussed with autism in mind (see here) although seemingly no one-size-fits-all genetic pattern related to all autism has yet been reported (see here).Questions and caveats still remain however. First is the continued focus on structural genetics over and above other influences on gene expression such as that suggested by the science of epigenetics. I know there is a lot of hype in this area but there is also some good science emerging on aspects like the methylome and autism (see here) and some important links between the epigenome and autism and immune function for example (see here). I might also direct you to some interesting research suggesting that those fossil viruses that we all carry around in our genome might also exert some effect (see here). In short, variations in the structure of the genome are probably not the whole story when it comes to the presentation of autism or any other label (or anything sub-threshold-wise, around the diagnostic edges).Second, and added to the first point, is the idea that 'genes for autism' are probably not exclusive 'genes for autism' insofar as their potential links to other behaviours/labels. We know from other research (see here) that genes perform lots of functions either working as individuals or more likely working as groups. Combined with the idea that some of the behaviours/symptoms noted in cases of autism might have other 'associations' (see here) and the idea of pleiotropy comes to the forefront [3]. This also combines with the idea that autism rarely exists in some sort of diagnostic vacuum (see here). I might add that I'll be coming to the paper by Wen and colleagues soon enough...Finally, although it is tempting to use the Robinson findings as 'proof' that blurred genetic edges might mean 'we're all a little bit autistic', I'm happy to see that some commentators have countered such an assertion. As I hinted at earlier, the behaviours noted in autism are not somehow totally unconnected to the human experience insofar as all can be seen at some time or other during typical development. But... and it is an important point, autism is a diagnosis based on how said behaviours go well beyond that 'typical' categorisation in terms of their intensity, duration and importantly, effect on a person's life. Much like the pop quizzes asking 'are you autistic?' to say 'we're all a little autistic' potentially belittles what autism means to many, many people day-after-day-after day. And with recent reports on where autism in the extreme can sometimes lead (see here), caution is very much advised in this context.----------[1] Robinson EB. et al. Genetic risk for autism spectrum disorders and neuropsychiatric variation in the general population. Nat Genet. 2016 Mar 21.[2] Robinson EB. et al. Autism spectrum disorder severity reflects the average contribution of de novo and familial influences. Proc Natl Acad Sci U S A. 2014 Oct 21;111(42):15161-5.[3] Hagenaars SP. et al. Shared genetic aetiology between cognitive functions and physical and mental health in UK Biobank (N=112 151) and 24 GWAS consortia. Mol Psychiatry. 2016 Jan 26.----------Robinson EB, St Pourcain B, Anttila V, Kosmicki JA, Bulik-Sullivan B, Grove J, Maller J, Samocha KE, Sanders SJ, Ripke S, Martin J, Hollegaard MV, Werge T, Hougaard DM, iPSYCH-SSI-Broad Autism Group, Neale BM, Evans DM, Skuse D, Mortensen PB, Børglum AD, Ronald A, Smith GD, & Daly MJ (2016). Genetic risk for autism spectrum disorders and neuropsychiatric variation in the general population. Nature genetics PMID: 26998691... Read more »

Robinson EB, St Pourcain B, Anttila V, Kosmicki JA, Bulik-Sullivan B, Grove J, Maller J, Samocha KE, Sanders SJ, Ripke S.... (2016) Genetic risk for autism spectrum disorders and neuropsychiatric variation in the general population. Nature genetics. PMID: 26998691  

  • April 11, 2016
  • 11:15 PM

Choosing units of size for populations of cells

by Artem Kaznatcheev in Evolutionary Games Group

Recently, I have been interacting more and more closely with experiment. This has put me in the fortunate position of balancing the design and analysis of both theoretical and experimental models. It is tempting to think of theorists as people that come up with ideas to explain an existing body of facts, and of mathematical […]... Read more »

Shnerb, N.M., Louzoun, Y., Bettelheim, E., & Solomon, S. (2000) The importance of being discrete: life always wins on the surface. Proceedings of the National Academy of Sciences, 97(19), 10322-4. PMID: 10962027  

  • April 11, 2016
  • 04:19 PM

ZIKV pathogenesis: development of animal models

by thelonevirologist in Virology Tidbits

Zika Virus (ZIKV) is a emerging positive strand RNA virus that belongs to the genus of Flaviviridae. Human infections are mostly asymptomatic although a causative link to microcephaly and Guillan-Barre Syndrome (GBS) have been proposed.
So far however no reliable animal model to study ZIKV associated disease has been identified but in order to test a potential vaccine and order to gain a better understanding of ZIKV pathogenesis animal models are being developed. Similar to DENV, these models may involve immunocompetent and humanized mice as well nonhuman primates.
Here recent advances to establish a mouse model are presented. ... Read more »

Musso D, & Gubler DJ. (2016) Zika Virus. Clinical microbiology reviews, 29(3), 487-524. PMID: 27029595  

Chan KW, Watanabe S, Kavishna R, Alonso S, & Vasudevan SG. (2015) Animal models for studying dengue pathogenesis and therapy. Antiviral research, 5-14. PMID: 26304704  

DICK GW. (1952) Zika virus. II. Pathogenicity and physical properties. Transactions of the Royal Society of Tropical Medicine and Hygiene, 46(5), 521-34. PMID: 12995441  

Rossi SL, Tesh RB, Azar SR, Muruato AE, Hanley KA, Auguste AJ, Langsjoen RM, Paessler S, Vasilakis N, & Weaver SC. (2016) Characterization of a Novel Murine Model to Study Zika Virus. The American journal of tropical medicine and hygiene. PMID: 27022155  

Lazear, H., Govero, J., Smith, A., Platt, D., Fernandez, E., Miner, J., & Diamond, M. (2016) A Mouse Model of Zika Virus Pathogenesis. Cell Host . DOI: 10.1016/j.chom.2016.03.010  

Bell TM, Field EJ, & Narang HK. (1971) Zika virus infection of the central nervous system of mice. Archiv fur die gesamte Virusforschung, 35(2), 183-93. PMID: 5002906  

Hamel R, Dejarnac O, Wichit S, Ekchariyawat P, Neyret A, Luplertlop N, Perera-Lecoin M, Surasombatpattana P, Talignani L, Thomas F.... (2015) Biology of Zika Virus Infection in Human Skin Cells. Journal of virology, 89(17), 8880-96. PMID: 26085147  

Tang H, Hammack C, Ogden SC, Wen Z, Qian X, Li Y, Yao B, Shin J, Zhang F, Lee EM.... (2016) Zika Virus Infects Human Cortical Neural Progenitors and Attenuates Their Growth. Cell stem cell. PMID: 26952870  

Lefèvre F, Guillomot M, D'Andréa S, Battegay S, & La Bonnardière C. (1998) Interferon-delta: the first member of a novel type I interferon family. Biochimie, 80(8-9), 779-88. PMID: 9865499  

Lazear HM, Daniels BP, Pinto AK, Huang AC, Vick SC, Doyle SE, Gale M Jr, Klein RS, & Diamond MS. (2015) Interferon-λ restricts West Nile virus neuroinvasion by tightening the blood-brain barrier. Science translational medicine, 7(284). PMID: 25904743  

Rowland, A., Washington, C., Sheffield, J., Pardo-Villamizar, C., & Segars, J. (2016) Zika virus infection in semen: a call to action and research. Journal of Assisted Reproduction and Genetics, 33(4), 435-437. DOI: 10.1007/s10815-016-0684-6  

  • April 11, 2016
  • 02:19 AM

Levels of paranoia are higher in autism: systematic review

by Paul Whiteley in Questioning Answers

Paranoia, defined as the unfounded or exaggerated idea that something or someone is deliberately trying to psychologically, physically or financially harm you, is not an uncommon transient sentiment among the general population at one time or another. On a more pathological level, paranoid schizophrenia perhaps represents the archetypal label where paranoia assumes an altogether more persistent and 'life-changing' effect; also potentially escalating into more extreme behaviour/s.The idea that levels of paranoia might also be elevated as and when a diagnosis of autism spectrum disorder (ASD) is received is discussed in a recent review paper by Debbie Spain and colleagues [1]. Looking at the available peer-reviewed literature on the topic, researchers reported that those with ASD "were consistently found to have higher levels of paranoia compared to non-clinical controls, and lower levels than individuals with current psychotic experiences manifesting in the context of schizophrenia." They further speculated that: "core ASD characteristics and associated neurocognitive impairments also serve to precipitate and perpetuate paranoia."Accepting that cultural views of paranoia or paranoid behaviour are not generally all that 'positive' and how this may have potentially the same impact on autism as it has had on the perception of schizophrenia, the Spain paper is an important addition to the research literature. I say this not solely because of how issues such as perseveration and rumination potentially linked to the perpetuation of paranoia are not uncommon in cases of autism [2] but also because of the still evolving story around how autism and schizophrenia might, on occasion [3], overlap (see here). The idea that social anxiety and depression might be something else important to the clinical regions of paranoid thought [4] also ties in with evidence on the over-representation of these labels/behaviours alongside some autism (see here).Appropriate clinical screening is, once more, implied as and when any suspicions about the presence of chronic paranoid thinking occur when autism is diagnosed; not least because of the potential for progression into the clinical realms of schizophrenia (with caveats) and related labels. That paranoia combined with ruminative thinking and/or worry [5] for example, can in some circumstances be absolutely disabling for a person is also a good reason why intervention should be very, very seriously considered...----------[1] Spain D. et al. Conceptualising paranoia in ASD: A systematic review and development of a theoretical framework. Research in Autism Spectrum Disorders. 2016; 25: 97-111.[2] Pugliese CE. et al. The role of anger rumination and autism spectrum disorder-linked perseveration in the experience of aggression in the general population. Autism. 2015 Aug;19(6):704-12.[3] Woodbury-Smith MR. et al. Autism spectrum disorders, schizophrenia and diagnostic confusion. Journal of Psychiatry & Neuroscience : JPN. 2010;35(5):360.[4] Carroll A. Are you looking at me? Understanding and managing paranoid personality disorder. Advances in Psychiatric Treatment. 2009; 15: 40-48.[5] Startup H. et al. Worry processes in patients with persecutory delusions. Br J Clin Psychol. 2016 Mar 20.----------Spain, D., Sin, J., & Freeman, D. (2016). Conceptualising paranoia in ASD: A systematic review and development of a theoretical framework Research in Autism Spectrum Disorders, 25, 97-111 DOI: 10.1016/j.rasd.2016.02.002... Read more »

  • April 11, 2016
  • 02:00 AM

Week 14 In Review: Open-Access Science | 4 to 10 April

by TakFurTheKaffe in Tak Fur The Kaffe

River flooding boosts carbon emissions, six new species of Chinese dragon millipedes discovered, how ancient animals adapted to climate change, maths tell palaeontologists where to find fossils, and the Arctic Ocean was ice-free ten million years ago. Here are five of the latest scientific studies published open-access this week.... Read more »

Stegen, J., Fredrickson, J., Wilkins, M., Konopka, A., Nelson, W., Arntzen, E., Chrisler, W., Chu, R., Danczak, R., Fansler, S.... (2016) Groundwater–surface water mixing shifts ecological assembly processes and stimulates organic carbon turnover. Nature Communications, 11237. DOI: 10.1038/ncomms11237  

Botha-Brink, J., Codron, D., Huttenlocker, A., Angielczyk, K., & Ruta, M. (2016) Breeding Young as a Survival Strategy during Earth’s Greatest Mass Extinction. Scientific Reports, 24053. DOI: 10.1038/srep24053  

Stein, R., Fahl, K., Schreck, M., Knorr, G., Niessen, F., Forwick, M., Gebhardt, C., Jensen, L., Kaminski, M., Kopf, A.... (2016) Evidence for ice-free summers in the late Miocene central Arctic Ocean. Nature Communications, 11148. DOI: 10.1038/ncomms11148  

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