Post List

  • July 29, 2014
  • 01:15 PM
  • 14 views

Can’t Handle the Stress? Blame your Brain

by Gabriel in Lunatic Laboratories

Do you rise to the occasion, or do you fold under the pressure? No matter which side of the fence you’re, you can thank [or blame] your brain. Some people […]... Read more »

  • July 29, 2014
  • 12:32 PM
  • 11 views

Are silly superstitions useful because they are silly?

by neuroecology in Neuroecology

(Attention warning: massive speculation ahead.) Auguries often seem made up, useless. Is that why they are useful? Dove figured that the birds must be serving as some kind of ecological indicator. Perhaps they gravitated toward good soil, or smaller trees, or some other useful characteristic of a swidden site. After all, the Kantu’ had been […]... Read more »

  • July 29, 2014
  • 12:02 PM
  • 9 views

When Mom and Dad Have Different Migratory Routes, Kids Fly Right Down the Middle

by Elizabeth Preston in Inkfish

It sounds like the setup to a bad joke told by zoologists: What do you get when you cross a bird that always flies to the west with one that always flies east? But the punch line is weirder than you’d guess. Birds’ migratory routes are partly coded into their DNA. A baby that inherits […]The post When Mom and Dad Have Different Migratory Routes, Kids Fly Right Down the Middle appeared first on Inkfish.... Read more »

  • July 29, 2014
  • 11:55 AM
  • 11 views

Japanese Encephalitis Virus, Coronavirus, Autophagy, and the ER stress response

by thelonevirologist in Virology Tidbits

The accumulation of misfolded proteins in the ER lumen induces a stress response commonly known as the Unfolded Protein Response (UPR) or ER stress response, an adaptive signalling pathway increasing the expression of ER chaperones, inhibiting mRNA translation, and stimulating ER associated degradation (ERAD) of accumulated proteins. The degradation via the ERAD pathway in particular requires the formation of double membrane vesicles -more commonly referred to as autophagosomes - which subsequently fuse with lysosomes to form the autolysosome. The ERAD pathway can be induced by all three branches of the ER stress response -PERK, ATF6, and IRE1- which increase the expression of ER degradation enhancer, mannosidase alpha-like-1/-2 (EDEM1/2) proteins in addition to other components of the ERAD pathway either by ATF4 (in conjunction with sXBP1) by cleaved ATF6α. Binding of cytosolic misfolded proteins to components of the ERAD pathway allows the retrotranslocation of these protein into the ER lumen where ER chaperones may assist these proteins to be folded correctly and/or be glycosylated in a process which involves binding to EDEM1/2/3. JEV induces autophagy early in the infection but apoptosis at later stages. The pathways linking autophagy and apoptosis to ER stress response are discussed and the role of JEV proteins in the induction of both apoptosis and autophagy via CHOP is highlighted and compared to Coronavirus nsp -3/-4/-6.... Read more »

Rzymski T, Milani M, Pike L, Buffa F, Mellor HR, Winchester L, Pires I, Hammond E, Ragoussis I, & Harris AL. (2010) Regulation of autophagy by ATF4 in response to severe hypoxia. Oncogene, 29(31), 4424-35. PMID: 20514020  

Li JK, Liang JJ, Liao CL, & Lin YL. (2012) Autophagy is involved in the early step of Japanese encephalitis virus infection. Microbes and infection / Institut Pasteur, 14(2), 159-68. PMID: 21946213  

Cottam EM, Whelband MC, & Wileman T. (2014) Coronavirus NSP6 restricts autophagosome expansion. Autophagy, 10(8). PMID: 24991833  

  • July 29, 2014
  • 11:17 AM
  • 9 views

Treating Sleep Problems Following Traumatic Brain Injury

by William Yates, M.D. in Brain Posts

Sleep problems are common following traumatic brain injury (TBI).In a previous post, I reviewed a study of the risk factors for sleep disorders following TBI.The most severe TBI is a risk factor for hypersomnia. Anxiety and depression following TBI increase risk for insomnia complaints.Few large studies of treatment for sleep problems after TBI exist. However, a recent manuscript outlined the potential benefit of treatment of sleep disorders in a series of 12 subjects.Catherine Wiseman-Hakes and colleagues from the University of Toronto described their experience with sleep and TBI in a manuscript in the journal Brain Injury.Their study examined the impact of sleep disorder treatment in TBI on recovery of cognitive function including speech/communication. Treatment included sleep hygiene education, pharmacological treatment and continuous positive airway pressure (CPAP) for those with sleep apnea.Twelve subjects with TBI completed a baseline assessment for presence of insomnia, communication function and neuropsychological performance. Subjects also completed a laboratory sleep study (polysomnography) for accurate diagnosis of specific sleep disorders.Subjects then had treatment for sleep problems individualized to the specific sleep disorders diagnoses. After 2 to 4 months ofleep disorder treatment, follow up neuropsychological assessment was completed.The key findings from the study included:Sleep disorder diagnoses were diverse and included hypersomnia, obstructive sleep apnea, restless leg syndrome, circadian rhythm disturbances and insomniaTreatment of sleep disorders produced a robust subjective reduction in insomnia severity ratingsTreatment of sleep disorders produced a reduction in depression, improved language function and increased speed of language processingPharmacological treatments selected by the treating physicians included modafanil, methylphendiate and fluoxetine for hypersomnia, trazodone for insomnia, pregabablin, gabapentin and pramipexole for restless leg syndromeThe authors note their findings "reinforce the necessity for routine screening for sleep disorders in persons with TBI".Given the diversity of diagnoses in this study, screening in TBI needs to be linked to comprehensive sleep laboratory assessment.This study supports sleep assessment and sleep disorder treatment as a key component of TBI rehabilitation. This component appears to have significant benefit to global cognitive and communication recovery after TBI.Weaknesses of this clinical trial are the small sample size, lack of a control group and non-standardized pharmacological treatment.Nevertheless, the results are impressive and point to the need for additional larger randomized clinical trials of treatment for sleep disorders in TBI.Readers with more interest in this study can access the free full-text manuscript by clicking on the PMID link in the citation below.Photo of juvenile great blue heron is from the author's files. Follow the author on Twitter WRY999.Wiseman-Hakes C, Murray B, Moineddin R, Rochon E, Cullen N, Gargaro J, & Colantonio A (2013). Evaluating the impact of treatment for sleep/wake disorders on recovery of cognition and communication in adults with chronic TBI. Brain injury : [BI], 27 (12), 1364-76 PMID: 24070180... Read more »

  • July 29, 2014
  • 10:37 AM
  • 6 views

STING-associated autoinflammatory disease

by Aurelie in The Immuno Blog

A study published in the New England Journal of Medicine describes an autoinflammatory syndrome associated with mutations in the gene encoding STING. Dubbed SAVI, for STING-associated vasculopathy with onset in infancy, the disease is characterized by systemic inflammation, severe cutaneous … Continue reading →... Read more »

Liu, Y., Jesus, A., Marrero, B., Yang, D., Ramsey, S., Sanchez, G., Tenbrock, K., Wittkowski, H., Jones, O., Kuehn, H.... (2014) Activated STING in a Vascular and Pulmonary Syndrome. New England Journal of Medicine, 2147483647. DOI: 10.1056/NEJMoa1312625  

  • July 29, 2014
  • 09:00 AM
  • 9 views

Finding the Missing Stories: The Prior Cemetery’s Unmarked Slave Graves

by Katy Meyers in Bones Don't Lie

One of the more common (though often frustrating) questions we get in archaeology is “Why are you doing historic archaeology? We already know what happened”. To some extent, for eras […]... Read more »

  • July 29, 2014
  • 07:35 AM
  • 14 views

Is Twitter Ruining Our Proper English?

by Katja Keuchenius in United Academics

“Hey al im on my way 2wrk but i totes 4got 2bring ur ipod sori il hav 2 bring it nxt tym ur workin. Hav a nice day xo”
Gives you the cramps? Maybe you should read this article.... Read more »

  • July 29, 2014
  • 07:30 AM
  • 16 views

Is homosexuality "natural"?

by Bill Sullivan in The 'Scope

In the beginning, there was no sex. That’s because in the beginning, there was no Barry White. A playful look at examples of homosexuality in nature.... Read more »

Van Houdenhove E, Gijs L, T'sjoen G, & Enzlin P. (2014) Asexuality: A Multidimensional Approach. Journal of sex research, 1-10. PMID: 24750031  

  • July 29, 2014
  • 04:04 AM
  • 17 views

Ketogenic diet and the valproate mouse model of autism

by Paul Whiteley in Questioning Answers

A brief entry today and yet another blog post that starts with a quote (sorry)... "The offspring exposed to VPA [valproic acid] prenatally demonstrated a significant decrease in the number of play initiations/attacks and this was reversed with the KD [ketogenic diet]".Gloucester Old Spot @ Wikipedia That finding reported in the paper by Ahn and colleagues [1] continues my interest in all-things related to prenatal VPA exposure and the reported effects on some offspring (see here). The added bonus of including some discussion about how the use of a ketogenic diet might reverse some of the effects of VPA exposure (in rats at least) is also worthwhile mentioning.A couple of pointers perhaps...Rats, Sprague-Dawley mother rats, were given VPA or saline (as a control) during pregnancy and their pups (VPA-exposed vs. controls) were subjected to measures looking at "juvenile play behavior" and eventually "mitochondrial bioenergetic analysis" as a function of the use of a ketogenic or standard diet.Results: "Prenatal VPA exposure also disrupted the pattern of play responses". Not a great surprise there given everything else that has been linked to VPA exposure in-utero. But.. use of the ketogenic diet "was able to modify complex social behaviors and mitochondrial respiration". As noted previously, the reduction in play initiations made by the VPA exposed mice was to some degree rescued following use of the ketogenic diet.Yes, I know that this was a study of rats, and whilst useful, rats are rats not humans. But I am nevertheless intrigued by the suggestion that something like a ketogenic diet - more typically indicated for some types of treatment resistant epilepsy - might to some degree, affect the behaviour and physiology of animals exposed to a traditional anticonvulsant like valproate during the nine months that made them. Does anyone else find that a little ironic? Also throw in mention of the words 'autism spectrum disorder' alongside that animal VPA exposure model alongside the ketogenic diet (see here) and I'm sure there's some more research to be done in this area.Mode of action? I dunno. I will draw your attention to some interesting work on carnitine homoeostasis as a function of valproate administration [2] which might be relevant. Carnitine plays a role in mitochondrial function [3] and there is some suggestion that a ketogenic diet might help maintain carnitine levels in the presence of VPA [4]. Whether this applies to brain structures or neurochemistry potentially already affected by prenatal exposure to VPA is a question not yet asked or answered. Bearing in mind the gastrointestinal (GI) effects also noted in VPA exposure models (see here) I might also be inclined to 'look to the bowels' in terms of any potential effects from the ketogenic diet in that organ too.Music to close and I was taken aback by the performance from Pumeza at the opening to the 2014 Commonwealth Games and her version of Freedom Come All Ye...----------[1] Ahn Y. et al. The Ketogenic Diet Modifies Social and Metabolic Alterations Identified in the Prenatal Valproic Acid Model of Autism Spectrum Disorder. Dev Neurosci. 2014 Jul 8.[2] Morand R. et al. Effect of short- and long-term treatment with valproate on carnitine homeostasis in humans. Ther Drug Monit. 2012 Aug;34(4):406-14.[3] Zammit VA. et al. Carnitine, mitochondrial function and therapy. Adv Drug Deliv Rev. 2009 Nov 30;61(14):1353-62.[4] Coppola G. et al. Plasma free carnitine in epilepsy children, adolescents and young adults treated with old and new antiepileptic drugs with or without ketogenic diet. Brain Dev. 2006 Jul;28(6):358-65.----------Ahn Y, Narous M, Tobias R, Rho JM, & Mychasiuk R (2014). The Ketogenic Diet Modifies Social and Metabolic Alterations Identified in the Prenatal Valproic Acid Model of Autism Spectrum Disorder. Developmental neuroscience PMID: 25011527... Read more »

  • July 28, 2014
  • 07:55 PM
  • 35 views

Attention Deficit Hyperactivity Disorder & Eating Disorders: Is There a Link?

by Tetyana in Science of Eating Disorders


Attention deficit hyperactivity disorder (ADHD), characterized by inattention, hyperactivity, and impulsivity, is a common childhood disorder. ADHD can often persist into adolescence and adulthood. The prevalence of ADHD is thought to be between 6-7% among children and adolescents and ~5% among adults (Willcutt, 2012).
Increasingly, evidence from multiple studies has pointed to comorbidity between ADHD and eating disorders (EDs). For example, one study found that young females with ADHD were 5.6 times more likely to develop clinical (i.e., diagnosable according to DSM-5) or subthreshold (i.e., sub-clinical) bulimia nervosa (BN) (Biederman et al., 2007). Another study found that found that 21% of female inpatients at an ED unit had six or more ADHD symptoms (Yates et al., 2009).
However, most previous studies are limited by the fact that they assessed comorbidity between ADHD and EDs among patients. This limits our ability to generalize these findings to community samples, where many may experience symptoms of the disorders at subthreshold levels. Moreover, most studies focused on bingeing/purging behaviours and did not investigate differences between ADHD subtypes.
In the current study, Jennifer Bleck …

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  • July 28, 2014
  • 03:10 PM
  • 80 views

This Month In Blastocystis Research (JUL 2014)

by Christen Rune Stensvold in Blastocystis Parasite Blog

A new study from Colombia sees Blastocystis as a quasi-ubiquitous organism.... Read more »

  • July 28, 2014
  • 02:44 PM
  • 55 views

Watch ALL the neurons in a brain: Ahrens and Freeman continue their reign of terror

by neuroecology in Neuroecology

Okay, not quite all of them. But it looks like Misha Ahrens and Jeremy Freeman are going to continue their reign of terror, imaging the whole zebrafish brain as if it’s no big deal. Yeah they’ve got almost every neuron of a vertebrate, so what? Besides figuring out that not shooting light at the eyes might […]... Read more »

Freeman, J., Vladimirov, N., Kawashima, T., Mu, Y., Sofroniew, N., Bennett, D., Rosen, J., Yang, C., Looger, L., & Ahrens, M. (2014) Mapping brain activity at scale with cluster computing. Nature Methods. DOI: 10.1038/nmeth.3041  

Vladimirov, N., Mu, Y., Kawashima, T., Bennett, D., Yang, C., Looger, L., Keller, P., Freeman, J., & Ahrens, M. (2014) Light-sheet functional imaging in fictively behaving zebrafish. Nature Methods. DOI: 10.1038/nmeth.3040  

  • July 28, 2014
  • 01:13 PM
  • 40 views

A New Hepatitis C Treatment offers Hope

by Gabriel in Lunatic Laboratories

Well this might seem weird, but today is world hepatitis day. I guess I should qualify weird with the fact that it’s only weird because no one really knows. What […]... Read more »

  • July 28, 2014
  • 09:14 AM
  • 41 views

Glasses-Free Computers

by Viputheshwar Sitaraman in Draw Science

Looking at computers with eyeglasses strains your eyes, so scientists are making computers that help your eyes out.... Read more »

Huang, F., Wetzstein, G., Barsky, B., & Raskar, R. (2014) Eyeglasses-free display. ACM Transactions on Graphics, 33(4), 1-12. DOI: 10.1145/2601097.2601122  

  • July 28, 2014
  • 09:05 AM
  • 60 views

The mistakes that lead therapists to infer psychotherapy was effective, when it wasn't

by Christian Jarrett in BPS Research Digest

How well can psychotherapists and their clients judge from personal experience whether therapy has been effective? Not well at all, according to a paper by Scott Lilienfeld and his colleagues. The fear is that this can lead to the continued practice of ineffective, or even harmful, treatments.The authors point out that, like the rest of us, clinicians are subject to four main biases that skew their ability to infer the effectiveness of their psychotherapeutic treatments. This includes the mistaken belief that we see the world precisely as it is (naive realism), and our tendency to pursue evidence that backs our initial beliefs (the confirmation bias). The other two are illusory control and illusory correlations - thinking we have more control over events than we do, and assuming the factors we're focused on are causally responsible for observed changes.These features of human thought lead to several specific mistakes that psychotherapists and others commit when they make claims about the effectiveness of psychological therapies. Lilienfeld's team call these mistakes "causes of spurious therapeutic effectiveness" or CSTEs for short. The authors have created a taxonomy of 26 CSTEs arranged into three categories.The first category includes 15 mistakes that lead to the perception that a client has improved, when in fact he or she has not. These include palliative benefits (when the client feels better about their symptoms without actually showing any tangible improvement); confusing insight with improvement (when the client better understands their problems, but does not actually show recovery); and the therapist's office error (confusing a client's presentation in-session with their behaviour in everyday life).The second category consists of errors that lead therapists and their clients to infer that symptom improvements were due to the therapy, and not some other factor, such as natural recovery that would have occurred anyway. Among these eight mistakes are a failure to recognise that many disorders are cyclical (periods of recovery interspersed with phases of more intense symptoms); ignoring the influence of events occurring outside of therapy, such as an improved relationship or job situation; and the influence of maturation (disorders seen in children and teens can fade as they develop).The third and final category of errors are those that lead to the assumption that improvements are causes by unique features of a therapy, rather than factors that are common to all therapies. Examples here include not recognising placebo effects (improvements stemming from expectations) and novelty effects (improvements due to initial enthusiasm).To counter the many CSTEs, Lilienfeld's group argue we need to deploy research methods including using well-validated outcome measures, taking pre-treatment measures, blinding observers to treatment condition, conducting repeated measurements (thus reducing the biasing impact of irregular everyday life events), and using control groups that are subjected to therapeutic effects common to all therapies, but not those unique to the treatment approach under scrutiny. "CSTEs underscore the pressing need to inculcate humility in clinicians, researchers, and students," conclude Lilienfeld and his colleagues. "We are all prone to neglecting CSTEs, not because of a lack of intelligence but because of inherent limitations in human information processing. As a consequence, all mental health professionals and consumers should be sceptical of confident proclamations of treatment breakthroughs in the absence of rigorous outcome data."_________________________________ Lilienfeld, S., Ritschel, L., Lynn, S., Cautin, R., & Latzman, R. (2014). Why Ineffective Psychotherapies Appear to Work: A Taxonomy of Causes of Spurious Therapeutic Effectiveness Perspectives on Psychological Science, 9 (4), 355-387 DOI: 10.1177/1745691614535216 --further reading--When therapy causes harmPost written by Christian Jarrett (@psych_writer) for the BPS Research Digest.

... Read more »

  • July 28, 2014
  • 07:45 AM
  • 48 views

Plastic bags responsible for outrageous lack of cute pink piglets

by Stephanie Swift in mmmbitesizescience

Most of us now subscribe to the idea that plastic bags are bad for the environment. Hence, droves of people turn up at their local supermarket with a sturdy jute bag in tow. Now, there’s evidence that the items that … Continue reading →... Read more »

  • July 28, 2014
  • 06:56 AM
  • 36 views

Model Predicts Carbon Components’ Performance as Electrodes

by dailyfusion in The Daily Fusion

Researchers at the Lawrence Livermore National Laboratory and Rice University have created a theoretical model that predicts how carbon components will perform as anodes in lithium-ion batteries.... Read more »

  • July 28, 2014
  • 04:24 AM
  • 74 views

Prenatal and neonatal blood mercury levels and autism

by Paul Whiteley in Questioning Answers

Acknowledging that some topics have the ability to furrow brows when it comes to autism research, mercury and autism is becoming something of a frequent talking point on this blog as a function of a whole slew of articles appearing in the peer-reviewed domain. If I were to [very tentatively] summarise the collected literature so far, it would be to say something like:Mosaic of mercury @ Wikipedia (i) there is quite a bit more research to be done on some sources of mercury being 'linked' to cases of autism i.e. air pollution, fish consumption (see here),and(ii) the body burden of mercury for some on the autism spectrum is elevated (see here) compared to other groups and potentially linked to "a decreased ability to excrete mercury due to a combination of lowered reduced glutathione, emergence of oxidative stress, and excessive use of oral antibiotics" according to the review by Francesca Gorini and colleagues [1] (open-access).I know some people may not like hearing that summary but that's my interpretation of the various reviews and meta-analyses conducted so far. I should add that I'm not though passing any specific comment on whether mercury 'causes' autism bearing in mind what we know about the developmental consequences of exposure.The paper by Vincent Yau and colleagues [2] looking at maternal serum and infant newborn bloodspot levels of mercury adds to that literature with their conclusion: "levels of total mercury in serum collected from mothers during mid-pregnancy and from newborn bloodspots were not significantly associated with risk of ASD [autism spectrum disorder]". I believe we had seen this data presented before at the 2011 IMFAR conference too (see here).A few details first:Based on data obtained from the EMA (Early Markers of Autism) study, a cohort "identified from the California Department of Developmental Services (DDS)" records, mid-pregnancy maternal serum samples and the wonderful resource that is the neonatal bloodspots related to some 84 children diagnosed with an ASD were analysed for total mercury content (inorganic and organic mercury). Blinded results were compared with 159 population controls (asymptomatic) and 49 children diagnosed with a learning (intellectual) disability or developmental delay.ICP mass spectrometry was the name of the analytical game, which as I've talked about before, is one of the methods of choice when it comes to the analysis of the metallome. Archived blood spot samples were subject to laser ablation as a function of their mounting. Results: "Maternal serum and infant blood mercury levels were significantly correlated among all study groups". In other words, maternal mercury burden seemed to be associated with neonatal offspring burden (albeit with a correlation coefficient ~0.4 which is OK but not exactly great).Further: "Results for mercury levels in newborn blood samples were similar" across the groups. Ergo, at birth, levels of total mercury from neonatal bloodspots "were not significantly associated with risk of ASD". That's not to say that there weren't some differences in average levels of blood mercury levels across the groups, just that such differences were not deemed to elevate the risk of ASD overall.Like quite a lot of the science in this area, there are several ways you could interpret these results. You could, for example say that the maternal burden of mercury during pregnancy was not associated with offspring risk of autism. You could also say that 'at or shortly after birth' (remember those words), blood mercury levels do not seem to correlate with the risk of autism. Therefore mercury is not a factor in relation to autism as per other results in this area [3]. You could say those things, as you might for several other variables supposedly related to autism... vitamin D for example? (see here and then see here).But you might also consider the bank of research which has reported elevated levels of mercury in various biofluids and tissues particularly focused on slightly older infants and children with autism as illustrative of something potentially important: increasing exposure to mercury with age. Take for example the paper by Majewska and colleagues [4] and their findings reporting: "Autistic children significantly differed from healthy peers in the concentrations of mercury in hair: younger autistics had lower levels, while older - higher levels than their respective controls". The results from Hertz-Picciotto and colleagues [4] (open-access here) also implied that behaviour might play a role in blood mercury levels: "Interestingly, although few children had Hg amalgams, those who did and who also either chewed gum or had bruxism appeared to have experienced sufficient release of inorganic Hg to be measurable in blood". I say this noting that not every child with autism has mercury amalgams, as neither do they all partake in teeth grinding.The Yau results make an important contribution to the issue of mercury and autism in terms of maternal contribution and mercury load at birth. As part of some further investigations, and bearing in mind that participants in the EMA initiative might also be involved in other State initiatives (beincharge!), I would like to see further follow-up of participants and if and how their mercury load might have changed as they matured. Analysis of other parameters mentioned in that Gorini review paper - such as glutathione measures for example - might also offer some important accompanying data on whether excretion factors are part of the issue here and what might be done to help relieve any excess burden of the troublesome heavy metal that is mercury. Oh, and given that genetic factors might also play some role in mercury accumulation as per the findings by Llop and colleagues [5] (open-access), there may also be more research to do here too...----------[1] Gorini F. et al. The Role of Heavy Metal Pollution in Neurobehavioral Disorders: a Focus on Autism. Review Journal of Autism... Read more »

Yau VM, Green PG, Alaimo CP, Yoshida CK, Lutsky M, Windham GC, Delorenze G, Kharrazi M, Grether JK, & Croen LA. (2014) Prenatal and neonatal peripheral blood mercury levels and autism spectrum disorders. Environmental research, 294-303. PMID: 24981828  

  • July 27, 2014
  • 02:17 PM
  • 77 views

Holy Grail of Battery Design: A lithium anode

by Gabriel in Lunatic Laboratories

Technology has been racing forward at an ever increasing rate. Unfortunately, anyone who owns a smartphone will tell you that the battery life doesn’t match the advancements. That is probably […]... Read more »

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