Serum levels of dipeptidyl peptidase (DPP) IV were found to be lower in children with autism compared to asymptomatic controls according to the study by Shahid Bashira & Laila AL-Ayadhi . Based on analysis by ELISA, researchers concluded that "alterations in the plasma level of DPP IV play a role in the pathophysiology of autism".A sailor went to sea, sea, sea... @ Wikipedia Anyone who has followed the autism research scene for any length of time might have already heard about DPP-IV and autism. The paper by Hunter and colleagues  (open-access here) and subsequent response  highlights some of the discussions in this area relating to the use of the opioid-excess hypothesis  as a means to potentially explain some autism. The idea stemming from some earlier work (see here) being that a defect in the functioning of DPP-IV with regards to its ability to degrade proline-rich proteins such as gliadin (gluten) might account for the build-up of gluten derived opioid peptides suggested as part of the opioid-excess theory. Earlier accounts of issues with DPP-IV in relation to the classic gluten-related autoimmune condition coeliac disease (see here for an overview) kinda set the tone  for some analysis with autism in mind. Indeed, at least one trial of enzyme-based therapy has also talked about the potential involvement of DPP-IV in some cases of autism .The Bashira paper did not specifically set out to look at the relationship between DPP-IV and dietary elements potentially linked to autism. Instead their focus seemed to be on the involvement of this peptidase in brain physiology and "its possible link to neuroinflammation in autism". DPP-IV has, for example, been discussed with cerebral ischemia in mind as per the results from Röhnert and colleagues  although I hasten to add that I am not equating autism and brain ischemia.I personally feel that quite a bit more research effort is needed in the area of DPP-IV. Lower plasma levels of DPP-IV have been noted in cases of other conditions such as depression . The recent results from Simone Peters and colleagues  which talked about "Short-term exposure to gluten specifically induced current feelings of depression" in their cohort (see this post) could fit well with the reduction in gluten peptide degrading abilities potentially present as a consequence of something like lower DPP-IV levels. Indeed, one might also speculate that the suggestion of non-coeliac gluten sensitivity (NCGS) may actually reflect involvement of opioid peptides on the basis of such a correlation...I'm also taken back to some work by Vojdani and colleagues  which talked about anti-CD26 autoantibodies being present in a "significant percentage of children with autism". CD26, a surface glycoprotein used synonymously with DPP-IV, was suggested to show involvement as a function of "dietary peptides, bacterial toxins and xenobiotics bind[ing] to lymphocyte receptors and/or tissue enzymes, resulting in autoimmune reaction in children with autism". Their follow-up study  further added to the literature in this area and how "Dysfunctional membrane peptidases and autoantibody production may result in neuroimmune dysregulation and autoimmunity" in relation to autism. Autoimmunity and autism y'say?As per the cycles of scientific research, where research areas fall in and out of favour, it does appear that there is a resurgence of interest in elements of the opioid-excess theory with a specific focus on the role of food-derived peptides in relation to at least some autism. The Roy review looking at naltrexone for autism (see here) is one element given the opioid antagonistic effects of this pharmaceutic. The Sokolov paper (with its flaws) looking at beta-casomorphin - the opioid peptide derived from the casein protein - in relation to autism is another. The Trivedi paper (see here) on exogenous opioid peptides and DNA methylation levels adds to the research bundle. Dare I even mention the camel milk and autism connection also being made in the research literature too as a function of different milks and different protein/peptide configurations?Music to close. Epic by Faith No More.---------- Bashir S. & AL-Ayadhi L. Alterations in plasma dipeptidyl peptidase IV in autism: A pilot study. Neurology, Psychiatry and Brain Research. 2014; 20: 41-44. Hunter LC. et al. Opioid peptides and dipeptidyl peptidase in autism. Dev Med Child Neurol. 2003 Feb;45(2):121-8. Shattock P. et al. Opioid peptides and dipeptidyl peptidase in autism. Dev Med Child Neurol. 2004 May;46(5):357. Shattock P. & Whiteley P. Biochemical aspects in autism spectrum disorders: updating the opioid-excess theory and presenting new opportunities for biomedical intervention. Expert Opin Ther Targets. 2002 Apr;6(2):175-83. Smith MW. & Phillips AD. Abnormal expression of dipeptidylpeptidase IV activity in enterocyte brush-border membranes of children suffering from coeliac disease. Exp Physiol. 1990 Jul;75(4):613-6. Brudnak MA. et al. Enzyme-based therapy for autism spectrum disorders -- is it worth another look? Med Hypotheses. 2002 May;58(5):422-8. Röhnert P. et al. Dipeptidyl peptidase IV, aminopeptidase N and DPIV/APN-like proteases in cerebral ischemia. J Neuroinflammation. 2012 Feb 28;9:44. Maes M. et al. Alterations in plasma dipeptidyl peptidase IV enzyme activity in depression and schizophrenia: effects of antidepressants and antipsychotic drugs. Acta Psychiatr Scand. 1996 Jan;93(1):1-8. Peters SL. et al. Randomised clinical trial: gluten may cause depression in subjects with non-coeliac gluten sensitivity - an exploratory clinical study. Aliment Pharmacol Ther. 2014 May;39(10):1104-12. Vojdani A. et al. Infections, toxic chemicals and dietary peptides binding to lymphocyte receptors and tissue enzymes are major instigators of autoimmunity in autism. Int J Immunopathol Pharmacol. 2003 Sep-Dec;16(3):189-99. Vojdani A. et al. Heat shock protein and gliadin peptide promote development of peptidase antibodies in children with autism and patients with aut... Read more »
Bashir, S., & AL-Ayadhi, L. (2014) Alterations in plasma dipeptidyl peptidase IV in autism: A pilot study. Neurology, Psychiatry and Brain Research, 20(2), 41-44. DOI: 10.1016/j.npbr.2014.03.001
Kamil GodulaCreditEmbryonic stem cells can develop into virtually all kinds of cells. However, researchers still don't understand how to guide their development into the specific types of mature cells that make up the organs and other structures of living organisms. Now, researchers say that one key to guiding the differentiation process are long chains of sugars that dangle from proteins on surfaces of cells. Kamil Godula's group at the University of California, San Diego, has created synthetic molecules that can stand in for the natural sugars, but can be more easily manipulated to direct the process, they report in the Journal of the American Chemical Society.A variety of growth factors influence the fate of embryonic stem cells. All bind to specific receptors on the surface of the cell, but many must also bind to these sugars to exert their influence.Read More... Read more »
Huang ML, Smith RA, Trieger GW, & Godula K. (2014) Glycocalyx Remodeling with Proteoglycan Mimetics Promotes Neural Specification in Embryonic Stem Cells. Journal of the American Chemical Society. PMID: 25019314
If you’ve been watching the news recently, you’ll probably have seen reports on the Ebola outbreak in West Africa. Around 673 people in Guinea and Liberia have died so far (including one case of a Liberian government employee who died shortly after arriving at Lagos airport in Nigeria), making this the most deadly outbreak to date. So what exactly is Ebola, and why is it so deadly?
Ebola virus disease (EVD) has an incredibly high mortality rate – while the current outbreak has a mortality rate of about 60%, EVD can be fatal in up to 90% of cases. It is caused by members of the genus Ebolavirus (part of the Filoviridae family), which includes five different species: Bundibugyo ebolavirus, Zaire ebolavirus, Reston ebolavirus, Sudan ebolavirus, and Taï Forest ebolavirus. The current outbreak was caused by Zaire ebolavirus. Fruit bats of the Pteropodidae family are the natural reservoir of the virus, and eating the bats can cause the virus to be transmitted to humans. In response to the outbreak, the Guinean government has banned the sale of bats for culinary purposes. Contact with infected chimpanzees (alive or dead) is another route of zoonotic transmission. Once a human becomes infected, they can transfer it to others via bodily fluids such as sweat, blood, and breast milk. Human-to-human transfer can occur from the febrile stage onwards, including after death – many people catch EVD while preparing bodies for funerals.... Read more »
Gatherer, D. (2014) The 2014 Ebola virus disease outbreak in West Africa. Journal of General Virology, 95(Pt_8), 1619-1624. DOI: 10.1099/vir.0.067199-0
I tried to kill myself, more than once in fact. It was a troubling time for me and as a former active duty Marine that might not be too surprising […]... Read more »
Guintivano, J., Brown, T., Newcomer, A., Jones, M., Cox, O., Maher, B., Eaton, W., Payne, J., Wilcox, H., & Kaminsky, Z. (2014) Identification and Replication of a Combined Epigenetic and Genetic Biomarker Predicting Suicide and Suicidal Behaviors. American Journal of Psychiatry. DOI: 10.1176/appi.ajp.2014.14010008
Guintivano, J., Arad, M., Gould, T., Payne, J., & Kaminsky, Z. (2013) Antenatal prediction of postpartum depression with blood DNA methylation biomarkers. Molecular Psychiatry, 19(5), 560-567. DOI: 10.1038/mp.2013.62
Anecdotal reports have linked traumatic brain injury with later violent death including death by suicide.Few large epidemiological studies have been published on this association.However, a recent Swedish population study published in JAMA Psychiatry provides valuable insight into this issue.Seena Fazel and colleagues from the University of Oxford, University College London and the Karolinksa Institute examined a large database of over 200,000 patients with TBI.Cases of TBI were identified from all Swedish persons born in or after 1954 who received a ICD diagnosis of TBI. These diagnoses were assigned by physicians treating hospitalized or clinic patients.TBI cases were then examined for cause of death using the Swedish National Cause-of-Death Register. Death rates for TBI were compared to two control groups in the period at least six months following TBI. One control group was an age and sex-matched general population group without a TBI diagnosis.A second control group was comprised of siblings of the TBI group who themselves had not suffered a TBI. This type of control group is helpful in controlling for important sociodemographic variables. The key findings from the study included:TBI cases had significantly higher rates of death during follow up with odds ratios estimates of 2.6 using sib controls and 3.2 using population controlsViolent death causes were key contributors to increased mortality in TBI including (sib OR, population control OR)motor vehicle accidents (2.5, 3.2)non-motor vehicle accidents (3.4, 5.2)assault (2.7, 3.9)suicide (2.3, 3.3) The research team examined potential mortality co-factors including pre-existing and post-TBI depression diagnosis, alcohol abuse and drug abuse. Additionally they examined effects of sex, TBI severity, brain imaging abnormalities and presence of concussion.TBI cases had higher rates compared to controls for pre-existing any psychiatric diagnosis, depression, alcohol abuse and drug abuse.TBI cases also had higher rates for a new diagnosis of any psychiatric diagnosis, depression, alcohol abuse and drug abuse.In the TBI sample with premature mortality, 61% had a lifetime diagnosis of a psychiatric or substance abuse diagnosis.Medical factors contributing to violent death including suicide were presence of a TBI-related brain imaging abnormality (edema, focal changes, hemorrhage), more severe TBI and presence of concussion.This study confirms that TBI is an independent contributor to increased premature violent death including suicide. However, pre-existing psychiatric and substance abuse problems may contribute both to risk of TBI and risk of premature violent death. Additionally, the increased rate for developing a post-TBI depression, alcohol abuse or drug abuse may also contribute to violent death risk.The highest rates for suicide were those with TBI and depression as well as for those with TBI and substance abuse.The take home message here is pretty clear. Clinicians treating and following TBI populations need to monitor closely for co-occurring psychiatric illness, depression and substance abuse. Close monitoring and intervention for these co-occurring disorders may reduce premature mortality due to suicide and other violent death in TBI.Readers with more interest in this research can access the free full-text manuscript by clicking on the PMID link in the citation below.Photo of osprey is from the author's files.Follow the author on Twitter WRY999.Fazel S, Wolf A, Pillas D, Lichtenstein P, & Långström N (2014). Suicide, fatal injuries, and other causes of premature mortality in patients with traumatic brain injury: a 41-year Swedish population study. JAMA psychiatry, 71 (3), 326-33 PMID: 24430827... Read more »
Fazel S, Wolf A, Pillas D, Lichtenstein P, & Långström N. (2014) Suicide, fatal injuries, and other causes of premature mortality in patients with traumatic brain injury: a 41-year Swedish population study. JAMA psychiatry, 71(3), 326-33. PMID: 24430827
The Great War helped create the influenza pandemic of 1918, which eventually brought an early end to the Great War. Continue reading...... Read more »
Gamblin S. J. (2004) The Structure and Receptor Binding Properties of the 1918 Influenza Hemagglutinin. Science, 303(5665), 1838-1842. DOI: http://dx.doi.org/10.1126/science.1093155
Barry John M. (2004) The site of origin of the 1918 influenza pandemic and its public health implications (Commentary). Journal of Translational Medicine, 2(3). DOI: 10.1186/1479-5876-2-3
Humphries M. O. (2014) Paths of Infection: The First World War and the Origins of the 1918 Influenza Pandemic. War in History, 21(1), 55-81. DOI: http://dx.doi.org/10.1177/0968344513504525
The dbGaP, database of Genotypes and Phenotypes, repository at NCBI collects information from research projects that link genotype and phenotype information and human variation, across many different types of studies, providing leads on variation that may be important to understand clinical issues. Some of the data is publicly available de-identified patient information, and some of the […]... Read more »
Doan Son, Lin Ko-Wei, Conway Mike, Ohno-Machado Lucila, Hsieh Alex, Feupe Stephanie Feudjio, Garland Asher, Ross Mindy K, Jiang Xiaoqian, & Farzaneh Seena. (2013) PhenDisco: phenotype discovery system for the database of genotypes and phenotypes. Journal of the American Medical Informatics Association : JAMIA. PMID: 23989082
Tryka K. A., A. Sturcke, Y. Jin, Z. Y. Wang, L. Ziyabari, M. Lee, N. Popova, N. Sharopova, M. Kimura, & M. Feolo. (2013) NCBI's Database of Genotypes and Phenotypes: dbGaP. Nucleic Acids Research, 42(D1). DOI: http://dx.doi.org/10.1093/nar/gkt1211
Is there a minimum size for life? How would you measure it, cell volume or genome size? People do both. The current minimum example of life is Mycoplasma genitalium, at just 200 nm by 600 nm in well-fed cultures. M. genitalium also has the smallest known genome for a free-living organism (520 genes, we have about 27,000). Some organisms have fewer genes (137 or so) but are endosymbionts, so they can get away with trashing some of their DNA. New research shows that M. genitalium is a pathogenic organism as well, being sexually transmitted and more common than N. gonorrhoeae.
There are smaller structures, like nanobacteria, but we don’t know they are alive. Found in many disease states, nanobacteria are claimed to be pathogenic, but a late 2013 study showed that they are mineral formations that are generated spontaneously from many biological fluids. We’ll have to keep looking for small stuff.
... Read more »
Manhart LE. (2013) Mycoplasma genitalium: An emergent sexually transmitted disease?. Infectious disease clinics of North America, 27(4), 779-92. PMID: 24275270
Wu CY, Young L, Young D, Martel J, & Young JD. (2013) Bions: a family of biomimetic mineralo-organic complexes derived from biological fluids. PloS one, 8(9). PMID: 24086546
Gibson DG, Glass JI, Lartigue C, Noskov VN, Chuang RY, Algire MA, Benders GA, Montague MG, Ma L, Moodie MM.... (2010) Creation of a bacterial cell controlled by a chemically synthesized genome. Science (New York, N.Y.), 329(5987), 52-6. PMID: 20488990
The findings from Jai Eun Choi and colleagues  suggesting that use of the antipsychotic risperidone may impact on levels of certain cytokines - messenger cells of the immune system - in some cases of autism spectrum disorder (ASD) grabbed my attention recently. I've always been pretty interested in the complexity of the immune system when it comes to something like autism (see here) as well as the various examples of how many of the medications used to 'manage' aspects of autism appear to have quite a few more biological effects over and above those listed on the patient information leaflet. Think melatonin for example, and what a molecular handyperson this pharmaceutic has turned out to be (see here).Could it be magic... @ Wikipedia The Choi paper worked on the assumption that use of risperidone and other antipsychotics have previously been shown to correlate with changes to serum levels of certain cytokines as per examples of work in the area of schizophrenia  and here . Some of this research even hinted that part of the reason why antipsychotics might 'work' in some cases of schizophrenia was to do with their potential effect on "the inflammatory-like situation" present . Certainly it's been noted before on this blog how inflammation may very well play some role when it comes to psychiatry (see here) particularly in light of some of the research on the various inflammatory markers (see here) accepting the chicken-and-egg question of what comes first: inflammation or symptoms?Anyhow, based on a small-ish sample (n=45), Choi et al looked at plasma levels of "27 different cytokines" both before risperidone treatment was introduced and after 8 weeks on the drug. Interestingly the words 'responders' and 'nonresponders' were included in the analyses undertaken to look for any changes/trends following antipsychotic use (something which I think more studies should head towards). As it happens, "2 of the 27 plasma cytokines showed statistically significant decreases in median levels" - eotaxin and monocyte chemoattractant protein-1 (MCP-1). Further, when those responders and non-responders were separated out "the median values of interleukin (IL)-5 were significantly higher (p=0.005) in the overall responder group than in nonresponders".Obviously one has to be a little bit guarded about the conclusions reached from this fairly small and fairly short study. Whilst risperidone does have a place in the medicines cabinet for some people with autism (see here), paediatric use (as was the case in the Choi study) is not without risks as per a recent entry on the SFARI website (see here). The guidance from NICE here in the UK (well, England at least) also mentioned how cautious physicians must be when using antipsychotics "for behaviour that challenges" with autism in mind.I was quite interested in the Choi findings particularly that of the elevations in IL-5 in the responder group. I'm no expert on IL-5 but some light reading around the topic (see here) seems to imply that elevations of this cytokine are probably not going to be a great thing from the point of view of their involvement in the activation of eosinophils . I've talked before on this blog about some of the work looking at eosinophils and autism (see here) and some potentially interesting correlations with other research (see here). I'd perhaps like to see more about this correlation in future studies particularly building on other findings in relation to IL-5 and autism  (open-access here) including as part of being a risk factor for offspring autism  (open-access here).Insofar as the eotaxin and MCP-1 findings, well, again there is probably a lot more work to do on these compounds as a function of their mention in other autism research  (open-access here). The paper by Paul Ashwood  (who incidentally was an author on the Choi paper) looking at Fragile X syndrome (FXS) with and without autism also caught my eye: "significant differences were observed between the FXS group with autism and the FXS without autism for IL-6, eotaxin, MCP-1" as another avenue for further study.So then... somewhere the drinks are free (or should that be all-inclusive).---------- Choi JE. et al. Change in Plasma Cytokine Levels During Risperidone Treatment in Children with Autism. J Child Adolesc Psychopharmacol. 2014 May 14. Zhang XY. et al. Changes in serum interleukin-2, -6, and -8 levels before and during treatment with risperidone and haloperidol: relationship to outcome in schizophrenia. J Clin Psychiatry. 2004 Jul;65(7):940-7. Kim DJ. et al. Effect of risperidone on serum cytokines. Int J Neurosci. 2001;111(1-2):11-9. Cazzullo CL. et al. Cytokine profiles in schizophrenic patients treated with risperidone: a 3-month follow-up study. Prog Neuropsychopharmacol Biol Psychiatry. 2002 Jan;26(1):33-9. Takatsu K. & Nakajima H. IL-5 and eosinophilia. Curr Opin Immunol. 2008 Jun;20(3):288-94. Suzuki K. et al. Plasma cytokine profiles in subjects with high-functioning autism spectrum disorders. PLoS One. 2011;6(5):e20470. Goines PE. et al. Increased midgestational IFN-γ, IL-4 and IL-5 in women bearing a child with autism: A case-control study. Mol Autism. 2011 Aug 2;2:13. Ashwood P. et al. Associations of impaired behaviors with elevated plasma chemokines in autism spectrum disorders. J Neuroimmunol. 2011 Mar;232(1-2):196-9.[... Read more »
Choi JE, Widjaja F, Careaga M, Bent S, Ashwood P, & Hendren RL. (2014) Change in Plasma Cytokine Levels During Risperidone Treatment in Children with Autism. Journal of child and adolescent psychopharmacology. PMID: 24828014
Over 75% of surveyed collegiate athletes, who believed they sustained a concussion in the past year, reported not seeking proper medical attention for that concussion. The most common reason athletes reported not seeking proper medical attention was not believing the concussion was severe enough to warrant stopping the activity to seek out a medical professional.... Read more »
Delaney, J., Lamfookon, C., Bloom, G., Al-Kashmiri, A., & Correa, J. (2014) Why University Athletes Choose Not to Reveal Their Concussion Symptoms During a Practice or Game. Clinical Journal of Sport Medicine, 1. DOI: 10.1097/JSM.0000000000000112
Gabapentin and pregabalin misuse are problems that are not going to go away. My post on gabapentin is one of the most-read on this site. While these are useful medicines, workers in drug treatment and support see patients regularly on gabapentin or pregabalin who have misused the drugs or who are misusing them. Guidance is [...]
The post Gabapentin and pregabalin misuse appeared first on Recovery Review.
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Schifano, F. (2014) Misuse and Abuse of Pregabalin and Gabapentin: Cause for Concern?. CNS Drugs, 28(6), 491-496. DOI: 10.1007/s40263-014-0164-4
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 »
Kumar, S., Hultman, R., Hughes, D., Michel, N., Katz, B., & Dzirasa, K. (2014) Prefrontal cortex reactivity underlies trait vulnerability to chronic social defeat stress. Nature Communications. DOI: 10.1038/ncomms5537
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 »
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
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
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  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  which might be relevant. Carnitine plays a role in mitochondrial function  and there is some suggestion that a ketogenic diet might help maintain carnitine levels in the presence of VPA . 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...---------- 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. 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. Zammit VA. et al. Carnitine, mitochondrial function and therapy. Adv Drug Deliv Rev. 2009 Nov 30;61(14):1353-62. 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 »
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
Miguel Ramalho-Santos, PhDA new stem-cell discovery might one day lead to a more streamlined process for obtaining stem cells, which in turn could be used in the development of replacement tissue for failing body parts, according to UC San Francisco scientists who reported the findings in the current edition of Cell.The research builds on a strategy that involves reprogramming adult cells back to an embryonic state in which they again have the potential to become any type of cell.The efficiency of this process may soon increase thanks to the scientists' identification of biochemical pathways that can inhibit the necessary reprogramming of gene activity in adult human cells. Removing these barriers increased the efficiency of stem-cell production, the researchers found.Read More... Read more »
Qin, H., Diaz, A., Blouin, L., Lebbink, R., Patena, W., Tanbun, P., LeProust, E., McManus, M., Song, J., & Ramalho-Santos, M. (2014) Systematic Identification of Barriers to Human iPSC Generation. Cell, 158(2), 449-461. DOI: 10.1016/j.cell.2014.05.040
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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Eating Disorders and Psychiatric Comorbidities in Female Inpatients
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Bleck, J., DeBate, R., & Olivardia, R. (2014) The Comorbidity of ADHD and Eating Disorders in a Nationally Representative Sample. The Journal of Behavioral Health Services . DOI: 10.1007/s11414-014-9422-y
A new study from Colombia sees Blastocystis as a quasi-ubiquitous organism.... Read more »
Londoño-Franco AL, Loaiza-Herrera J, Lora-Suárez FM, & Gómez-Marín JE. (2014) [Blastocystis sp . frequency and sources among children from 0 to 5 years of age attending public day care centers in Calarcá, Colombia]. Biomedica : revista del Instituto Nacional de Salud, 34(2), 218-27. PMID: 24967927
Klimeš V, Gentekaki E, Roger AJ, & Eliáš M. (2014) A large number of nuclear genes in the human parasite Blastocystis require mRNA polyadenylation to create functional termination codons. Genome biology and evolution. PMID: 25015079
Lukeš J, Kuchta R, Scholz T, & Pomajbíková K. (2014) (Self-) infections with parasites: re-interpretations for the present. Trends in parasitology. PMID: 25033775
Tomasini N, Lauthier JJ, Ayala FJ, Tibayrenc M, & Diosque P. (2014) How often do they have sex? A comparative analysis of the population structure of seven eukaryotic microbial pathogens. PloS one, 9(7). PMID: 25054834
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 »
Lawitz, E., Sulkowski, M., Ghalib, R., Rodriguez-Torres, M., Younossi, Z., Corregidor, A., DeJesus, E., Pearlman, B., Rabinovitz, M., Gitlin, N.... (2014) Simeprevir plus sofosbuvir, with or without ribavirin, to treat chronic infection with hepatitis C virus genotype 1 in non-responders to pegylated interferon and ribavirin and treatment-naive patients: the COSMOS randomised study. The Lancet. DOI: 10.1016/S0140-6736(14)61036-9
C. Ronald KahnIn 2012, Japanese biologist Shinya Yamanaka won a Nobel Prize for discovering the so-called induced pluripotent stem cells" (iPSCs), cells derived from normal adult cells that have the ability to differentiate into almost any other kind of cells. Now, researchers at Joslin Diabetes Center say they have created the first iPSCs line that offers a human model for insulin resistance, a key driver of type 2 diabetes. "This is one of the very first studies of human iPSC models for type 2 diabetes, and it points out the power of this technology to look at the nature of diabetes, which is complex and may be different in different individuals." said C. Ronald Kahn, MD, Joslin's Chief Academic Officer and the Mary K. Iacocca Professor of Medicine at Harvard Medical School.Until now, scientists examining the causes and effects of insulin resistance have struggled with a general lack of human cell lines from tissues such as muscle, fat and liver that respond significantly to insulin, Kahn says. Studying insulin resistance as it progresses through pre-clinical stages of type 2 diabetes has been particularly challenging.Read More... Read more »
Iovino S, Burkart AM, Kriauciunas K, Warren L, Hughes KJ, Molla M, Lee YK, Patti ME, & Kahn CR. (2014) Genetic Insulin Resistance is a Potent Regulator of Gene Expression and Proliferation in Human iPS Cells. Diabetes. PMID: 25059784
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