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  • September 20, 2014
  • 04:51 AM

Antibiotics and risk of pediatric Crohn's disease

by Paul Whiteley in Questioning Answers

I couldn't let the meta-analysis from Ryan Ungaro and colleagues [1] pass without a brief mention. Concluding that: "Exposure to antibiotics appears to increase the odds of being newly diagnosed with CD [Crohn's disease] but not UC [ulcerative colitis]" and further: "This risk is most marked in children diagnosed with CD", the implications from this and other findings in this area may be far-reaching.I've talked before on this blog about antibiotic exposure and risk of inflammatory bowel disease (IBD) (see here) and how, bearing in mind risk is risk, there may be quite a bit more to see in the whole gut bacteria - disease risk arena. Acknowledging that science is still feeling it's way around this area and in particular, whether the use of probiotics might offset any risk or mitigate symptoms [2], the meta-analytic contribution of Ungaro et al represent another important driver for further investigation into those trillions of beasties which call us home [3]. Oh and then there is the gut-brain axis too?Music to close... Be Happy.----------[1] Ungaro R. et al. Antibiotics Associated With Increased Risk of New-Onset Crohn’s Disease But Not Ulcerative Colitis: A Meta-Analysis. The American Journal of Gastroenterology. 2014. 16 September.[2] Orel R. & Trop TK. Intestinal microbiota, probiotics and prebiotics in inflammatory bowel disease. World J Gastroenterol. Sep 7, 2014; 20(33): 11505–11524.[3] Wu GD. Diet, the Gut Microbiome and the Metabolome in IBD. Nestle Nutr Inst Workshop Ser. 2014;79:73-82.----------Ungaro R, Bernstein CN, Gearry R, Hviid A, Kolho KL, Kronman MP, Shaw S, Van Kruiningen H, Colombel JF, & Atreja A (2014). Antibiotics Associated With Increased Risk of New-Onset Crohn's Disease But Not Ulcerative Colitis: A Meta-Analysis. The American journal of gastroenterology PMID: 25223575... Read more »

Ungaro R, Bernstein CN, Gearry R, Hviid A, Kolho KL, Kronman MP, Shaw S, Van Kruiningen H, Colombel JF, & Atreja A. (2014) Antibiotics Associated With Increased Risk of New-Onset Crohn's Disease But Not Ulcerative Colitis: A Meta-Analysis. The American journal of gastroenterology. PMID: 25223575  

  • September 19, 2014
  • 07:28 PM

Nanosponges Clean up Antibody-mediated Autoimmune Disease

by Gabriel in Lunatic Laboratories

What does lupus, rheumatoid arthritis, type I diabetes, multiple sclerosis, and rheumatic heart disease have in common? All of these (and many other) apparently unrelated disorders are caused by autoimmunity, in which the immune system produces antibodies that attack normal, healthy cells and tissues. Currently considered incurable, these autoimmune diseases can be managed, but to varying degrees and not without serious side effects. Moreover, autoimmune diseases include a wide range of dysfunctional immune responses known as type II, type III, and type IV immune hypersensitivity reactions.... Read more »

Copp JA, Fang RH, Luk BT, Hu CM, Gao W, Zhang K, & Zhang L. (2014) Clearance of pathological antibodies using biomimetic nanoparticles. Proceedings of the National Academy of Sciences of the United States of America, 111(37), 13481-6. PMID: 25197051  

  • September 19, 2014
  • 01:21 PM

New test for Diagnosing Alzheimer’s Early

by Gabriel in Lunatic Laboratories

Alzheimer’s diagnosis is important, like the famous slogan “with a stroke, time lost is brain lost,” detecting alzheimer’s is important in order to stave off cognitive decline. A just like a stroke time lost is brain lost. Unfortunately early diagnosis has been hard to come by, but now researchers say a simple test that combines thinking and movement can help to detect heightened risk for developing Alzheimer’s disease in a person. The best part, they say this will work even before there are any telltale behavioural signs of dementia.... Read more »

  • September 19, 2014
  • 04:08 AM

Increasing parental age and autism severity?

by Paul Whiteley in Questioning Answers

An interesting paper by David Geier and colleagues [1] (open-access here) caught my eye recently, concluding that there was a lack of support for the suggestion that: "increasing parental age was associated with increasing autism spectrum disorder phenotypic severity"."the snozzberries taste like snozzberries".Before progressing through the paper and its possible implications, the eagle-eyed out there might have already spotted the name Dr Brian Hooker on the authorship list of the Geier paper. Outside of his other peer-reviewed work [2], I probably only need to mention the letters 'CDC' and everything that has [so far] followed including (at the time of writing) a removal statement for another paper [3]...Anyhow, the idea behind the Geier paper stems from the quite widely disseminated notion that there may be a connection between increasing parental age at conceiving and an increased risk of offspring autism. I've covered it a few times on this blog (see here and see here). The authors elaborate about a recent hypothesis suggesting that "there must be a linkage between increasing genetic load and increasing parental age in autism spectrum disorder pathogenesis" based on studies like the one from Kong and colleagues [4] (covered in a previous post) and Lampi and colleagues [5]. Further, that as a consequence of an increasing genetic load (all those SNPs et al), "there should be a significant relationship between increasing parental age and increasing autism spectrum disorder phenotypic severity of subjects diagnosed with an autism spectrum disorder".The paper is open-access but maybe a few details are in order:Participants (N=351), diagnosed with DSM-IV autism, were drawn from "patients presenting for outpatient genetic consultations at the ASD Centers, LLC". Mean age was approximately 9 years of age, most male and most reporting developmental regression following birth. Details of age of parents at time of offspring birth were analysed alongside use of the ATEC (Autism Treatment Evaluation Checklist) at initial clinical presentation. These variables formed the crux of the study.Results: "Overall, it was observed that no significant relationships were observed between increasing autism spectrum disorder phenotypic severity and increasing maternal or paternal age". Except, that is, for something that seemed to suggest that older maternal age at birth of child seemed to correlates with "improved sociability" in offspring. The authors report that their observations: "provide important insights into the apparent lack of a relationship between increasing parental age and increasing autism spectrum disorder phenotypic severity".Of course one has to be careful with any study of correlation/association, particularly when it comes to something as simple as just looking at ATEC scores of severity of behaviours in the autism domains and parents age at time of birth of their children. I personally would also have liked to see some further discussion on whether the broader autism phenotype (BAP) for example, might have been an influencing variable too in light of studies like the one from Hasegawa and colleagues [6]. Also, the participant group is quite large - as the authors note - but even there I think back to the sort of sample numbers that those [big data] studies in Taiwan are including (see here) as to where we should be heading.That all being said, I don't want to downplay the Geier results. Another quote might be useful here: "most observed de novo genetic events are unconnected to an autism spectrum disorder diagnosis, and those that do confer risk are distributed across many genes and are not necessarily sufficient for disease". This ties in rather nicely with the recent discussions on common variations and autism risk (see here) and how Gaugler and colleagues [7] questioned how much weight to give to de novo mutations in the grand scheme of autism 'causation'. This also might imply that non-genetic events, or at least non-structural genetic events headed under the general banner of environment might also play some contributory role to at least some cases of autism. Again, something which has cropped up on this blog before (see here).Music to close. Given the recent vote near these parts, one of Scotland's most famous exports... Franz Ferdinand and Do You Want To.----------[1] Geier DA. et al. An Evaluation of the Effect of Increasing Parental Age on the Phenotypic Severity of Autism Spectrum Disorder. J Child Neurol. 2014 Aug 27. pii: 0883073814541478.[2] Hooker B. et al. Methodological issues and evidence of malfeasance in research purporting to show thimerosal in vaccines is safe. Biomed Res Int. 2014;2014:247218.[3] Hooker BS. Measles-mumps-rubella vaccination timing and autism among young african american boys: a reanalysis of CDC data. Transl Neurodegener. 2014; 3: 16.[4] Kong A. et al. Rate of de novo mutations and the importance of father's age to disease risk. Nature. 2012 Aug 23;488(7412):471-5.[5] Lampi KM. et al. Parental age and risk of autism spectrum disorders in a Finnish national birth cohort. J Autism Dev Disord. 2013 Nov;43(11):2526-35.[6] Hasegawa C. et al. Broader autism phenotype in mothers predicts social responsiveness in young children with autism spectrum disorders. Psychiatry Clin Neurosci. 2014 Jun 6. doi: 10.1111/pcn.12210.[7] Gaugler T. et al. Most genetic risk for autism resides with common variation. Nature Genetics. 2014. July 20.----------... Read more »

  • September 18, 2014
  • 11:45 PM

Experimental and comparative oncology: zebrafish, dogs, elephants

by Artem Kaznatcheev in Evolutionary Games Group

One of the exciting things about mathematical oncology is that thinking about cancer often forces me to leave my comfortable arm-chair and look at some actually data. No matter how much I advocate for the merits of heuristic modeling, when it comes to cancer, data-agnostic models take second stage to data-rich modeling. This close relationship […]... Read more »

Gallaher, J., & Anderson, A.R. (2013) Evolution of intratumoral phenotypic heterogeneity: the role of trait inheritance. Interface Focus, 3(4), 20130016. arXiv: 1305.0524v1

  • September 18, 2014
  • 05:00 PM

Trunk biomechanics, hip and knee kinematics in patellofemoral pain

by Craig Payne in Running Research Junkie

Trunk biomechanics, hip and knee kinematics in patellofemoral pain... Read more »

  • September 18, 2014
  • 05:00 PM

The influence of running speed on ankle and knee joint moments

by Craig Payne in Running Research Junkie

The influence of running speed on ankle and knee joint moments... Read more »

  • September 18, 2014
  • 12:58 PM

Is Stress Eating Away at You? No, Literally…

by Gabriel in Lunatic Laboratories

Ever wonder why, when people are too stressed, they are often grouchy, grumpy, nasty, distracted or forgetful? It may not be something you’ve done, in fact it turns out stress is literally tearing apart the brain. By this I mean that researchers have just highlighted a fundamental synaptic mechanism that explains the relationship between chronic stress and the loss of social skills and cognitive impairment. When triggered by stress, an enzyme attacks a synaptic regulatory molecule in the brain. In other words, when people use the colloquialism “what’s eating you?” the answer might just be, stress.... Read more »

van der Kooij, M., Fantin, M., Rejmak, E., Grosse, J., Zanoletti, O., Fournier, C., Ganguly, K., Kalita, K., Kaczmarek, L., & Sandi, C. (2014) Role for MMP-9 in stress-induced downregulation of nectin-3 in hippocampal CA1 and associated behavioural alterations. Nature Communications, 4995. DOI: 10.1038/ncomms5995  

  • September 18, 2014
  • 11:11 AM

Genetics of Social Skills: Oxytocin Receptor Gene

by William Yates, M.D. in Brain Posts

Social neuroscience is an emerging emphasis in the field of neuroscience research.Social cognition is the subset of cognitive functions related to social processes and includes factors such as facial recognition, social memory and ability to form friendships and other social bonds.Impairment in social cognition is a known feature in autism, schizophrenia and other mental disorders. This type of impairment can produce significant problems in life adjustment, employment and human attachment.Genetic features appear to be important in human social cognition. Biological factors influence social behavior including the action of the hormone oxytocin.Dave Skuse along with colleagues in England, Finland and the U.S. recently published an important study examining the oxytocin receptor gene and social cognition.Their study used a family study design of 198 families from the U.K. and Finland with a single identified with high-functioning autism.This strategy was used with recognition that social cognition deficits are common in family members of those with autism and autism spectrum disorder.Probands with autism and family members had genetic testing for oxytocin gene polymorphism status along with the related vasopression gene. All participants completed a standardized test known as the Facial Recognition Memory Test (FRMT). Facial recognition and memory are key elements in social cognition and social function.The key findings from the study included the following:Oxytocin receptor polymorphism SNP rs237887 was strongly linked to deficits in facial recognition memoryHomozygous status for this SNP was associated with approximately a one standard deviation reduction in performance on the FRMT.This deficit was found in the autism group along with a significant number of undiagnosed family membersThe authors note their finding is consistent with other studies linking this specific SNP polymorphism with measures of empathy, autism traits and emotional responsivity to betrayal cues. The authors also note their results add to rodent animal model studies finding a key role for the oxytocin and vasopressin system in modulating social cognition and social behavior.These types of studies hold promise for potential drug development to reduce social impairment in those with autism and other disorders of social cognition.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 from the Dingle peninsula in Ireland is from the author's files.Follow the author on Twitter WRY999Skuse DH, Lori A, Cubells JF, Lee I, Conneely KN, Puura K, Lehtimäki T, Binder EB, & Young LJ (2014). Common polymorphism in the oxytocin receptor gene (OXTR) is associated with human social recognition skills. Proceedings of the National Academy of Sciences of the United States of America, 111 (5), 1987-92 PMID: 24367110... Read more »

Skuse DH, Lori A, Cubells JF, Lee I, Conneely KN, Puura K, Lehtimäki T, Binder EB, & Young LJ. (2014) Common polymorphism in the oxytocin receptor gene (OXTR) is associated with human social recognition skills. Proceedings of the National Academy of Sciences of the United States of America, 111(5), 1987-92. PMID: 24367110  

  • September 18, 2014
  • 04:50 AM

Anxiety and sensory over-responsivity linked to gut issues in autism

by Paul Whiteley in Questioning Answers

"The name's Lonnegan! Doyle Lonnegan!"Consider this micropost an extension of some previous discussions on this blog about how gastrointestinal (GI) issues present in cases of autism might show some connection to the presence of anxiety and sensory issues (see here). Today I'm discussing further research by Micah Mazurek and colleagues [1] which follows a previous publication by this author [2] on this topic.In the latest paper, Dr Mazurek and colleagues describe the course of abdominal pain in 225 children diagnosed with an autism spectrum disorder (ASD). Of the quarter of participants who presented with "chronic abdominal pain at baseline", the majority (over 80%) still had the same GI issue at 1-year follow-up. Indeed, a further 25% of those who did not present with abdominal pain at the start of the study finished the study with such an issue. The authors conclude: "Abdominal pain appears to be common and persistent among children with ASD". Further, anxiety and sensory over-responsivity also seemed to correlate with bowel features which is probably not unexpected.Yes, you might indeed say that this study was based on "the parent-reported GI Symptom Inventory Questionnaire" among other things and so one has to be slightly cautious about inferring states. But as I've mentioned before on this blog, parents/primary caregivers tend to be pretty good at picking up when such issues are present in their children (see here) if not precise to all the technical details [3].Perhaps the most important detail about the Mazurek study is their mention of the word 'pain' and how so many of their cohort seemed to be enduring quite a bit of it for such a long period of time. You wouldn't think that there was guidance on identifying and managing these issues [4] would you? And whilst we are on the topic of GI issues and autism, I might as well bring your attention to the potentially important question asked by Heitzer and colleagues [5]: Should clinical trial research of psychotropic medication in autism control for gastrointestinal symptoms? Answers on a postcard please (although I will blogging about this paper in times to come).So then, how about William Shatner singing Pulp to close. Replacing a Sheffield accent with a Montreal one... mmm, maybe he needs a little Henderson's Relish with that cheese?----------[1] Mazurek MO. et al. One-year course and predictors of abdominal pain in children with autism spectrum disorders: The role of anxiety and sensory over-responsivity. Research in Autism Spectrum Disorders. 2014; 8: 1508-1515.[2] Mazurek MO. et al. Anxiety, sensory over-responsivity, and gastrointestinal problems in children with autism spectrum disorders. J Abnorm Child Psychol. 2013 Jan;41(1):165-76.[3] Gorrindo P. et al. Gastrointestinal dysfunction in autism: parental report, clinical evaluation, and associated factors. Autism Res. 2012 Apr;5(2):101-8.[4] Buie T. et al. Evaluation, Diagnosis, and Treatment of Gastrointestinal Disorders in Individuals With ASDs: A Consensus Report. Pediatrics. 2010; 125: S1-S18.[5] Heitzer AM. et al. Should clinical trial research of psychotropic medication in autism control for gastrointestinal symptoms? J Clinical Pharmacology. 2014. 6 May.----------Mazurek, M., Keefer, A., Shui, A., & Vasa, R. (2014). One-year course and predictors of abdominal pain in children with autism spectrum disorders: The role of anxiety and sensory over-responsivity Research in Autism Spectrum Disorders, 8 (11), 1508-1515 DOI: 10.1016/j.rasd.2014.07.018... Read more »

  • September 17, 2014
  • 05:00 PM

Custom made vs sham foot orthotics for achilles tendinopathy

by Craig Payne in Running Research Junkie

Custom made vs sham foot orthotics for achilles tendinopathy... Read more »

  • September 17, 2014
  • 01:24 PM

Biofilms: Using Bacteria for new Designer Nanomaterials

by Gabriel in Lunatic Laboratories

For most people biofilms conjure up images of slippery stones in a streambed and dirty drains. While there are plenty of "bad" biofilms around – they are even the same stuff that causes pesky dental plaque and a host of other more serious medical problems – a team of researchers sees biofilms as a robust new platform for designer nanomaterials that could clean up polluted rivers, manufacture pharmaceutical products, fabricate new textiles, and more.... Read more »

Peter Q. Nguyen,, Zsofia Botyanszki,, Pei Kun R. Tay,, & Neel S. Joshi. (2014) Programmable biofilm-based materials from engineered curli nanofibres. Nature Communications. info:/10.1038/ncomms5945

  • September 17, 2014
  • 11:28 AM

Antidepressants Modulate Memory in the Healthy Brain

by William Yates, M.D. in Brain Posts

The mechanism of antidepressant drug response is not well understood.One theory posits antidepressant effects are only seen in those with clinical depression leaving the healthy brain unchanged.In a previous post, I outlined a study demonstrating effects of antidepressants on brain connectivity measures in the healthy brain.A recent fMRI study extends our understanding of the potential mechanisms for antidepressant drugs.CT Cerqueira and colleagues from Brazil studied the effects of the antidepressant clomipramine in a series of human subjects without a personal or family history of depression or other major psychiatric disorder.Subjects were started on a trial of clomipramine 10 mg increasing to 40 mg daily as tolerated.These healthy subjects then rated whether they noted any positive subjective response to clomipramine as defined by:increased mental efficiency and cogntive functionimproved mood and sense of well-beingawareness of significant change from usual subjective stateFour of sixteen subjects were rated as "responders" to the low dose clomipramine trial. Subjects provided a report of autobiographical memories in the previous six months that were grouped into positive (happy) versus negative (dysphoria/irritability).The key findings from the study included:Clomipramine "responders" showed enhanced blood flow (BOLD changes) with negative emotion cuesThis enhanced blood flow was located in the left tempero-parieto-occipital cortex and the left frontoparietal cortexNo differences were noted in blood flow between responders and non-responders with positive emotional cuesThe authors note there findings support a modulation of negative autobiographical memory in some individuals with healthy brains without an active mood disorder.It is unclear why this effect was limited to only about 25% of the healthy subject group. It is possible these "responders" to clomipramine had a form of sub-clinical depression.Alternately, the study supports the possibility of a more generalized effect of antidepressants not limited to those with a clinical mood disorder.Reduction of distress to negative emotional memories is a known clinical effect of an antidepressant effect in those with mood disorder.The enhanced brain activity in this study with clomipramine is located in brain regions known to be active in processing emotional stimuli and modulation of the negative response to dysphoric memories.The current study is limited by a small sample size but supports further study of antidepressant brain effects in healthy versus depressed subjects. This type of research may provide insight into designing more effective antidepressant drugs.Readers with more interest in this research can access the free full-text article by clicking on the PMID link below.Landscape of Dingle peninsula in Ireland is from the author's files.Follow the author on Twitter WRY999Cerqueira CT, Sato JR, de Almeida JR, Amaro E Jr, Leite CC, Gorenstein C, Gentil V, & Busatto GF (2014). Healthy individuals treated with clomipramine: an fMRI study of brain activity during autobiographical recall of emotions. Translational psychiatry, 4 PMID: 24984192... Read more »

  • September 17, 2014
  • 08:28 AM

Builders and Blocks – Engineering Blood Vessels with Stem Cells

by Jalees Rehman in The Next Regeneration

Back in 2001, when we first began studying how regenerative cells (stem cells or more mature progenitor cells) enhance blood vessel growth, our group as well as many of our colleagues focused on one specific type of blood vessel: arteries. Arteries are responsible for supplying oxygen to all organs and tissues of the body and arteries are more likely to develop gradual plaque build-up (atherosclerosis) than veins or networks of smaller blood vessels (capillaries). Once the amount of plaque in an artery reaches a critical threshold, the oxygenation of the supplied tissues and organs becomes compromised. In addition to this build-up of plaque and gradual decline of organ function, arterial plaques can rupture and cause severe sudden damage such as a heart attack. The conventional approach to treating arterial blockages in the heart was to either perform an open-heart bypass surgery in which blocked arteries were manually bypassed or to place a tube-like "stent" in the blocked artery to restore the oxygen supply. The hope was that injections of regenerative cells would ultimately replace the invasive procedures because the stem cells would convert into blood vessel cells, form healthy new arteries and naturally bypass the blockages in the existing arteries.... Read more »

Paul JD, Coulombe KL, Toth PT, Zhang Y, Marsboom G, Bindokas VP, Smith DW, Murry CE, & Rehman J. (2013) SLIT3-ROBO4 activation promotes vascular network formation in human engineered tissue and angiogenesis in vivo. Journal of molecular and cellular cardiology, 124-31. PMID: 24090675  

  • September 17, 2014
  • 08:05 AM

Should I Stay Or Should I Go

by Mark Lasbury in As Many Exceptions As Rules

Bacteria can swarm to conquer new territory or settle into structured biofilms, not unlike tribes that are nomadic versus those that build cities. New research indicates has shed light on the mechanics of swarming and biofilm production, including the function of extracellular DNA and secreted polysaccharides. Both biofilms and swarming depend on quorum sensing, and several new papers have identified chemicals that can interrupt quorum sensing in pathogenic bacteria and therefore prevent disease development.... Read more »

Gloag ES, Turnbull L, Huang A, Vallotton P, Wang H, Nolan LM, Mililli L, Hunt C, Lu J, Osvath SR.... (2013) Self-organization of bacterial biofilms is facilitated by extracellular DNA. Proceedings of the National Academy of Sciences of the United States of America, 110(28), 11541-6. PMID: 23798445  

Alteri CJ, Himpsl SD, Pickens SR, Lindner JR, Zora JS, Miller JE, Arno PD, Straight SW, & Mobley HL. (2013) Multicellular bacteria deploy the type VI secretion system to preemptively strike neighboring cells. PLoS pathogens, 9(9). PMID: 24039579  

  • September 17, 2014
  • 06:29 AM

Autoimmune disease risk and eating disorders

by Paul Whiteley in Questioning Answers

"We were set up. The cops were waiting for us.""We observed an association between eating disorders and several autoimmune diseases with different genetic backgrounds. Our findings support the link between immune-mediated mechanisms and development of eating disorders".So said the paper by Anu Raevuori and colleagues [1] (open-access) based on an analysis of over 2300 people "treated at the Eating Disorder Unit of Helsinki University Central Hospital between 1995 and 2010" compared with nearly 10,000 control participants (so yes, this was quite a well-powered study).The Raevuori paper is open-access but if you want a few choice details, here goes...Based on a body of research literature looking at a possible association between eating disorders and autoimmune conditions like type 1 diabetes [2], authors set about testing the hypothesis on a large scale on whether "the risk of autoimmune diseases would be increased in individuals with eating disorders both prior and after the onset of the treatment for an eating disorder".Having already mentioned how large a scale the authors' participants groups were, various eating disorder diagnoses were confirmed based on ICD-10 criteria [3] and both research and control populations were assessed for some 30 autoimmune conditions based on existing hospital discharge registry. "Period and lifetime prevalences" were calculated from the data. Results: "Participants with BN [bulimia nervosa] made up the largest patient group (54.0%), followed by those with AN [anorexia nervosa] (38.8%), and those with BED [binge eating disorder] (7.3%)". Over 5% of those diagnosed with an eating disorder had been diagnosed with one or more autoimmune conditions compared with just under 3% of controls when it came to looking at period prevalence (at the onset of treatment). Long quote coming up... "The risk of prior diagnosis of endocrinological autoimmune diseases (OR 3.3, 95% CI 2.4–4.6, P<0.001), of gastroenterological immune-mediated diseases (OR 2.0, 95% CI 1.3–3.1, P = 0.002), and of autoimmune diseases combined (OR 2.1 95% CI 1.7–2.7, P<0.001) was significantly higher among patients than among matched controls".With regards to lifetime prevalence (over the whole study period) "8.9% (N = 209) of patients and 5.4% of control individuals (N = 509) had ever been diagnosed with one or more autoimmune disease". Whilst only looking like a relatively small percentage difference in the rates of autoimmune conditions between the groups, it is the scale of the Raevuori study in terms of participant numbers which gives the data some 'edge'. As the authors also note, their use of the category BED - binge eating disorder - is also another plus to their study given it's recent inclusion into DSM-5 (see here).As I always seem to be about papers mentioned on this blog, I was really quite interested in the results presented by Raevuori et al and their potential implications for how we describe eating disorders and the potential mechanisms involved in onset. Research into autoimmune conditions has recently been producing some rather important associations as per my covering of things like a [possible] link between autoimmune disorders following trauma and PTSD (see here) and even a suggested connection with some epilepsy (see here).Raevuori and colleagues discuss several pertinent mechanisms potentially linking their findings including the ever-present issue of inflammation and: "Pro-inflammatory cytokines and antibodies/autoantibodies against neuronal antigens". They also mention some possible role for "intestinal microflora contributing to the development of cross-reactive neuronal autoantibodies [providing] a link between gut and brain" and the growing fascination with all-things gut microbiome. Their finding of a greater frequency of the inflammatory bowel disease (IBD), Crohn's disease in their eating disorder cohort offers some evidence for this assertion as a function of the growing interest in gut bacteria and IBDs [4].Without hopefully going too far off tangent from the Raevuori paper, I started to think about how these results might also fit in with some of the research done on autism and whether there may be a bigger picture here. Eating disorders have been mentioned alongside the label autism quite a few times in the research literature [5]. My previous discussions on signs of autism in cases of eating disorders (see here) is one example. Likewise, autoimmune conditions and autism also seem to have something of a connection (see here) alongside presented data on markers of autoimmunity in cases of autism (see here and see here). One can perhaps see how the various elements - immune function, inflammation, gut bacteria, gut permeability? - might be intertwined, albeit in a rather complex fashion...?Music then, and Naive by The Kooks.----------[1] Raevuori A. et al. The increased risk for autoimmune diseases in patients with eating disorders. PLoS One. 2014 Aug 22;9(8):e104845.[2] Young V. et al. Eating problems in adolescents with Type 1 diabetes: a systematic review with meta-analysis. Diabet Med. 2013 Feb;30(2):189-98.[3] Herpetz S. et al. The Diagnosis and Treatment of Eating Disorders. Dtsch Arztebl Int. Oct 2011; 108(40): 678–685.[4] Manichanh C. et al. The gut microbiota in IBD. Nat Rev Gastroenterol Hepatol. 2012 Oct;9(10):599-608.[5] Huke V. et al. Autism spectrum disorders in eating disorder populations: a systematic review. Eur Eat Disord Rev. 2013 Sep;21(5):345-51.----------Raevuori A, Haukka J, Vaarala O, Suvisaari JM, Gissler M, Grainger M, Linna MS, & Suokas JT (2014). The increased risk for autoimmune diseases in patients with eating disorders. PloS one, 9 (8) PMID: 25147950... Read more »

Raevuori A, Haukka J, Vaarala O, Suvisaari JM, Gissler M, Grainger M, Linna MS, & Suokas JT. (2014) The increased risk for autoimmune diseases in patients with eating disorders. PloS one, 9(8). PMID: 25147950  

  • September 17, 2014
  • 06:09 AM

Unwelcome colonisers: biofilm formation on voice prostheses

by socgenmicro in Microbe Post

A human being’s voice is one of their most distinguishing and individual features. Most of us have experienced the frustration of temporarily losing our voices – but for many survivors of laryngeal cancer (cancer of the voice box), this loss … Continue reading →... Read more »

Talpaert, M., Balfour, A., Stevens, S., Baker, M., Muhlschlegel, F., & Gourlay, C. (2014) Candida Biofilm Formation on Voice Prostheses. Journal of Medical Microbiology. DOI: 10.1099/jmm.0.078717-0  

  • September 17, 2014
  • 12:05 AM

Not So Competitive Return Rates to Activity Following ACL Reconstruction

by Nicole Cattano in Sports Medicine Research (SMR): In the Lab & In the Field

Only 55% of athletes returned to competitive sport following anterior cruciate ligament (ACL) reconstruction. The debate continues as to whether hamstring or patellar tendon autograft is better. However, factors that may favor return to competitive sport include younger age, male gender, elite sport, and a positive psychological response. ... Read more »

  • September 16, 2014
  • 10:15 PM

Colon cancer, mathematical time travel, and questioning the sequential mutation model.

by Artem Kaznatcheev in Evolutionary Games Group

On Saturday, I arrived in Columbus, Ohio for the the MBI Workshop on the Ecology and Evolution of Cancer. Today, our second day started. The meeting is an exciting combination of biology-minded mathematicians and computer scientists, and math-friendly biologist and clinicians. As is typical of workshops, the speakers of the first day had an agenda […]... Read more »

Baker AM, Cereser B, Melton S, Fletcher AG, Rodriguez-Justo M, Tadrous PJ, Humphries A, Elia G, McDonald SA, Wright NA.... (2014) Quantification of crypt and stem cell evolution in the normal and neoplastic human colon. Cell reports, 8(4), 940-7. PMID: 25127143  

  • September 16, 2014
  • 01:20 PM

New Cocktail Turns Adult Cells into Stem Cells

by Gabriel in Lunatic Laboratories

For those of us who were following stem cell news, recently the field had a huge setback when a paper, that offered a cheap and novel way to create stem cells, was retracted from publication. Regenerative medicine aims to replace lost or damaged cells, tissues or organs through cellular transplantation, but the promise to a better life has been hampered. Because stem cells derived from human embryos can trigger ethical concerns, a good solution is reprogramming adult cells back to an embryo-like state using a combination of reprogramming factors. Unfortunately that has been easier said than done.... Read more »

Buganim Y, Markoulaki S, van Wietmarschen N, Hoke H, Wu T, Ganz K, Akhtar-Zaidi B, He Y, Abraham BJ, Porubsky D.... (2014) The Developmental Potential of iPSCs Is Greatly Influenced by Reprogramming Factor Selection. Cell stem cell, 15(3), 295-309. PMID: 25192464  

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