Children with HIV who can resist the disease progressing could point the way to new treatments for HIV infection that are more widely applicable to infected adults and children alike, an international team of researchers has found.
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Muenchhoff, M., Adland, E., Karimanzira, O., Crowther, C., Pace, M., Csala, A., Leitman, E., Moonsamy, A., McGregor, C., Hurst, J.... (2016) Nonprogressing HIV-infected children share fundamental immunological features of nonpathogenic SIV infection. Science Translational Medicine, 8(358), 358-358. DOI: 10.1126/scitranslmed.aag1048
When extremely happy or relaxed, rats will display a behavior known as boggling where their eyes vibrate and bulge. ... Read more »
Froberg-fejko, Karen. (2014) Give a rat a bone: satisfying rodents' need to gnaw. Lab animal. info:/
Some comments on early animal evolution fossil record and Indian Peninsular Proterozoic Basins... Read more »
Kale, V. (2016) Proterozoic Basins of Peninsular India: Status within the Global Proterozoic Systems. Proceedings of the Indian National Science Academy, 82(3). DOI: 10.16943/ptinsa/2016/48461
Mathur, V., Shome, S., Nath, S., & Babu, R. (2014) First record of metazoan eggs and embryos from early Cambrian Chert Member of Deo ka Tibba Formation, Tal Group, Uttarakhand Lesser Himalaya. Journal of the Geological Society of India, 83(2), 191-197. DOI: 10.1007/s12594-014-0031-4
Stone tools and fossils suggest that an early wave of Homo sapiens may have migrated into India as early as 100K years ago. Did these migrants leave a genetic trace in present day Indians.. ... Read more »
Mallick, S., Li, H., Lipson, M., Mathieson, I., Gymrek, M., Racimo, F., Zhao, M., Chennagiri, N., Nordenfelt, S., Tandon, A.... (2016) The Simons Genome Diversity Project: 300 genomes from 142 diverse populations. Nature. DOI: 10.1038/nature18964
They've finally arrived. The results of the English Adult Psychiatric Morbidity Survey 2014 have been published by NHS Digital (yes, our Nation's healthcare services has a digital arm) and when it comes to autism (adult autism 18 years+), some rather peculiar statistics have been produced.OK, for those who want/need a quick heads-up on all-things Adult Psychiatric Morbidity Survey (APMS), I'll refer you to a previous post I wrote covering this prevalence survey with autism in mind (see here). APMS provides estimates of the numbers of various mental health diagnoses among adults living in private households in England.The 2014 data report some key facts, not least that: "One in three adults aged 16-74 (37 per cent) with conditions such as anxiety or depression, surveyed in England, were accessing mental health treatment, in 2014." This figure is an increase on the 2007 APMS data (24%). There are also some other important data derived from the 2014 survey too with regards to sex differences in relation to "common mental disorder (CMD)" in diagnosis and in symptoms. Lessons need to be learned.It is however with autism in mind (see here for the section covering autism), that I'm concentrating on in this post and the observation that: "The estimated prevalence of autism in 2014, using the threshold of a score of 10 on the ADOS [autism diagnostic observation schedule] to indicate a positive case, was 0.7% of the adult population in England (equivalent to a rate of 7 per thousand). The estimated prevalence of autism in the 2007 data (1.0%) was similar to the 2014 estimate; with largely overlapping confidence intervals." A separate 'additional notes' document accompanies the APMS 2014 autism findings (see here).1% in 2007 and 0.7% in 2014? Accepting that when it comes to prevalence estimates there is always a degree of 'error' expected (as per the comment on 'overlapping confidence intervals') I'm a little bit puzzled by this latest data and the idea that the figures are described as 'similar'. Puzzled because as well as suggesting that adult autism prevalence estimates might have actually dipped between the years, the authors note that their search of 3 quite populous areas of England ("Leicestershire, Lambeth and Sheffield") across both the 2007 and 2014 data combined only found "31 participants identified with autism."So what's going on with the APMS and autism?A question indeed and I assume that the 'combining' of the 2007 and 2014 datasets reveals quite a bit more than just the very small number of participants identified in the studies. I have to say that my brow is furrowing a little at the sight of the Autism Spectrum Quotient (AQ) as retaining an 'autism screener' role in the APMS 2014. If I've learned anything about the AQ in recent times it is that whilst measuring something, it may not be a particularly great exclusive screen for autism (see here). Even the authors attached to the APMS 2014 autism data have said so : "The AQ-20 was only a weak predictor of ADOS-4 cases." I've also mentioned about the ADOS module situation and the whys and wherefores with APMS in mind in that previous post on the topic (see here again).So we're left with a quandary. The much heralded '1% of adults may have autism' statistic is replaced by a lower value (with appropriate caveats on confidence intervals) of 0.8% when the APMS 2007 and 2014 data are combined. Is this a true reflection of adult autism in England in recent times? How does this tally with the suggestion that child and adolescent rates of autism are on the increase as per that seen in other parts of the UK (see here)?Or, are the processes pertinent to estimating adult autism used by the APMS not really cutting the statistical/methodological mustard?Which one is it?---------- Brugha TS. et al. Validating two survey methods for identifying cases of autism spectrum disorder among adults in the community. Psychol Med. 2012 Mar;42(3):647-56.----------Brugha TS, McManus S, Smith J, Scott FJ, Meltzer H, Purdon S, Berney T, Tantam D, Robinson J, Radley J, & Bankart J (2012). Validating two survey methods for identifying cases of autism spectrum disorder among adults in the community. Psychological medicine, 42 (3), 647-56 PMID: 21798110... Read more »
Brugha TS, McManus S, Smith J, Scott FJ, Meltzer H, Purdon S, Berney T, Tantam D, Robinson J, Radley J.... (2012) Validating two survey methods for identifying cases of autism spectrum disorder among adults in the community. Psychological medicine, 42(3), 647-56. PMID: 21798110
"School-based interventions should address malleable factors such as the number of peer connections and received friendships that predict the best social outcomes for children with ASD [autism spectrum disorder]."So said the study findings reported by Jill Locke and colleagues  looking at "the stable (unlikely to change) and malleable (changeable) characteristics of socially successful children with ASD."Mindful that the phrase 'socially successful children' is perhaps not one that I'm particularly enamoured with, and certainly not one that necessarily opens the doors to 'successful' academic outcomes in childhood for example (see here), the Locke paper makes for interesting reading.Looking at nearly 150 "elementary-aged children with ASD" authors listed a number of factors linked to 'playground peer engagement' and 'social network salience ' a.k.a playing with other children in the school yard and "inclusion in informal peer groups." The severity of autistic symptoms was unsurprisingly a key feature as was those numbers of 'peer connections' and 'received friendships'.What do these results mean? Well, minus sweeping generalisations, there may be some pretty easy ways that 'social outcomes' can be positively influenced for at least some children on the autism spectrum; not least one important variable: friends. Yes, a shocker I know.I've used the term 'easy ways' and 'friends' in that previous sentence to denote how [sometimes] complicated and expensive/resource intensive interventions to 'increase social outcomes' when it comes to the label of autism really might not be the most effective use of resources. I however understand that friends, real friends, are not just something that can be magically produced on demand and that also friendships, whilst in the end generally worthwhile, are not without their own stresses and strains (some of which might be even more stressful and strainful(!) for a child on the autism spectrum).One approach that does seem to be finding some favour in the peer-reviewed domain at least is that of employing a buddy system. The findings reported by Laushey & Heflin  whilst not without their methodological issues, provide some important assertions that a peer buddy approach might be something for schools to consider for some pupils with autism. I know some people might argue that a buddy is not the same as a friend but I'm not one of the them: opportunity (not necessity) is the mother of invention. Visit most schools (at least in here in the UK) and you will see similar arrangements being made for pupils whether diagnosed with autism or not. That and use of 'buddy/friendship stops' in certain parts of the playground and you'll see how important socialisation is viewed for all school pupils.I'm also a greater believer that sport and exercise can be an important part of inclusion practices when it comes to autism - something equally applicable to school. Y'know, those team games that help build and forge important bonds between children particularly when it comes to competitive team games, also introducing the important concept of 'belonging'. I appreciate that finding the right sport is important in terms of likes/dislikes and ability but there are quite a few options out there. Indeed, drilling further down into the concept of 'belonging', one can perhaps see how even at elementary school age, finding your social niche can open up a whole world of new friends/associates thus implying that school clubs (e.g. Lego club, ICT club) might also be an important intervention tool too.I don't want to come across too formulaic or mechanical when it comes to how to improve social outcomes for children on the autism spectrum because there is not one-size-fits-all 'flowchart' to this issue. Appreciating also that some children on the autism spectrum might not necessarily want to be 'social butterflies' there has to be some indication from the child as to the extent of their wants and wishes when it comes to social interaction also taken into account.I should also remind readers that when it comes to friendships, children can be a rather fickle bunch...---------- Locke J. et al. Characteristics of socially successful elementary school-aged children with autism. J Child Psychol Psychiatry. 2016 Sep 13. Laushey KM. & Heflin LJ. Enhancing social skills of kindergarten children with autism through the training of multiple peers as tutors. J Autism Dev Disord. 2000 Jun;30(3):183-93.----------Locke J, Williams J, Shih W, & Kasari C (2016). Characteristics of socially successful elementary school-aged children with autism. Journal of child psychology and psychiatry, and allied disciplines PMID: 27620949... Read more »
Locke J, Williams J, Shih W, & Kasari C. (2016) Characteristics of socially successful elementary school-aged children with autism. Journal of child psychology and psychiatry, and allied disciplines. PMID: 27620949
A couple of years ago, I mused here on Language on the Move what linguistic theory would look like if...... Read more »
Piller, I. (2016) Dubai: Language in the ethnocratic, corporate and mobile city. Smakman, D. and P. Heinrich. Eds. Metrolinguistics: Urban Language Ecologies around the World. info:/
A team of researchers has observed what they believe are the building blocks of memories in a mouse brain. In their paper, the researchers describe how they caused certain neurons to become illuminated when they fired, allowing them to watch in real time as memories were made and then later as they were replayed while the mouse was sitting idle.
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Malvache, A., Reichinnek, S., Villette, V., Haimerl, C., & Cossart, R. (2016) Awake hippocampal reactivations project onto orthogonal neuronal assemblies. Science, 353(6305), 1280-1283. DOI: 10.1126/science.aaf3319
One clinical challenge is making an accurate diagnosis in patients with dementia.Alzheimer's disease is typically the predominant diagnosis in dementia. However a significant number of patients will present with dementia due to Lewy Body disease, Parkinson's dementia, frontotemporal dementia or vascular dementia.A recent study helps clinicians to distinguish Lewy Body from Alzheimer's dementia and Parkinson's disease.Douglas Scharre and collegues from Ohio State University conducted a matched pair analysis of 21 patients with Lewy Body dementia with 21 patients with Alzheimer's disease and 21 patients with Parkinson's disease.Parkinson's disease subjects in this study had higher cognitive function scores than the Lewy Body disease subjects but were matched on level of motor impairment.Subject groups were assessed on a variety of motor, cognitive and neuropsychological domains. Lewy Body dementia subjects differed from the Alzheimer's group in the following areas:Higher impairment scores on executive function and visuospatial functionLower impairment on memory and orientationHigher scores on measures of sleepinessHigher scores on fluctuation of cognitive and behavior deficitsMore hallucinationsMore sleep apneaLewy body dementia subjects differed from the Parkinson's disease group in the following areas:More impairment in axial motor functionMore impairment in gait and balance functionHigher scores on measures of sleepinessHigher scores on fluctuation of cognitive and behavior deficitsMore hallucinationsMore sleep apneaThe authors noted that measures of axial motor, gait and balance impairment correlated higher with level of executive function impairment, visuomotor function impairment and global cognitive impairment.This is an important study and highlights the need for specific neuropsychological testing along with assessment of motor, gait and balance domains dementia evaluations.Readers with more interest in this study can access the author's uncorrected proofs by clicking on the DOI link in the citation below.Follow me on Twitter WRY999Photo of brown thrasher from my back yard is from my files.Scharre, D., Chang, S., Nagaraja, H., Park, A., Adeli, A., Agrawal, P., Kloos, A., Kegelmeyer, D., Linder, S., Fritz, N., Kostyk, S., & Kataki, M. (2016). Paired Studies Comparing Clinical Profiles of Lewy Body Dementia with Alzheimer’s and Parkinson’s Diseases Journal of Alzheimer's Disease, 1-10 DOI: 10.3233/JAD-160384... Read more »
Scharre, D., Chang, S., Nagaraja, H., Park, A., Adeli, A., Agrawal, P., Kloos, A., Kegelmeyer, D., Linder, S., Fritz, N.... (2016) Paired Studies Comparing Clinical Profiles of Lewy Body Dementia with Alzheimer’s and Parkinson’s Diseases. Journal of Alzheimer's Disease, 1-10. DOI: 10.3233/JAD-160384
Cancer metastasis occurs when cancer cells leave a primary tumor and invade other tissues. Generally, this leads to a poor prognosis for patients. Underlying epigenetic mechanisms of tumor progression are poorly understood but are of great interest for developing new approaches of treatment in the clinic. Cancer etiology is highly correlated with alterations in the histone code1-5 and protein methyltransferases are frequently dysregulated in cancer, implicating them as compelling novel targets for chemotherapy. Arginine methylation in particular regulates biological function3,6,7 as well as oncogenesis and tumor progression.1,2,6 The protein arginine methyltransferases (PRMT) family targets a range of substrates, including histones, spliceosomal factors, and ribosomal proteins.9-11 Recent reports have linked the dysregulation of arginine methylation to numerous cancers and our recent paper Chen et al. investigates the role of PRMT5, a histone arginine methyltransferase, in cancer metastasis and tumor progression... Read more »
Chen H, Lorton B, Gupta V, & Shechter D. (2016) A TGFβ-PRMT5-MEP50 axis regulates cancer cell invasion through histone H3 and H4 arginine methylation coupled transcriptional activation and repression. Oncogene. PMID: 27270440
Chi P, Allis CD, & Wang GG. (2010) Covalent histone modifications--miswritten, misinterpreted and mis-erased in human cancers. Nature reviews. Cancer, 10(7), 457-69. PMID: 20574448
Stopa N, Krebs JE, & Shechter D. (2015) The PRMT5 arginine methyltransferase: many roles in development, cancer and beyond. Cellular and molecular life sciences : CMLS, 72(11), 2041-59. PMID: 25662273
Cha B, & Jho EH. (2012) Protein arginine methyltransferases (PRMTs) as therapeutic targets. Expert opinion on therapeutic targets, 16(7), 651-64. PMID: 22621686
Yang XJ, & Seto E. (2008) Lysine acetylation: codified crosstalk with other posttranslational modifications. Molecular cell, 31(4), 449-61. PMID: 18722172
Greenblatt SM, Liu F, & Nimer SD. (2016) Arginine methyltransferases in normal and malignant hematopoiesis. Experimental hematology, 44(6), 435-41. PMID: 27026282
Wilczek C, Chitta R, Woo E, Shabanowitz J, Chait BT, Hunt DF, & Shechter D. (2011) Protein arginine methyltransferase Prmt5-Mep50 methylates histones H2A and H4 and the histone chaperone nucleoplasmin in Xenopus laevis eggs. The Journal of biological chemistry, 286(49), 42221-31. PMID: 22009756
Ho MC, Wilczek C, Bonanno JB, Xing L, Seznec J, Matsui T, Carter LG, Onikubo T, Kumar PR, Chan MK.... (2013) Structure of the arginine methyltransferase PRMT5-MEP50 reveals a mechanism for substrate specificity. PloS one, 8(2). PMID: 23451136
Burgos ES, Wilczek C, Onikubo T, Bonanno JB, Jansong J, Reimer U, & Shechter D. (2015) Histone H2A and H4 N-terminal tails are positioned by the MEP50 WD repeat protein for efficient methylation by the PRMT5 arginine methyltransferase. The Journal of biological chemistry, 290(15), 9674-89. PMID: 25713080
Chan-Penebre E, Kuplast KG, Majer CR, Boriack-Sjodin PA, Wigle TJ, Johnston LD, Rioux N, Munchhof MJ, Jin L, Jacques SL.... (2015) A selective inhibitor of PRMT5 with in vivo and in vitro potency in MCL models. Nature chemical biology, 11(6), 432-7. PMID: 25915199
Liu F, Cheng G, Hamard PJ, Greenblatt S, Wang L, Man N, Perna F, Xu H, Tadi M, Luciani L.... (2015) Arginine methyltransferase PRMT5 is essential for sustaining normal adult hematopoiesis. The Journal of clinical investigation, 125(9), 3532-44. PMID: 26258414
Ikushima H, & Miyazono K. (2010) TGFbeta signalling: a complex web in cancer progression. Nature reviews. Cancer, 10(6), 415-24. PMID: 20495575
Lamouille, S., Xu, J., & Derynck, R. (2014) Molecular mechanisms of epithelial–mesenchymal transition. Nature Reviews Molecular Cell Biology, 15(3), 178-196. DOI: 10.1038/nrm3758
For the first time, an antibody was able to target and disrupt the Aβ plaques in the brain.... Read more »
Sevigny, J., Chiao, P., Bussière, T., Weinreb, P., Williams, L., Maier, M., Dunstan, R., Salloway, S., Chen, T., Ling, Y.... (2016) The antibody aducanumab reduces Aβ plaques in Alzheimer’s disease. Nature, 537(7618), 50-56. DOI: 10.1038/nature19323
Dietary intake in young athletes seem to meet most recommendations, therefore supplementing may only be necessary for a few select micronutrients based on age and gender. ... Read more »
Parnell, J., Wiens, K., & Erdman, K. (2016) Dietary Intakes and Supplement Use in Pre-Adolescent and Adolescent Canadian Athletes. Nutrients, 8(9), 526. DOI: 10.3390/nu8090526
Please use your full stops wisely.I believe that this is the first time that I've talked about postural tachycardia syndrome (PoTS) on this blog as I bring to your attention some rather intriguing findings reported by Hugo Penny and colleagues  on how PoTS and gluten-related disorders might not be unstrange diagnostic bedfellows.PoTS by the way, describes symptoms where standing upright / sitting down induces dizziness, fainting and other symptoms. As well as being quite prevalent in a certain condition called Ehlers-Danlos syndrome (see here), PoTS is also described fairly frequently in cases of chronic fatigue syndrome / myalgic encephalomyelitis (CFS/ME) too.Describing how "patients with postural tachycardia syndrome (PoTS) were placing themselves on a gluten-free diet without medical consultation" the authorship team (mentioned previously on this blog) residing in the great city of Sheffield decided to look-see whether there may be underlying medical reasons why such gluten-free moves seemed to be used in cases of PoTS. They screened their 100 participants with PoTS "for gluten sensitivity, related symptoms and dietary habits" as well as assessing for coeliac disease, the archetypal gluten-related autoimmune condition.Results: compared with a couple of control groups numbering in total above 1500 local participants, coeliac disease (CD) seemed to be more common in the PoTS groups - "serology and biopsy-proven coeliac disease." Alongside: "PoTS patients also had a higher prevalence of self-reported gluten sensitivity... compared with age-matched and sex-matched controls." The authors conclude that there may be more to see when it comes to the presence of classical and non-classical gluten-related disorders in relation to PoTS.This is potentially important stuff. Accepting that outside of the immediate dizziness and fainting symptoms associated with PoTS there may be other 'gastrointestinal' involvement  the intriguing idea that [certain] symptoms might be to some degree alleviated by use of a dietary change is worthy of greater inspection. Indeed, set within the context of an associated diagnostic label, orthostatic intolerance, where an upright posture provokes related symptoms, also being potentially linked to gastrointestinal issues  one has an interesting template as to how gut and brain might show some important links. That a gluten-free diet will most likely target both gut and brain (yes, it might) provides plenty of food for thought as to possible mechanisms.I'm also pretty interested in the growing research base looking at a possible autoimmune component to at least some cases of PoTS . I know this takes us into some 'brow-furrowing' areas of peer-reviewed science  (indeed, complicated science) but the potential importance of cases of autoimmune PoTS intersecting with cases of autoimmune coeliac disease provides yet another example of how birds of an autoimmune feather tend to flock together (see here). The implication being that cases of PoTS should perhaps be screened for CD and other autoimmune disease/features and perhaps treated accordingly, offers some new directions for research and clinical practice.And just in case you are still convinced that use of a gluten-free diet outside of CD is all bunk, the worm still continues to turn...To close, 'Shatner's Bassoon'. That is all.---------- Penny HA. et al. Is there a relationship between gluten sensitivity and postural tachycardia syndrome? Eur J Gastroenterol Hepatol. 2016 Sep 7. Wang LB. et al. Gastrointestinal dysfunction in postural tachycardia syndrome. J Neurol Sci. 2015 Dec 15;359(1-2):193-6. Sullivan SD. et al. Gastrointestinal symptoms associated with orthostatic intolerance. J Pediatr Gastroenterol Nutr. 2005 Apr;40(4):425-8. Thieben MJ. et al. Postural orthostatic tachycardia syndrome: the Mayo clinic experience. Mayo Clin Proc. 2007 Mar;82(3):308-13. Blitshteyn S. & Brook J. Postural tachycardia syndrome (POTS) with anti-NMDA receptor antibodies after human papillomavirus vaccination. Immunol Res. 2016 Aug 25.----------Penny, H., Aziz, I., Ferrar, M., Atkinson, J., Hoggard, N., Hadjivassiliou, M., West, J., & Sanders, D. (2016). Is there a relationship between gluten sensitivity and postural tachycardia syndrome? European Journal of Gastroenterology & Hepatology DOI: 10.1097/MEG.0000000000000740... Read more »
Penny, H., Aziz, I., Ferrar, M., Atkinson, J., Hoggard, N., Hadjivassiliou, M., West, J., & Sanders, D. (2016) Is there a relationship between gluten sensitivity and postural tachycardia syndrome?. European Journal of Gastroenterology , 1. DOI: 10.1097/MEG.0000000000000740
A new study using aerial imagery across the state of California has found that converting land to grow almonds between 2007 and 2014 has led to a 27% annual increase in irrigation demands—despite the state's historic drought. The expansion of almonds has also consumed 16,000 acres of wetlands and will likely put additional pressure on already stressed honeybee populations.
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WATKINS, Larissa, WATSON, Kelly, & HUFFMAN, F. Tyler. (2016) MONITORING CHANGE IN AGRICULTURAL LAND AND WATER USAGE IN CALIFORNIA’S CENTRAL VALLEY USING GEOSPATIAL TECHNIQUES. Geological Society of America. info:/10.1130/abs/2016AM-285205
‘Overpronation’ and achilles tendon blood flow... Read more »
Karzis, K., Kalogeris, M., Mandalidis, D., Geladas, N., Karteroliotis, K., & Athanasopoulos, S. (2016) The effect of foot overpronation on Achilles tendon blood supply in healthy male subjects. Scandinavian Journal of Medicine . DOI: 10.1111/sms.12722
We might think of animal mating being as simple as 1 male and 1 female, like on Noah's Ark. But many types of fish undergo sex changes throughout their lives. My goal is to open people's eyes to the diversity among sex in animals.... Read more »
Tsuboi, M., & Sakai, Y. (2016) Polygamous mating system and protogynous sex change in the gobiid fish Fusigobius neophytus. Journal of Ethology, 34(3), 263-275. DOI: 10.1007/s10164-016-0472-x
What do you see in the picture? An elephant, right?
Some will say that they see an African elephant, or perhaps an elephant in the savannah protecting from the sun in the shade of a tree. But who sees an elephant and a majestic flowering baobab surrounded by savannah shrubs in a dry grass meadow?
If your answer is the latter, congratulations, you are a quite unique case. If in the picture you just see “an elephant” then you are just like most of the people around you.
This phenomenon was first described in the 90s by two American botanists with the name of plant blindness. We are unable to see, notice and pay attention to plants surrounding us and therefore we have an hard time understanding their essential ecological role. We fail to appreciate the aesthetic features of these living organisms and the uniqueness of their biological characteristics, to the point of not being able to recognize plant species growing in our neighborhood or knowing what a plant really needs to survive.... Read more »
"Elevated peripheral pro-NT [neurotensin] levels reflect more severe forms of active celiac disease, indicating a potential role of NT in intestinal inflammation."The suggestion, from Caroline Montén and colleagues , that the neuropeptide called neurotensin might play a role in paediatric coeliac disease is an interesting one that caught my eye recently. Interesting not only because of the potential implications for the archetypal 'gluten-causing' autoimmune condition called coeliac disease, but also because neurotensin might have some rather important links to [some] autism too .OK, a quick recap is perhaps useful. Neurotensin when it comes to autism typically means one name, Theoharis Theoharides, he of mast cells fame (see here). The idea is that neurotensin (NT) is, among other things, quite a 'potent trigger' of mast cells and when activated these mast cells can release their inner contents that include quite a few substances linked to allergic inflammation. At least some of the talk linking 'inflammation' and autism might include a role for mast cells  and so hey presto, a potentially important chain of biological events might therefore be linked.Going back to the original Montén paper on NT and coeliac (celiac) disease, researchers set about investigating "if plasma pro-NT levels correlated with the degree of intestinal mucosal damage and tissue transglutaminase autoantibody (tTGA) levels in children with celiac disease." They did find elevated levels of one of the NT precursor fragments in a coeliac disease group (n=96) compared with controls (n=89) and there did seem to be something of a possible connection between pro-NT levels and tTGA. On these basis, they concluded that NT might indeed be linked to the intestinal inflammation noted in cases of coeliac disease. Mast cells might also be important to coeliac disease too according to recent findings.Accepting that coeliac disease is not autism (even though in some individual cases they may be linked ), there are a few further studies that might be required on this topic with autism in mind. As I've already mentioned, inflammation - particularly inflammation of the gastrointestinal (GI) tract - is not something unheard of in autism research/practice circles (see here). I know furrowed brows can be associated with this area of discussion but I'm talking about peer-reviewed science not anecdote and speculation. One might for example, see an investigation whereby those with autism and GI-related issues (including an inflammatory component) might be more closely inspected for something like NT to see if it is something important. You could even include those potentially falling into the grey area of non-coeliac gluten sensitivity (NCGS) if you so wished (see here). Given also related findings for some on the autism spectrum in relation to tTGA too (see here) and the possibility of another link there with NT, some brave research team might also wish to inspect this parameter. I might also suggest that looking at gut motility patterns in relation to NT levels could be another area ripe for further investigation with autism in mind (see here) given some previous discussions on the effects of NT.Just a few suggestions for how a little more work in this area might prove illuminating.Insofar as what to do about a possible link between NT and autism, well someone it seems has already started that conversation  and discussions are seemingly continuing in the peer-reviewed domain ...---------- Montén C. et al. Role of pro-neurotensin as marker of paediatric celiac disease. Clin Exp Immunol. 2016 Sep 10. Angelidou A. et al. Neurotensin is increased in serum of young children with autistic disorder. J Neuroinflammation. 2010 Aug 23;7:48. Theoharides TC. et al. Atopic diseases and inflammation of the brain in the pathogenesis of autism spectrum disorders. Transl Psychiatry. 2016 Jun 28;6(6):e844. Genuis SJ. & Bouchard TP. Celiac disease presenting as autism. J Child Neurol. 2010 Jan;25(1):114-9. Ghanizadeh A. Targeting neurotensin as a potential novel approach for the treatment of autism. Journal of Neuroinflammation. 2010; 7:58. Patel AB. et al. Neurotensin stimulates sortilin and mTOR in human microglia inhibitable by methoxyluteolin, a potential therapeutic target for autism. Proc Natl Acad Sci U S A. 2016 Sep 23. pii: 201604992.----------Montén C, Torinsson Naluai Å, & Agardh D (2016). Role of pro-neurotensin as marker of paediatric celiac disease. Clinical and experimental immunology PMID: 27612962... Read more »
Montén C, Torinsson Naluai Å, & Agardh D. (2016) Role of pro-neurotensin as marker of paediatric celiac disease. Clinical and experimental immunology. PMID: 27612962
by Piter Kehoma Boll One of the most difficult concepts to explain in biology is certainly life itself. But I am not here today to talk about the definition of life, but rather of another puzzling concept: behavior. Behavior is the … Continue reading →... Read more »
Bergner, R. (2016) What is behavior? And why is it not reducible to biological states of affairs?. Journal of Theoretical and Philosophical Psychology, 36(1), 41-55. DOI: 10.1037/teo0000026
Levitis, D., Lidicker, W., & Freund, G. (2009) Behavioural biologists do not agree on what constitutes behaviour. Animal Behaviour, 78(1), 103-110. DOI: 10.1016/j.anbehav.2009.03.018
Why do more men die when they attempt suicide than women? The answer could lie in four traits, finds scientists. There are over 6,000 British lives lost to suicide each year, and nearly 75 per cent of those are male. However, research has found women are more likely to suffer from depression, and to attempt to take their own life.
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Deshpande, G., Baxi, M., Witte, T., & Robinson, J. (2016) A Neural Basis for the Acquired Capability for Suicide. Frontiers in Psychiatry. DOI: 10.3389/fpsyt.2016.00125
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