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  • September 18, 2016
  • 03:01 PM

The new findings heart repair research

by Dr. Jekyll in Lunatic Laboratories

Scientists trying to find ways to regenerate a damaged heart have shed more light on the molecular mechanisms that could one day make this a reality. Whilst other organs such as the liver can regenerate, the heart muscle has very little ability to do so after suffering damage, such as a heart attack.
In the womb the body is able to produce heart muscle cells but soon after birth it effectively stops producing them.... Read more »

  • September 18, 2016
  • 07:03 AM

5 Things We Learned This Week | Open-Access Science | Week 37, 2016

by TakFurTheKaffe in Tak Fur The Kaffe

New theories in ocean circulation and acidification, shorter sea ice season in polar bear habitats, and new tools to track bird migrations and hair protein analysis in forensic IDs. Here are five of the latest scientific studies published open-access this week.... Read more »

Stern, H., & Laidre, K. (2016) Sea-ice indicators of polar bear habitat. The Cryosphere, 10(5), 2027-2041. DOI: 10.5194/tc-10-2027-2016  

Shamoun-Baranes, J., Farnsworth, A., Aelterman, B., Alves, J., Azijn, K., Bernstein, G., Branco, S., Desmet, P., Dokter, A., Horton, K.... (2016) Innovative Visualizations Shed Light on Avian Nocturnal Migration. PLOS ONE, 11(8). DOI: 10.1371/journal.pone.0160106  

Parker, G., Leppert, T., Anex, D., Hilmer, J., Matsunami, N., Baird, L., Stevens, J., Parsawar, K., Durbin-Johnson, B., Rocke, D.... (2016) Demonstration of Protein-Based Human Identification Using the Hair Shaft Proteome. PLOS ONE, 11(9). DOI: 10.1371/journal.pone.0160653  

  • September 17, 2016
  • 01:50 PM

Largest-ever study reveals environmental impact of genetically modified crops

by Dr. Jekyll in Lunatic Laboratories

According to new research, widespread adoption of genetically modified crops has decreased the use of insecticides, but increased the use of weed-killing herbicides as weeds become more resistant. This is the largest study of genetically modified crops and pesticide use to date. The team of economists studied annual data from more than 5,000 soybean and 5,000 maize farmers in the U.S. from 1998 to 2011, far exceeding previous studies that have been limited to one or two years of data.

... Read more »

  • September 17, 2016
  • 08:27 AM

Comorbidities surrounding paediatric chronic fatigue syndrome / myalgic encephalomyelitis (CFS / ME)

by Paul Whiteley in Questioning Answers

"This large nationwide registry linkage study confirms that the clinical picture in CFS/ME [chronic fatigue syndrome / myalgic encephalomyelitis] is complex."That sentence, taken from the paper by Inger Bakken and colleagues [1] (open-access available here), is perhaps the under-statement of the year as authors sought to "describe comorbidities diagnosed in primary care in children diagnosed with CFS/ME in specialist health care" and "describe the timing of the diagnoses from primary care in relation to the timing of the CFS/ME diagnosis."I grow tired of saying this but yet again, one of those very useful Scandinavian population registries was the starting point for the study - this time based in Norway - as some 1600 children diagnosed with CFS/ME were identified. Their data were compared against nearly 5000 children diagnosed with type 1 diabetes (T1DM) and a little over 1.3 million control - general child population - children. You could say that this was an adequately powered study.A couple of important points were identified from the analysis of patient records. First: "Among children with CFS/ME, the most frequently observed primary care diagnosis was “weakness / general tiredness”." This is probably not unexpected given the nature of CFS/ME. Despite such weakness/general tiredness being initially identified in the vast majority of those with CFS/ME, sleep disturbances were also found more commonly among this group compared to other participants. Rather interestingly, asthma was also reported to be more common in the CFS/ME group than either of the control groups potentially reinforcing a role for atopy in the course/onset of at least some CFS/ME [2].Next: "we found higher frequencies of depression and anxiety in the CFS/ME group." This is an important point that one has to be slightly careful with in terms of the introduction of psychological/psychiatric elements to a diagnosis of CFS/ME. I'll come back to this shortly.Next: "Elevated frequencies of all diagnoses related to infection were observed in the CFS/ME group. In particular, infectious mononucleosis was far more frequent in this group (17.2 %) than in the control groups (T1DM: 3.7 %, general child population: 2.9 %). Influenza, acute tonsillitis, “strep throat”, and pneumonia were also more frequent in the CFS/ME group." Minus any sweeping generalisations, the suggestion that an infection illness might be part and parcel of at least some cases of CFS/ME is potentially borne out by this data. Infectious mononucleosis a.k.a glandular fever as a 'trigger' for CFS/ME is not unknown to the research [3] and other literature for example.Finally: "The time span from the first primary care diagnosis of weakness / general tiredness to the specialist health care diagnosis of CFS/ME was 1 year or longer for 47.8 %." Whilst everyone would love to see a timely diagnosis of CFS/ME made, particularly when it comes to children, this data kinda suggest that diagnosis in Norway can still a long and drawn out process. Yes, I understand that many of the numerous diagnostic criteria used to diagnose CFS/ME rely on symptoms being present for an extended period of time but this does little to aid the child and their family and the important effects of such symptoms on things like schooling and other important facets of childhood.The Bakken findings provide an important research snapshot of CFS/ME in children. The themes of (i) infection being potentially important to quite a few cases and (ii) the quite long time lag between primary care (i.e. General Practitioner, GP) diagnosis of weakness / general tiredness and specialist diagnosis of CFS/ME are important ones that research and practice can/should perhaps learn some lessons from.Insofar as the observation of depression and/or anxiety being more frequently present in cases of CFS/ME, the authors make reference to the paper by Winger and colleagues [3] (see this post for more information). Winger et al reported that depressive symptoms in their group did not seemingly link/explain the reduction of health-related quality of life scores they reported for their cohort of adolescents with CFS. Taken together with the Bakken results, the implication is that whilst more commonly reported in CFS/ME, depression (and anxiety) issues are important to cases. They cannot however at this point be described as anything more than comorbid. I say this because, unfortunately, there are still opinions out there that might see depression, anxiety and other psychiatric manifestations as 'causative' of CFS/ME rather than, as I see it, being a symptom stemming from the effects of CFS/ME. If you are bed-bound, not able to go to school, not able to socialise properly and not able to do all the things your peers are doing, it is highly likely that your psychology will eventually be affected to some degree."The long time spans observed from the first diagnosis of weakness / general tiredness in primary care to a specialist health care diagnosis of CFS/ME might indicate that the treatment of these patients is sometimes not optimal." I also struggle to disagree with that sentence.----------[1] Bakken IJ. et al. Comorbidities treated in primary care in children with chronic fatigue syndrome / myalgic encephalomyelitis: A nationwide registry linkage study from Norway. BMC Fam Pract. 2016 Sep 2;17(1):128.[2] Yang TY. et al. Increased Risk of Chronic Fatigue Syndrome Following Atopy: A Population-Based Study. Medicine (Baltimore). 2015 Jul;94(29):e1211.[3] Winger A. et al. Health related quality of life in adolescents with chronic fatigue syndrome: a cross-sectional study. Health Qual Life Outcomes. 2015 Jul 3;13:96.----------Bakken IJ, Tveito K, Aaberg KM, Ghaderi S, Gunnes N, Trogstad L, Magnus P, Stoltenberg C, & Håberg SE (2016). Comorbidities treated in primary care in children with chronic fatigue syndrome / myalgic encephalomyelitis: A nationwide registry linkage study from Norway. BMC family practice, 17 (1) PMID: 27590471... Read more »

  • September 16, 2016
  • 07:00 AM

Friday Fellow: Samambaiaçu

by Piter Boll in Earthling Nature

by Piter Kehoma Boll It’s more than time to bring a fern as a Friday Fellow, and I decided to start with one of my favorites, the Neotropical tree fern Dicksonia sellowiana, known in Brazil as Samambaiaçu or Xaxim. The samambaiaçu … Continue reading →... Read more »

  • September 16, 2016
  • 05:01 AM

Air travel and diving possibly increase risk of pneumothorax in BHD patients

by Joana Guedes in BHD Research Blog

Birt–Hogg–Dubé syndrome is caused by germline mutations in the FLCN gene and characterized by skin fibrofolliculomas, lung cysts, spontaneous pneumothorax (SP) and renal cancer. Because sudden changes in air pressure can increase the chances of developing a collapsed lung, a concern many BHD patients have is whether it is safe to air travel and scuba dive, or whether this increases the chances of a pneumothorax. In a new study, Johannesma et al. (2016) evaluate the incidence of SP in patients with BHD during or shortly after air travel and diving. The study was conducted by sending a survey to a cohort of BHD patients. The authors assessed SP episodes occurring within 1 month after air travel or diving and concluded that exposure to changes in air pressure associated with flying and diving may increase the risk of developing pneumothorax.... Read more »

Johannesma, P., van de Beek, I., van der Wel, J., Paul, M., Houweling, A., Jonker, M., van Waesberghe, J., Reinhard, R., Starink, T., van Moorselaar, R.... (2016) Risk of spontaneous pneumothorax due to air travel and diving in patients with Birt–Hogg–Dubé syndrome. SpringerPlus, 5(1). DOI: 10.1186/s40064-016-3009-4  

  • September 16, 2016
  • 04:24 AM

Anxiety disorders and mortality risk: implications for autism?

by Paul Whiteley in Questioning Answers

"Anxiety disorders significantly increased mortality risk. Comorbidity of anxiety disorders and depression played an important part in the increased mortality."So said the findings reported by Sandra Meier and colleagues [1] looking to assess any relationship between the presence of an anxiety disorder and mortality risk. Based on data from one of those oh-so-useful Scandinavian population registries (Denmark this time), researchers reported that: "The risk of death by natural and unnatural causes was significantly higher among individuals with anxiety disorders... compared with the general population." Death by unnatural causes was also linked in quite a few cases to "comorbid diagnoses of depression."Although making sombre reading, the data from Meier et al provide further evidence [2] that a psychiatric/behavioural diagnosis might have far-reaching implications when it comes to the risk of early mortality, be that based on natural causes or something rather more unnatural such as death by suicide or an enhanced risk of accidental death or death because of illness. This also follows a trend suggesting that severe mental illness also has social implications such as an increased risk of becoming a victim of crime too (see here). Quality of life, health-related or otherwise, is nearly always affected by such diagnoses.I introduced the 'implications for autism' bit to this post simply because (a) when it comes to comorbidity surrounding the diagnosis of autism, anxiety and depression (various types) pretty much come top with regards to psychiatric labels applied (see here and see here respectively) and (b) enhanced risk of early mortality is also an unfortunate feature when it comes to autism too (see here). Putting these findings together and well, I'm sure you can understand the need for quite a bit more study in this area and in particular, a reiteration of how utterly disabling anxiety and/or depression can be when it comes to autism.If and when possible roles for anxiety and/or depression are found to contribute to some of the excess risk of early mortality when it comes to autism, the bright side is that this could have implications for intervention and management and onwards a reduction in mortality risk. I might also introduce the findings reported by Butnoriene and colleagues [3] at this point, who suggested that sex differences might also be relevant to the type of risk factors associated with mortality. Discussions in this area should also probably include discussions on a related topic based on a particularly extreme path being selected by some on the autism spectrum (see here).Without trying to make connections where none might exist, I'm also inclined to suggest that outside of psychological and pharmacological interventions to tackle anxiety and/or depression comorbid to autism, one might also look to treating certain somatic correlates also potentially exerting an effect (see here). There is potentially lots to examine across such comorbidities as yet again, another very important line of study opens up that intersects with autism.Finally, dare I also add that other labels such as obsessive-compulsive disorder (OCD) that may also intersect with some autism (see here - yes, this is another Meier paper) might also increase the risk of early mortality when it comes to autism too [4]?----------[1] Meier SM. et al. Increased mortality among people with anxiety disorders: total population study. The British Journal of Psychiatry. 2016; 209: 216-221.[2] Pratt LA. et al. Excess mortality due to depression and anxiety in the United States: results from a nationally representative survey. Gen Hosp Psychiatry. 2016 Mar-Apr;39:39-45.[3] Butnoriene J. et al. Metabolic syndrome, major depression, generalized anxiety disorder, and ten-year all-cause and cardiovascular mortality in middle aged and elderly patients. Int J Cardiol. 2015;190:360-6.[4] Fernández de la Cruz L. et al. Suicide in obsessive-compulsive disorder: a population-based study of 36 788 Swedish patients. Mol Psychiatry. 2016 Jul 19.----------Meier SM, Mattheisen M, Mors O, Mortensen PB, Laursen TM, & Penninx BW (2016). Increased mortality among people with anxiety disorders: total population study. The British journal of psychiatry : the journal of mental science PMID: 27388572... Read more »

Meier SM, Mattheisen M, Mors O, Mortensen PB, Laursen TM, & Penninx BW. (2016) Increased mortality among people with anxiety disorders: total population study. The British journal of psychiatry : the journal of mental science. PMID: 27388572  

  • September 15, 2016
  • 05:15 PM

Badass bacteria are thriving in your washing machine

by Piter Boll in Earthling Nature

by Piter Kehoma Boll You probably have heard of bacteria (and archaeans) that live in extreme environments on Earth, such as hot springs or lakes with high salinity, where most lifeforms would die horribly in a few seconds. We usually … Continue reading →... Read more »

Savage, A., Hills, J., Driscoll, K., Fergus, D., Grunden, A., & Dunn, R. (2016) Microbial diversity of extreme habitats in human homes. PeerJ. DOI: 10.7717/peerj.2376  

  • September 15, 2016
  • 02:22 PM

MRI scanner sees emotions flickering across an idle mind

by Dr. Jekyll in Lunatic Laboratories

As you relax and let your mind drift aimlessly, you might remember a pleasant vacation, an angry confrontation in traffic or maybe the loss of a loved one. And now a team of researchers say they can see those various emotional states flickering across the human brain.

... Read more »

  • September 15, 2016
  • 09:10 AM

Paralympic athletes and the rise of the cyborgs

by gdw in FictionalFieldwork

Para and super? The Olympics are over. They’ve brought us some good stories, some nice records, and (self-citation alert!) a humble blog post about the ethics of doping. But the Paralympics, their less mediatized cousin, are in full swing. Paralympians from all over the world gather to wow us with their athletic prowess in the Paralympic […]... Read more »

  • September 15, 2016
  • 04:41 AM

How to Hold Scientific Journals Accountable?

by Neuroskeptic in Neuroskeptic_Discover

Writing in PLoS Biology, neurobiologist Thomas C. Südhof discusses Truth in Science Publishing: A Personal Perspective. Südhof is a Professor in the Department of Molecular and Cellular Physiology at Stanford. A veteran scientist, he's been publishing since 1982.

So what's the state of science publishing as Südhof sees it?

He first notes that "scientists, public servants, and patient advocates alike increasingly question the validity of published scientific results, endangering the publi... Read more »

  • September 15, 2016
  • 04:25 AM

Eicosapentaenoic acid (EPA)-predominant fatty acid supplements and the treatment of depression

by Paul Whiteley in Questioning Answers

"Further RCTs [randomised-controlled trials] should be conducted on study populations with diagnosed or clinically significant depression of adequate duration using EPA [eicosapentaenoic acid] -predominant omega-3 HUFA [highly unsaturated fatty acids] formulations."So went the conclusions of the review article published by Brian Hallahan and colleagues [1] who searched the peer-reviewed science literature for clinical trials "evaluating efficacy of omega-3 highly unsaturated fatty acids (HUFAs) in major depressive disorder." They found over 30 trials of omega-3 supplementation vs. placebo published between 1980 and 2014 that together included participant numbers in the thousands.They reported that among those diagnosed with depression, the type of fatty acid supplement used might matter: "eicosapentaenoic acid (EPA)-predominant formulations (>50% EPA) demonstrated clinical benefits compared with placebo." When it came to that other commonly discussed omega-3 fatty acid - docosahexaenoic acid (DHA) - the results were not so great for those diagnosed with depression in terms of changes to symptom presentation(s). Importantly too, the authors noted that: "EPA failed to prevent depressive symptoms among populations not diagnosed for depression."Interesting. More so when read alongside another recent review paper by Husted & Bouzinova [2] who similarly suggest that more targeted research is needed to "clarify an optimal dosage of EPA and DHA in [the] prevention of depression." They also described the idea that various processes particularly pertinent to the concept of inflammation (yes, depression and inflammation do seem to have some commonalities) might be a target for certain omega-3 fatty acids and onwards the presentation of depression. There may even be 'critical windows' where such supplementation might be more useful (see here) than others.What's the critical difference between EPA and DHA that could account for the Hallahan findings? Well, there are a few good articles on how not all omega-3 fatty acids are the same, but I found one that is pretty informative (see here). Chemically-speaking, there are differences in structure which might account for where and when these compounds might fit when it comes to various chemical reactions in the body. Going back to the whole inflammation thing, I understand that EPA might also have some important effects on an enzyme called delta-5-desaturase (D5D) but I'd guess this is not the only difference that might be important.I'll be keeping a watch out for developments in this area of study but for now, yet more evidence that food and nutrition might have some important influences on behaviour and psychiatry. Nutritional psychiatry is starting to come out from the clinical shadows perhaps...Music: The Fall and Eat Y'Self Fitter ('Up the stairs mister').----------[1] Hallahan B. et al. Efficacy of omega-3 highly unsaturated fatty acids in the treatment of depression. The British Journal of Psychiatry. 2016; 209: 192-201.[2] Husted KS. & Bouzinova EV. The importance of n-6/n-3 fatty acids ratio in the major depressive disorder. Medicina (Kaunas). 2016;52(3):139-47.----------Hallahan B, Ryan T, Hibbeln JR, Murray IT, Glynn S, Ramsden CE, SanGiovanni JP, & Davis JM (2016). Efficacy of omega-3 highly unsaturated fatty acids in the treatment of depression. The British journal of psychiatry : the journal of mental science PMID: 27103682... Read more »

Hallahan B, Ryan T, Hibbeln JR, Murray IT, Glynn S, Ramsden CE, SanGiovanni JP, & Davis JM. (2016) Efficacy of omega-3 highly unsaturated fatty acids in the treatment of depression. The British journal of psychiatry : the journal of mental science. PMID: 27103682  

  • September 14, 2016
  • 08:00 PM

ZIKV: antivirals and the cell cycle, TBK-1 relocalisation and immune signalling

by thelonevirologist in Virology Tidbits

Zika Virus (ZIKV) is an emerging flavivirus that was first isolated in 1947 from a sentinel monkey in Uganda as part of study that aimed to identify novel pathogens and despite sporadic local outbreaks in countries such as Gabon, Nigeria, Cambodia, Malaysia and Indonesia followed by the first major outbreak in Yap/Federal States of Micronesia 2007 only caused mild disease in humans with up to 80% of asymptomatic cases. Here the repurposing of drugs for treating Zika as well as the effect of relocalising TBK-1 to mitochondria in ZIKV infected cells on immune signalling is discussed. ... Read more »

Bonaldo MC, Ribeiro IP, Lima NS, Dos Santos AA, Menezes LS, da Cruz SO, de Mello IS, Furtado ND, de Moura EE, Damasceno L.... (2016) Isolation of Infective Zika Virus from Urine and Saliva of Patients in Brazil. PLoS neglected tropical diseases, 10(6). PMID: 27341420  

Campos Rde M, Cirne-Santos C, Meira GL, Santos LL, de Meneses MD, Friedrich J, Jansen S, Ribeiro MS, da Cruz IC, Schmidt-Chanasit J.... (2016) Prolonged detection of Zika virus RNA in urine samples during the ongoing Zika virus epidemic in Brazil. Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology, 69-70. PMID: 26921737  

Chatel-Chaix L, Cortese M, Romero-Brey I, Bender S, Neufeldt CJ, Fischl W, Scaturro P, Schieber N, Schwab Y, Fischer B.... (2016) Dengue Virus Perturbs Mitochondrial Morphodynamics to Dampen Innate Immune Responses. Cell host , 20(3), 342-56. PMID: 27545046  

Costa F, Sarno M, Khouri R, de Paula Freitas B, Siqueira I, Ribeiro GS, Ribeiro HC, Campos GS, Alcântara LC, Reis MG.... (2016) Emergence of Congenital Zika Syndrome: Viewpoint From the Front Lines. Annals of internal medicine, 164(10), 689-91. PMID: 26914810  

Cugola FR, Fernandes IR, Russo FB, Freitas BC, Dias JL, Guimarães KP, Benazzato C, Almeida N, Pignatari GC, Romero S.... (2016) The Brazilian Zika virus strain causes birth defects in experimental models. Nature, 534(7606), 267-71. PMID: 27279226  

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

DICK GW, KITCHEN SF, & HADDOW AJ. (1952) Zika virus. I. Isolations and serological specificity. Transactions of the Royal Society of Tropical Medicine and Hygiene, 46(5), 509-20. PMID: 12995440  

Garcez PP, Loiola EC, Madeiro da Costa R, Higa LM, Trindade P, Delvecchio R, Nascimento JM, Brindeiro R, Tanuri A, & Rehen SK. (2016) Zika virus impairs growth in human neurospheres and brain organoids. Science (New York, N.Y.), 352(6287), 816-8. PMID: 27064148  

Jurado KA, Simoni MK, Tang Z, Uraki R, Hwang J, Householder S, Wu M, Lindenbach BD, Abrahams VM, Guller S.... (2016) Zika virus productively infects primary human placenta-specific macrophages. JCI insight, 1(13). PMID: 27595140  

Lazear HM, Govero J, Smith AM, Platt DJ, Fernandez E, Miner JJ, & Diamond MS. (2016) A Mouse Model of Zika Virus Pathogenesis. Cell host , 19(5), 720-30. PMID: 27066744  

Li H, Saucedo-Cuevas L, Regla-Nava JA, Chai G, Sheets N, Tang W, Terskikh AV, Shresta S, & Gleeson JG. (2016) Zika Virus Infects Neural Progenitors in the Adult Mouse Brain and Alters Proliferation. Cell stem cell. PMID: 27545505  

Miner JJ, Sene A, Richner JM, Smith AM, Santeford A, Ban N, Weger-Lucarelli J, Manzella F, Rückert C, Govero J.... (2016) Zika Virus Infection in Mice Causes Panuveitis with Shedding of Virus in Tears. Cell reports, 16(12), 3208-18. PMID: 27612415  

Nowakowski TJ, Pollen AA, Di Lullo E, Sandoval-Espinosa C, Bershteyn M, & Kriegstein AR. (2016) Expression Analysis Highlights AXL as a Candidate Zika Virus Entry Receptor in Neural Stem Cells. Cell stem cell, 18(5), 591-6. PMID: 27038591  

Oehler E, Watrin L, Larre P, Leparc-Goffart I, Lastere S, Valour F, Baudouin L, Mallet H, Musso D, & Ghawche F. (2014) Zika virus infection complicated by Guillain-Barre syndrome--case report, French Polynesia, December 2013. Euro surveillance : bulletin Europeen sur les maladies transmissibles , 19(9). PMID: 24626205  

Onorati M, Li Z, Liu F, Sousa AM, Nakagawa N, Li M, Dell'Anno MT, Gulden FO, Pochareddy S, Tebbenkamp AT.... (2016) Zika Virus Disrupts Phospho-TBK1 Localization and Mitosis in Human Neuroepithelial Stem Cells and Radial Glia. Cell reports, 16(10), 2576-92. PMID: 27568284  

Qian X, Nguyen HN, Song MM, Hadiono C, Ogden SC, Hammack C, Yao B, Hamersky GR, Jacob F, Zhong C.... (2016) Brain-Region-Specific Organoids Using Mini-bioreactors for Modeling ZIKV Exposure. Cell, 165(5), 1238-54. PMID: 27118425  

Ribeiro LS, Marques RE, Jesus AM, Almeida RP, & Teixeira MM. (2016) Zika crisis in Brazil: challenges in research and development. Current opinion in virology, 76-81. PMID: 27179929  

Tang H, Hammack C, Ogden SC, Wen Z, Qian X, Li Y, Yao B, Shin J, Zhang F, Lee EM.... (2016) Zika Virus Infects Human Cortical Neural Progenitors and Attenuates Their Growth. Cell stem cell, 18(5), 587-90. PMID: 26952870  

Weaver SC, Costa F, Garcia-Blanco MA, Ko AI, Ribeiro GS, Saade G, Shi PY, & Vasilakis N. (2016) Zika virus: History, emergence, biology, and prospects for control. Antiviral research, 69-80. PMID: 26996139  

Zhang F, Hammack C, Ogden SC, Cheng Y, Lee EM, Wen Z, Qian X, Nguyen HN, Li Y, Yao B.... (2016) Molecular signatures associated with ZIKV exposure in human cortical neural progenitors. Nucleic acids research. PMID: 27580721  

Zhu Y, Zhao L, Liu L, Gao P, Tian W, Wang X, Jin H, Xu H, & Chen Q. (2010) Beclin 1 cleavage by caspase-3 inactivates autophagy and promotes apoptosis. Protein , 1(5), 468-77. PMID: 21203962  

Chattopadhyay S, Marques JT, Yamashita M, Peters KL, Smith K, Desai A, Williams BR, & Sen GC. (2010) Viral apoptosis is induced by IRF-3-mediated activation of Bax. The EMBO journal, 29(10), 1762-73. PMID: 20360684  

Richter B, Sliter DA, Herhaus L, Stolz A, Wang C, Beli P, Zaffagnini G, Wild P, Martens S, Wagner SA.... (2016) Phosphorylation of OPTN by TBK1 enhances its binding to Ub chains and promotes selective autophagy of damaged mitochondria. Proceedings of the National Academy of Sciences of the United States of America, 113(15), 4039-44. PMID: 27035970  

  • September 14, 2016
  • 08:00 AM

5-Formlycytosine (5fC): A new base?

by Eliza Bacon in EpiBeat

DNA methylation and hydroxymethylation are well-established key players in gene regulation. Although many would agree that 5hmC also plays a critical role, there is still some debate over whether it serves a functional role, or is merely an artifact of DNA de-methylation. Even still, other intermediates of de-methylation are actively being investigated. In a recent paper by Iuilaro et al. 2016, a group of scientists argue that 5-formlycytosine (5fC), an intermediate of DNA de-methylation, is a stable and detectable base within the genome and may have an epigenetic function in its own right.

Active DNA de-methylation in mammals involves oxidation of 5-methylcytosine (5mC) by one or more of the TET enzymes to generate 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC). 5fC and 5caC are then excised by the thymine DNA glycosylase (TDG) enzyme, initiating base excision repair (BER). 5fC has been detected in a variety of tissues and cell systems, at relatively low levels compared to 5mC and 5hmC. Recently, scientists at The Babraham Institute have shown that not only is 5fC is detectable and stable in vivo, but that several proteins have been found to specifically bind 5fC in various cell lines.... Read more »

Iurlaro M, McInroy GR, Burgess HE, Dean W, Raiber EA, Bachman M, Beraldi D, Balasubramanian S, & Reik W. (2016) In vivo genome-wide profiling reveals a tissue-specific role for 5-formylcytosine. Genome biology, 17(1), 141. PMID: 27356509  

  • September 14, 2016
  • 04:26 AM

Unexpected improvement in core autism symptoms following a probiotic?

by Paul Whiteley in Questioning Answers

The paper by Enzo Grossi and colleagues [1] (open-access) is definitely worthy of a post today and the suggestion that the "appropriate use of probiotics" might be something to consider for at least some diagnosed as being on the autism spectrum.Accepting that I'm slightly curious as to what would be considered 'inappropriate use of probiotics', the Grossi paper describes the clinical journey of a boy aged 12 diagnosed with an autism spectrum disorder (ASD) accompanied by learning (intellectual) disability who was concurrently diagnosed with coeliac disease (CD). The CD diagnosis was a slightly complicated affair given that whilst he presented with the relevant 'genetics' of CD (HLA genotypes) and "a slight elevation of transglutaminase antibodies" a gluten-free diet seemingly did very little in terms of clinical benefits and when it came to the "blood-specific tests for celiac disease" they were always negative. I'll come back to some of these points shortly but his chronic gastrointestinal (GI) symptoms that were first thought to be CD related were subsequently put down to irritable bowel syndrome (IBS).In light of the IBS diagnosis and given some pretty important research suggesting that specific probiotic formulations might have treatment-potential for some IBS (see here), a probiotic intervention was prescribed: VSL#3. What happened next is intriguing...After a few weeks of probiotic treatment, some 'apparent improvements' were noted in the boy's behavioural presentation. This led the authors to start looking more systematically at whether said improvements could be charted and possibly tied into his probiotic use. We are told that the various components of his behavioural plan that had been in place for some 6 years were continued without "any particular change." Use of the gold-standard assessment tool that is the ADOS - Autism Diagnostic Observation Schedule - was employed over a period of about a year-and-a-half to covering the period of probiotic use. Data for two ADOS assessments were available before the probiotic was installed and four assessments were carried out during and post-intervention. The results suggested that scores relevant to social affect (the DSM-5 term describing issues with social and communicative domains) changed over the intervention period in line with some of the observations made of this boy. Further: "This change was surprising since in our assessment records over several years, the patient status had remained steadily unchanged." It should also be noted that the GI symptoms, the initial target of probiotic use, also reduced "as expected."Yes, I know that this is a case report (and N=1) and given what we (think we) know about autism, such results can by no means be generalised to all autism. There could also be a million and one other variables potentially accounting for the results including something called puberty potentially playing a role (see here) given the age of the boy. One needs to be cautious.But... these are still potentially important results for quite a few different reasons. Going back to the description of CD being diagnosed and then un-diagnosed, regular readers might know about my interest in something called non-coeliac gluten sensitivity (NCGS) when it comes to something like autism (see here). The suggestion being that although a diagnosis of autism is not protective against a diagnosis of CD, the still emerging peer-reviewed data seems to suggest something slightly more gluten-fuzzy when it comes to at least some autism. That elevated levels of tissue transglutaminase are also not an uncommon finding in relation to [some] autism (see here) adds to the curiosity in this area.Bowel or GI issues occurring alongside autism? Well, I've said it before and I'll say it again: GI issues (both functional and pathological) are over-represented when  it comes to autism (see here). You can call it IBS or similar other bowel related label but the fact of the matter is that such issues are not uncommon and lots more resources need to be poured into looking at and importantly, treating such issues save any further health inequalities appearing alongside the label of autism. It makes good sense that if something like IBS is diagnosed, and the various meta-analyses suggest that probiotics might be one part of an intervention strategy for IBS, their use where IBS clusters with autism should be the same as when autism is not part of the equation. Simple as.The Grossi case report also highlights how gut and brain, with a healthy portion of gut microbiome, might show some important links for some on the autism spectrum [2]. This is by no means 'a new thing' (see here) and to some extent, justifies the various studies where gut bacteria for example, have been looked at in the context of autism (see here for example). That such a connection might also include issues with gut permeability (see here) is another important detail and is evidenced by the possibility that probiotics may also work on the gut membrane [3] as well as those trillions of wee beasties that call us home.In short, more research on the use of probiotics with autism is very much implied (and indeed is already in progress). Watch this space.To close, first we had Mr Pharmacist from The Fall. Now we have Oxymoronic from NOFX. Spot the difference...----------[1] Grossi E. et al. Unexpected improvement in core autism spectrum disorder symptoms after long-term treatment with probiotics. SAGE Open Medical Case Reports. 2016; 4: 2050313X16666231.[2] Inoue R. et al. A preliminary investigation on the relationship between gut microbiota and gene expressions in peripheral mononuclear cells of infants with autism spectrum disorders. Biosci Biotechnol Biochem. 2016 Sep 1:1-9.[3] Mennigen R. et al. Probiotic mixture VSL#3 protects the epithelial barrier by maintaining tight junction protein expression and preventing apoptosis in a murine model of colitis. Am J Physiol Gastrointest Liver Physiol. 2009 May;296(5):G1140-9.----------... Read more »

  • September 13, 2016
  • 04:27 AM

A 'characteristic chemical signature' to chronic fatigue syndrome?

by Paul Whiteley in Questioning Answers

Today I'm (belatedly) talking about the paper by Robert Naviaux and colleagues [1] (open-access) and some further peer-reviewed discussion concerning the metabolomics of chronic fatigue syndrome (CFS). Suggesting that "targeted, broad-spectrum metabolomics of plasma not only revealed a characteristic chemical signature but also revealed an unexpected underlying biology" when it comes to CFS, it is not surprising that this work has attracted some media interest (indeed, quite a lot of media interest).I don't want to regurgitate all the findings given that (a) they are numerous, and (b) the paper is open-access, but there are a few details worth noting.So:Some readers might recognise the names Robert and Jane Naviaux listed as authors on this current paper as one and the same team involved in all that suramin for [mouse] autism work (see here). Their previous focus on the application of metabolomics (specifically the use of mass spectrometry) following the use of suramin hints at the skills and expertise this group have in that field.Their research attention was turned to CFS with the aim to put further flesh on the idea that there may be some important biochemistry happening in cases of the condition.Eighty-four adults were included for study; 45 diagnosed with CFS by various criteria (yes, there are quite a few of them). They provided blood samples that were subject to analysis: "Targeted, broad-spectrum, chemometric analysis of 612 metabolites from 63 biochemical pathways was performed."Results: well, first various 'trigger' factors were linked to onset of CFS participants' symptoms. Biological triggers - "viral, bacterial, fungal/mold, and parasitic infections" - were most common but "no single infectious agent or other stressor was statistically more prevalent." There appear to be many [organic] roads to the development of CFS.'A characteristic chemical signature' is something that many media outlets have jumped on to based on these results. Indeed, with some very pretty Venn diagrams included, there did appear to be some chemical 'signatures' that defined CFS vs. not-CFS.  The sorts of compounds seemingly involved related to the: "Sphingolipids, glycosphingolipids, phospholipids, purines, microbiome aromatic amino acid and branch chain amino acid metabolites." I'm particularly interested in the amino acid chemistry detected and how it may overlap with other findings [2].The relevance of those chemical signatures in terms of biological processes were quite diverse but led authors to conclude that "the metabolic features of CFS are consistent with a hypometabolic state." Some media outlets have referred to this as a 'semi-hibernation like state' where metabolism is somehow slowed down. I'm not so sure this is the most accurate definition given that hibernation normally implies a time-limit to such a state. Unfortunately, for many, CFS does not magically stop come the biological Spring. There is also mention of how the findings might relate to other research in CFS including a role for mitochondrial function (see here) and NAD (see here).With some cautions attached to this line of work (see here), not least the quite small participant groups included for study and, I believe, the use of a single blood sample at one specific time point, this is interesting work. Added to a growing tide of research suggesting that if one looks, one might indeed find some biological issues associated with a diagnosis of CFS (see here for example), this is yet another stop in the journey towards understanding CFS is terms of biology not psychology. The next stop is of course independent replication."The study of larger cohorts from diverse geographical areas, and comparison with related medical disorders like depression and posttraumatic stress disorder, will be needed to validate the universality and specificity of these findings. The finding of an objective chemical signature in CFS helps to remove diagnostic uncertainty, will help clinicians monitor individualized responses to treatment, and will facilitate multicenter clinical trials." Big words that indeed require that independent replication, but the research future for CFS is already looking a little brighter as a result of the Naviaux findings.----------[1] Naviaux RK. et al. Metabolic features of chronic fatigue syndrome. Proc Natl Acad Sci U S A. 2016 Aug 29. pii: 201607571.[2] Georgiades E. et al. Chronic fatigue syndrome: new evidence for a central fatigue disorder. Clin Sci (Lond). 2003 Aug;105(2):213-8.----------Naviaux RK, Naviaux JC, Li K, Bright AT, Alaynick WA, Wang L, Baxter A, Nathan N, Anderson W, & Gordon E (2016). Metabolic features of chronic fatigue syndrome. Proceedings of the National Academy of Sciences of the United States of America PMID: 27573827... Read more »

Naviaux RK, Naviaux JC, Li K, Bright AT, Alaynick WA, Wang L, Baxter A, Nathan N, Anderson W, & Gordon E. (2016) Metabolic features of chronic fatigue syndrome. Proceedings of the National Academy of Sciences of the United States of America. PMID: 27573827  

  • September 12, 2016
  • 02:19 PM

Learning to turn down your amygdala can modify your emotions

by Dr. Jekyll in Lunatic Laboratories

Training the brain to treat itself is a promising therapy for traumatic stress. The training uses an auditory or visual signal that corresponds to the activity of a particular brain region, called neurofeedback, which can guide people to regulate their own brain activity. However, treating stress-related disorders requires accessing the brain's emotional hub, the amygdala, which is located deep in the brain and difficult to reach with typical neurofeedback methods.

... Read more »

  • September 12, 2016
  • 04:31 AM

The force is strong with autism?

by Paul Whiteley in Questioning Answers

"Tablet and phone games could help diagnose autism, study suggests" went the BBC headline covering the paper by Anna Anzulewicz and colleagues [1] (open-access). The idea being that the way that touch screens are used on tablet and smart phones could potentially 'separate out' those with autism from those with not-autism.Based on a small participant number of "37 children 3–6 years old with autism and 45 age- and gender-matched children developing typically" researchers set about examining "autism-specific motor patterns in the gameplay of children as they engaged with a smart tablet computer (iPad mini) under natural conditions and with minimal instructions." Motor issues accompanying autism are something gaining some renewed (and welcomed) research attention in recent times (see here). Specifically, researchers were utilising the astounding technology that goes into all those swipes and taps that we're also used to these days, and whether under 'serious' game conditions, aspects like force impact and gesture pressure could differentiate the two groups.As per the headline and the rather cheesy title to this post, there were some differences picked up between the autism and control groups based on touch and swiping responses being put through their machine-learning paces (something else that has a growing following in autism research circles). So: "The inertial data indicate children with autism engaged in gameplay with greater force of impact than those developing typically." This and other potential differences led researchers to conclude that: "children with autism applied a significantly different distribution of forces into the device during gameplay than the typically developing children did."Whilst interesting research there is quite a bit more to do before anyone starts using taps and swipes as a means to diagnose autism (or anything else). I don't really need to say that this was a study including a relatively small participant group nor that whilst "All participants had normal or corrected-to-normal vision and no other sensory or motor deficits" this does not preclude the possibility that subtle issues might also be at work (see here). That also recent discussions have suggested moving away from the singular diagnosis of autism as a research starting point is also worth reiterating (see here).Still, I can see some opportunities arising from this area of research and how perhaps combined with other innovative areas of screening and diagnosis there may be much more to see including how subtle differences in movement might also influence variables such as interaction [2]. Yes indeed, "smart tablet technology offers an attractive, new paradigm for clinical autism assessment and bio-behavioural research of pre-school children, enabling engaging, ecological testing of children’s motor behaviour in a fun, accessible format fit for precise computational analysis of neuropsychological function."To close: Danny Boy (from the Proms 2013 although this years version was pretty good too).----------[1] Anzulewicz A. et al. Toward the Autism Motor Signature: Gesture patterns during smart tablet gameplay identify children with autism. Scientific Reports. 2016; 6: 31107.[2] Edey R. et al. Interaction Takes Two: Typical Adults Exhibit Mind-Blindness Towards Those With Autism Spectrum Disorder. J Abnorm Psychol. 2016 Sep 1.----------Anzulewicz A, Sobota K, & Delafield-Butt JT (2016). Toward the Autism Motor Signature: Gesture patterns during smart tablet gameplay identify children with autism. Scientific reports, 6 PMID: 27553971... Read more »

  • September 11, 2016
  • 03:12 PM

A microRNA plays role in major depression

by Dr. Jekyll in Lunatic Laboratories

A tiny RNA appears to play a role in producing major depression, the mental disorder that affects as many as 250 million people a year worldwide. Major depression, formally known as major depressive disorder, or MDD, brings increased risk of suicide and is reported to cause the second-most years of disability after low-back pain.

... Read more »

  • September 10, 2016
  • 04:27 AM

Prevalence of self-injurious behaviors among children with autism

by Paul Whiteley in Questioning Answers

Just over a quarter of children diagnosed with an autism spectrum disorder (ASD) present with self-injurious behaviour (SIB).That was the headline finding reported by Gnakub Soke and colleagues [1] who surveyed the 8000+ children "in the Autism and Developmental Disabilities Monitoring (ADDM) Network during the 2000, 2006, and 2008 surveillance years." THE ADDM network, as some people might know, is one and the same network that comes up with the [estimated] prevalence of autism in the United States (see here) and so carries quite a lot of statistical and clinical clout when it comes to data production. The actual figure for SIB was 27% when taking all the various ADDM sites into consideration but, much like the estimated prevalence stats, "with some variation between sites."SIB is a topic that has been discussed on this blog a few times before (see here and see here for example). It's not something that generally makes for polite dinner table conversation and not something that many people would say makes for 'good PR' when it comes to the public perception of autism. Nevertheless, these and other estimates of SIB in autism (including its persistence) are one of the more pressing issues for those that present with such behaviours given not only the damage and distress that SIB can do to a person but also the effect(s) on family and loved ones too."Clinicians should inquire about SIB during assessments of children with ASD." I think that sentence is taken as read in light of the coincidence of autism and SIB. More than that however I think many people would like to see a lot more research into the potential hows and whys of SIB [2] and what can be done to minimise such 'challenging behaviour'. Yes, such acts may in some way be communicative for some people on the autism spectrum (i.e. pain, discomfort, etc), and if so, the use of a 'chemical cosh' is likely to have repercussions for such possible communication attempts. But where such SIB acts place someone at risk of permanent physical injury and/or increase the likelihood of extremes such as the need for corrective surgery, I don't think many people would hold back with the idea of appropriate management for such extreme behaviours.----------[1] Soke GN. et al. Brief Report: Prevalence of Self-injurious Behaviors among Children with Autism Spectrum Disorder-A Population-Based Study. J Autism Dev Disord. 2016 Aug 26.[2] Yuan X. & Devine DP. The role of anxiety in vulnerability for self-injurious behaviour: studies in a rodent model. Behavioural Brain Research. 2016; 311: 201-209.----------Soke GN, Rosenberg SA, Hamman RF, Fingerlin T, Robinson C, Carpenter L, Giarelli E, Lee LC, Wiggins LD, Durkin MS, & DiGuiseppi C (2016). Brief Report: Prevalence of Self-injurious Behaviors among Children with Autism Spectrum Disorder-A Population-Based Study. Journal of autism and developmental disorders PMID: 27565654... Read more »

Soke GN, Rosenberg SA, Hamman RF, Fingerlin T, Robinson C, Carpenter L, Giarelli E, Lee LC, Wiggins LD, Durkin MS.... (2016) Brief Report: Prevalence of Self-injurious Behaviors among Children with Autism Spectrum Disorder-A Population-Based Study. Journal of autism and developmental disorders. PMID: 27565654  

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