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  • October 13, 2014
  • 05:30 PM

Yes folks... broccoli chemical impacts on autism presentation

by Paul Whiteley in Questioning Answers

Please do not adjust your set. Broccoli, or least a chemical found in broccoli called sulforaphane has, under placebo-controlled, double-blind experimental conditions, been reported to impact on the presentation of autism according to the paper by Kanwaljit Singh and colleagues [1] (open-access).Eat your greens @ Fir0002/FlagstaffotosI had to do a bit of a double-take myself when I first read about these results (see here). Indeed, even the authors themselves seemed to be a little taken aback by their own findings if other media on this study is to be believed (see here). Still peer-reviewed science is peer-reviewed science and that goes just as much for this study as any other.The paper is open-access but a few details might be useful:The study was previously registered in the US database (see here). It involved comparing "capsules of sulforaphane-rich broccoli sprout extracts" with "indistinguishable placebo capsules" containing microcrystalline cellulose (wood pulp) in a small group of young men (aged 13-27 years) diagnosed with an autism spectrum disorder (ASD) administered daily over 18 weeks. As I mentioned, the study was also double-blind.Various measures - behavioural and physiological - were recorded at baseline (prior to study start) and at choice points during the 18 week study period. The results of the behavioural measures including the Aberrant Behaviour Checklist (ABC) and Social Responsiveness Scale (SRS) completed by parents/caregivers and the Clinical Global Impression Severity (CGI-S) and the Clinical Global Impression Improvement (CGI-I) scales completed by "study physicians" are included in the main paper results and conclusions.Results: well, first and foremost there were a few adverse events reported during the trial. The authors note that: "Sulforaphane treatment effectively improved core aberrant behaviors of ASD, and was safe and well-tolerated". But... "the sulforaphane group gained significantly more weight over the 18-wk period, compared with placebo" and there was mention of "single unprovoked seizures" occurring in two participants taking the active treatment. These seizures may well be unconnected to the sulforaphane capsules but one cannot rule out the possibility that they were connected.Forty participants completed the trial, or at least "part of the outcome measure evaluations" boiling down to "14 placebo and 26 sulforaphane". The statistical evaluation undertaken involved looking at "the differences between scores of individuals at 4, 10, 18, and 22 wk from their respective average pretreatment values". But the authors also undertook a separate intention-to-treat analysis that "included all 44 participants".The headlines: "many of the participants who were treated with sulforaphane in this study had statistically significant and clinically meaningful improvements during treatment with sulforaphane". With all due respect to parent/caregiver reports, I was particularly drawn to the fact that study physicians although blinded to who was on active treatment and who was taking a placebo were able to rate "13 of the 40 participants" as showing noticeable improvements in behaviour and sociability and "all were receiving sulforaphane". That's quite a feat by any study's standard.The authors conclude: "The substantial improvements of individual ASD patients’ trajectories were conspicuous and suggest that further investigation of sulforaphane in ASD is promising".These are interesting results crying out for further independent [longer term] replication. The fact also that this was a trial of adolescents and adults with autism also fills a gap in the autism research market alluded to in previous posts on this blog (see here). Mechanism of effect? Well, there does seem to be quite a bit more to do in this area. The authors note that sulforaphane "was selected because it upregulates genes that protect aerobic cells against oxidative stress, inflammation, and DNA-damage, all of which are prominent and possibly mechanistic characteristics of ASD". Oxidative stress does indeed appear on the research radar when it comes to autism, at least some autism (see here) and sulforaphane fits the bill in terms of its potential 'protective' effects [2]. I've also talked about such mechanisms with another source of sulforaphane in mind (see here). That all being said, I don't doubt that there may be other biological processes at work.So, in conclusion 'eat your greens' might very well be an important phrase for some on the autism spectrum. Whether eating the source material carries the same effect or will be equally well received as taking a daily pill is another matter...----------[1] Singh K. et al. Sulforaphane treatment of autism spectrum disorder (ASD). PNAS. 2014. October 13.[2] Guerrero-Beltrán CE. et al. Protective effect of sulforaphane against oxidative stress: recent advances. Exp Toxicol Pathol. 2012 Jul;64(5):503-8.-----------Kanwaljit Singh, Susan L. Connors, Eric A. Macklin, Kirby D. Smith, Jed W. Fahey, Paul Talalay, & Andrew W. Zimmerman (2014). Sulforaphane treatment of autism spectrum disorder (ASD) PNAS : 10.1073/pnas.1416940111... Read more »

Kanwaljit Singh, Susan L. Connors, Eric A. Macklin, Kirby D. Smith, Jed W. Fahey, Paul Talalay, & Andrew W. Zimmerman. (2014) Sulforaphane treatment of autism spectrum disorder (ASD). PNAS. info:/10.1073/pnas.1416940111

  • October 13, 2014
  • 05:27 PM

Free Radicals and Wound Healing

by Gabriel in Lunatic Laboratories

Free radicals, said in the right crowd and you might hear someone scream for their life. Of course, to be perfectly transparent antioxidants have already shown to be bad in plenty of cases, so maybe it’s just bad PR. Still they were long assumed to be destructive to tissues and cells causing a host of age related problems with them. Well new research is showing that “free radicals” generated by the cell’s mitochondria—the energy producing “powerhouse” structures in the cell—are actually beneficial to healing wounds.... Read more »

Suhong Xu,, & Andrew D. Chisholm. (2014) C. elegans Epidermal Wounding Induces a Mitochondrial ROS Burst that Promotes Wound Repair . Developmental Cell. info:/

  • October 13, 2014
  • 10:18 AM

Guiding light to boost algae biofuel production

by This Science is Crazy! in This Science Is Crazy!

New study uses waveguides dotted with SU-8 pillars to scatter light in a tank of algae. By varying the spacing of the pillars, light intensity across the tank was approximately uniform and increased algae growth by 'at least 40%' compared to scheme with uniformly-distributed pillars... Read more »

  • October 13, 2014
  • 04:46 AM

Cognitive-Behavioural Therapy (CBT) for anxiety in autism

by Paul Whiteley in Questioning Answers

I'll readily admit that despite having a tinge of psychology running through my research career, I'm not overly enthused about the impact of the discipline on the autism spectrum down the years. I'm not necessarily just talking about the Freudian effect which set autism research back decades and shamefully added needless worry and stigma to those on the spectrum and their loved ones, but also the grand over-arching psychological theories which seemed, for example, to completely miss the 'heterogeneity' aspect to the condition(s) nor seemingly took into account the importance of comorbidity. Thankfully psychology is trying to make amends for its past sins when it comes to autism as per the article by Happé and colleagues [1] which also featured in a recent special edition of The Psychologist (see here). That being said, old habits still seemingly die hard [2] and 'unifying' generalisations still abound..."Farewell and adieu to you, fair Spanish ladies"With all this in mind, I've always been a little hesitant when it comes to the application of psychological therapies to autism. I'm not necessarily talking about the various behavioural/educational interventions [rightly or wrongly] put forward with autism in mind, but more the 'talking therapies' and in particular, the idea that cognitive-behavioural therapy (CBT) might be something to consider for at least some of those on the autism spectrum.The paper by Danielle Ung and colleagues [3] has kinda restored my faith in how psychology might yet be useful to helping some aspects of daily living for some on the spectrum; specifically with a focus on abating the often crippling effects of comorbidity such as anxiety. Based on their review and meta-analysis, the authors concluded that: "CBT demonstrates robust efficacy in reducing anxiety symptoms in youth with high-functioning ASD [autism spectrum disorder]".I've talked before on this blog about anxiety and how, for some on the autism spectrum, the effects of anxiety seem to take precedent over and above the effects of autism in a persons day-to-day life. I can't overstate the impact that anxiety can have on a person with autism and how, alongside physiological consequences, there may well be some new triads to look at when it comes to such issues (see here). With all this in mind, anything that can be done to alleviate excessive anxiety from the lives of people with autism should be looked into outside the roads which some might have already travelled. CBT already has some practical use with certain types of anxiety outside of anything directly linked to autism so pairing CBT with anxiety in autism seems like a logical step to take.The Ung paper is not the first however to report on how CBT might be useful for anxiety comorbid to autism:Sukhodolsky and colleagues [4] similarly meta-analysed the peer-reviewed literature up to 2012 (see here) and found some pretty good effect sizes based on their re-analysis of the cumulative data.Storch and colleagues [5] actually carried out a trial of CBT (versus treatment as usual) with children with autism and "clinically significant anxiety" and suggested that: "CBT adapted for anxious youth with high-functioning ASD demonstrates large effects in reducing anxiety symptoms".Reaven and colleagues [6] concluded similar things based on their group CBT intervention "specifically developed for children with ASD".That being said, the result from Sung and colleagues [7] are also worth mentioning because of their comparison of CBT with a "Social Recreational (SR) program". They reported: "lower levels of generalized anxiety and total anxiety symptoms at 6-month" for both CBT and SR programs and concluded that: "factors such as regular sessions in a structured setting, consistent therapists, social exposure and the use of autism-friendly strategies are important components of an effective framework in the management of anxiety in children and adolescents with ASD". The indication there is that the specific effects of CBT on anxiety in autism may very well turn out not be the whole story as per other activities potentially indicated for some on the autism spectrum (see here).Psychology still needs to tread carefully when it comes to autism and perhaps hold back from trying to over-psychologise(?) any effect noted from CBT for certain people on the autism spectrum. As per those Sung results, the idea of comparing CBT to interventions outside of just 'treatment as usual' is an area where more investigation needs to be focused so as not to imply that CBT is the be-all-and-end-all for anxiety when present in cases of autism. Further inquiry perhaps also needs to be undertaken into various types of CBT available and whether specific programs [8] might show greater benefits for specific people or groups of people on the spectrum. Also how more physiological measures linked to anxiety, might need to be included in those further investigations to represent something of a more objective measure of effectiveness. All this to make sure that CBT for anxiety in autism does not go the same way as CBT for schizophrenia [9] for example.Oh, and just before I go, I'm gonna be blogging soon about some of the work on intolerance of uncertainty linked to anxiety in autism as something of a potentially new dimension for looking at the presentation of anxiety in relation to at least some autism.And now for some (hopefully relaxing) music ... Passenger and Let Her Go.----------[1] Happé F. et al. Time to give up on a single explanation for autism. Nat Neurosci. 2006 Oct;9(10):1218-20.[2] Fletcher-Watson S. et al. Interventions based on the Theory of Mind cognitive model for autism spectrum disorder (ASD). Cochrane Database Syst Rev. 2014 Mar 21;3:CD008785.[3] Ung D. et al. A Systematic Review and Meta-Analysis of Cognitive-Behavioral Therapy for Anxiety in Youth with High-Functioning Autism Spectrum Disorders. Child Psychiatry Hum Dev. 2014 Sep 23.[4] Sukhodolsky DG. et al. Cognitive-behavioral therapy for anxiety in children with high-functioning autism: a meta-analysis. Pediatrics. 2013 Nov;132(5):e1341-50.[5] Storch EA. et al. The effect of cognitive-behavior... Read more »

  • October 12, 2014
  • 02:57 PM

Nothing Sticks to a new Bioinspired coating for medical devices

by Gabriel in Lunatic Laboratories

Putting things in the body can be tricky, I mean we need things from joint replacements to cardiac implants and dialysis machines, these medical devices are needed to enhance or save lives on a daily basis. However, any device implanted in the body or in contact with flowing blood faces two critical challenges that can threaten the life of the patient the device is meant to help: blood clotting and bacterial infection. Problems that sound easier to fix than they actually are.... Read more »

Don Ingber et. al. (2014) A bioinspired omniphobic surface coating on medical devices prevents thrombosis and biofouling. Nature Biotechnology. info:/10.1038/nbt.3020

  • October 12, 2014
  • 11:30 AM

Your Artificial Sweeteners, Your Bacteria, and Your Health

by Geoffrey Hannigan in Prophage

It seems like one cannot help hearing about this paper throughout the microbiome and related fields. The paper "Artificial Sweeteners Induce Glucose Intolerance by Altering the Gut Microbiota" was recently published in Nature, and it has had a lot of press...... Read more »

Suez, J., Korem, T., Zeevi, D., Zilberman-Schapira, G., Thaiss, C., Maza, O., Israeli, D., Zmora, N., Gilad, S., Weinberger, A.... (2014) Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature. DOI: 10.1038/nature13793  

  • October 12, 2014
  • 10:55 AM

Is EV-D68 causing mysterious polio-like symptoms in children?

by EE Giorgi in CHIMERAS

Bubble fun at the Santa Fe Renaissance Fair © EEG One of the twists in my latest book, Gene Cards, is an unknown pathogen threatening the fictional city of Liasis. I confess that when I came up with the idea I was a little nervous. My story is set in the future, and with all the state-of-the-art technology we already have, is it feasible to think that we will still deal with diseases without a known causative agent? The thing is, new viruses and new pathogens arise all the time. Take the flu, for example. Every time it jumps from one species to another, it has the potential to recombine in new strains and create a new virus. Influenza viruses are usually recognizable from their surface proteins, hemagglutinin and neuraminidase. But the point is that for as long as there are pathogen that thrive in animal reservoirs and then suddenly jump to humans, these pathogens could potentially lead to unknown organisms. And it's hard to test for something you don't know. Another issue with viruses is that they can "hide" in cells (like neurons) that are not accessible through standard test, making them harder to detect unless one resolves to invasive techniques.One thing is to theorize that it's possible, and one thing is to find it's happening, as you can read in this post from TWiV: "In February 2014 I wrote about children in California who developed a poliomyelitis-like paralysis, also called acute flaccid paralysis or AFP. However, the cause of this paralysis was not known. The CDC has released its study of these cases and concludes 'The etiology of AFP with anterior myelitis in the cases described in this report remains undetermined'."The CDC report is available online, and perhaps the most striking quote is the following:"Additional laboratory testing for infectious diseases conducted at the CDPH Viral and Rickettsial Disease Laboratory did not identify a causative agent to explain the observed clinical syndrome reported among the patients."So, what is the story, here?Acute flaccid paralysis happens when muscles become weak or limp and can no longer contract. In order to be diagnosed as AFP, the symptoms must arise spontaneously and not be caused by a trauma. A number of viruses can cause this condition, including polio. When caused by polio, the paralysis is associated with inflammation of the spinal cord, and the whole condition takes the name of "acute flaccid paralysis associated with anterior myelitis." A total of 23 cases of acute flaccid paralysis associated with anterior myelitis have been reported in California between June 2012 and May 2014."Affected patients resided in diverse geographic areas throughout California with no indication of clustering. During the 30-month inquiry, no indication of seasonality or temporal trends in disease onset was established."Twelve patients had been vaccinated against polio, two hadn't, and for the rest no information was available. Nineteen of the 23 patients had been tested for the "usual suspects" (polio, enteroviruses, West Nile virus, rabies, etc.), but only two tested positive for Enterovirus EV-D68, which in most cases actually manifests as a respiratory disease. The CDC report excludes polio as a cause of the 23 cases in the study and concludes that no common etiology could be found.[. . .] whether these cases represent an actual increase from baseline incidence of AFP with anterior myelitis in this population is unclear. A study examining AFP in children aged 15 years in California during 1992-1998 reported an incidence of 1.4 AFP cases per 100,000 children per year, with the most common diagnoses being Guillain-Barre syndrome (23%), unspecified AFP (21%), and botulism (12%). None of the 245 reviewed cases had recognized anterior myelitis, which is characteristic of paralytic poliomyelitis.If you do a quick search on PubMed, you'll see that the most common etiology for AFP is polio, and in those cases it's usually associated with anterior myelitis. A Korean study carried over the span of 10 years (from 2001 to 2010) found a total of 285 AFP cases, for which Guillain-Barre syndrome was the major leading causes [1]. Usually triggered by an infection, Guillain-Barre syndrome is a disorder that affects the peripheral nervous system. With prompt treatment, it is 100% curable, though if not treated promptly, it can cause life-threatening complications.What about the two patients who tested positive for Enterovirus D68? EV-D68 was first isolated in 1962. Since then, there have been rare reports of clustered cases, particularly in summer. However, this summer, there has been an unusual increase in reported cases of severe respiratory diseases, and most of these cases tested positive for EV-D68. Here are the latest numbers from the CDC:"From mid-August to October 8, 2014, CDC or state public health laboratories have confirmed a total of 664 people in 45 states and the District of Columbia with respiratory illness caused by EV-D68."What makes this virus worrisome is that it affects young children (usually under the age of 10) and that currently there is no vaccine or treatment against it. And while it normally manifests as a respiratory disease, in some rare instances, the virus can affect the nervous system. In the two California AFP cases that tested positive for EV-D68, the virus was found through nasal swabs. There is a possibility that in the other cases the virus was not found because it was elsewhere, namely in the nervous system (where it would be found only through invasive procedures).In a different report, the CDC describes "a cluster of nine children evaluated at Children's Hospital Colorado with acute neurologic illness characterized by extremity weakness, cranial nerve dysfunction (e.g., diplopia, facial droop, dysphagia, or dysarthria), or both. Neurologic illness onsets occurred during August 8‚ September 15, 2014."Four of eight Colorado children tested were positive for EV-D68. And even though these symptoms are not quite equivalent to AFP, they still fall within the spectrum of acute neurologic illnesses. Bottom line: we can't quite hold EV-D68 as responsible of the mysterious AFP cases, but we can't exclude it either. Viruses tend to target specific cells in the body, and sometimes they can spread beyond their usual "hunting grounds." When a pathogen is symptomatic (or manifests certain symptoms) only in one particular subset of the population, the reported cases appear to be unrelated, making it very hard to reconstruct the etiology of the outbreak.[1] Kim H, Kang B, Hwang S, Lee SW, Cheon DS, Kim K, Jeong YS, & Hyeon JY (2014). Clinical and enterovirus findings associated with acute flaccid paralysis in the Republic of Korea during the recent decade. Journal of medical virology, 86 (9), 1584-9 PMID: 24114945[2] ... Read more »

Zangwill KM, Yeh SH, Wong EJ, Marcy SM, Eriksen E, Huff KR, Lee M, Lewis EM, Black SB, & Ward JI. (2010) Paralytic syndromes in children: epidemiology and relationship to vaccination. Pediatric neurology, 42(3), 206-12. PMID: 20159431  

  • October 11, 2014
  • 04:14 PM

Poop Pills, Yeah they are a Thing Now

by Gabriel in Lunatic Laboratories

When someone is lying it isn't too abnormal to hear someone say, "you're full of sh..." well you get the idea. Our poop defines us, the microbes that live in our digestive tract make it possible for us to digest food, absorb nutrients, and stay healthy. Heck they may even cause your cravings! Unfortunately sometimes --whether due to abuse of antibiotics or some medical condition like C. diff infection-- gut bacteria can work against us, leading to all sorts of problems. As of now, the only real way to fix it is a poop transplant, which can be invasive and the most effective poop transplants are not done anally, but orally.... Read more »

Ilan Youngster, MD,, George H. Russell, MD,, Christina Pindar, Tomer Ziv-Baran, PhD, Jenny Sauk, MD, & Elizabeth L. Hohmann, MD. (2014) Oral, Capsulized, Frozen Fecal Microbiota Transplantation for Relapsing Clostridium difficile Infection. Journal of the American Medical Association . info:/10.1001/jama.2014.13875

  • October 11, 2014
  • 12:06 PM

Efficacy of foetal stem cell transplantation in autism...

by Paul Whiteley in Questioning Answers

The recent news that researchers might be one step closer to 'curing' type 1 diabetes following the publication of the paper by Pagliuca and colleagues [1] brought back into focus how stem cell therapy might hold some promise for all manner of conditions. The idea that researchers could generate "hundreds of millions of glucose-responsive β cells from hPSC [human pluripotent stem cells] in vitro" still faces a few challenges, including overcoming the immune assault central to the autoimmune condition that is type 1 diabetes. I have but one comment to make about the immune system and autoimmunity in this context: worm pills (see here)...The question of whether an advance has been similarly made following the publication of the paper by Jeff Bradstreet and colleagues [2] is perhaps open to some discussion with their observations that: "Statistically significant differences (p<0.05) were shown on ATEC/ABC scores for the domains of speech, sociability, sensory and overall health, as well as reductions in the total scores when compared to pre-treatment values" based on the use of foetal stem cells (FSCs) "in treating children diagnosed with ASDs [autism spectrum disorders]". Further details about the study can also be found in the latter slides of the presentation shown here.Stem cell therapy in the context of autism is still a scientific hot potato. I've covered previous, very preliminary, forays into this research area before on this blog (see here). It is with the same cautions and caveats that I discuss the latest paper from Bradstreet et al.So:This was a study of some 45 children diagnosed with an autism spectrum disorder (ASD) (mean age = 6-7 years). Diagnosis was confirmed by some of the gold-standard assessment instruments including ADOS and ADI. There were quite a few exclusion criteria applied to study entrants such that those with epilepsy, or "a neurological or co-morbid psychiatric disorder" were not examined. Learning disability without autism was also "considered exclusion criteria" as was a diagnosis of Asperger syndrome.The study was based in Kiev in the Ukraine where "stem cells harvested from 5-9 weeks old human fetuses following voluntarily – elective pregnancy terminations (legally available in the Ukraine)" were used. I don't doubt that there may be some who have strong views about this practice as per commentary from other authors (see here). Hematopoietic stem cells (HSCs) after harvesting were tested for various bacterial, fungal and viral infections as were the women who previously carried.Long quote coming up... "Stem cell transplantation of suspensions containing cryopreserved fetal stem cells were preceded by pre-medication of the subject via intravenous slow infusion of diphenylhydramine (Darnitsa, Ukraine) 10 mg and prednisone (Darnitsa, Ukraine) 15 mg on Day 1 and diphenhydramine (Darnitsa, Ukraine) 10 mg on Day 2". At this point, I'll draw your attention to some other work previously discussed on this blog on a possible role for corticosteroid therapy for some types of autism (see here) which included the use of prednisolone, the active metabolite of prednisone. After which the stem cells were administered...Results: "Early post-transplantation effects were reported in 78% of children: 26% of these children became calmer; eye contact was improved in 9%, while 29% had better appetite and 23% had an improved affect". Importantly, the authors report that no adverse effects were initially noted and "No transmittable diseases were noted during the 12 month follow-up". They also make mention of how initial effects may well have been [partly] as a consequence of the corticosteroid and other medication initially administered.Scores on the ATEC and ABC bore out the positive group changes noted between baseline (before stem cell therapy) and at 6 and 12 month follow-up which were also accompanied by various immunological changes "indicative of improved cell-mediated immunity in children".OK. Despite these results the authors themselves are still cautious about their findings and stress: "future research studies are urgently needed and larger randomized -placebo controlled trials are needed to further characterize potential FSC-associated improvements in ASDs". This was a straight forward observational trial (before and after) which lacked control groups and in particular a placebo-controlled element so one has to be slightly hesitant about the strength of any findings. For those however who might be pulling on this study because of the use of something like the ATEC to measure autistic presentation, I'll draw your attention to some work suggesting that this instrument might be rather useful for monitoring intervention options for autism (see here).As previously described, feelings run deep about the use or not of stem cells when it comes to autism not least because of the lack of data on long-term safety (and efficacy) in this context, the source 'material' for stem cells and the lack of information on just what might be going on in biological terms consequent to the behavioural results described. Examining this research from a cold, dispassionate, scientific point of view, I have to say that I'm becoming rather interested in what might be potentially going on during this and other studies [3] if not just as a function of other work by the late Paul Patterson and colleagues overlapping with this area [4] (discussed in a previous post). That being said, I'd like to see a lot more research done in this area before this kind of intervention enters anything like mainstream autism practice...----------[1] Pagliuca FW. et al. Generation of Functional Human Pancreatic β Cells In Vitro. Cell. 2014 Oct 9;159(2):428-439.[2] Bradstreet JJ. et al. Efficacy of fetal stem cell transplantation in autism spectrum disorders: an open-labeled pilot study. Cell Transplant. 2014 Oct 9.[3] Lv YT. et al. Transplantation of human cord blood mononuclear cells and umbilical cord-derived mesenchymal stem cells in autism. J Transl Med. 2013 Aug 27;11:196.[4] Hsiao EY. et al. Modeling an autism risk factor in mice leads to permanent immune dysregulation. Proc Natl Acad Sci U S A. 2012 Jul 31;109(31):12776-81.----------Bradstreet JJ, Sych N, Antonucci N, Klunnik M, Ivankova O, Matyashchuk I, Demchuk M, & Siniscalco D (2014). Efficacy of fetal stem cell transplantation in autism spectrum disorders: an open-labeled pi... Read more »

Bradstreet JJ, Sych N, Antonucci N, Klunnik M, Ivankova O, Matyashchuk I, Demchuk M, & Siniscalco D. (2014) Efficacy of fetal stem cell transplantation in autism spectrum disorders: an open-labeled pilot study. Cell transplantation. PMID: 25302490  

  • October 11, 2014
  • 11:39 AM

Saying NO to Our Food Craving Is Not as Simple as It Seems

by Wiley Asia Blog in Wiley Asia Blog - Life Sciences

Fitness junkies would not believe this, but our road to obesity could be greatly affected by the number and type of bacteria living within us. Researchers from UC San Francisco, Arizona State University and University of New Mexico suggest that a power struggle inside our gut happens daily. As it is a game of ‘survival-of-the-fittest’, our gut microbes would compete with each other over the availability of their preferred nutrient (e.g. sugar or fats). As a result, they influence our eating habits or cravings by releasing signaling molecules into our gut which activate our endocrine and nervous systems to set off the trigger for a specific type of food. Unknowingly, this vicious cycle goes on without us taking notice and can lead us to binge on food that is not the best for our waistlines.... Read more »

  • October 11, 2014
  • 04:48 AM

Yet more air pollution and autism risk research

by Paul Whiteley in Questioning Answers

Air pollution and autism risk. It's a topic which has cropped up a few times on this blog (see here and see here and see here) with the majority of the research (but not all) suggesting that there may be something to see when it comes to such a correlation.Enter then the paper by Amy Kalkbrenner and colleagues [1] to proceedings, and their conclusion: "Our study adds to previous work in California showing a relation between traffic-related air pollution and autism, and adds similar findings in an eastern US state, with results consistent with increased susceptibility in the third-trimester". I might add that Dr Kalkbrenner has some research form when it comes to looking at environment and autism and has appeared on this blog before (see here).Based on two datasets covering the east and west coasts of the United States (North Carolina and "the San Francisco Bay Area in California") including nearly 1000 children diagnosed with an autism spectrum disorder (ASD) and some 14,000 asymptomatic controls, researchers compared estimated exposure patterns based on birth addresses. Specifically, they looked at exposure to particulates "less than 10 μm (PM10)" within a period starting from preconception through to the child's first birthday. They also took into account a whole slew of geographic and demographic variables which potentially may have influenced results. They reported odds ratios (ORs) - adjusted ORs - which seemed to indicate that exposure, "a 10 μg/m increase in PM10", particularly during the third trimester of pregnancy was associated with increased susceptibility to autism. Ergo, more evidence for a potential link between prenatal air pollution exposure and offspring autism risk.If I'm reading the Kalkbrenner paper correctly however, PM10 exposure during the first and second trimesters of pregnancy was not associated with autism. Indeed for the first trimester at least (bearing in mind the confidence intervals) the adjusted OR was "0.86 (95% CI = 0.74-0.99)" which I'll leave to readers to decide whether it was important or not.There's little more for me to say about this area of autism research aside from the usual caveats applying regarding the use of estimated exposure patterns over and above actual individual exposure levels and the further requirement to elaborate on any mechanism potentially pertinent aside from any general description such as a role for oxidative stress or inflammatory markers [2]. I say this acknowledging the preliminary observations made about genotype, air pollution and autism risk [3] which still require independent follow-up.In light of the my recent discussions on asthma being a potential risk factor for autism (see here) and further research on atopy and autism [4] which I'll be blogging about soon, one wonders whether other manifestations of air pollution exposure might also play some role in such findings. That combined with the more general developmental effects thought to be had as a result of air pollution exposure [5], and the whole thing starts to get rather complicated and in need of much greater scrutiny...Music then and at the risk of [musically] repeating myself: Alice Cooper and No More Mr Nice Guy...----------[1] Kalkbrenner AE. et al. Particulate Matter Exposure, Prenatal and Postnatal Windows of Susceptibility, and Autism Spectrum Disorders. Epidemiology. 2014 Oct 3.[2] Volk HE. et al. Residential proximity to freeways and autism in the CHARGE study. Environ Health Perspect. 2011 Jun;119(6):873-7.[3] Volk HE. et al. Autism spectrum disorder: interaction of air pollution with the MET receptor tyrosine kinase gene. Epidemiology. 2014 Jan;25(1):44-7.[4] Chen MH. et al. Is atopy in early childhood a risk factor for ADHD and ASD? A longitudinal study. J Psychosom Res. 2014 Oct;77(4):316-21.[5] Calderón-Garcidueñas L. et al. Air pollution and detrimental effects on children's brain. The need for a multidisciplinary approach to the issue complexity and challenges. Front Hum Neurosci. 2014 Aug 12;8:613.----------Kalkbrenner AE, Windham GC, Serre ML, Akita Y, Wang X, Hoffman K, Thayer BP, & Daniels JL (2014). Particulate Matter Exposure, Prenatal and Postnatal Windows of Susceptibility, and Autism Spectrum Disorders. Epidemiology (Cambridge, Mass.) PMID: 25286049... Read more »

  • October 10, 2014
  • 11:26 PM

The red of bearded vultures—allure or cure?

by Yao-Hua Law in TORCH

[This story first appeared on Earth Touch News] Soaring high among the mountains from Europe to China and to Africa, the bearded vulture (Gypaetus barbatus) commands attention at any lunch party. It likes to gate crash into the frenzy around carrion, pushing other scavengers aside with wings that could stretch the height of Michael Jordan, […]... Read more »

  • October 10, 2014
  • 05:49 PM

How the Brain Heals After a Stroke

by Gabriel in Lunatic Laboratories

You have all the brain cells you'll ever have when you reach adulthood. That was the science lesson I was taught in high school from, maybe a misguided teacher, or maybe just misinformed, I do not know. That statement however is not true, we know that the brain is very plastic and ever changing. It's resilience still amazes us, even today with all that we know about it. Now a previously unknown mechanism through which the brain produces new nerve cells after a stroke has been discovered, showing us just how resilient the brain truly is.... Read more »

Magnusson, J., Goritz, C., Tatarishvili, J., Dias, D., Smith, E., Lindvall, O., Kokaia, Z., & Frisen, J. (2014) A latent neurogenic program in astrocytes regulated by Notch signaling in the mouse. Science, 346(6206), 237-241. DOI: 10.1126/science.346.6206.237  

  • October 10, 2014
  • 11:54 AM

A "parsimonious" Bayesian supertree model for estimating species trees

by Leonardo Martins in bioMCMC

When we have sequence alignments regarding several genes from a group of taxa, we usually want to extract the phylogenetic information common to all of them. However, in many cases such phylogenomic analyses depend on selecting one sequence from each species per gene family (=alignment), or excluding paralogs, or partitioning these paralogous sequences into loci, or utilizing only gene families without apparent paralogs. If we want to analyse all our data at once, without excluding sequences or whole alignments, we are left with few options.We just published such an alternative, which is based on the idea that we can measure the disagreement between the phylogenetic trees representing each gene and a putative tree representing the species. Therefore, by using disagreement measures that allow for arbitrary mappings between the trees, we can handle gene trees with paralogs, multiple individuals from the same population or missing data. These measures we call "distances" [1], and we developed a probability distribution describing how these distances can work as penalties against very dissimilar gene and species tree pairs. We can use any combination of the reconciliation distances, the recently developed mulRF distance, and (very experimentally) an approximate SPR distance to include into our multivariate penalty distribution. We are also experimenting with other distances, as we implement them. This penalty distribution is then incorporated into a hierarchical Bayesian model, which I call "parsimonious" since it doesn't use a fully probabilistic model to describe the coalescent processes, or the birth and death of new loci. It assumes instead that only the most parsimonious reconciliations are relevant to the model. (I was advised, however, that calling it a "parsimonious Bayesian model" could be confusing...)The distance supertree model is based on several distance measures d(G,S) between each gene family tree G and the species tree S. A species trees that is more similar to all gene trees is more likely than a more distant one. Notice that d(G,S) can in fact be a vector with several distances.We implemented this model into the software guenomu, which is available under a GPL license at The input to the software is a set of files with the distribution of gene trees as estimated for each gene family, independently, and the output will be the posterior distribution of these gene family trees together with the distribution of species trees.  We tested our model on many data sets simulated with the SimPhy software -- which is able to simulate the evolution of gene families with duplications, losses, and the multispecies coalescent fully probabilistically -- followed by a quick-and-dirty emulation of a Bayesian phylogenetic inference [2].The difference between the input and output (posterior) distribution of trees for each gene family is that the input trees were estimated independently -- let's say, by running MrBayes for each alignment representing a gene family -- while the posterior takes into account the other gene families through their common species tree. Therefore the posterior distribution is a re-sampled version of the input, and as we see in the figure below it improves the gene tree estimation.Input and posterior distributions if gene trees across many simulations (average values over gene families, per simulated data set). The simulations were pooled by species tree size, where we can see that guenomu can reduce the uncertainty of the gene trees. The accuracy is the fraction of splits (=branches) successfully reconstructed. Figure adapted from doi:10.1093/sysbio/syu082Our model was successful in reconstructing the species tree even for high levels of incomplete lineage sorting (short species tree branches, in coalescent units) coupled with duplications and losses. It also fared a bit better than iGTP, and much better than our implementation of distance matrix-based species tree inference methods [3]. Notice that only software that accepts gene trees with several tips from the same species can be compared. We were gladly surprised to see that iGTP under the duplication-loss cost also performed well, provided we use the gene tree frequencies as weights.Violin plots showing the distribution of accuracies in species tree estimation, over all simulations. The two red distributions are for the consensus and MAP tree estimates using guenomu, while the brown and blue plots are for other reconstruction methods. The dendrogram at the top classifies the methods by accuracy. Figure adapted from doi:10.1093/sysbio/syu082Notes:[1] They are not proper metrics since they are not symmetric, for instance.[2] Since our simulated gene families have hundreds of tips, simulating the alignments and then sampling the gene tree distributions with MrBayes or friends would take too long (we did this for smaller data sets only). We therefore created a program (available with guenomu) that would copy many times each tree, replacing randomly short branches by one of its alternative bipartitions.[3] We must take into account that these matrix-based methods (like GLASS, SD, etc.) assume that all disagreement is due to the coalescent, which is not true under our simulations. Furthermore our implementation may not be as good as some established software. Therefore our results are not evidence against these methods. (I particularly love their idea of being able to work with the distance matrices.)Reference:de Oliveira Martins L., Mallo D. & Posada D. (2014). A Bayesian Supertree Model for Genome-Wide Species Tree Reconstruction, Systematic Biology, DOI: supplementary material is not available yet at DataDryad, as of today Oct 10, 2014. I assume it will go online soon, but if you want it please drop me a line)... Read more »

  • October 10, 2014
  • 10:00 AM

Ebola Virus VP40 -A protein straight out of “transformers”

by Clay Clark in Biochem Blogs

  Ebola. Just the word is enough to make people panic. Well “Ebola” is actually just a river in the Democratic Republic of the Congo. Of course when they hear the word, most people think about the deadly virus discovered near this river in 1976. To clarify the terminology, “Ebola” is the river; “Ebolavirus” is […]... Read more »

Bornholdt Zachary A., Dafna M. Abelson, Peter Halfmann, Malcolm R. Wood, Yoshihiro Kawaoka, & Erica Ollmann Saphire. (2013) Structural Rearrangement of Ebola Virus VP40 Begets Multiple Functions in the Virus Life Cycle. Cell, 154(4), 763-774. DOI:  

Feldmann Heinz. (2011) Ebola haemorrhagic fever. The Lancet, 377(9768), 849-862. DOI:  

  • October 10, 2014
  • 08:00 AM

For Disguise, Female Squid Turn On Fake Testes

by Elizabeth Preston in Inkfish

Did you know this week is International Cephalopod Awareness Days? I’ll assume your gifts are in the mail. Today is dedicated to squid, and you can’t have total cephalopod awareness without discussing fake squid testes. This post was first published in September 2013. The best way to stay out of trouble, if you’re a shimmery, […]The post For Disguise, Female Squid Turn On Fake Testes appeared first on Inkfish.... Read more »

DeMartini DG, Ghoshal A, Pandolfi E, Weaver AT, Baum M, & Morse DE. (2013) Dynamic biophotonics: female squid exhibit sexually dimorphic tunable leucophores and iridocytes. The Journal of experimental biology, 216(Pt 19), 3733-41. PMID: 24006348  

  • October 10, 2014
  • 07:55 AM

The Friday Five for 10/10/14

by Bill Sullivan in The 'Scope

Paralyzed rats walk again, origins of AIDS, science of touching and kissing, and how to tell if you're dying.... Read more »

Wenger N, Moraud EM, Raspopovic S, Bonizzato M, DiGiovanna J, Musienko P, Morari M, Micera S, & Courtine G. (2014) Closed-loop neuromodulation of spinal sensorimotor circuits controls refined locomotion after complete spinal cord injury. Science translational medicine, 6(255). PMID: 25253676  

Pinto, J., Wroblewski, K., Kern, D., Schumm, L., & McClintock, M. (2014) Olfactory Dysfunction Predicts 5-Year Mortality in Older Adults. PLoS ONE, 9(10). DOI: 10.1371/journal.pone.0107541  

Faria, N., Rambaut, A., Suchard, M., Baele, G., Bedford, T., Ward, M., Tatem, A., Sousa, J., Arinaminpathy, N., Pepin, J.... (2014) The early spread and epidemic ignition of HIV-1 in human populations. Science, 346(6205), 56-61. DOI: 10.1126/science.1256739  

  • October 10, 2014
  • 04:40 AM

Vitamin D supplement improves autistic behaviours?

by Paul Whiteley in Questioning Answers

I don't want to get too ahead of myself with this post talking about the paper by Feiyong Jia and colleagues [1] (open-access) who concluded: "Vitamin D supplementation may be effective in ameliorating the autistic behavioral problems in children with autism spectrum disorders [ASDs]".The idea however that issues with vitamin D seemingly present in quite a few cases of ASD [2] (see here too) but not all [3] might actually have more direct consequences for behavioural presentation is something which is deserving of quite a bit more experimental study. I'm minded to suggest that the paper by Frighi and colleagues [4] might also be relevant here given the heightened prevalence of intellectual disability associated with (some) autism."The light that burns twice as bright burns half as long"I'll admit that I have not been able to fully take in all the details of the Jia paper given that it is published in Chinese. But looking at the abstract and using a translation tool for the full-text version ("OK Google, translate..."), a few things were seemingly apparent:This is a case report detailing the clinical experiences of a young boy aged 32 months who fitted the DSM-IV criteria for an ASD. Apparently there is some interest in vitamin D and autism at the authors' affiliated institution (see here).As part of some biological work-up the young boy was found to present with low levels of vitamin D (serum 25 (OH) D) (14.3 ng/ml). Depending on how you would define adequate vitamin D levels, this value would probably reflect deficiency (see here).Treatment of the vitamin D deficiency followed involving an injection of 150,000 IU (international units) of vitamin D3 combined with daily 400 IU of vitamin D3 administered by mouth. The authors note that no other treatment was provided at this time.At 2 months, behaviour was reassessed by CARS and M-CHAT among things, and serum 25 (OH) D levels examined again. Vitamin D levels had increased to 51.8 ng/ml which put him within the normal concentration range. Allied to this increase, autistic symptoms were also noted to have improved. The authors suggest that their results warrant further, larger and more controlled, study, something which appears to have already started [5].Before anyone gets the idea that I'm advocating vitamin D3 injections for autism or anything else, I would very much like to reiterate the authors' point about needing further research in this area bearing in mind the more typical relationship between vitamin D and something like bone health for example. The recent guidance from the American Academy of Pediatrics (AAP) on optimising bone health in children and adolescents [6] might also be pertinent. The use of 150,000 IU of vitamin D has also been discussed previously in the more general peer-reviewed literature [7] particularly if and when compliance to an oral treatment regime might be poor. But that still does not mean that I'm advocating anything at this time.I'm afraid that I cannot readily offer any specific biological reasons why vitamin D supplementation might tie into the symptom improvements noted in the Jia study given the seemingly wide range of systems showing some involvement for the sunshine vitamin/hormone. I could speculate about certain processes being potentially affected (see here) which might be relevant to cases of autism but won't say too much more about that at this time. This might be a good point to also drop in the paper by Sarah Hanieh and colleagues [8] (open-access) talking about maternal vitamin D levels and offspring language scores as potentially being pertinent.I should reiterate that the Jia paper was based on an individual case report so one has to perhaps be slightly weary of any effect being potentially applicable to others nor solely due to vitamin D. This, particularly given the receipt of a diagnosis of ASD at baseline and what this might have meant for things like education and the use of less-formal intervention options over the course of the study period.That all being said, I continue to find the reported results interesting [9] if not just from the perspective of autism to more general health and wellbeing...Classical music to close and since we're not so far from there: remember, remember the 5th of November, the gunpowder treason and plot... (and the world according to 'V').----------[1] Jia F. et al. Vitamin D Supplementation Improves Autistic Symptoms in a Child with AutismSpectrum Disorder. Asian Case Reports in Pediatrics. 2014; 2: 21-24.[2] Pioggia G. et al. Autism and lack of D3 vitamin: A systematic review. Research in Autism Spectrum Disorders. 2014; 8: 1685-1698.[3] Uğur C. & Gürkan CK. Serum vitamin D and folate levels in children with autism spectrum disorders. Research in Autism Spectrum Disorders. 2014; 8: 1641-1647.[4] Frighi V. et al. Vitamin D deficiency in patients with intellectual disabilities: prevalence, risk factors and management strategies. Br J Psychiatry. 2014 Sep 25. pii: bjp.bp.113.143511.[5] Ucuz II. et al. The relationship between Vitamin D, autistic spectrum disorders, and cognitive development: do glial cell line-derived neurotrophic factor and nerve growth factor play a role in this relationship? International Journal of Developmental Disabilities. 2014. DOI:[6] Golden NH. et al. Optimizing Bone Health in Children and Adolescents. Pediatrics. 29 Sept.[7] Munns C. et al. Prevention and treatment of infant and childhood vitamin D deficiency in Australia and New Zealand: a consensus statement. Med J Aust. 2006 Sep 4;185(5):268-72.[8] Garland CF. et al. Meta-analysis of all-cause mortality according to serum 25-hydroxyvitamin D. Am J Public Health. 2014 Aug;104(8):e43-50.[9] Hanieh S. et al. Maternal vitamin D status and infant outcomes in rural Vietnam: a prospective cohort study. PLoS One. 2014 Jun 26;9(6):e99005.----------... Read more »

  • October 10, 2014
  • 03:00 AM

The Amsterdam Patient Charter for Global Kidney Cancer Care

by Lizzie Perdeaux in BHD Research Blog

Kidney cancer patients face a number of challenges, such as lack of awareness both by patients and their doctors, difficulty getting a diagnosis, limited access to treatment, inappropriate treatment, lack of information and lack of support. Given that there were … Continue reading →... Read more »

Giles RH, Maskens D, & the International Kidney Cancer Coalition. (2014) Amsterdam Patient Charter for Global Kidney Cancer Care. European urology. PMID: 25257033  

  • October 9, 2014
  • 10:15 PM

Ecology of cancer: mimicry, eco-engineers, morphostats, and nutrition

by Artem Kaznatcheev in Evolutionary Games Group

One of my favorite parts of mathematical modeling is the opportunities it provides to carefully explore metaphors and analogies between disciplines. The connection most carefully explored at the MBI Workshop on the Ecology and Evolution of Cancer was, as you can guess from the name, between ecology and oncology. Looking at cancer from the perspective […]... Read more »

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