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  • November 4, 2014
  • 05:46 PM

Steak is bad for the Heart and now We Know why

by Gabriel in Lunatic Laboratories

“Red meat is bad for your heart”, that is typically the story we hear from people. While some might take this as meat is bad for us, or that it is wrong to eat red meat, science has been trying to find a better answer to that question. After all it wouldn’t do for science to say, it just does. Well as luck may have it, new research provides details on how gut bacteria turn a nutrient found in red meat into metabolites that increase the risk of developing heart disease. The findings may lead to new strategies for safeguarding individuals’ cardiovascular health.... Read more »

Koeth RA, Wang Z, Levison BS, Buffa JA, Org E, Sheehy BT, Britt EB, Fu X, Wu Y, Li L.... (2013) Intestinal microbiota metabolism of L-carnitine, a nutrient in red meat, promotes atherosclerosis. Nature medicine, 19(5), 576-85. PMID: 23563705  

Robert A. Koeth, Bruce S. Levison, Miranda K. Culley, Jennifer A. Buff, Zeneng Wang, Jill C. Gregory, Elin Org, Yuping Wu, Lin Li, Jonathan D. Smith, W.H. Wilson Tang, Joseph A. DiDonato.... (2014) g-Butyrobetaine is a proatherogenic intermediate in gut microbial metabolism of L-carnitine to TMAO. Cell Press. info:/10.1016/j.cmet.2014.10.006.

  • November 4, 2014
  • 10:52 AM

Anorexia Nervosa: Fasting and Starvation Brain Effects

by William Yates, M.D. in Brain Posts

Brain research in anorexia nervosa presents several challenges.Current knowledge of cognitive function in anorexia supports impairment in set shifting and global brain processing or central coherence.However, there are two issues that complicate understanding the underlying brain effects in anorexia nervosa.First, individuals with anorexia nervosa often have additional anxiety and mood disorders. It can be difficult to tease out the specific effects of anorexia nervosa from the effects of these comorbid conditions.Second, fasting and starvation are common metabolic issues in anorexia. These metabolic stresses can also influence brain function.Sarah Pender and colleagues from University College London and Spain recently published a research study on the neuropsychology of starvation.The key elements of their study included the following elements:Subjects: Healthy females recruited by poster in a university sample. Subjects were required to not have a lifetime history of any psychiatric disorder including anorexia nervosa.Measures: A test of set-shifting ability using a test called the rule-change task. A test of local versus global cognitive processing style. A second test of global processing known as the group embedded figures task.Metabolic status: Each subject was studied on the above measures after eating and following a period of 18 hours of fasting.  The authors then compared performance on these neuropsychology tests in the fasting versus satiated state. The main findings from the study included findings in set-shifting and central coherence.Set-shifting: Performance on set-shifting was not slowed or impaired in the fasting state compared to the satiated state. However, fasting appeared to increase the difficulty (or effort) to set shift.Central coherence: During the fasting state, subjects shifted processing to a stronger local processing style and a weaker global processing style. This is consistent with reduced central coherence with fasting.A relevant potential confounding variable in this type of task is the contribution of anxiety and depression in neuropsychological task performance.I previously collaborated with Dr. Rebecca Marshall and other colleagues at the Laureate Institute of Brain Research in a study of neuropsychological function in a group of women with a variety of eating disorders. In this study, we found subjective anxiety ratings contributed to a significant about of variance in neuropsychological performance in eating disorders. Additionally, we found executive function impairment, a component of central coherence in 30 % of the clinical sample.Pender and colleagues looked for effects of anxiety and depression in their study and did not find any confounding effects. Obviously, their sample was likely to only have minimal sub-clinical levels of anxiety/depression given the requirement for no current or lifetime psychiatric problem for enrollment.The authors conclude even short-term fasting "might trigger weak central coherence, and thus play a role in maintaining behaviors characteristic of AN". The authors also note the brain effects of fasting, starvation and anorexia nervosa may have difficulty participating in psychotherapy. Psychotherapy requires a more global processing style to be effective.Readers with more interest in this research can access the free full-text manuscripts by clicking on the PMID link in the citations below.Photo of brain corpus callosum activated during right-left brain coherence is from an iPad screen shot from the 3D Brain app.Follow the author on Twitter WRY999Pender, S., Gilbert, S., & Serpell, L. (2014). The Neuropsychology of Starvation: Set-Shifting and Central Coherence in a Fasted Nonclinical Sample PLoS ONE, 9 (10) DOI: 10.1371/journal.pone.0110743Billingsley-Marshall RL, Basso MR, Lund BC, Hernandez ER, Johnson CL, Drevets WC, McKee PA, & Yates WR (2013). Executive function in eating disorders: the role of state anxiety. The International journal of eating disorders, 46 (4), 316-21 PMID: 23354876... Read more »

Billingsley-Marshall RL, Basso MR, Lund BC, Hernandez ER, Johnson CL, Drevets WC, McKee PA, & Yates WR. (2013) Executive function in eating disorders: the role of state anxiety. The International journal of eating disorders, 46(4), 316-21. PMID: 23354876  

  • November 4, 2014
  • 08:00 AM

Where Do All Those Leaves Come From?!

by Mark E. Lasbury in The 'Scope

You rake leaves and lug them to the curb, or you push them into your neighbor’s yard with your blower. Either way, do you know where the matter/mass in all those leaves comes from? You won’t believe the answer. But the leaf may be passé. New research is showing how artificial leaves can produce oxygen for space travel and hydrogen for fuel cells.... Read more »

Pijpers, J., Winkler, M., Surendranath, Y., Buonassisi, T., & Nocera, D. (2011) Light-induced water oxidation at silicon electrodes functionalized with a cobalt oxygen-evolving catalyst. Proceedings of the National Academy of Sciences, 108(25), 10056-10061. DOI: 10.1073/pnas.1106545108  

  • November 4, 2014
  • 05:01 AM

Producers and consumers of autism research: never the twain shall meet?

by Paul Whiteley in Questioning Answers

I was interested to read the paper by Elizabeth Pellicano and colleagues [1] (open-access) investigating "the views of community involvement in autism research both from the perspectives of autism researchers and of community members, including autistic adults, family members and practitioners". Quite a few results are reported including the idea that researchers "were skeptical about the possibilities of dramatically increasing community engagement, while community members themselves spoke about the challenges to fully understanding and influencing the research process".I'm made of wax, Larry. What are you made of?I believe this research links into a previous study by the same authors [2] which has also been discussed on this blog (see here) asking the question: what should autism research focus upon? The results on that occasion implied that depending on who was asked: "There was a clear disparity between the United Kingdom’s pattern of funding for autism research and the priorities articulated by the majority of participants". As an addition to that work, I'll take this opportunity to direct you to the paper by Jina Jang and colleagues [3] reporting that most autism research seems to be centred on the "younger population".The most recent Pellicano work is again open-access but a few details are worth mentioning:Two instruments/methods were reported on: (i) the results of an on-line questionnaire completed by over 1500 respondents "aged 18 and over who could be divided into four key stakeholder groups: autistic adults, immediate family members, practitioners and researchers", and (ii) focus groups / individual interviews, again including people representative of those key stakeholder groups (albeit much reduced in terms of participant numbers). The idea being to ask "both researchers and members of the autism community about their experiences of engagement in research".Several themes are reported based on either researcher views or autism community views. "The majority of autistic adults, parents of children with autism and professionals wanted to be more involved in the research process". A nice position for autism researchers to be in by all accounts, but... "community members felt that researchers aren't proactive enough" when it came to approaching the autism community to take part in research. Even when taking part in autism research there were "largely asymmetric interactions with researchers" according to the autism community in terms of research wanting/needing study volunteers but not much after that in terms of engagement.Researchers also had a few issues with the whole research engagement process too. Some wanted a more inclusive relationship when it came to research engagement with the autism community. But, there was also some caution about how far this engagement should go insofar as "they [the autism community] might not be the appropriate people to decide what and how issues should be researched and... it risks “politicizing” scientific issues".Perhaps of potential importance to how you are reading about this study was some mention on how some members of the autism community felt that autism research was "indigestible" when it came to writing up in science papers and the use of "scientific jargon". One of the first thoughts that crossed my mind on reading such results was an article I'd read not so long ago by Steven Pinker (see here) and what this could mean for peer-reviewed science writing. That and the value of science blogging...Alongside quite a few other snippets of potentially important information, the authors conclude that: "There is no ‘one size fits all’ approach to community engagement" (no real surprise there) but with a little innovation, autism researchers and the autism community can reach some middle ground mutually beneficial to both camps. What's more to say on this topic? Well, not a great deal really, aside from that which Pellicano et al cover in their collective papers on this topic and where autism research should perhaps be heading. Of course, I would advocate for more people to get interested and involved in science - autism science - even if this means spending a few hours a week looking through something like PubMed or joining social media sites like Twitter and following those interested in the various autism research being produced. The caveats to that are that: (i) science is all about probability not absolutes, (ii) not all science is equal, and (iii) when it comes to autism, the issues of heterogeneity and all that enhanced risk of various comorbidity, need to be kept in mind when reading about any 'scientific breakthrough' or 'wonder-study' which purports to definitively answer any research question.Insofar as resources, at least here in the UK, where people can participate in autism research, the National Autistic Society (NAS) hold a directory of research projects looking for participants (I assume other countries have similar resources). I do wonder if any such international database might exist which could act as a central autism research point drawing on resources like the US facility and other research databases for those wishing to take part?Finally, blog. Yes, you heard me correct. People with autism, parents, professionals and even researchers, put pen to paper and start your own blog... it's normally free and pretty easy to do once you get the hang of it. Who knows, perhaps one day, every study will have its own blog or blog entry.A little song to close... Danke Schoen.----------[1] Pellicano E. et al. Views on Researcher-Community Engagement in Autism Research in the United Kingdom: A Mixed-Methods Study. PLoS ONE. 2014; 9: e109946.[2] Pellicano E. et al. What should autism research focus upon? Community views and priorities from the United Kingdom. Autism. 2014 Oct;18(7):756-70.[3] Jang J. et al. What are the ages of persons studied in autism research: A 20-year review. Research in Autism Spectrum Disorders. 2014; 8: 1756–1760.----------Pellicano E, Dinsmore A, & Charman T (2014). Views on Researcher-Community Engagement in Autism Research in the United Kingdom: A Mixed-Methods Study. PloS one, 9 (10) PMID: 25303222... Read more »

  • November 3, 2014
  • 05:55 PM

Reshaping the Limits of Synthetic Biology

by Gabriel in Lunatic Laboratories

Ever think you could have built something better if you had a hand in the design? Sometimes people just have a desire to make, after all the maker movement is huge for a reason. Well geneticists have a new toy tool to play with —dubbed “the telomerator”—that could redefine the limits of synthetic biology and advance how successfully living things can be engineered or constructed in the laboratory based on an organism’s genetic, chemical base-pair structure. How cool is that?!... Read more »

J. Boeke et al. (2014) Circular permutation of a synthetic eukaryotic chromosome with the telomerator. Proceedings of the National Academy of Sciences. info:/10.1073/pnas.1414399111

  • November 3, 2014
  • 04:13 AM

Probiotics to counter heavy metal toxicity?

by Paul Whiteley in Questioning Answers

"In summary, this work has demonstrated the potential value of long-term probiotic-based interventions to counter mercury and arsenic exposure in vulnerable populations, particularly in pregnant women".Sounds like an '80s man to me...That was one of the primary conclusions reported by Jordan Bisanz and colleagues [1] (open-access) examining "at-risk populations of pregnant women and in children in Mwanza, Tanzania". The idea being that alongside the use of metal chelating medicines such as dimercaptosuccinic acid (DMSA) and ethylenediaminetetraacetic acid (EDTA) indicated for 'acute' exposure to heavy metals, there may be other ways and means of treating heavy metal exposure over longer periods and where resources may not be as plentiful. Some media about this study can be seen here.The Bisanz paper is open-access but a few pointers might be in order:The study was based on the idea that certain strains of bacteria are known to have "an affinity for many toxic metals, including lead and cadmium" as documented in papers such as the one by Monachese and colleagues [2]. Further, that so-called "probiotic yogurt kitchens that service economically disadvantaged people" as a source of potentially beneficial bacteria are already working at the particular location selected by the study authors.So, two studies were implemented: (a) looking at school-aged children (SAC) (initial N=44) randomised to receive either a probiotic yoghurt containing "1 × 1010 CFU Lactobacillus rhamnosus GR-1 per 250 g" or "an equivalent portion of ultra-heat-treated milk as a control devoid of lactic acid bacteria" daily for 24 days; and (b) "60 pregnant women [PW] were recruited, of which 26 received a probiotic yogurt containing 1 × 1010 CFU L. rhamnosus GR-1 per 250 g and supplemented with 4.3 g of Moringa, a micronutrient-rich plant, to enhance maternal nutrition". The study entries in the US National Institutes of Health (NIH) database can be found here and here respectively. Analysis of blood metal levels ("blood lead, total mercury, total arsenic, and cadmium") were undertaken at enrolment and follow-up for all participants across the two studies. Analysis of fecal samples for children in study (a) was also undertaken pre- and post-intervention to test for any differences across the yoghurt vs. milk groups. Local fish were also analysed for heavy metal content to ascertain dietary exposure alongside dietary patterns of participants.Results: there were quite a few... levels of heavy metals in SAC and PW studied were elevated compared to "levels present in a developed country (Canada)" somewhere in the order of over 6 times greater for lead and mercury. Children (SAC) were particularly vulnerable to an increased heavy metal burden. The authors noted: "Metal exposure from dietary fish intake likely explains why we saw elevated blood levels of mercury in both the SAC and PW groups"."The studies provided the first positive evidence for the use of probiotics to combat toxic heavy metal exposure in vulnerable human populations". Well, sort of, is probably the best way that I can comment on this assertion, as the authors noted: "no statistically significant differences were detected in blood metal levels in SAC receiving the probiotic or milk control, although we noted that there was a weak trend of reduced blood levels of lead and arsenic". They did find that in the control group in receipt of milk, "blood levels of mercury and arsenic increased" between the testing occasions "but remained stable in the probiotic group". So concluding that levels of certain heavy metals didn't get any worse following the use of a probiotic is probably a more accurate way of looking at things.Insofar as the gut bacteria analysis side of things: "Administration of the probiotic was not observed to have an effect on the gut bacterial community composition". But the authors did report that: "Elevated blood lead was associated with increases in Succinivibrionaceae and Gammaproteobacteria relative abundance levels in stool".There are some important results to be derived from the Bisanz paper but not necessarily in the way that I think the authors hoped, bearing in mind this was a very short study limited to one specific probiotic strain. That being said, the idea that probiotics might have some kind of protective effect - "probiotic administration may be especially advocated at peak exposure times" - is an interesting one, worthy of quite a bit more investigation. I know discussions in certain quarters about the use of chelation therapy for certain conditions have the ability to furrow brows (see here). This despite the fact that when clinically indicated, chelation can provide some powerful results as demonstrated in the recent paper by Thurtle and colleagues [2] (open-access) on the use of oral DMSA for severe lead poisoning in Northern Nigeria. If we are to assume that certain types of bacteria might potentially be able to prevent or reduce uptake of something like heavy metals in the gastrointestinal (GI) tract from oral sources (i.e. food), I'd be minded to say that such inexpensive and potentially safer methods protecting against heavy metal poisoning, might be something to explore. And hopefully I'm talking out of turn when I mention some of the literature on lead and mercury exposure when it comes to autism (see here) as another possible avenue for more formal investigation.Next up: probiotics and influenza anyone? (With the need for a lot more research and certainly nothing like medical or clinical advice given or intended by me on this topic).Music then. Domino by Jessie J.----------[1] Bisanz JE. et al. Randomized Open-Label Pilot Study of the Influence of Probiotics and the Gut Microbiome on Toxic Metal Levels in Tanzanian Pregnant Women and School Children. mBio. 2014. 7 October.[2] Thurtle N. et al. Description of 3,180 Courses of Chelation with Dimercaptosuccinic Acid in Children ≤5 y with Severe Lead Poisoning in Zamfara, Northern Nigeria: A Retrospective Analysis of Programme Data. PLoS Medicine. 2014; 11: e1001739.-----------... Read more »

Jordan E. Bisanz, Megan K. Enos, Joseph R. Mwanga, John Changalucha, Jeremy P. Burton, Gregory B. Gloor, & Gregor Reid. (2014) Randomized Open-Label Pilot Study of the Influence of Probiotics and the Gut Microbiome on Toxic Metal Levels in Tanzanian Pregnant Women and School Children. mBio. info:/10.1128/mBio.01580-14

  • November 3, 2014
  • 12:05 AM

See All About It! New Set of Tests to Add to the Concussion Assessment Protocol

by Jane McDevitt in Sports Medicine Research (SMR): In the Lab & In the Field

The vestibular/ocular motor screening (VOMS) is valid assessment to identify young patients with concussions.... Read more »

Mucha A, Collins MW, Elbin RJ, Furman JM, Troutman-Enseki C, DeWolf RM, Marchetti G, & Kontos AP. (2014) A Brief Vestibular/Ocular Motor Screening (VOMS) Assessment to Evaluate Concussions: Preliminary Findings. The American Journal of Sports Medicine, 42(10), 2479-86. PMID: 25106780  

  • November 1, 2014
  • 01:14 PM

Where HIV hides

by Gabriel in Lunatic Laboratories

HIV is hard to get rid of,not because it primarily resides in the blood, but because of where it hides when antiretrovirals drop HIV levels. So the real question is where does HIV hide? Unfortunately those antiretroviral drugs can usually control the virus, but can’t completely eliminate it. So any strategy to eradicate HIV from the body has to take into account not only the main group of immune cells the virus targets, called CD4 or helper T cells, but other infected cells as well.... Read more »

  • November 1, 2014
  • 06:07 AM

Early childhood atopy and autism risk

by Paul Whiteley in Questioning Answers

De profundis clamo ad te, domineRegular readers will probably have heard something like this before so I'm sorry if I'm repeating myself: "The presence of any atopic disease in early childhood increased the risk of developing ADHD [attention deficit hyperactivity disorder]... and ASD [autism spectrum disorder]... in later life".So said Mu-Hong Chen and colleagues [1] with yet another 'big data' paper coming out of Taiwan.There is little point in me turning this research into some sort of mega-post given that this topic has featured so heavily on this blog. In case you missed them, here are some of the relevant posts:Allergic and autoimmune diseases and autism (2012) (see here)Asthma increases risk of ADHD? (2013) (see here)Asthma as a risk factor for autism? (2014) (see here)Autism, ADHD and allergy: Taiwan and big data (again) (2014) (see here)Lazy? Yes, I am being a bit lazy in this post by just supplying older links but what more can I say apart from that there seems to be a complicated relationship between immune function and behaviour. Oh, and other research from this group might also be worthwhile looking at as per studies linking epilepsy and atopic dermatitis [2] and major depression and/or bipolar disorder and asthma [3] knowing about the various comorbidity relationships with autism (see here and see here).And here is some lazy music to accompany my lazy post...----------[1] 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.[2] Chen MH. et al. Risk of epilepsy among patients with atopic dermatitis: a nationwide longitudinal study. Epilepsia. 2014 Aug;55(8):1307-12.[3] Chen MH. et al. Higher risk of developing major depression and bipolar disorder in later life among adolescents with asthma: a nationwide prospective study. J Psychiatr Res. 2014 Feb;49:25-30.----------Chen MH, Su TP, Chen YS, Hsu JW, Huang KL, Chang WH, Chen TJ, Pan TL, & Bai YM (2014). Is atopy in early childhood a risk factor for ADHD and ASD? A longitudinal study. Journal of psychosomatic research, 77 (4), 316-21 PMID: 25280829... Read more »

Chen MH, Su TP, Chen YS, Hsu JW, Huang KL, Chang WH, Chen TJ, Pan TL, & Bai YM. (2014) Is atopy in early childhood a risk factor for ADHD and ASD? A longitudinal study. Journal of psychosomatic research, 77(4), 316-21. PMID: 25280829  

  • October 31, 2014
  • 04:05 PM

New Genetic Editing Technique Offers Novel Treatment of Defects

by Gabriel in Lunatic Laboratories

The promises of genetic modifications are endless, longer life, better health, cures for genetic based diseases that would otherwise cause an unimaginable amount of suffering all wiped out. We’ve come a long way in genetic alteration thanks, in part, to the ever faster moving pace of science. While genetic modification is the thing of horror movies, it also can change the world in ways we cannot even imagine — unfortunately getting genome-editing proteins into cells, where they need to be to access the genome, is a major challenge, especially in live animals or human patients.... Read more »

  • October 31, 2014
  • 12:05 PM

I Need How Many Calories? Caloric Needs in Bulimia Nervosa Patients

by Tetyana in Science of Eating Disorders

In the 1980s, a few studies came out suggesting that patients with bulimia nervosa (BN) require fewer calories for weight maintenance than anorexia nervosa patients (e.g., Newman, Halmi, & Marchi, 1987) and healthy female controls (e.g., Gwirtsman et al., 1989).
Gwirtsman et al. (1989), after finding that patients with bulimia nervosa required few calories for weight maintenance than healthy volunteers, had these suggestions for clinicians:
When bulimic patients are induced to cease their binging and vomiting behavior, we suggest that physicians and dietitians prescribe a diet in which the caloric level is lower than might be expected. Our experience suggests that some patients will tend to gain weight if this is not done, especially when hospitalized. Because patients are often averse to any gain in body weight, this may lead to grave mistrust between patient and physician or dietitian.
Among many things, this ignores the fact that patients with bulimia nervosa, despite being in the so-called “normal” weight range may not be at their healthy weight.
It is not possible to determine at this point whether the abnormality in …

You May Also Like:
Energy Expenditure in Anorexia Nervosa Patients
Hypermetabolism in Anorexia Nervosa
The “Double Life” of Bulimia Nervosa: Patients’ Perspectives

... Read more »

de Zwaan, M., Aslam, Z., & Mitchell, J.E. (2002) Research on energy expenditure in individuals with eating disorders: a review. International Journal of Eating Disorders, 31(4), 361-9. PMID: 11948641  

Gwirtsman, H.E., Kaye, W.H., Obarzanek, E., George, D.T., Jimerson, D.C., & Ebert, M.H. (1989) Decreased caloric intake in normal-weight patients with bulimia: comparison with female volunteers. American Journal of Clinical Nutrition, 49(1), 86-92. PMID: 2912015  

  • October 31, 2014
  • 05:06 AM

Caesarean section births and autism risk?

by Paul Whiteley in Questioning Answers

It was a familiar story. Big media headlines such as: Caesarean sections 'may increase risk of autism' appearing all over, but when it came to finding the study behind the headlines, the publishing journal seemed to be trailing a little way behind. We've been in a similar situation before."As the flames rose to her Roman nose"Anyhow, the paper by Eileen Curran and colleagues [1] (open-access) has finally made it to the research table and hence is fodder for today's ramblings with the suggestion that the way we make our grand entrance into the world might correlate with some heightened risk for autism spectrum disorder (ASD).I have to say that I was initially quite interested in the Curran findings for quite a few reasons. Primary among them is some curiosity I have about the gut microbiota in relation to quite a few states and diagnoses (see here) and how our mode of entry into the world can seemingly impact on our first exposure to the bacterial passengers which eventually call us home. It is perhaps one of the lesser known observations, that the voyage down our dear mothers birth canal is also a great meet-and-greet opportunity for baby and bacteria. For those who don't get to experience such wonders, there is a suggestion that different types of bacteria might make friends which are then 'programmed' to be accepted by our developing immune systems [2] with onwards possible significance for future health and wellbeing. That being said, there is still a way to go to understanding such a relationship more thoroughly despite some intriguing results specifically with autism and the gut microbiome in mind (see here). I might also add that some of the authors on the Curran paper seemingly have some interest in the whole gut bacteria - behaviour relationship as per another recent paper [3].The Curran paper is a systematic review of the literature which looked at: "mode of delivery on autism spectrum disorders (ASD) and attention-deficit/hyperactivity disorder (ADHD)". They concluded that: "Thirteen studies reported an adjusted estimate for CS-ASD [Caesarean section-ASD], producing a pooled odds ratio (OR) of 1.23 (95% CI: 1.07, 1.40)". Said studies were analysed up to February 2014. The population attributable fraction calculated by authors implied that: "5.36% of cases of ASD may be attributable to delivery by CS assuming the observed association is causal".The lead author is rightly cautious about their findings, as per some other comment in the media: “Parents should be reassured that the overall risk of a child developing ASD (Autism Spectrum Disorder) is very small and that Caesarean section is largely a very safe procedure and when medically indicated, it can be lifesaving,”. I wouldn't disagree with those sentiments allowing for the fact that (a) a fair proportion of deliveries these days are by C-section, and (b) not every child diagnosed with autism is delivered via C-section.That being said, there does seem to be more to do in this area of science. Subsequent studies published after the cut-off point set by Curran have reported C-sections as a 'risk factor' for autism. The paper by Salhia and colleagues [4] for example, looking at the epidemiology of autism in [some] Arab Gulf countries found as much, alongside some other quite frequently reported variables potentially influencing autism risk (e.g. advanced maternal and paternal age).I'm going to drop in a few additional papers and then I'm done. Chien and colleagues [5] also talked about C-sections as a risk factor for autism but with the added twist that the use of a general anaesthetic during said procedure might be implicated in any relationship. You might scoff at the suggestion that anaesthetic has anything to do with autism but before you do, perhaps have a read through the paper by DiMaggio and colleagues [6] first and slightly more speculatively, the paper by Johnson and colleagues [7]. The study by Chudal and colleagues [8] - mentioned by Curren et al - looking at various perinatal factors in the context of bipolar disorder is also worthwhile introducing bearing in mind that interest in such comorbidity is increasing in the context of some autism (see here). As with many other variables 'correlated' to autism risk, to shut the door on any association with comorbidity outside of just the diagnosis of autism is foolhardy.Irrespective of your opinion about whether C-sections might be linked to autism risk and the other possible reasoning behind said suggestion [9], the Curran paper joins a growing list of variables potentially associated with autism. Systematic reviews and meta-analyses are consolidating quite a bit of this data, although as always the heterogeneity covered under the label of autism and the important issue of comorbidity need to be kept in mind. As with the growing idea that many small genetic issues might cumulatively be linked to [some] autism further compounded by more recent data [10] (see here for some media), so one might assume that multiple small contributions from the 'environment' might likewise also influence offspring risk of autism too. Determining how and when these genetic and environmental variables come together seems to be to be the next logical step...Music to close: The Specials and Ghost Town. Have a spooky day!----------[1] Curran EA. et al. Research Review: Birth by Caesarean section and development of autism spectrum disorder and attention-deficit/hyperactivity disorder: a systematic review and meta-analysis. Journal of Child Psychology and Psychiatry. 2014. October 27.[2] Weng M. & Walker WA. The role of gut microbiota in programming the immune phenotype. J Dev Orig Health Dis. 2013 Jun;4(3):203-14.[3] Stilling RM. et al. Friends with social benefits: host-microbe interactions as a driver of brain evolution and development? Front. Cell. Infect. Microbiol. 2014. October 29.[4] Salhia HO. et al. Systemic review of the epidemiology of autism in Arab Gulf countries. Neurosciences (Riyadh). ... Read more »

  • October 30, 2014
  • 03:45 PM

Zombies: Science Fiction vs. Fact

by Gabriel in Lunatic Laboratories

Well in the spirit of Halloween I thought I would make a nice little zombie post. Zombies, those brain loving little guys, [and girls] are everywhere. From shows like The Walking […]... Read more »

Lafferty KD. (2006) Can the common brain parasite, Toxoplasma gondii, influence human culture?. Proceedings. Biological sciences / The Royal Society, 273(1602), 2749-55. PMID: 17015323  

Vyas A, Kim SK, Giacomini N, Boothroyd JC, & Sapolsky RM. (2007) Behavioral changes induced by Toxoplasma infection of rodents are highly specific to aversion of cat odors. Proceedings of the National Academy of Sciences of the United States of America, 104(15), 6442-7. PMID: 17404235  

Thomas, F., Schmidt-Rhaesa, A., Martin, G., Manu, C., Durand, P., & Renaud, F. (2002) Do hairworms (Nematomorpha) manipulate the water seeking behaviour of their terrestrial hosts?. Journal of Evolutionary Biology, 15(3), 356-361. DOI: 10.1046/j.1420-9101.2002.00410.x  

W. Wesołowska T. Wesołowski. (2014) Do Leucochloridium sporocysts manipulate the behaviour of their snail hosts?. Journal of Zoology , 292(3), 151-155. info:/10.1111/jzo.12094

  • October 30, 2014
  • 11:20 AM

Alcoholism as a Reward System Dysfunction

by William Yates, M.D. in Brain Posts

Alcoholism and other addictive behaviors often occur together within individual patients.For example, individuals with alcoholism commonly also are smokers and meet criteria for a diagnosis of nicotine dependence.This co-occurrence suggests multiple types of addiction may share genetic and environmental risk factors. Additionally, there might be a common neurobiological mechanism in play for many addictions.Kenneth Blum and other leading alcoholism researchers recently published a review that proposed a theory of addiction they labelled the "Reward Deficiency Solution System".Here are some of my notes on the key points outlined in their literature review:IntroductionThe goal of the review was to find common mechanisms for addictions--both those related to a substance and those not substance related, i.e. obesity or pathological gamblingGenetic studies linking alcoholism to the dopamine 2 receptor (DRD2) date back to 1990Over 3000 studies have been published on the DRD2 receptor and addictions since 1990Studies have not universally supported a DRD2 link to addictions but many do support the linkIs Dopamine Deficit or Over Supply at Fault?Dopamine transporter gene one (DAT1) deficit status has been linked to obesity possibly through a dysregulation in food rewardPolymorphisms that involve D2 and D4 reduce reward response to food and lead to weight gainfMRI research in children and adolescents have shown that an increased dopamine-related neurotransmission in the striatum may be a risk factor for obesitySo, both deficit and oversupply of dopamine may influence addiction risk including risk for obesityIs There a Solution to Reward Deficiency Syndrome (RDS)?Dopamine antagonists such as naltrexone and acamprosate have had limited successStudies of a newly developed drug KB220Z, a dopamine agonist are promisingKB220Z studies in mice show increased brain enkephalin and reduced alcohol-seeking behavior KB220Z studies in humans has been linked to reduced alcohol withdrawal, lower addiction treatment drop out rates and reduced craving scores across multiple substance types including alcohol, cocaine, heroin and nicotineKB220Z activates the brain reward center known as the nucleus accumbens and increases activation of the prefrontal-cerebellar-occipital brain circuitGenetic and Functional Mechanisms in RDSWe lack understanding of how genes regulate functional networks related to addiction circuitryAddicts do show reduced fMRI resting state network connectivityKB220Z appears to reverse these resting state connectivity deficits in addictsStudying genomic contributions to brain connectivity patterns in reward may be a powerful strategy for addiction drug developmentMy Comments: This review highlights the weakness of our current state of knowledge for understanding how genetics, brain neurochemistry and brain circuitry influence addition. However, I do agree with the reviewers that progress is being made and that brain circuitry imaging may be a valuable tool in future progress.Readers with more interest in this topic can access the free full-text manuscript by clicking on the PMID link in the citation below.Molecular model of dopamine is from a Wikepedia Commons file authored by sbroolsFollow the author on Twitter @WRY999Blum K, Febo M, McLaughlin T, Cronjé FJ, Han D, & Gold SM (2014). Hatching the behavioral addiction egg: Reward Deficiency Solution System (RDSS)™ as a function of dopaminergic neurogenetics and brain functional connectivity linking all addictions under a common rubric. Journal of behavioral addictions, 3 (3), 149-56 PMID: 25317338... Read more »

  • October 30, 2014
  • 07:59 AM

Fright Week: The Stranger in the Mirror

by The Neurocritic in The Neurocritic

In the mirror we see our physical selves as we truly are, even though the image might not live up to what we want, or what we once were. But we recognize the image as “self”. In rare instances, however, this reality breaks down.In Black Swan, Natalie Portman plays Nina Sayers, a ballerina who auditions for the lead in Swan Lake. The role requires her to dance the part of the innocent White Swan (for which she is well-suited), as well as her evil twin the Black Swan — which is initially outside the scope of her personality and technical abilities. Another dancer is favored for the role of the Black Swan. Nina's drive to replace her rival, and her desire for perfection, lead to mental instability (and a breathtaking performance). In her hallucinations she has become the Black Swan.1The symbolic use of mirrors to depict doubling and fractured identity was very apparent in the film:Perhaps Darren Aronofsky [the director's] intentions for the mirror was its power to reveal hidden identities. If you noticed the scenes where Nina saw herself in the mirror, it reflected the illusion of an evil. The mirror presented to her the darkness within herself that metaphorically depicted the evolution into the black swan. How can the recognition of self in a mirror break down?Alterations in mirror self-recognitionThere are at least seven main routes to dissolution or distortion of self-image:psychotic disordersdementiaright parietal-ish or otherwise right posterior cortical strokes and lesionsthe ‘strange-face in the mirror' illusion hypnosisdissociative disorders (e.g., depersonalization, dissociative identity disorderbody image issues (e.g., anorexia, body dysmorphic disorder) Professor Max Coltheart and colleagues have published extensively on the phenomenon of mirrored-self misidentification, defined as “the delusional belief that one’s reflection in the mirror is a stranger.” They have induced this delusion experimentally by hypnotizing highly suggestible participants and planting the suggestion that they would see a stranger in the mirror (Barnier et al., 2011): Following a hypnotic suggestion to see a stranger in the mirror, high hypnotizable subjects described seeing a stranger with physical characteristics different to their own. Whereas subjects' beliefs about seeing a stranger were clearly false, they had no difficulty generating sensible reasons to explain the stranger's presence. The authors tested the resilience of this belief with clinically inspired challenges. Although visual challenges (e.g., the hypnotist appearing in the mirror alongside the subject) were most likely to breach the delusion, some subjects maintained the delusion across all challenges. Ad campaign for the Exelon Patch (rivastigmine, a cholinesterase inhibitor) used to treat Alzheimer's disease. Photographer Tom Hussey did a series of 10 award-winning portraits depicting Alzheimer's patients looking at their younger selves in a mirror (commissioned by Novartis).Mendez et al. (1992) published a retrospective study of 217 patients with Alzheimer's disease. They searched the medical records for caregiver reports of disturbances in person identification of any kind. The most common type was transient confusion of family members that resolved when reminded of the person's identity (found in 33 patients). The charts of five patients contained reports of mirror misidentification, which was always associated with paranoia and delusions. Although not exactly systematic, this fits with other studies reporting that 2–10% of Alzheimer's patients have problems recognizing themselves in a mirror.A very thorough investigation of the topic was actually published 50 years ago, but largely neglected because it was in French. Connors and Coltheart (2011) translated the 1963 paper of Ajuriaguerra, Strejilevitch, & Tissot into English. The Introduction is quite eloquent:The vision of our image in the mirror is a discovery that is perpetually renewed, one in which our being is isolated from the world, from the objects surrounding it, and assumes, despite the fixed quality of reflected images, the significance of multiple personal and potential expressions. The image reflected by the mirror furnishes us not only with that which is, but also how our real image might be changed. It therefore inextricably combines awareness, indulgence and critique.They examined how 30 hospitalized dementia interacted with mirrors in terms of  (1) recognition of their own reflection; (2) use of reflected space; and (3) identifying body parts. The patients sat in front of a mirror and answered the following questions:What is this?Who is that?How old would you say that person is?How do you think you look?Then the experimenter stood behind them and asked questions about himself (e.g., “who is that man?”), and showed them objects in a mirror (e.g., an orange or a pipe – very funny).Eight patients did not recognize themselves in the mirror:Three didn't understand the concept of a mirror. They didn't pay attention to any reflections until directed to do so, and then they became transfixed. They also failed to recognize photos of themselves or their caretakers.Another three eventually admitted it might be themselves when prodded several times.These individuals had severe Alzheimer's disease.The final two recognized themselves the second time, and displayed considerably more anxiety. This sounds terribly frightening:These patients were attentive to their own reflections and those of the researchers, whom they identified. The first patient seemed a bit anxious; she began by touching herself, then laughed, then proclaimed “that is not quite me, it sort of looks like me, but it's not me.” When she was shown her photo head-on and then from the side, she immediately identified herself when the photo was head-on but from the side said “that's not quite me.” These individuals were in an earlier state of dissolution and likely had more awareness of what was happening to them.Other patients with mirrored-self misidentification show greater sparing of cognitive abilities. Chandra and Issac (2014) presented brief case summaries of five mild to moderate dementia patients with “mirror image agnosia, a new observation involving failure to recognize reflected self-images.” This is obviously not a new observation, but the paper includes two videos, one of which is embedded below. Sixty-two-year-old female was brought to the hospital with features of forgetfulness and getting... Read more »

Barnier AJ, Cox RE, Connors M, Langdon R, & Coltheart M. (2011) A stranger in the looking glass: developing and challenging a hypnotic mirrored-self misidentification delusion. The International journal of clinical and experimental hypnosis, 59(1), 1-26. PMID: 21104482  

Chandra SR, & Issac TG. (2014) Mirror image agnosia. Indian journal of psychological medicine, 36(4), 400-3. PMID: 25336773  

Mendez MF, Martin RJ, Smyth KA, & Whitehouse PJ. (1992) Disturbances of person identification in Alzheimer's disease. A retrospective study. The Journal of nervous and mental disease, 180(2), 94-6. PMID: 1737981  

  • October 30, 2014
  • 04:44 AM

Pain and adolescent Chronic Fatigue Syndrome

by Paul Whiteley in Questioning Answers

"We found a higher prevalence of severe pain among adolescents with CFS [Chronic Fatigue Syndrome] and lowered pain thresholds compared with HCs [healthy controls]".That was the headline generated by the study from Anette Winger and colleagues [1] (open-access) looking to describe several parameters tied into experience of pain in the context of CFS. Further: "The total sum of bodily symptoms represented a heavy burden with great functional consequences".Your hokey pokey dragon is out helpin' Santa Claus pull his sled!The Winger paper is open-access, and pretty self-explanatory in terms of the hows and whys of the study (including strengths and limitations) so no need for me to further complicate things. As part of the NorCAPITAL project (The Norwegian Study of Chronic Fatigue Syndrome in Adolescents: Pathophysiology and Intervention Trial) ( entry here) which has already reported on the use of clonidine for CFS [2], the latest publication is an important add-on.There are a few details included in the results which do however merit some additional highlighting. So:"In the present study, almost three-quarters of the adolescents with CFS suffered from weekly pain, and pain on a daily basis was a problem for half of the patients". This was "highly significant" when compared with reports from controls, particularly where two-thirds of CFS participants reported weekly headaches. Muscle and joint pain were also recorded by adolescents with CFS alongside almost half reporting abdominal pain. Indeed, joint pain showed the most disparity between the groups with reports of such pain tipping 70% in the CFS group compared with only 10% of controls reporting this more frequently than once a month.When looking at result examining the pressure pain threshold (PPT) - "the minimum intensity of a stimulus that is perceived as painful" - and examining scores based on completion of the Brief Pain Inventory (BPI), authors concluded that: "At all measure points, PPTs were significantly lower (all p<0.001) among patients with CFS than HCs"."In our study, the adolescents reported that pain interfered with school, general activity and mood; however, we cannot conclude from this study that pain has a causal effect, because it could be the other way around". What's more to say about this research? Well, the very important message that the presentation of CFS might go well beyond just 'chronic fatigue' is paramount. This is not new news to science and practice as per the various reviews on the topic of pain exemplified by Nijs and colleagues [3]. I dare say that some public perceptions of CFS/ME would also change if more people understood that pain is a seemingly important manifestation of the condition. Oh and that CFS and pain sensation might not just be all in the mind...I'm also inclined to introduce the condition fibromyalgia (FM) into proceedings, given the many and varied reports talking about key symptoms overlapping [4]. I'm not altogether sure of the hows and whys of FM and CFS connecting, but certainly the primary FM symptom of widespread pain and extreme sensitivity strikes me as being potentially important. With no medical advice given or intended and perhaps somewhat counter-intuitive to analgesia, the increasing body of work looking at the use of something like low-dose naltrexone (see here for some of my interest in this area) for pain in FM [5] may also very well be something in need of a little more study with pain in CFS in mind, alongside other possible pain relief options.So then, The White Stripes with Ball and Biscuit.----------[1] Winger A. et al. Pain and pressure pain thresholds in adolescents with chronic fatigue syndrome and healthy controls: a cross-sectional study. BMJ Open. 2014; 4(10): e005920.[2] Fagermoen E. et al. Clonidine in the treatment of adolescent chronic fatigue syndrome: a pilot study for the NorCAPITAL trial. BMC Research Notes 2012, 5:418 [3] Nijs J. et al. Pain in patients with chronic fatigue syndrome: time for specific pain treatment? Pain Physician. 2012 Sep-Oct;15(5):E677-86.[4] Aaron LA. et al. Overlapping Conditions Among Patients With Chronic Fatigue Syndrome, Fibromyalgia, and Temporomandibular Disorder. Arch Intern Med. 2000;160(2):221-227.[5] Younger J. et al. Low-dose naltrexone for the treatment of fibromyalgia: findings of a small, randomized, double-blind, placebo-controlled, counterbalanced, crossover trial assessing daily pain levels. Arthritis Rheum. 2013 Feb;65(2):529-38.----------Winger, A., Kvarstein, G., Wyller, V., Sulheim, D., Fagermoen, E., Smastuen, M., & Helseth, S. (2014). Pain and pressure pain thresholds in adolescents with chronic fatigue syndrome and healthy controls: a cross-sectional study BMJ Open, 4 (10) DOI: 10.1136/bmjopen-2014-005920... Read more »

  • October 29, 2014
  • 03:19 PM

More Genetic Links Behind Autism

by Gabriel in Lunatic Laboratories

Vaccines do NOT cause autism. One more time, vaccines DO NOT cause autism. So what does cause autism, that problem has been plaguing scientists for awhile now. Thankfully two major genetic studies of autism and involving more than 50 laboratories worldwide, have newly implicated dozens of genes in the disorder. The research shows that rare mutations in these genes affect communication networks in the brain and compromise fundamental biological mechanisms that govern whether, when, and how genes are activated overall.... Read more »

Iossifov, I., O’Roak, B., Sanders, S., Ronemus, M., Krumm, N., Levy, D., Stessman, H., Witherspoon, K., Vives, L., Patterson, K.... (2014) The contribution of de novo coding mutations to autism spectrum disorder. Nature. DOI: 10.1038/nature13908  

De Rubeis, S., He, X., Goldberg, A., Poultney, C., Samocha, K., Ercument Cicek, A., Kou, Y., Liu, L., Fromer, M., Walker, S.... (2014) Synaptic, transcriptional and chromatin genes disrupted in autism. Nature. DOI: 10.1038/nature13772  

  • October 29, 2014
  • 01:45 PM

This Month in Blastocystis Research (OCT 2014) - Trick or Treat Edition

by Christen Rune Stensvold in Blastocystis Parasite Blog

October was mostly about conferences and funding. And why is no one studying endosymbiosis in Blastocystis?... Read more »

Fletcher S, Caprarelli G, Merif J, Andresen D, Hal SV, Stark D, & Ellis J. (2014) Epidemiology and geographical distribution of enteric protozoan infections in sydney, australia. Journal of public health research, 3(2), 298. PMID: 25343139  

Nowack EC, & Melkonian M. (2010) Endosymbiotic associations within protists. Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 365(1541), 699-712. PMID: 20124339  

Prodeus TV, Zelia OP, Khlebnikova TA, & Pikul' DA. (2014) [Extraenteric infection caused by Blastocystis spp. in a female patient with liver abscess]. Meditsinskaia parazitologiia i parazitarnye bolezni, 6-9. PMID: 25296418  

  • October 29, 2014
  • 08:00 AM

Almost This Or Almost That? Must Be The Other

by Mark Lasbury in As Many Exceptions As Rules

The protists are a catch-all kingdom, neither characteristics nor cladistics can easily group them, or even tell you what one is. Recent studies have begun to identify histories of the plant-like protist phyla based on their flagella. Rhodophyta are a basal phylum, and yet they have no flagella at all, while genomic studies have identified 495 different proteins in chromista flagella, with some being specific to each of the two dissimilar flagella on the organisms. Such diversity within one grouping of one kingdom is amazing, and frustrating.... Read more »

  • October 29, 2014
  • 04:36 AM

The stability of an Asperger syndrome diagnosis

by Paul Whiteley in Questioning Answers

"Asperger Syndrome, when considered as an ASD/PDD [autism spectrum disorder/pervasive developmental disorder] diagnosis, was fairly stable into adulthood, but there was a significant increase over time in cases no longer meeting criteria for an ASD diagnosis according to the DSM-IV, or AS according to the Gillberg criteria".The night is darkest just before the dawn.That was one of the primary conclusions made in the paper by Adam Helles and colleagues [1] who prospectively followed a group of males diagnosed with Asperger syndrome (AS) in childhood into adulthood covering a period of some 20 years. I believe the starting point of this study has been seen before in the peer-reviewed literature in the paper by Cederlund & Gillberg [2] (open-access here) (a paper which takes me back to my own PhD days with it's important influence to some of my work). Other follow-ups have also been reported [3].Looking at the diagnostic stability of AS, Helles et al noted that compared with baseline where all participants fulfilled diagnostic criteria, at follow-up (two follow-ups actually) there was a "significant decrease in the rate of cases fulfilling any PDD diagnosis according to the DSM-IV, from 91% at T1 [time 1] to 76% at T2 [time 2] in the 47 cases followed up twice". The decline in cases according to the Gillberg criteria was even more stark (82% at T1 and 44% at T2).Researchers also noted a few other potentially important points in their findings such that: "Severity of autism spectrum symptoms at T1 was the main predictor of diagnostic stability at T2" and a fifth of those who met criteria for DSM-IV criteria for a PDD diagnosis "did not meet DSM-5 ASD criteria although they had marked difficulties in everyday life". This last point has been mentioned by other authors (see here).There are a few ways one could take the Helles findings. One could see it as further evidence of the fluidity of presented symptoms when it comes to the autism spectrum as per other discussions in this area (see here). You might even view it as an extension of all that chatter on something like differing developmental trajectories along the autism spectrum (see here) or 'optimal outcome' and autism (see here) albeit without the focus on early intervention as potentially being involved (see here) as far as we know. Indeed, one has to wonder whether for those not meeting the diagnostic criteria as they age and mature, this may in part be because of the various strategies learned over a lifetime to overcome some of the barriers posed by the diagnosis?But I can also see how for some people such research might be less well-received particularly when added to the 'disappearance' of the term Asperger syndrome from the latest revision of DSM (DSM-V). The paper by Spillers and colleagues [4] described concerns about "identity, community, the cure movement, and services" following the DSM-5 changes when talking to people on the autism spectrum. I wonder how the Helles findings on 'falling out of the spectrum' diagnostically speaking for some, might have similar tones if and when discussed.Accepting that the Helles findings were eventually based on quite a small participant group and their insinuation that not reaching the diagnostic thresholds for something like Asperger syndrome does not imply a life free of some of the more 'disabling' aspects on and around the diagnosis (yes, including various comorbidity), I do think there is more to see in this area. The realisation that we know so little about the autism spectrum in the long-term [5] and how behaviours ebb and flow, that our systems of diagnosis might not necessarily be as robust as we want them to be (see here) and the continued alliance between diagnosis and service receipt excluding many at the diagnostic periphery all come into play. With all the research data collected down the years, one suspects that with a little bit of organisation and willingness to plough some financial and other resources into this issue, further insight into exactly how stable an autism diagnosis might be and for who should be fairly readily available...Music to close, and having enjoyed the impressive tones of Sheryl Crow last evening, a song most parents will have a heard a few times: Real Gone.----------[1] Helles A. et al. Asperger syndrome in males over two decades: stability and predictors of diagnosis. Journal of Child Psychology and Psychiatry. 2014. 3 October.[2] Cederlund M. & Gillberg C. One hundred males with Asperger syndrome: a clinical study of background and associated factors. Dev Med Child Neurol. 2004 Oct;46(10):652-60.[3] Cederlund M. et al. Asperger syndrome and autism: a comparative longitudinal follow-up study more than 5 years after original diagnosis. J Autism Dev Disord. 2008 Jan;38(1):72-85.[4] Spillers JL. et al. Concerns about identity and services among people with autism and Asperger's regarding DSM-5 changes. J Soc Work Disabil Rehabil. 2014;13(3):247-60.[5] Howlin P. et al. Cognitive and language skills in adults with autism: a 40-year follow-up. J Child Psychol Psychiatry. 2014 Jan;55(1):49-58.----------Adam Helles, Carina I. Gillberg, Christopher Gillberg, & Eva Billstedt (2014). sperger syndrome in males over two decades: stability and predictors of diagnosis Journal of Child Psychology and Psychiatry : doi: 10.1111/jcpp.12334... Read more »

Adam Helles, Carina I. Gillberg, Christopher Gillberg, & Eva Billstedt. (2014) sperger syndrome in males over two decades: stability and predictors of diagnosis. Journal of Child Psychology and Psychiatry. info:/doi: 10.1111/jcpp.12334

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