Post List

  • December 5, 2016
  • 04:30 AM

Is Normative Data the New Normal?

by Sam Walton in Sports Medicine Research (SMR): In the Lab & In the Field

Individual differences may be seen in baseline SCAT3 data between sex, history of concussion, and history of comorbidities. Therefore, using the patient’s personal medical history may add value to the SCAT3 sideline screening.... Read more »

  • December 5, 2016
  • 02:58 AM

Double-blind randomised, placebo-controlled trial of vitamin D in autism

by Paul Whiteley in Questioning Answers

It was inevitable ("it is your destiny") that I would formulate a post about the paper published by Khaled Saad and colleagues [1] reporting results based on "a double-blinded, randomized clinical trial (RCT)" looking at the potential usefulness of a vitamin D supplement on "the core symptoms of autism in children." Inevitable because the peer-reviewed research literature looking at the sunshine vitamin/hormone in relation to autism is getting rather voluminous (see here and see here for examples) with the promise of lots more to come (see here). The fact that the name Saad in relation to this area of autism research has appeared before on this blog (see here) indicates that this researcher/research group are no strangers to this area of autism science.First, thanks to Alex for the Saad paper. And so... utilising the premier research design, where 109 children* (aged 3-10 years old) diagnosed with an autism spectrum disorder (ASD) were randomly allocated to receive vitamin D drops - "300 IU [international units] vitamin D3/kg/day, not to exceed 5,000 IU/day" - or a placebo drops over 4 months and then tested blind "by the Childhood Autism Rating Scale (CARS), Aberrant Behavior Checklist (ABC), Social Responsiveness Scale (SRS), and the Autism Treatment Evaluation Checklist (ATEC)" before and after their vitamin D or placebo, some interesting results emerged. Their trial and protocol, by the way, was also registered. [*Actually, 120 children were initially allocated to vitamin D or placebo but 11 were lost to follow-up or discontinued participation in the study.]Results: well first and foremost the tenet 'do no harm' seemed to be adhered to as we are told that "vitamin D was well tolerated by the ASD children" at least for the study duration. This is particularly important in light of that case report a few weeks back talking about vitamin D toxicity in the context of autism (see here). Indeed: "The serum levels of 25-hydroxycholecalciferol (25 (OH)D) were measured at the beginning and at the end of the study" kinda shows that authors were probably mindful of possible toxicity issues [2] alongside wanting to get a little more information about baseline vs. endpoint levels of the stuff. Having said all that the use of vitamin D was not completely side-effect free as 5 children taking the vitamin D drops reported symptoms such as "skin rashes, itching, and diarrhea."Further: "The autism symptoms of the children improved significantly, following 4-month vitamin D3 supplementation, but not in the placebo group." Scores on the CARS (Total scores) showed a "significant decrease" in the vitamin D group compared with the group taking the placebo drops. This was in the direction of vitamin D supplementation positively impacting on the presentation of autistic symptoms. Scores on the ATEC also showed something akin to improvement for those taking the vitamin D drops. As one might expect, measured levels of vitamin D - "serum levels of 25 (OH)D" - rose in the vitamin D supplemented group compared to those in the placebo group.These are interesting results providing some of the first double-blind RCT findings in relation to vitamin D supplementation and autism. I particularly like the fact that alongside well-validated instruments such as the CARS for 'measuring autism', the authors also included the ATEC, an instrument that I have growing fondness for (see here). They also measured functional vitamin D levels (albeit via an ELISA assay - I'd prefer via mass spec!) so it's not difficult to see that minus any unknown variables, the behavioural changes seem to match the biological changes to vitamin D status.There is more to do and indeed, more research in this area is already underway. Larger groups of participants still following that gold standard research methodology will give a more accurate picture and perhaps provide some details about potential best responders to such an intervention (something already hinted at in the Saad data). And then there is the question of 'how' vitamin D might be affecting the presentation of [some] autism. Well, far be it from me to speculate too much, and also taking into account what Saad et al have to say on this matter, I suggest that we might learn a thing or two from looking at vitamin D use in other areas of medicine (see here) and taking things from there...For now, here is what the UK Government says about vitamin D and the population at large although not everyone is convinced...Music: Kate Bush and This Woman's Work....----------[1] Saad K. et al. Randomized controlled trial of vitamin D supplementation in children with autism spectrum disorder. J Child Psychol Psychiatry. 2016 Nov 21.[2] Vogiatzi MG. et al. Vitamin D supplementation and risk of toxicity in pediatrics: a review of current literature. J Clin Endocrinol Metab. 2014 Apr;99(4):1132-41.----------Saad K, Abdel-Rahman AA, Elserogy YM, Al-Atram AA, El-Houfey AA, Othman HA, Bjørklund G, Jia F, Urbina MA, Abo-Elela MG, Ahmad FA, Abd El-Baseer KA, Ahmed AE, & Abdel-Salam AM (2016). Randomized controlled trial of vitamin D supplementation in children with autism spectrum disorder. Journal of child psychology and psychiatry, and allied disciplines PMID: 27868194... Read more »

Saad K, Abdel-Rahman AA, Elserogy YM, Al-Atram AA, El-Houfey AA, Othman HA, Bjørklund G, Jia F, Urbina MA, Abo-Elela MG.... (2016) Randomized controlled trial of vitamin D supplementation in children with autism spectrum disorder. Journal of child psychology and psychiatry, and allied disciplines. PMID: 27868194  

  • December 4, 2016
  • 03:34 PM

Do Synapses Really Store Memories?

by Neuroskeptic in Neuroskeptic_Discover

Most neuroscientists will tell you that long-term memories are stored in the brain in the form of synapses, the connections between neurons. On this view, memory formation occurs when synaptic connections are strengthened, or entirely new synapses are formed.

However, in a new piece in Frontiers in Systems Neuroscience, Austrian researcher Patrick C. Trettenbrein critiques the synapse-memory theory: The Demise of the Synapse As the Locus of Memory.

Trettenbrein acknowledges that "t... Read more »

  • December 3, 2016
  • 06:25 AM

19th Century DIY Brain Stimulation

by The Neurocritic in The Neurocritic

Fig. 4 (Wexler, 2016). Lindstrom's Electro-Medical Apparatus (ca. 1895), courtesy of the Bakken.

Think the do-it-yourself transcranial direct current stimulation movement (DIY tDCS) is a technologically savvy and hip creation of 21st century neural engineering? MIT graduate student Anna Wexler has an excellent and fun review of late 19th and early 20th century electrical stimulation

... Read more »

  • December 3, 2016
  • 04:23 AM

Parent-mediated interventions for young children with autism meta-analysed

by Paul Whiteley in Questioning Answers

Do not mess with  Lois.Today I'm posting on the topic of the paper by Rose Nevill and colleagues [1] concluding: "that while most outcome domains of parent-delivered intervention are associated with small effects, the quality of research is improving."Parent-mediated interventions in relation to autism have been covered on this blog quite recently (see here) accompanied by that 'super-parenting' headline fail. Such approaches work on the idea that helping parents to "develop strategies for interaction and management of behaviour" [2] might be one route of early intervention when it comes to autism. The research road has however not been smooth when it comes to this class of intervention (see here) and despite some positives (see here) has perhaps not been the overwhelming success that many had hoped for.Nevill and colleagues reviewed 19 trials of parent-mediated interventions for autism ("randomized clinical trials") looking at various outcomes in relation to core symptoms of autism and aspects such as communication and cognitive functions. The results kinda reiterate what we already know that so far, parent-mediated interventions aren't really cutting the statistical mustard when it comes to outcomes and important statistics related to effect sizes. Indeed, the [weighted] Hedge's g statistics produced by the authors on the cumulative data in this area can, at best, be described as 'modest' (and I mean at best). As a comparison, have a look at the Hedge's g stats produced by a meta-analysis of the placebo response when it came to autism [3]: "a moderate effect size for overall placebo response (Hedges' g=0.45, 95% confidence interval (0.34-0.56), P<0.001)" (based on "25 data sets (1315 participants)"). This bearing in mind that the parent-mediated intervention trials don't usually include a placebo condition (and indeed, typically don't even blind - how could you?)I don't want to poo-poo all of this area of autism science because it may still be pretty important. A few things do however worry me about the attention here based on the ideas that parent-child interactions are somehow the be-all-and-end-all of autism (also harking back to the bad 'ole days) and that in these times of continued cost-savings and austerity, parents are being expected to carry out the same services as other professionals. On that first point focused on parent-child interactions, I've always been a little cautious about what this means. Certainly in light of the primary focus on this blog, looking at genetics, epigenetics and biochemistry when it comes to autism, parent-mediated interventions are to be seen as a reactive strategy attempting to deal with 'symptoms' not necessarily causes. Yes, I know 'symptoms' are what parents and other family members see and deal with day in day out, but I'm wondering how successful parent-mediated intervention would be if used in the context of autism secondary to an inborn error of metabolism for example? Surely it makes more sense to spend a little more time ruling out some of the potential reasons why autism or particular autistic features might come about (i.e. screening - see here and see here for some other examples) rather than universally providing a parent-mediated intervention manual and hoping for the best? I might also add that a greater recognition that among 'the autisms' (see here) there may be some important waxing and waning of presentation(s) (see here) potentially influenced by things like the presence of comorbidity too reiterates that every person is an individual and set manuals on parent-child interactions don't necessarily cover all that heterogeneity. And there's also the suggestion that some parent-mediated intervention options are also seemingly failing when it comes to important comorbidities such as anxiety (knowing how disabling these can be) as being something else that needs to be kept in mind.We'll have to see how this area develops further but for now, I don't think anyone can seriously say the existing research on this topic has shown anything like the successes that everyone hoped for. And whilst we should celebrate the fact that "the quality of research is improving" I'm not sure one can blame the limited success of such an approach on previous poor quality research.To close, today is a really, really big day for some of my brood who have their 1st Dan black belt grading. After several years of training, hard work and effort pertinent to their voyages through Shotokan karate it all comes down to examination this evening. Thanks and credit need to go to their Sensei for all their efforts in getting them this far, as well as a certain practitioner who is Shotokan YouTube royalty. Whoever you are, thank you.----------[1] Nevill RE. et al. Meta-analysis of parent-mediated interventions for young children with autism spectrum disorder. Autism. 2016. Nov 14.[2] Oono IP. et al. Parent-mediated early intervention for young children with autism spectrum disorders (ASD). Cochrane Database Syst Rev. 2013 Apr 30;(4):CD009774.[3] Masi A. et al. Predictors of placebo response in pharmacological and dietary supplement treatment trials in pediatric autism spectrum disorder: a meta-analysis. Transl Psychiatry. 2015 Sep 22;5:e640.----------Nevill, R., Lecavalier, L., & Stratis, E. (2016). Meta-analysis of parent-mediated interventions for young children with autism spectrum disorder Autism DOI: 10.1177/1362361316677838... Read more »

  • December 2, 2016
  • 08:30 PM

This Month in Blastocystis Research (NOV 2016)

by Christen Rune Stensvold in Blastocystis Parasite Blog

Lab protocols on Blastocystis culture, cryopreservation, and subtyping are now available in Wiley Online Library.... Read more »

  • December 2, 2016
  • 01:40 PM

Parkour Athletes Teach Scientists about Swinging Apes

by Elizabeth Preston in Inkfish

"I was at a conference, and a colleague was talking about the locomotion of great apes in the trees," says Lewis Halsey, a physiologist at the University of Roehampton in London. The colleague mentioned that it's tough to measure how these animals use energy. That's when Halsey had an epiphany. "I was working with parkour athletes on another project," he says, studying how much energy the athletes used while jumping and climbing around a city. Why not use these human athletes to stand in for... Read more »

  • December 2, 2016
  • 07:48 AM

Case studies: BHD syndrome associated with pulmonary malformation and with lung neoplasm

by Joana Guedes in BHD Research Blog

Matsutani et al. (2016) reported for the first time BHD syndrome accompanied by pulmonary arteriovenous malformation. The patient, a young male with no significant medical history, presented with chest pain. Chest X-ray and CT revealed emphysematous changes in both lungs and a tumour with pleural fluid. A thoracoscopy revealed dark red pleural fluid and multiple cysts in the lung. The tumour lesion was resected and identified as a non-malignant intrapulmonary hematoma caused by a significant haemorrhage in the pulmonary parenchyma, which was diagnosed as intrapulmonary hematoma. ... Read more »

Matsutani, N., Dejima, H., Takahashi, Y., Uehara, H., Iinuma, H., Tanaka, F., & Kawamura, M. (2016) Birt-Hogg-Dube syndrome accompanied by pulmonary arteriovenous malformation. Journal of Thoracic Disease, 8(10). DOI: 10.21037/jtd.2016.09.68  

Gunji-Niitsu, Y., Kumasaka, T., Kitamura, S., Hoshika, Y., Hayashi, T., Tokuda, H., Morita, R., Kobayashi, E., Mitani, K., Kikkawa, M.... (2016) Benign clear cell “sugar” tumor of the lung in a patient with Birt-Hogg-Dubé syndrome: a case report. BMC Medical Genetics, 17(1). DOI: 10.1186/s12881-016-0350-y  

  • December 2, 2016
  • 06:18 AM

Friday Fellow: Indian shot

by Piter Boll in Earthling Nature

by Piter Kehoma Boll Today’s Friday Fellow may not seem to be such an astonishing plant, but it has its peculiarities, some of them quite interesting. Commonly known as Indian shot, African arrowroot, purple arrowroot, and many other names, it … Continue reading →... Read more »

  • December 2, 2016
  • 03:18 AM

The prebiotic galactooligosaccharide (B-GOS) and autism: just add to poo(p)

by Paul Whiteley in Questioning Answers

Yes, it is childish but...With all the continued chatter on a possible role for the collected gut microbiota - those wee beasties that inhabit our deepest, darkest recesses - in relation to some autism (see here for example), the paper by Roberta Grimaldi and colleagues [1] (open-access available here) provides yet more potentially important information.So, poo(p) samples were the starring material in the paper - "obtained from three non-autistic children and three autistic child donors"- and specifically what happened when something called B-GOS "a prebiotic galactooligosaccharide" was added to samples following their journey through a "Three stage continuous culture gut model system" otherwise known as an artificial gut. Said gut model based at Reading University has already been the topic of other news (see here).As well as looking at the initial bacterial profile of those stool samples, researchers plotted the changes to the stool's inhabitants (or what was left of the stool) over the course of B-GOS addition, as well as looking at things like the "production of SCFAs [short-chain fatty acids] in the fermentations" and other metabolites via the gold-standard chemical analytical technique called 1H-NMR (see here for more details).Results: "Consistent with previous studies, the microbiota of ASD [autism spectrum disorder] children contained a higher number of Clostridium spp. and a lower number of bifidobacteria compared to non-autistic children." With the addition of B-GOS to the 'mixture', researchers reported on a significant increase in bifidobacterial populations at the different stages of their gut model and in samples from both those with autism and those without autism. Such "bifidogenic properties of B-GOS" are not unheard of.As to the metabolites of those bacteria present in the poo(p) samples, there were some interesting knock-on effects noted in both raw and B-GOS supplemented samples. "Our data show a lower concentration of butyrate and propionate in autistic models, compared to non-autistic models, but nodifferences in acetate before adding B-GOS into the system." Propionic acid (propionate) has some research history with autism in mind (see here). Butyric acid (butyrate) is something of a rising star in quite a few domains, having also been mentioned in the context of autism too (see here). Indeed it's interesting to note that B-GOS administration "mediated significant production of... butyrate... simulating the transverse and distal colon respectively. There was no effect on propionate." The findings of lower starting levels of butyrate in samples from children with autism were also substantiated by the NMR analyses undertaken. Increases in butyrate and changes to various other metabolites ("increasing ethanol, lactate, acetate and butyrate and decreasing propionate and trimethylamine") were also noted via this analytical method for this group.A long quote coming up: "This in vitro study showed promising and positive results in that supplementing the microbiota of ASD children with 65%B-GOS may manipulate the gut bacterial population and alter metabolic activity towards a configuration that might represent a health benefit to the host. However, further work will be required to assess such changes in an in vivo human intervention study."Just before anyone makes a run on B-GOS or any similar product however, I do need to stress a few important points. First, this was a study of poo(p) samples from 3 autistic children compared with samples from 3 non-autistic children. Aside from the small participant numbers, we don't know anything about participants' various comorbidities (although we know they were "free of any metabolic and gastrointestinal diseases") and only limited information on their dietary habits and medication history. Second, poo(p) was the target material included for analysis and what happened when B-GOS was supplemented during the journey through the artificial gut model. This study said nothing about what happens when real people with autism take B-GOS orally for example, and how it might affect gut bacterial populations and metabolites as it progresses down a real gastrointestinal (GI) tract. This also includes a lack of information on any potential side-effects in a real-world situation. We are also assuming that any supplement survives the stomach. There is quite a bit more to do in this area.But for now, I stick to the idea that the Grimaldi paper provides some potentially important information and certainly, some new routes/methods for further study of the link between prebiotics, probiotics and synbiotics in the context of the gut microbiota and autism...----------[1] Grimaldi R. et al. In vitro fermentation of B-GOS: Impact on faecal bacterial populations and metabolic activity in autistic and non-autistic children. FEMS Microbiol Ecol. 2016 Nov 16. pii: fiw233.----------Grimaldi R, Cela D, Swann JR, Vulevic J, Gibson GR, Tzortzis G, & Costabile A (2016). In vitro fermentation of B-GOS: Impact on faecal bacterial populations and metabolic activity in autistic and non-autistic children. FEMS microbiology ecology PMID: 27856622... Read more »

  • December 1, 2016
  • 04:30 AM

Neurological or Mechanical – Cross-over Effects of Foam Rolling on Ankle Dorsiflexion

by Richard Shaw in Sports Medicine Research (SMR): In the Lab & In the Field

Foam rolling may lead to small improvements in dorsiflexion range of motion in the contralateral limb. ... Read more »

  • December 1, 2016
  • 02:57 AM

Dietary fibre deficiency and gut barrier integrity

by Paul Whiteley in Questioning Answers

"Dietary fiber deprivation, together with a fiber-deprived, mucus-eroding microbiota, promotes greater epithelial access and lethal colitis by the mucosal pathogen, Citrobacter rodentium."So said the findings reported by Mahesh Desai and colleagues [1] meriting an editorial in the publishing journal [2] as the sentiments of 'eating your greens' applies to some rather interesting [mouse] findings.Fibre (UK spelling) comes in various different forms typically categorised as soluble and insoluble depending on their relationship with water. Using a "gnotobiotic mouse model" - where mice were "colonized with a synthetic human gut microbiota composed of fully sequenced commensal bacteria" - Desai et al reported on the effects of different diets with different fibre content. Their results make for important reading as a fibre-deprived gut was associated with the rise of some rather potent bacteria that seemed to enjoy dining out on the "colonic mucus barrier, which serves as a primary defense against enteric pathogens." Yes, mice gut barriers - or some of their components at least - were being eaten by the very bacteria they contain. Enjoy your lunch.I'm not dwelling too much on the Desai findings, bearing in mind their focus on mice not humans, but I do want to raise a couple of potentially relevant points. First is the focus on the intestinal barrier and how that so-called 'leaky gut' seems to show a connection to dietary fibre intake. Yet more research bringing this woo-like term in from the scientific cold (see here). Next is the idea that if the Desai results are transferable from mouse to humans, they could be relevant to quite a lot of people who perhaps don't enjoy as much dietary fibre as they should. Further, there may be particular groups of people who might be particularly prone to a poor diet [3] (see here too) where the already discussed term 'leaky gut' is also relevant (see here); also bringing in the idea of a role for those trillions of wee beasties (the gut microbiota) that call us home.I'll be watching for how this research area pans out...----------[1] Desai MS. et al. A Dietary Fiber-Deprived Gut Microbiota Degrades the Colonic Mucus Barrier and Enhances Pathogen Susceptibility. Cell. 2016 Nov 17;167(5):1339-1353.e21.[2] Gazzaniga FS. & Kasper DL. Veggies and Intact Grains a Day Keep the Pathogens Away. Cell. 2016 Nov 17;167(5):1161-1162.[3] Bandini LG. et al. Changes in Food Selectivity in Children with Autism Spectrum Disorder. J Autism Dev Disord. 2016 Nov 19.----------Desai MS, Seekatz AM, Koropatkin NM, Kamada N, Hickey CA, Wolter M, Pudlo NA, Kitamoto S, Terrapon N, Muller A, Young VB, Henrissat B, Wilmes P, Stappenbeck TS, Núñez G, & Martens EC (2016). A Dietary Fiber-Deprived Gut Microbiota Degrades the Colonic Mucus Barrier and Enhances Pathogen Susceptibility. Cell, 167 (5), 1339-2147483647 PMID: 27863247... Read more »

Desai MS, Seekatz AM, Koropatkin NM, Kamada N, Hickey CA, Wolter M, Pudlo NA, Kitamoto S, Terrapon N, Muller A.... (2016) A Dietary Fiber-Deprived Gut Microbiota Degrades the Colonic Mucus Barrier and Enhances Pathogen Susceptibility. Cell, 167(5), 1339-2147483647. PMID: 27863247  

  • November 30, 2016
  • 01:41 PM

Open and Post Peer Review: New Trends in Open Access Publications

by Nesru Koroso in United Academics

Among the academic community, there a growing feeling that traditional peer review is failing at accomplishing its core objective: ensuring scientific quality.... Read more »

  • November 30, 2016
  • 10:30 AM

Playtime After Training Improves a Dog's Memory

by CAPB in Companion Animal Psychology Blog

Making time for play immediately after a dog training session improves the dog’s memory.New research by Nadja Affenzeller (University of Lincoln) et al investigates whether play following learning leads to better performance the next day. The scientists wanted to know whether this effect, previously found in humans, would also apply to dogs.In people, it is thought that the hormonal response during positive arousal acts on parts of the brain called the hippocampus and amygdala and leads to better memory. The effect applies to a type of memory called declarative memory, which is our memory for facts and events (for example, the President of the United States, or the capital of Denmark).Now we can’t expect dogs to tell us who is the President of the United States, but it is possible to get them to do a task very similar to one used in some of the human memory research: learning to tell the difference between two objects.The results show that the dogs who got to play immediately after learning needed fewer trials in the task the next day, compared to the dogs who had rested instead.First of all, each dog had a pre-training session, in which the dog was taught to approach an object. In the very early stages, food was placed on the object, and when the dog approached, s/he was allowed to eat it.For those interested in the food canine scientists use as rewards, it was either a piece of pork or chicken sausage, depending on the dog’s dietary preferences.In the training session, the dogs were taught to distinguish between two objects and choose the right one by putting their two front paws on a cardboard square on which the object was placed. If they went to the correct object, the researcher clicked and then gave them a reward. If they picked the wrong object, the researcher used a no-reward marker (“wrong” said in a neutral tone of voice).The objects were not things the dogs were used to. There was a blue basket with white dots which contained a layer of woodchips, and a green box with black stripes on that had a layer of cat litter at the bottom.The dogs were trained in sessions of 10 trials, until they had got 80% right in two sessions in a row.Immediately after doing this, dogs either had a play session or a rest session, depending which group they were in.The 8 dogs in the play session had a 10 minute walk to an enclosed area where they had a 10 minute play session, followed by the walk back. Dogs had a choice between fetching a ball or Frisbee, or playing tug.The 8 dogs in the rest session were given a bed to lie on while the owner and researcher engaged in a 30 minute conversation. The researcher kept an eye on the dog and said their name or distracted them to prevent them from going to sleep.The next day, the dogs came back to learn the same task again.Dogs that had taken part in the play session re-learned the object discrimination much more quickly, taking 26 trials on average (plus or minus 6), compared to 43 trials (plus or minus 19) for the dogs who had rested.The researchers took measures of heart rate, which differed between play/rest sessions as you would expect, but otherwise was the same for both groups of dogs. They also found that salivary cortisol was lower after the play sessions, which they found surprising (if you’re interested in salivary cortisol research, see this post by Julie Hecht).19 Labrador Retrievers, aged between 1 and 9 years old, took part. The study focussed only on purebred Labrador Retrievers so that breed could not affect the results. Their prior training levels were also taken into account and evenly distributed across the two groups.This turned out to be important, because the ‘experienced’ dogs who had previously taken part in cognitive tasks like this learned the task much more quickly. The gundogs need more trials, perhaps because they had previous experience of following human cues in the field, which didn’t happen in the lab. Some of the dogs were ‘naïve’ and had only basic obedience, did not work or participate in trials, and had never taken part in similar research before.This shows it is important to take prior training experience into account when designing canine research studies.Three of the dogs had to be excluded (two because of motivation issues, and one because of a preference for one of the objects), so only 16 took part in the full study.The study does not show the mechanism by which memory is improved, but it is thought to relate to the hormones produced during the play session. However, the play also included exercise, and further research is needed to confirm whether it is play per se or exercise that caused the effect.The scientists write,“The results show that engaging in playful activity for 30 min after successfully learning the task improved re-training performance, evidenced by fewer trials needed to meet task criteria 24 h after initial acquisition. This significant difference between the two groups not only suggests that the intervention is affecting long-term memory rather than an improved short-term memory, but also that pleasant arousal post-learning has similar effects on enhancing memory in dogs as it does in humans.” This study asked dogs to discriminate between two objects that looked and smelled different. A similar real-life training task is scent detection. Further research to investigate the best ways to improve performance in the training of scent dogs for drug or explosives detection, or in medical testing, could be very exciting.It’s nice to know another way in which dogs are like people. And next time someone says they’d like to end a dog training session on a positive note, perhaps a game of tug or fetch is in order.If you're interested in the research on dog training, check out my dog training research resources page or my post about why canine science is better than common sense.Reference: Affenzeller, N., Palme, R., & Zulch, H. (2017). Playful activity post-learning improves training performance in Labrador Retriever dogs (Canis lupus familiaris) Physiology & Behavior, 168, 62-73 DOI: 10.1016/j.physbeh.2016.10.014Photos: dezi (top) and Dmussman (both Read more »

  • November 30, 2016
  • 07:00 AM

A Better Model System for Ovarian Cancer: Patient-derived tumor xenografts (PDXs) are suitable for epigenetic methylome-based cancer research

by Tushar Tomar in EpiBeat

Ovarian cancer is the most lethal gynecologic malignancy. After epigenomic analysis of patient tumors, aberrant DNA methylation patterns are universally observed in the most abundant histological subtype of ovarian cancer, high-grade serous ovarian cancer (HGSOC). These epigenetic modifications like DNA methylation are known to frequently affect gene regulation involved in cancer-related processes. Since epigenetic alterations are reversible in nature, these changes have emerged as attractive targets for epigenetic therapy for cancer. However, modelling this cancer type for epigenomic research is a great challenge for preclinical researcher.1 Recent genomic analyses showed that most commonly used HGSOC cell lines, like SKOV3 and A2780, are less representative models of HGSOC. Recently, patient-derived tumor xenografts (PDXs) i.e., patient tumor tissues transplanted directly into immune-deficient mice have appeared as better representative preclinical models than cell lines-based xenograft models. They recapitulate histological type, as well as maintain genomic features and the reminiscent heterogeneity of the corresponding patient’s primary tumor.2 Furthermore, treatment results of ovarian cancer PDXs have a good predictive value for standard platinum-based chemotherapy and novel therapeutic agents. Recently, a panel of about 50 ovarian cancer PDXs with different histological subtypes have been established and genomically characterized for future cancer research at University Medical Centre Groningen, The Netherlands.3 Although several comparative gene expression and mutational studies have been performed for HGSOC PDXs, comparable studies on the epigenome are not yet available.... Read more »

Alkema NG, Wisman GB, van der Zee AG, van Vugt MA, & de Jong S. (2016) Studying platinum sensitivity and resistance in high-grade serous ovarian cancer: Different models for different questions. Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy, 55-69. PMID: 26830315  

Hidalgo M, Amant F, Biankin AV, Budinská E, Byrne AT, Caldas C, Clarke RB, de Jong S, Jonkers J, Mælandsmo GM.... (2014) Patient-derived xenograft models: an emerging platform for translational cancer research. Cancer discovery, 4(9), 998-1013. PMID: 25185190  

  • November 30, 2016
  • 03:10 AM

Restless leg syndrome in parents of children with autism

by Paul Whiteley in Questioning Answers

The findings reported by Maureen Russell and colleagues [1] provide some blogging fodder today and the observation that: "Biological caregivers of children with ASD [autism spectrum disorder] demonstrated a high prevalence of RLS [Restless Legs Syndrome] symptoms and poorer mental health."OK, I know some people might be asking 'just what is Restless Legs Syndrome'? It is a recognised condition complete with 'disease' title (Willis-Ekbom disease). Symptoms, as the name suggests, centre on 'an overwhelming, irresistible urge to move the legs'. But things might not just stop at 'jittery legs' when it comes to this condition, as various other parts of the body can also be involved and indeed, affect important functions such as sleep.Russell et al surveyed 50 biological caregivers (parents) of children diagnosed with an autism spectrum disorder (ASD) with regards to sleep habits "that included RLS as determined by four questions." They also "compared the sleep quality and daytime behaviors of children with ASD in caregivers with and without symptoms of RLS."They observed that just over a fifth of their caregiver cohort "fit the criteria for RLS symptomatology." They also reported that those 'biological caregivers' who reported RLS symptoms also reported "poorer mental health" based on responses to the "Medical Outcomes Survey (MOS) 12-Item Short Form (SF-12)." When it came to offspring parameters, authors reported that: "Caregivers with RLS described more night waking and greater internalized behavior problems in their children with ASD than the caregivers without RLS." They interpret this 'association' in the context that there is a degree of heritability attached to RLS and some of those sleeping issues noted in offspring could mean that the symptoms of RLS are also present in children diagnosed with ASD too.Noting the relatively small scale of the Russell study in participant number terms, the very preliminary method of reporting on mental health and the fact that there isn't a single test for RLS, these are interesting findings. I note the lead author has her PhD online (see here) showing how this research fits into a larger scheme of work on sleep and quality of life in caregivers of children with autism.Looking at the Russell findings in the context of 'hows and whys' there are some potentially important correlations that might be noteworthy. RLS has been linked with the presentation of attention-deficit hyperactivity disorder (ADHD), a not insignificant comorbidity noted in quite a bit of autism (see here). I don't want to make any connections where none might exist but it is reasonable to assume that an over-represented occurrence of ADHD in autism could be important. Insofar as the heritability of ADHD specifically across families, there is more to do in this area but it's not unheard of for ADHD symptoms to be present in other family members including parents. This could impact on the results reported by Russell et al.Although certain medicines have been associated with the symptoms of RLS, there is also a body of peer-reviewed science suggesting that a deficiency in iron might also be important [2]. There is still a degree of debate specifically as to how iron deficiency might 'cause' RLS but one of the primary lines of thinking revolves around how iron is an important co-factor for the biological reactions that turn the amino acid tyrosine [eventually] into the neurotransmitter dopamine. Again, minus any 'I know all the answers' sentiments, iron levels in relation to autism have been a source of some investigation down the years (see here). Some researchers have also talked about maternal iron intake potentially affecting the 'risk' of offspring autism too (see here) (with appropriate caveats).Whatever the reason(s) to account for the Russell findings, there is a requirement for further research in this area, for a start to assess just how prevalent RLS might be in both people diagnosed on the autism spectrum and their significant others. Knowing how much comorbidity seems to follow a diagnosis of autism (see here) I wouldn't be surprised to see yet another connection; this one however, might provide some rather important clues as to overlapping genetics and biology...Music, and Gotye still has an amazing song...----------[1] Russell M. et al. Symptoms of Restless Legs Syndrome in Biological Caregivers of Children with Autism Spectrum Disorders. J Clin Sleep Med. 2016 Oct 28. pii: jc-00043-16.[2] Li X. et al. Brain iron deficiency in idiopathic restless legs syndrome measured by quantitative magnetic susceptibility at 7 tesla. Sleep Med. 2016 Jun;22:75-82.----------Russell M, Baldwin C, McClain D, Matthews N, Smith C, & Quan SF (2016). Symptoms of Restless Legs Syndrome in Biological Caregivers of Children with Autism Spectrum Disorders. Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine PMID: 27855729... Read more »

Russell M, Baldwin C, McClain D, Matthews N, Smith C, & Quan SF. (2016) Symptoms of Restless Legs Syndrome in Biological Caregivers of Children with Autism Spectrum Disorders. Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine. PMID: 27855729  

  • November 30, 2016
  • 02:00 AM

Chemical games and the origin of life from prebiotic RNA

by Eric Bolo in Evolutionary Games Group

From bacteria to vertebrates, life — as we know it today — relies on complex molecular interactions, the intricacies of which science has not fully untangled. But for all its complexity, life always requires two essential abilities. Organisms need to preserve their genetic information and reproduce. In our own cells, these tasks are assigned to […]... Read more »

Yeates JA, Hilbe C, Zwick M, Nowak MA, & Lehman N. (2016) Dynamics of prebiotic RNA reproduction illuminated by chemical game theory. Proceedings of the National Academy of Sciences of the United States of America, 113(18), 5030-5. PMID: 27091972  

  • November 29, 2016
  • 01:36 PM

Open Access article processing charges: a new serial publication crisis?

by SciELO in SciELO in Perspective

The financial and ethical implications that emerge from open access publishing through article processing fees in India are analyzed in a study that proposes the creation of a national open access journal platform such as SciELO in order to reduce costs, increase efficiency and facilitate the sharing of metadata among repositories. … Read More →... Read more »

  • November 29, 2016
  • 11:24 AM

Your Brain On God: Reward and Motivation

by William Yates, M.D. in Brain Posts

William James authored a seminal book titled The Varieties of Religious Experience: A Study in Human Nature that was published in 1902.In this work, James reviewed the nature of religious experiences and noted a lack of scientific inquiry into this human phenomenon.James would have been extremely interested in a recent scientific inquiry into the religious experience from brain researchers at the University of Utah and Harvard University.In this study, functional magnetic resonance imaging (fMRI) was used to study the brain during a religious experience cue in a group of 19 individuals who were devout Mormons.The key elements of this study design included:Subjects: 19 young adults (7 female, 12 male) reporting weekly church attendance and daily experience of spirtitual feelingsExperimental cues: Control cues: resting state and audiovisual control. Religious experience cues: quotations from religious authorities, a period of prayer and scripture readingBrain imaging/analysis: Standard fMRI imaging using a 3T MRI scanner with analysis of areas of activation with religious experience compared with control activationsThe research team was able to identify significant brain regional areas of activation with religious cue stimulation.The authors summarized their finding in the discussion section of the manuscript:"We demonstrated in a group of devout Mormons that religious experience, identified as "feeling the Spirit," was associated with consistent brain activation across individuals within bilateral nucleus accumbens, frontal attentional, and ventromedial prefrontal cortical loci."The figure above notes the location of the key nucleus accumbens region of the brain known to be important in the brain reward response network. This brain region has been identified as a key region activated by a variety of reward experiences including feeling love, music appreciation and the euphoria associated with euphoric states induced by stimulants such as cocaine and methamphetamine.The authors propose that the observed activation of the frontal and prefrontal cortex regions may indicate a network that includes individual perception of salience of religious experience and "representation of affective meaning for the religious stimuli".This is an important study of brain effects of the religious experience. The results show exposure to religious stimuli in devout individuals activates a non-specific powerful reward response. This reward response may contribute to the motivational mechanism for doctrinal beliefs and church attendance.It is likely this type of response is not limited to devout Mormons but similar in other Christian believers and non-Christian believers where a "spiritual experience" is part of the religious experience.Readers with more interest in this research can access the full free-text manuscript by clicking on the PMID link in the citation below.Figure is an iPad screenshot from the app 3D Brain.Follow me on Twitter @WRY999Ferguson MA, Nielsen JA, King JB, Dai L, Giangrasso DM, Holman R, Korenberg JR, & Anderson JS (2016). Reward, Salience, and Attentional Networks are Activated by Religious Experience in Devout Mormons. Social neuroscience PMID: 27834117... Read more »

Ferguson MA, Nielsen JA, King JB, Dai L, Giangrasso DM, Holman R, Korenberg JR, & Anderson JS. (2016) Reward, Salience, and Attentional Networks are Activated by Religious Experience in Devout Mormons. Social neuroscience. PMID: 27834117  

  • November 29, 2016
  • 07:02 AM

Simultaneous Submillimeter and Hard X-Ray Intermittent Processes during Flares by Guillermo Giménez de Castro et al.*

by CESRA in Solar Radio Science

Intermittency is a disruptive characteristic of a process, which can be associated, in many cases, with a sudden energy release. Intermittency is a key characteristic of flares that should become evident in the flux time evolution at many different wavelengths. We investigate the similarities and differences of the intermittency during [...]... Read more »

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