Post List

  • May 20, 2017
  • 06:12 AM
  • 103 views

Gastrin-releasing peptide and autism continued

by Paul Whiteley in Questioning Answers

Yet another 'continued' or 'part 2' short post for you today, building on some previous - very preliminary research - talking about the use of gastrin-releasing peptide (GRP) and autism (see here).The authors included on the paper by Josemar Marchezan and colleagues [1] are familiar ones to this part of the autism research landscape as per the other occasions that members of this group have looked at / talked about GRP and autism in the peer-reviewed domain.GRP is all about a compound that 'does what it says on the tin' insofar as stimulating the release of gastrin from specialist cells in the stomach. This in turn leads to the secretion of gastric acid among other things and onward aids the digestion of food.This time around Marchezan et al describe the results of a controlled trial on the use of GRP (vs. placebo) in a small group of boys (N=10) diagnosed with autism. This is a step-up from their previous research efforts in this area talking about a case series report and an open (non-blinded, non-placeboed?) study. Participants were given the same amount of GRP (160 pmol/kg) over the same number of days (4 consecutive days) as that detailed in their previous studies. This time around, the Aberrant Behavior Checklist (ABC) scale was the outcome measure of choice.Results: well, let's put it one way, they weren't exactly astounding in terms of any positive effects from the use of GRP over such a short space of time. This was exemplified by the authors use of "no statistical difference" when it came to looking at quite a lot of the data obtained during the investigation comparing GRP to placebo. On the plus side there were "no adverse effects, changes in vital signs, or laboratory abnormalities associated with the use of GRP" so the whole 'first do no harm' bit seems to be intact, at least in the short-term.Whilst it would be easy to sweep such results under the 'did not work' carpet, I am however minded to go with the authors' suggestion that "further research with other designs and a larger sample size to evaluate the efficacy and safety of GRP in children with autism" would be a step forward. I say this on the basis that hypochlorhydria - low levels of gastric acid - is not something completely unknown to parts of the autism spectrum (see here) and does suggest some *possible* involvement for something like GRP in specific cases of autism.----------[1] Marchezan J. et al. A Placebo-Controlled Crossover Trial of Gastrin-Releasing Peptide in Childhood Autism. Clin Neuropharmacol. 2017 Apr 27.----------Marchezan, J., Becker, M., Schwartsmann, G., Ohlweiler, L., Roesler, R., Renck, L., Gonçalves, M., Ranzan, J., & Riesgo, R. (2017). A Placebo-Controlled Crossover Trial of Gastrin-Releasing Peptide in Childhood Autism Clinical Neuropharmacology DOI: 10.1097/WNF.0000000000000213... Read more »

Marchezan, J., Becker, M., Schwartsmann, G., Ohlweiler, L., Roesler, R., Renck, L., Gonçalves, M., Ranzan, J., & Riesgo, R. (2017) A Placebo-Controlled Crossover Trial of Gastrin-Releasing Peptide in Childhood Autism. Clinical Neuropharmacology, 1. DOI: 10.1097/WNF.0000000000000213  

  • May 19, 2017
  • 10:21 PM
  • 83 views

The warmer the dangerouser, at least if you are a caterpillar

by Piter Boll in Earthling Nature

by Piter Kehoma Boll Scientist all over the world agree that species diversity is higher at the tropics than at polar regions, i.e., the closer you get to the equator, more species you will find. But apart from making food … Continue reading →... Read more »

Roslin, T., Hardwick, B., Novotny, V., Petry, W., Andrew, N., Asmus, A., Barrio, I., Basset, Y., Boesing, A., Bonebrake, T.... (2017) Higher predation risk for insect prey at low latitudes and elevations. Science, 356(6339), 742-744. DOI: 10.1126/science.aaj1631  

  • May 19, 2017
  • 07:00 AM
  • 88 views

Friday Fellow: Common Stinkhorn

by Piter Boll in Earthling Nature

by Piter Kehoma Boll Today things are getting sort of pornographic again. Some time ago I introduced a plant whose flowers resemble a woman’s vulva, the asian pigeonwing, and now is time to look at something of the other sex. … Continue reading →... Read more »

  • May 19, 2017
  • 05:13 AM
  • 102 views

Characterization of a FLCN mutation associated with RCC

by Joana Guedes in BHD Research Blog

Mutations in the FLCN gene are the cause of Birt-Hogg-Dubé (BHD) syndrome, a rare disease characterized by renal cell carcinoma (RCC), pneumothorax and fibrofolliculomas. In their new study, Bartram et al. (2017) identify a heterozygous mutation in the FLCN gene in a patient with RCC. DNA from tumour and a metastasis was analysed and the authors demonstrated skipping of exon 11 as the consequence of this mutation leading to a shift in the reading frame and the insertion of a premature stop codon. The FLCN protein was still expressed but it was strongly destabilized and had a different subcellular localization. Both altered protein stability and subcellular localization could be partly reversed by blocking proteasomal and lysosomal degradation.... Read more »

Bartram MP, Mishra T, Reintjes N, Fabretti F, Gharbi H, Adam AC, Göbel H, Franke M, Schermer B, Haneder S.... (2017) Characterization of a splice-site mutation in the tumor suppressor gene FLCN associated with renal cancer. BMC medical genetics, 18(1), 53. PMID: 28499369  

  • May 19, 2017
  • 04:26 AM
  • 90 views

Injury risk and ADHD: part 2

by Paul Whiteley in Questioning Answers

Consider this short post a sort of follow-on to a previous entry on this blog concerning the elevated risk of injury following a diagnosis of attention-deficit hyperactivity disorder (ADHD). The paper in question today is that by Wu-Chien Chien and colleagues [1] who yet again [2], brought the quite significant scientific weight of the "National Health Insurance Research Database in Taiwan" to bear on this topic.In this latest paper, Chien et al relied on data from a 'subset' of the main insurance research database and found some not unexpected things: "The patients with ADHD had a 143% increased risk of overall injuries than the controls after considering all the confounding factors" and "the use of methylphenidate was associated with a 22.6% decrease in the risk of injuries in the patients with ADHD."What's more to say? Well, yet again risk of adverse issues *correlating* with a diagnosis of ADHD comes to the forefront (see here for another example). Yet again the idea that 'tackling' ADHD is a worthy goal (for many reasons) if not only to mitigate such elevated risks being presented, bearing in mind that medication "approved solely for ADHD treatment" is not some sort of magic bullet [3]. There are also other potentially important intervention options to look at (see here for example). I'm minded at this point to also bring in the recent findings reported by Borschuk and colleagues [4] talking about how comorbid asthma accompanying ADHD (yes, there is a surprisingly strong relationship between the two diagnoses) might play a role in the expression of ADHD and onwards provide some 'interesting' directions when it comes to tackling ADHD and it's elevated risk for various adverse outcomes...To close, appreciating a talent...----------[1] Chien WC. et al. The risk of injury in adults with attention-deficit hyperactivity disorder: A nationwide, matched-cohort, population-based study in Taiwan. Res Dev Disabil. 2017 Apr 27;65:57-73.[2] Kang JH. et al. Attention-deficit/hyperactivity disorder increased the risk of injury: a population-based follow-up study. Acta Paediatr. 2013 Jun;102(6):640-3.[3] Fleming M. et al. Educational and Health Outcomes of Children Treated for Attention-Deficit/Hyperactivity Disorder. JAMA Pediatr. 2017. May 1.[4] Borschuk AP. et al. The influence of comorbid asthma on the severity of symptoms in children with attention-deficit hyperactivity disorder. J Asthma. 2017 May 1:1-7.----------Chien WC, Chung CH, Lin FH, Yeh CB, Huang SY, Lu RB, Chang HA, Kao YC, Chiang WS, Chou YC, Tsao CH, Wu YF, & Tzeng NS (2017). The risk of injury in adults with attention-deficit hyperactivity disorder: A nationwide, matched-cohort, population-based study in Taiwan. Research in developmental disabilities, 65, 57-73 PMID: 28458048... Read more »

  • May 18, 2017
  • 04:40 AM
  • 103 views

On vaccinated and un-vaccinated homeschooled children: the disappearing-reappearing-disappearing-reappearing studies

by Paul Whiteley in Questioning Answers

I originally began writing this post in the last week of November 2016 following first sight of the study abstract by Anthony Mawson and colleagues [1] and their journey into a topic that has had its fair share of discussion/argument* (*delete as appropriate) with autism in mind down the years: are vaccines or immunisation patterns potentially linked to [some] autism?As it happened, this post was shelved for some time because (a) only an abstract appeared despite a publication date accompanying the initial open-access submission in a Frontiers journal and (b) the subsequent sudden disappearance of the abstract from the publishers website following some discussions on social media about the paper and the review process (see here and see here for more information).The study then appeared in a different journal (April 2017) before once again disappearing.Now it's back - for now - in the same journal, so once again it's fodder for this blog...As I always do when it comes to any chatter specifically on this topic, I should reiterate a few things: (a) the prime directive of this blog - no clinical or medical advice is given or intended - and (b) that vaccines save lives. I know some people attribute other factors to that 'life-saving' angle when it comes to vaccines over the longer term (better health, better environment, etc), but one really only needs to look at the protective effect of the various meningitis vaccines for example, to see their results in something like real-time. I repeat again: vaccines save lives.What however does seem to be missing from at least some of the general discussion about vaccines as a whole and their very positive health effects is the fact that they are medicines. As such they are not somehow impervious to potentially producing side-effects for some people, albeit a small proportion of people who use them. The problem at the moment is, that we don't really know everything there is to know about which people might be at greater risk of side-effects than others (although some clues are emerging) and importantly, how all those side-effects may manifest. Science - metabolomic science - is however starting to tackle some aspects of these issues [2] minus too much hype at the present time.As per the title of this post, Mawson et al set about examining whether there were differences between those children who were vaccinated and those un-vaccinated across "a broad range of health outcomes." In line with the previous history hypothesising about autism and specific vaccination, the authors focused on any 'association' between vaccination status and neurodevelopmental disorders (NDD) taking into account other potentially confounding variables.The source data for those vaccinated / un-vaccinated children participants (N=666) was an anonymous online questionnaire completed by mothers of children who were members of various homeschooling organisations in four regions of the United States. Homeschooling refers to a situation where a child is educated at home outside of the mainstream education system choices. Homeschoolers were selected for study because, according to the authors, a "higher proportion are unvaccinated compared to public school children."Results: around 40% of the participants were indeed described as un-vaccinated in the Mawson cohort. This is quite a bit higher than other estimates [3] specifically looking at homeschooled children. Then to some of the details: "Vaccinated children were significantly less likely than the unvaccinated to have been diagnosed with chickenpox and pertussis." If you needed more evidence that vaccines work, that last sentence kinda provides you with it, particularly in light of what diseases like pertussis can potentially do to the most vulnerable.And then some potential controversies: vaccinated children were significantly more likely to have been diagnosed with pneumonia, otitis media, allergies and NDDs (defined as autism spectrum disorder, attention deficit hyperactivity disorder, and/or a learning disability). After some statistical adjustment for potentially confounding variables, authors reported that "vaccination, nonwhite race, and male gender were significantly associated with NDD after controlling for other factors." I might also draw your attention to the reported finding that: "preterm birth and vaccination combined was strongly associated with NDD in the final adjusted model with interaction, more than doubling the odds of NDD compared to vaccination alone." This might suggest that there are synergistic variables at work influencing any identified risk continuing a research theme [4]. Indeed, the same authors have devoted a whole other article to this finding [5] (this paper also went through the same disappearing-reappearing act too).Wearing the objective blinkers of science, this is by no means perfect research. Not only are there potential issues related to the use of an on-line questionnaire (and anonymous at that), the focus on subjective reports over inspection of more objective medical records (even though parents were asked to obtain and use their child's vaccination record(s) when completing the questionnaire), and problems associated with recall (including possible telescoping effects), there are a whole host of other issues that one could cite in relation to such research and potential biases that could/might have influenced the results (including factors such as this one). I might also add that the Mawson study did not appear to 'name names' when it came to which individual vaccines may or may not have been involved in their findings despite asking questions about if and when specific immunisations were administered to participants. Indeed authors noted: "We did not set out to test a specific hypothesis about the association between vaccination and health." Then there is also the 'reaction' angle to papers such as this one to mention; bearing in mind that science these days does not exist in some sort of social/cultural vacuum as per other very recent and very relevant examples. Cumulatively, you can see that there ... Read more »

Anthony R Mawson, Brian D Ray, Azad R Bhuiyan, & Binu Jacob. (2017) Pilot comparative study on the health of vaccinated and unvaccinated 6- to 12-year-old U.S. children. Journal of Translational Science. info:/10.15761/JTS.1000186

  • May 17, 2017
  • 03:08 PM
  • 134 views

Paper About Plagiarism Contains Plagiarism

by Neuroskeptic in Neuroskeptic_Discover

Regular readers will know that I have an interest in plagiarism. Today I discovered an amusing case of plagiarism in a paper about plagiarism.

The paper is called The confounding factors leading to plagiarism in academic writing and some suggested remedies. It recently appeared in the Journal of the Pakistan Medical Association (JPMA) and it's written by two Saudi Arabia-based authors, Salman Yousuf Guraya and Shaista Salman Guraya.



Here's an example of the plagiarism: a 2015 paper by ... Read more »

  • May 17, 2017
  • 12:00 PM
  • 110 views

Epigenetic Marks Associated to Severe Obesity

by Delphine Fradin in EpiBeat

There is growing evidence that DNA methylation might contribute to obesity. Candidate gene methylation studies in animal models and humans have demonstrated methylation changes in promoters of various genes that are implicated in obesity, appetite control and/or metabolism, insulin signaling, immunity, growth and circadian clock regulation.

Severe obesity in children is defined as greater than or equal to 99th percentile of body mass index (BMI) for age and gender or a BMI z-score ≥3.5. Population surveys demonstrate a significant increase in obesity prevalence among children, where severe obesity is the most rapidly growing paediatric obesity subgroup. Compared to youth with BMI in the obese range, those with severe obesity have higher rates of immediate and long-term diseases. It stands to reason that youth with obesity and severe obesity may also differ in aetiological factors and consequences, including epigenetic.... Read more »

Fradin, D., Boëlle, P., Belot, M., Lachaux, F., Tost, J., Besse, C., Deleuze, J., De Filippo, G., & Bougnères, P. (2017) Genome-Wide Methylation Analysis Identifies Specific Epigenetic Marks In Severely Obese Children. Scientific Reports, 46311. DOI: 10.1038/srep46311  

  • May 17, 2017
  • 11:24 AM
  • 107 views

Dad's Impact in Infant Development

by William Yates, M.D. in Brain Posts

Mother's interaction with their infants play a key role in infant development.The independent role of fathers in infant development is less well known and studied.A recent study from the United Kingdom supports a important role for father-child interactions in infant development.Here are the main elements of the design of this study:Subjects: Families of infants with typical deliveries were recruited from maternity wards in two hospitals in the United Kingdom.Design: Home assessments were completed at 3 months and 24 months following birth making this a longitudinal study design. Assesment at 3 months included observation of father-child interaction.Key outcome measures: 24 month score on the Mental Development Index (MDI) of the Bayley Scales of Infant DevelopmentStatistical analysis: Correlational analysis of paternal interaction measures at 3 and 24 months was completed. Additionally, independent simple linear analyses and PROCESS macro tool modeling were done to examine effects of covariates.The important finding from the study was that paternal-infant interaction at 3 months of age predicted important dimensions of infant mental development.Fathers who demonstrated more engagement, sensitivity and less control at 3 months had infants with greater scores on the Mental Development Index at 24 months.That authors note in the discussion section "The results of this study indicate that specific dimensions of father-child interactions at both time points are associated with MDI scores even when adjusting for paternal depression, age and education, and maternal sensitivity and infant age."The take home message in this study is that Dad's make a difference in infant development. As the authors note, supporting paternal interaction may be a key prevention measure in infant development.Readers with more interest in this study can access the free full-text manuscript by clicking on the PMID link in the citation below.Follow me on Twitter @WRY999Photo of paternal spider monkey and infant is from my photography files. Follow me on Instagram at WRY999You can find all my Brain Post blog posts and highlight Twitter posts on my Facebook Page Neuroscience Medicine.Sethna V, Perry E, Domoney J, Iles J, Psychogiou L, Rowbotham NEL, Stein A, Murray L, & Ramchandani PG (2017). FATHER-CHILD INTERACTIONS AT 3 MONTHS AND 24 MONTHS: CONTRIBUTIONS TO CHILDREN'S COGNITIVE DEVELOPMENT AT 24 MONTHS. Infant mental health journal PMID: 28449355... Read more »

  • May 17, 2017
  • 07:02 AM
  • 96 views

Those who only kill children are neuro-psychologically different from other murderers

by Doug Keene in The Jury Room

Of course it isn’t a surprise that they are gravely disturbed, but who knew it was neuropsychological?  This is an article from researchers at Northwestern University and looks very specifically at similarities and differences in the neuropsychological test scores of those who killed only children and those who killed some adults as well as children. […]... Read more »

Azores-Gococo, N., Brook, M., Teralandur, S., & Hanlon, R. (2017) Killing A Child. Criminal Justice and Behavior., 2147483647. DOI: 10.1177/0093854817699437  

  • May 17, 2017
  • 04:30 AM
  • 98 views

Another Feather in the Cap of the FIFA 11 Injury Prevention Program

by Kyle Harris in Sports Medicine Research (SMR): In the Lab & In the Field

Implementing the FIFA 11 injury prevention program decreases the risk of injury among collegiate male soccer players.... Read more »

Silvers-Granelli HJ, Bizzini M, Arundale A, Mandelbaum BR, & Snyder-Mackler L. (2017) Does the FIFA 11  Injury Prevention Program Reduce the Incidence of ACL Injury in Male Soccer Players?. Clinical orthopaedics and related research. PMID: 28389864  

  • May 17, 2017
  • 04:20 AM
  • 95 views

Carbon nanotubes, what are they good for?

by kylius wilkins in It Ain't Magic

Kylius Wilkins talks to Urs Frey and his paper that described his recent success manufacturing carbon nanotubes (CNTs).... Read more »

  • May 17, 2017
  • 02:48 AM
  • 77 views

EEG abnormalities and "high functioning" autism

by Paul Whiteley in Questioning Answers

I'm not a great fan of the term 'functioning' when it comes to autism (see here) hence the quote marks around high-functioning in the title of this post. Yes, I understand the message that it's trying to convey and that we don't have viable alternatives at the moment. It just however seems a little sweeping in terms of 'generalised' describing and labelling of people...No mind. Today I'd like to bring the paper by Özdem Ertürk Çetin and colleagues [1] to your attention and the observation that their results "support the fact that EEG abnormalities are observed at a higher rate also in ASD [autism spectrum disorder] with a better functionality." EEG - electroencephalographic or electroencephalogram - refers to the recording of electrical activity in the brain. Although in small amounts, our cells use electrical signals to message each other; said activity in the brain can be picked up and recorded using some rather sensitive equipment. EEGs are the method of choice when it comes to investigating epilepsy or related seizure disorders (such conditions are epitomised by abnormal electrical activity between cells).The connection between autism and epilepsy / seizure disorder is one that has persisted for many years (see here); even now to the point where research is starting to talk about autism / autistic traits being a feature of some cases of epilepsy (see here). Quite a bit of the research looking at autism and epilepsy has tended to suggest that epilepsy may be a little more over-represented for those towards the more severe end of the autism spectrum (i.e. in relation to presentation of symptoms and the presence of some degree of learning / intellectual disability). The Ertürk Çetin findings report that even in those with described 'better functionality' there may be disturbances in relation to the measurement of EEGs.Looking for "the presence of EEG abnormalities in sixteen children diagnosed with high-functioning ASD" researchers reported that whilst none of the participants had clinical seizures (the overt expression of epilepsy) "5 patients (31.3%) were detected to have EEG abnormalities." Bearing in mind the quite small participant numbers and the fact that no control groups (asymptomatic or otherwise) were included for comparisons, this is quite an important finding. I agree with the authors when they say that: "The potential impact of EEG abnormalities on cognition and behavior, and the risk of epilepsy should be considered during long-term follow-up of these patients." In other words, whenever a diagnosis of autism or ASD is received, one should always consider the possibility that a heightened risk of epilepsy / seizure / abnormal EEG patterns might also be a feature of presentation irrespective of "functioning" status.----------[1] Ertürk Çetin Ö. et al. EEG abnormalities and long term seizure outcome in high functioning autism. Acta Neurol Belg. 2017 Apr 26.----------Ertürk Çetin Ö, Korkmaz B, Alev G, & Demirbilek V (2017). EEG abnormalities and long term seizure outcome in high functioning autism. Acta neurologica Belgica PMID: 28447214... Read more »

  • May 16, 2017
  • 10:15 AM
  • 109 views

Fatal Attraction: Praying Mantises (A Guest Post)

by Miss Behavior in The Scorpion and the Frog

By Britta Bibbo We all know the character: an incredibly beautiful woman that seduces the rough-and-tumble action hero, only for him to later find himself chained up over a lava pit with sharks in it! …Or something like that. A “femme fatal” is the idea of a beautiful woman who leads men to their demise. None are more perfect for this role than the female praying mantis. Praying mantis females practice the art of deception through sexual cannibalism. It’s exactly how it sounds: the male is attracted to the female and tries to make some babies, but instead ends up being devoured. Sexual cannibalism hardly seems like a good strategy for keeping the mantis population up, but some argue it’s merely females taking advantage of every scrap of food they can find… even if it’s a loving male. False garden mantis (Pseudomantis albofimbriata). Image by Donald Hobern from Wikimedia Commons.When male mantises encounter a female in the wild they only have one thing on the brain, while a female may be more interested in self-preservation. If she hasn’t encountered food for a few days she will be VERY hungry and not all that interested in mating; in many species of mantises it is known that female mantises will eat males, even while having sex! So how do female mantises attract males? For most insects, females are able to attract males with pheromones, chemicals released from an individual that affect other individuals of the same species. For instance, females can emit pheromones that will be telling of their age, reproductive status, and body condition. Males are able to detect pheromones from great distances and these pheromones play a role in allowing a male to determine how attractive a female could be. Before any sexy time can begin, females have to show that they are open to male advances. Showing a male you’ve never met before that you’re interested can be a difficult task- so females typically emit pheromones that are known as honest signals. These signals accurately convey female interest in mating, as well as her reproductive status, age, and body condition. Because the majority of females are being honest, males don’t have to think twice about their mate’s intentions. This is where female deception comes into play. If a female takes advantage of the lack of male wariness, she could end up with an easy meal. This deception by the females is what scientists know as the Femme Fatale hypothesis. This hypothesis explains that female mantises are naturally selected to deceive male mantises, and exploit them as food. This idea hasn’t had much backing evidence until Dr. Kate Barry of Macquarie University in Sydney, Australia sought to test this hypothesis with the false garden mantis (Pseudomantis albofimbriata). After considering the test subjects and how the mantises communicate, Kate expected one of three possible outcomes: 1. There will be no pattern between female hunger and male attraction (if female false garden mantises are not femme fatales and false garden mantis pheromones do not communicate feeding-related information). 2. The well-fed females will attract the most males, while hungry females will attract the fewest males (if female false garden mantises are not femme fatales and females are always honest about their quality and willingness to mate). 3. The hungriest females will attract the most males, while well-fed females will still attract some males (if female false garden mantises are femme fatales and females are dishonest about their quality and willingness to mate when they are hungry). To test her expectations, Kate gathered juvenile mantises that were close to their adult forms to have many male and female mantises that have no previous mating experience. Once the mantises were adults, females were given different feeding regimens to have a range of hunger. Categories included Good (well-fed), Medium (slightly less fed), Poor (hungry), and Very Poor (very, very hungry). Adult mantises were housed in a circular cage that separated each female individually around the edge, while the males were kept in the center. Diagram of cage experiment was conducted in. Image by Britta Bibbo.To allow the males to smell the female pheromones, researchers separated males by special walls that the males could not see through, but could still detect the pheromones given off by a female. The number of males on a female’s side of the cage was used to measure how attractive her pheromones were to the males. The results of this study concluded that pheromones produced by the females that were very hungry were the most attractive to males. Through deception, the hungriest females are seen as sexier than well-fed, healthy females that are willing to mate! This result is surprising; normally females that are well-fed are seen as “sexier” because they have more nutrients available to them, making them more fertile. Hungry females have fewer nutrients available to them, making them less fertile, and therefore not as “sexy”. These hungry female mantises are advertising themselves as well-fed, fertile, and ready to rock when really, they’re not. Simply put, these results show that males are being catfished, and then consumed. Whether hungry females are actively trying to deceive males or if it’s just coincidental still needs to be looked into, but for now, be thankful for a partner who will see you as more than just a piece of meat! Literature Cited:Barry, K. (2014). Sexual deception in a cannibalistic mating system? Testing the Femme Fatale hypothesis Proceedings of the Royal Society B: Biological Sciences, 282 (1800), 20141428-20141428 DOI: 10.1098/rspb.2014.1428 ... Read more »

  • May 16, 2017
  • 07:04 AM
  • 18 views

Comparison of alternative zebra-structure models in solar radio emission by G.P. Chernov et al.*

by CESRA in Solar Radio Science

Discussion about the nature of zebra-structure (ZS) in type IV radio bursts continues, despite the ten proposed models. First of all, this is due to the wide variety of stripes in each new phenomenon, making the explanation of all the fine details by any one mechanism becomes impossible. The most widespread explanation is the emission at different levels of double plasma resonance (DPR), sequential on the height surfaces in the magnetic [...]... Read more »

G. P. Chernov, V. V. Fomichev, & R. A. Sych. (2017) Comparison of alternative zebra-structure models in solar radio emission. submitted to Astronomy Letter Journal. arXiv: 1704.02528v1

  • May 16, 2017
  • 05:02 AM
  • 97 views

IMFAR, the autism numbers game and 12% showing 'optimal outcome'

by Paul Whiteley in Questioning Answers

A post recently published on the Spectrum website led to my blogging entry today, and the observation that: 'Alternative screen finds high autism prevalence in U.S. state'.Discussing results delivered at IMFAR 2017 the research in question was that presented by Laura Carpenter and colleagues [1] (someone with quite a track record in autism research). This was a conference presentation and seemingly not yet peer-reviewed publication, so one needs to be a little cautious about making big claims just yet. That being said, there have been research hints that these results would be forthcoming [2] around this time.The headline finding was that the prevalence of autism spectrum disorder (ASD) in one particular part of the United States for the birth year 2004 was probably quite a bit higher than that previously reported/estimated based on initial screening for possible ASD and then actual assessment. Details of the initiative used in this research - the South Carolina Children’s Educational Surveillance Study (SUCCESS) - can be found here.Some 4100 children were "screened for ASD using the Social Communication Questionnaire." Those who were deemed 'at risk' for autism and a small proportion of those not hitting those *might be autism* thresholds were asked back for a more detailed interview. Although the number of children actually followed-up and interviewed who were eligible for further assessment was not particularly great, the authors were able to draw up an estimated prevalence of autism based on those who did complete the study. The figure: "ASD prevalence in this sample is 3.62%" roughly equivalent to 1 in 28 children. I say this in the context that in the United States and elsewhere, autism rates and/or numbers of cases are still high (see here and see here) and acknowledgement of the implications of such increases when it comes to services such as education, healthcare and the like.The Spectrum article focuses quite a bit on the participation rate noted in the Carpenter study but another snippet of information is also included in the conference abstract that is worthy of discussion. A detail that reads: "Six children (6/52; 12%) had a clear developmental history of ASD but did not display clinically significant symptoms at the time of participation in this study." Further: "12% with a history of ASD no longer had significant ASD-related symptoms, providing further support for the potential for optimal outcomes in some individuals."I'm rather interested in that 12% figure with 'optimal outcome'. Optimal outcome describes cases where a clear indication/diagnosis of autism has been seen/received, but for whatever reason(s) diagnostic thresholds are not longer met at a future assessment point. I've covered this group quite a few times on this blog, most notably in relation to a previous estimate of 9% of those diagnosed with autism potentially falling into this category (see here). Appreciating that such data challenges the assumption that *all* autism is a lifelong condition (indeed, stretching across the entire autism spectrum - see here), I'd reiterate that those described as being 'optimal outcomers' represent an important subgroup on the autism spectrum in these days of plural autisms (see here). Not least is the question: Why? Why do these children not maintain their diagnosis and what lessons (if any) can be learned for the wider autism spectrum, particularly also in the context that various quite disabling comorbidities might also be 'reduced' alongside core autism symptoms in this group.We await formal peer-reviewed publication of the Carpenter findings and perhaps some further details.To close, upon introducing my brood to the music of Kate Bush, I am yet again reminded just how good a singer/performer she really is...----------[1] Carpenter LA. et al. The Prevalence of Autism Spectrum Disorder in School Aged Children: Population Based Screening and Direct Assessment. IMFAR 2017.[2] Carpenter LA. et al. Screening and direct assessment methodology to determine the prevalence of autism spectrum disorders. Ann Epidemiol. 2016 Jun;26(6):395-400.----------Carpenter LA, Boan AD, Wahlquist AE, Cohen A, Charles J, Jenner W, & Bradley CC (2016). Screening and direct assessment methodology to determine the prevalence of autism spectrum disorders. Annals of epidemiology, 26 (6), 395-400 PMID: 27230493... Read more »

Carpenter LA, Boan AD, Wahlquist AE, Cohen A, Charles J, Jenner W, & Bradley CC. (2016) Screening and direct assessment methodology to determine the prevalence of autism spectrum disorders. Annals of epidemiology, 26(6), 395-400. PMID: 27230493  

  • May 15, 2017
  • 04:33 AM
  • 123 views

Intestinal dysbiosis, irritable bowel syndrome and ME/CFS

by Paul Whiteley in Questioning Answers

I don't want to spend too much time talking about yet another paper from the research tag-team that is Hornig & Lipkin [1] (open-access) on the topic of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). But this latest addition to their research repertoire (see here) is deserving of several comments.Not least are the observations made by the authors - including one Brent Williams who some might remember from autism research history (see here) and Jose Montoya who has also made a mark in CFS/ME research circles (see here) - on how the collected wee beasties that inhabit our gastrointestinal (GI) tract might have some role to play when it comes to at least some cases of CFS/ME. Yes it's gut microbiome research time again.The press release accompanying the paper by Dorottya Nagy-Szakal and colleagues can be seen here. The long-and-short of it was that: "Independent of IBS [irritable bowel syndrome], ME/CFS is associated with dysbiosis and distinct bacterial metabolic disturbances that may influence disease severity." Further: "Plasma cytokines did not define ME/CFS disease groups in our cohort." There could be some good reasons for that last sentence looking at immune-related molecules on the basis of other study results (see here) but further investigations are required.I have to say that outside of the observations that particular types of bacteria seem to be more or less prevalent in cases of CFS/ME (yet again) I was rather more interested in the finding that over 40% of the cohort also met criteria for IBS. I say that on the basis that I've already talked about 'abdominal discomfort syndrome' as a feature of some CFS/ME (see here) alongside findings that certain foods *might* also play a role in the bowel symptoms accompanying CFS/ME (see here).In these days of increasing pluralisation of spectrums (the autisms, the schizophrenias, etc) it is probably also quite useful to think about pluralising the diagnostic label CFS/ME too. Assuming we can get the diagnostic criteria right (see here) we could have a phenotype of CFS/ME that, for example, has a stronger bowel-related clinical signature than other forms. The further implications that the GI tract might play a role in CFS/ME in relation to either primary or secondary symptoms might also inform intervention. So, we kinda know that use of probiotics might be something to think about for some cases of IBS (see here). There is also some preliminary evidence that certain probiotics might also impact on some of the 'psychological' features (careful with that term) which can accompany CFS/ME [2]. The possibility of connections exist and therefore require further scientific exploration.----------[1] Nagy-Szakal D. et al. Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome. Microbiome. 2017; 5: 44.[2] Rao AV. et al. A randomized, double-blind, placebo-controlled pilot study of a probiotic in emotional symptoms of chronic fatigue syndrome. Gut Pathog. 2009 Mar 19;1(1):6.----------Nagy-Szakal D, Williams BL, Mishra N, Che X, Lee B, Bateman L, Klimas NG, Komaroff AL, Levine S, Montoya JG, Peterson DL, Ramanan D, Jain K, Eddy ML, Hornig M, & Lipkin WI (2017). Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome. Microbiome, 5 (1) PMID: 28441964... Read more »

Nagy-Szakal D, Williams BL, Mishra N, Che X, Lee B, Bateman L, Klimas NG, Komaroff AL, Levine S, Montoya JG.... (2017) Fecal metagenomic profiles in subgroups of patients with myalgic encephalomyelitis/chronic fatigue syndrome. Microbiome, 5(1), 44. PMID: 28441964  

  • May 15, 2017
  • 12:29 AM
  • 8 views

Looking for Empathy in All the Wrong Places: Bizarre Cases of Factitious Disorder

by The Neurocritic in The Neurocritic

art by Zdzisław Beksiński Factitious disorder is a rare psychiatric condition where an individual deliberately induces or fabricates an ailment because of a desire to fulfill the role of a sick person. This differs from garden variety malingering, where an individual feigns illness for secondary gain (drug seeking, financial gain, avoidance of work, etc.). The primary goal in factitious disorder is to garner attention and sympathy from caregivers and medical staff.The psychiatric handbook DSM-5 identifies two types of factitious disorder: Factitious Disorder Imposed on Self (formerly known as Munchausen syndrome when the feigned symptoms were physical, rather than psychological).  Factitious Disorder Imposed on Another: When an individual falsifies illness in another, whether that be a child, pet or older adult (formerly known as Munchausen syndrome by proxy).Since the desire to elicit empathy is one of the main objectives in this disorder, it is odd indeed when the “patient” feigns a frightening or repellent condition. A recent report by Fischer et al. (2016) discussed a particularly flagrant example: the case of a middle-aged man who falsely claimed to be a sexually sadistic serial killer to impress his psychotherapist. Not surprisingly, his ruse was a complete failure.The case report noted that Mr. S had been a loner his entire life: ... He described having anxiety growing up, mainly in social situations. ... Mr. S had a history of alcohol abuse starting in his mid-twenties and continuing into his early forties. He denied any significant medical history. He denied legal difficulties, psychiatric hospitalizations, and suicide attempts. He was single, had never been married, had no children, and reported having only one close friend for most of his life. He never had a close long-term romantic relationship and stated a clear preference for living a solitary life. Mr. S had served in the military but did not see combat, and afterwards worked the graveyard shift as a security guard (all the better to avoid people).One year prior to his admission to the psychiatric hospital, Mr. S sought outpatient therapy for depression and engaged in weekly supportive psychotherapy with a young female psychology intern. His psychiatrist started an SSRI antidepressant and a low dose of antipsychotic medication for “depression with psychotic features.” Mr. S's alleged psychosis consisted of “voices” of crowds of people saying things that he could not make out, which he experienced while working the night shift. He consistently attended his therapy sessions and was noted to be making progress. However, several months into his therapy, Mr. S told his therapist that he had been involved in of military combat and described himself as a decorated war hero. After several therapy sessions in which he [falsely] recounted his combat experiences, Mr. S was queried as to whether he ever killed anyone, to which Mr. S replied, “During the military or after the military?” He then told his therapist that he had followed, raped, and killed numerous women during the 20 years since leaving the military.He recounted his imaginary crimes to the young female intern:Mr. S reported that he would follow a potential female victim for several months before raping and strangling her to death with a rope. Although he claimed to rape and kill the women, he did not describe any sexual arousal from the subjugation, torture, or killing of his alleged victims. He refused to disclose how many women he had killed, where he had killed them, or how he had disposed of their bodies. He described having purchased various supplies to aid in abduction, which he kept in the back of his van while cruising for victims. These supplies included rope and two identical sets of clothes and shoes to help evade detection by the police. He described using various techniques to track his victims, as well as evade surveillance of his activities. He informed his therapist that he was actively following a woman he had encountered in a local public library several days earlier. Mr. S acknowledged that he studied the modus operandi of famous sexually sadistic serial killers by reading books. The patient's therapist, feeling frightened and threatened by these disclosures, transferred his case to her supervisor, who then saw the patient for a few therapy sessions. Mr. S reported worsening depression, hearing more “voices,” and attempting to self-amputate his leg using a tourniquet. Consequently, Mr. S was involuntarily detained as a “danger to self” and “danger to others” for evaluation in the local psychiatric hospital.He was diagnosed with major depressive disorder, single episode, unspecified severity, with psychotic features. His routine physical, neurological exam, and lab work all yielded normal results. ...The inpatient treatment team contacted the District Attorney's office in order to file for continued involuntary hospitalization due to the patient's homicidal ideation and history of violence. Subsequent police investigation and review of records could not substantiate any of the patient's claims of committing multiple homicides in the Pacific Northwest.. . .After the District Attorney accepted the application for the prolonged involuntary civil commitment (180-day hold), Mr. S was confronted with the inconsistencies between his self-reported symptoms and objective findings and the failure to corroborate his claims of prior homicides. In response, Mr. S then confessed that he “had made the whole thing up…about the killings…all of it” because he “wanted attention.” He said that he had never followed, raped, or killed anyone and never had an intention to do so. He said that he did not know why he claimed this, other than an “impulse came over me and I acted on it.” His false identity as a serial killer backfired, and he couldn't understand why his therapist had discontinued their sessions:He had believed that his feigned history and symptomatology would make him a “more interesting” patient to his therapist. He reported feeling rejected when his therapist transferred his care to her supervisor. He had little insight into why his therapist may have been frightened by his behavior. Mr. S revealed that following his initial fabrications, and despite his initial involuntary hospitalization, he had felt too embarrassed to admit the truth.His original diagnosis was revised to “factitious disorder with psychological symptoms, and cluster A traits (particularly schizoid and schizotypal traits) without meeting criteria for any one specific personality disorder.” Because of these personality traits, he had no insight into why his therapist might feel threatened by his terrifying stories. There are at least two other papers describing cases of factitious disorder with repugnant feigned symptoms: one reported a case of factitious pedophilia, and the other reported a case of factitious homicidal ideation.Thanks to Dr. Tannahill Glen for the link.References... Read more »

Porter, T., & Feldman, M. (2011) A Case of Factitious Pedophilia. Journal of Forensic Sciences, 56(5), 1380-1382. DOI: 10.1111/j.1556-4029.2011.01804.x  

Thompson CR, & Beckson M. (2004) A case of factitious homicidal ideation. The journal of the American Academy of Psychiatry and the Law, 32(3), 277-81. PMID: 15515916  

  • May 13, 2017
  • 04:42 AM
  • 160 views

Welcoming zonulin into autism research

by Paul Whiteley in Questioning Answers

I was VERY happy to read the paper published by Erman Esnafoglu and colleagues [1] suggesting that: "zonulin, which regulates intestinal permeability, plays a role in the development of symptoms of ASD [autism spectrum disorder]."Zonulin - something that "can be used as a biomarker of impaired gut barrier function for several autoimmune, neurodegenerative, and tumoral diseases" [2] - is a compound that I've been interested in for a while on this and other blogs (see here). The primary reason for the interest is that connection to intestinal permeability and how 'leaky gut' may well show some relevance to some autism (see here and see here). The thing that was up-to-now missing from the research chatter about intestinal hyperpermeability and autism was the measurement of zonulin on the basis that elevated levels of zonulin show a connection to dietary elements such as gliadin (a facet of gluten) [3]. This is particularly relevant because previous data has observed a possible link between use of a gluten-free diet and a reduction in intestinal permeability in relation to autism [4]. All this is [peer-reviewed] research music to my ears (see here)...Esnafoglu et al set about measuring serum levels of zonulin in 32 participants diagnosed with an autism spectrum disorder (ASD) compared with 33 not-autism controls. Yet again, the words 'healthy controls' are used by the authors to define the control group and yet again, the assumption is that those participants with autism are somehow 'unhealthy'. Researchers, please just call it what it is: not-autism controls (the term 'neurotypical' also tells us nothing about control groups either). Measurement of zonulin was via ELISA (enzyme-linked immunosorbent assay) and researchers also threw in a measure of autism severity based on use of the Childhood Autism Rating Scale (CARS).Results: well, the results seemed to be in the expected direction: "Serum zonulin levels were significantly higher in the patients with ASD (122.3 ± 98.46 ng/mL) compared with the healthy controls (41.89 ± 45.83 ng/mL)." Authors also identified a fairly healthy correlation between the CARS score and zonulin levels. These results imply that issues with intestinal permeability - leaky gut - seem to be present in relation to at least some autism. A shocker, I know.Obviously there is more research to do in this area; not least to increase the sample size, look at dietary intake/status as a function of zonulin measurement and explore the possibility that the genetics of zonulin production might also be *involved* in some autism [5]. I might add that other research on zonulin in relation to diagnoses not necessarily uncommon to autism might also be revealing (see here).Insofar as what to do about elevations in zonulin as and when detected in cases of autism, well the dietary link to zonulin production implies that the horror that is a gluten-free (GF) diet might be something to consider. The suggestion of a 'bacterial link' to zonulin production also suggests another possible intervention target in these days of gut microbiomes and autism (see here) although I think we have to be slightly careful about the use of some preparations. There is also another avenue for research speculation based on the development of zonulin (receptor) inhibitors such as Larazotide acetate [6] (otherwise known as AT-1001). With no medical or clinical advice given or intended, the evidence base for this zonulin-affecting compound is looking promising [7] with much more to come...In conclusion, zonulin has arrived on the autism research scene, and I'm expecting to see more peer-reviewed science on this topic in future times. Intestinal hyperpermeability, diet and [some] autism looks to be squarely back on the research agenda.----------[1] Esnafoglu E. et al. Increased Serum Zonulin Levels as an Intestinal Permeability Marker in Autistic Subjects. J Pediatrics. 2017. May 11.[2] Fasano A. Zonulin, regulation of tight junctions, and autoimmune diseases. Annals of the New York Academy of Sciences. 2012; 1258(1) :25-33.[3] Lammers KM. et al. Gliadin induces an increase in intestinal permeability and zonulin release by binding to the chemokine receptor CXCR3. Gastroenterology. 2008 Jul;135(1):194-204.e3.[4] de Magistris L. et al. Alterations of the intestinal barrier in patients with autism spectrum disorders and in their first-degree relatives. J Pediatr Gastroenterol Nutr. 2010 Oct;51(4):418-24.[5] Tripathi A. et al. Identification of human zonulin, a physiological modulator of tight junctions, as prehaptoglobin-2. Proc Natl Acad Sci U S A. 2009 Sep 29;106(39):16799-804.[6] Fasano A. Intestinal Permeability and its Regulation by Zonulin: Diagnostic and Therapeutic Implications. Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association. 2012;10(10):1096-1100.[7] Leffler DA. et al. Larazotide Acetate for Persistent Symptoms of Celiac Disease Despite a Gluten-Free Diet: A Randomized Controlled Trial. Gastroenterology. 2015; 148: 1311-1319.----------Esnafoglu, E., Cırrık, S., Ayyıldız, S., Erdil, A., Ertürk, E., Daglı, A., & Noyan, T. (2017). Increased Serum Zonulin Levels as an Intestinal Permeability Marker in Autistic Subjects The Journal of Pediatrics DOI: 10.1016/j.jpeds.2017.04.004... Read more »

Esnafoglu, E., Cırrık, S., Ayyıldız, S., Erdil, A., Ertürk, E., Daglı, A., & Noyan, T. (2017) Increased Serum Zonulin Levels as an Intestinal Permeability Marker in Autistic Subjects. The Journal of Pediatrics. DOI: 10.1016/j.jpeds.2017.04.004  

  • May 12, 2017
  • 10:43 AM
  • 141 views

A Cuttlefish Clash: The Strongest, Stripeyist Guy Gets the Girl

by Melissa Chernick in Science Storiented

I know what you’re thinking: “Why hasn’t she written about cuttlefish mating systems?” I understand, cuttlefish are ridiculously cool and you just need to know more about them. You are in luck as a brand new study has been published online about just that topic!Cuttlefish are cephalopods, which are all predatory marine animals that have at least eight arms, a siphon for jet-propulsion, and highly developed nervous and sensory systems (specifically the most sophisticated eye of all invertebrates). Those last characteristics make them highly intelligent, with complex learning behavior, to the point that many consider them to be “conscious.” Unlike other cephalopods, all of their hard parts (if any) are internal. That means all of their outside parts are soft, squishy and covered in color-changing skin. Their ability to change color is absolutely amazing, particularly in cuttlefish (just google ‘Flamboyant Cuttlefish’!). Located in their skin are tons of chromatophores (pigment filled bags) that expand or contract to reveal/hide their color. And it’s crazy-fast too. They can alter their appearance in as little as half a second! They use this color change for camouflage, courtship rituals, or just to show you how they feel about you interrupting them with your dive camera (a little personal experience with a mama octopus thrown in there).Cuttlefish are in the clade Coloidea that also includes squid and octopuses, and a sister group to the Nautilus. They look like squid but have stouter bodies and a fin fringe that runs around their body that they undulate to move. They have separate sexes and an often elaborate courtship ritual. Should a female find a male worthy, she accepts his spermatophore (sperm packet), which he transfers to her with a specially modified arm (hectocotylus). Then the females will use the contents of this packet to fertilize their eggs and lay them in clusters. Cuttlefish can be seasonal in their mating habits, with some species gathering in the hundreds to find their special someone. Where animals gather to mate, they also gather to strut their stuff. One of the ways they do this is through shear brawn. Basically, the strongest guy gets the girl. A study currently in press in The American Naturalist describes competition between male cuttlefish. Males compete vigorously for female mates. The researchers took a close look at the Common Cuttlefish (Sepia officinalis), a species “renowned for its visual capabilities, rapid adaptive camouflage, learning, and memory.” All those amazing qualities and yet oddly lacking in its ability to identify individual mates or rivals. Seriously, telling boy from girl is a challenge. This means that they must use a signal-response system to recognize each other. This system employs the use of intense zebra-stripe displays. Respond to a zebra with a zebra and you are male. If you don’t want to fight, darken your whole body (sign of alarm), ink and jet away. But extend your fourth arm, darken the skin around your eyes, and dilate your pupils and you know that shit is about to get real: inking, swiping, grappling, lunging, rolling, and biting. An all-out cuttlefish brawl.A lot of this information is known from lab studies of cuttlefish, but how do they act in their natural environment. To test this, the researchers went to the Aegean Sea near Çeşmealtı, Turkey and filmed a bunch of cuttlefish. They brought the footage back to the lab to analyze mate guarding and fighting behaviors, frequencies of a series of agnoistic behaviors in individual males, and aggressive behaviors (e.g., bar room brawl scenario). Since it all starts with the zebra stripes, they also compared the intensity between males. They found a generalized sequence of events that correlated to the amount of aggression. For example, just a dark ring around the eye is low-level aggression, adding a dilated pupil ramps it up to medium-level aggression, intensifying the zebra pattern and arching and tilting the body ramps it up even more. The more medium- to high-level aggressive behaviors the more likely the male was to win. The researchers summarize it this way: “weak zebra banding, fourth arm extension, dark eye ring > dark eye ring with dilated pupil, dark face, strong zebra banding, inking > intense zebra display > swiping, grappling > biting, rolling.” This makes sense if you think about it. Fighting may result in injury and injury is costly, sometimes fatal. So you need to make sure you can win. The series of stages allow each male to assess both themselves and their opponent to see if an actual brawl is worth it.Now, take what you’ve just learned and apply it to this video. It shows exactly the type of bout the authors describe. You may need to watch it twice, once to read the descriptions of what is going on and another to watch for the subtle differences described above. Can you see the color and eye changes? Just imagine what we will find out as camera systems get faster. Considering the extremely fast rate at which cuttlefish are able to change their colors, it is very likely that we are missing a lot of the more subtle details in communications between males (and probably with females too). We’ll have to revisit this subject in the future.Allen, J., Akkaynak, D., Schnell, A., & Hanlon, R. (2017). Dramatic Fighting by Male Cuttlefish for a Female Mate The American Naturalist DOI: 10.1086/692009Learn more about Cephalopods at the University of California Berkeley’s Museum of Palentology and the Monterey Bay AquariumImage from the Monterey Bay Aquarium... Read more »

Allen, J., Akkaynak, D., Schnell, A., & Hanlon, R. (2017) Dramatic Fighting by Male Cuttlefish for a Female Mate. The American Naturalist. DOI: 10.1086/692009  

join us!

Do you write about peer-reviewed research in your blog? Use ResearchBlogging.org to make it easy for your readers — and others from around the world — to find your serious posts about academic research.

If you don't have a blog, you can still use our site to learn about fascinating developments in cutting-edge research from around the world.

Register Now

Research Blogging is powered by SRI Technology.

To learn more, visit http://selfregulationinstitute.org/.