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  • March 26, 2017
  • 08:27 AM
  • 16 views

Multilingual neuromyths

by Madalena Cruz-Ferreira in Being Multilingual

P { margin-bottom: 0.08in; } Neuromyths are misconceptions about how the brain works. They are the topic of the Nature Neuroscience editorial The mythical brain, which highlights that they are as false as they are appealing, and that their appeal is what explains their resilience.Appealing seems to be the key word here, in its sense of ‘engaging’ with little or no rational engagement. Deena Skolnick Weisberg and colleagues showed this in The seductive allure of neuroscience explanations: when asked to choose between alternative nonsensical explanations of the same brain function, their informants systematically preferred the ones containing “logically irrelevant neuroscience information”. The mere mention of intimidating concepts like brain or neurology appears to lend credibility to any statement where they appear, in other words. Statements about the so-called ‘bilingual/multilingual brain’ are no exception, in the wake of the current exponential growth of academic and media news about brains and neuro-prefixed things. This growth reflects a shift in our ways of thinking about our brain along the past couple of decades. Late last century’s trends modelled the brain on the most sophisticated information gathering and processing device of the time, the computer. Since models naturally constrain our ways of thinking about what we’re modelling, our views of the brain came complete with computer-bound characteristics: brain space got allocated once and for all, and brains developed one way, towards decay. Related neuromyths had it that more than one language takes up brain space, or that aged brains lose language learning abilities. Early 21st century findings then spelled the death of brain death myths: ageing, which is what the brain and the rest of our bodies do from the moment we’re born, doesn’t entail brain decay. Brains were all but static, degenerative, limited-capacity CPUs: neural structures and functions evolve and regenerate themselves after all, in response to our experiences and needs, and both young and old brains retain the agility to do so. Brain plasticity duly became the new mantra and, not least, we could capture brains in action through imaging, our latest model. Related neuromyths have it that we now know what’s going on because we can see it, as Leonid Rozenblit and Frank Keil argue in The misunderstood limits of folk science: an illusion of explanatory depth. They show first, that we are experts at fooling ourselves that we “understand complex phenomena with far greater precision, coherence, and depth” than we actually do, and second, that “The illusion for explanatory knowledge is most robust where the environment supports real-time explanations with visible mechanisms.”Image © Thomas Schultz (Wikimedia Commons)Likewise, in What can functional neuroimaging tell the experimental psychologist?, Richard Henson warns us of the “real danger that pictures of blobs on brains seduce one into thinking that we can now directly observe psychological processes”. Blob-based evidence nevertheless continues to flourish, all the way from forensics, as Richard K. Sherwin observes in Visual jurisprudence, to education, as Sanne Dekker and colleagues show in Neuromyths in education: Prevalence and predictors of misconceptions among teachers or Paul A. Howard-Jones shows in Neuroscience and education: myths and messages. The seductive appeal of visual animations is irresistible, in sum, and it naturally sells very well, which is the topic of Diane M. Beck’s study The appeal of the brain in the popular press. But there are two problems. One is that the seduction is selective. Is it true, for example, that there is a bilingual/multilingual ‘advantage’, which may include inhibition of brain deterioration? Ellen Bialystok and colleagues say yes in Bilingualism, aging, and cognitive control: Evidence from the Simon Task, Shanna Kousaie and Natalie A. Phillips say no in Ageing and bilingualism: Absence of a “bilingual advantage” in Stroop interference in a nonimmigrant sample, and J. Bruce Morton and Sarah N. Harper, in What did Simon say? Revisiting the bilingual advantage, reserve judgement about whether multilingualism relates to brain performance at all until we understand what is really causing what. Meanwhile, Angela de Bruin and colleagues, in Cognitive Advantage in Bilingualism. An Example of Publication Bias?, conducted a meta-analysis of studies published between 1999 and 2012 on the so-called ‘bilingual advantage’, to conclude that the advantage may well lie in cherry-picking of findings. A recent issue of the Applied Psycholinguistics journal, dedicated to Bilingualism and neuroplasticity, reviews what (little) we know about this topic, but the myth that multilingualism is ‘good for your brain’ goes on making headlines: it’s simply too appealing to not be true. Apparently, it doesn’t sell to popularise research finding that multilingual brains may be as exciting as monolingual ones – which I, for one, find extremely appealing. The other problem is that academic and media reports don’t speak the same language. Media headlines stating that multilingualism “keeps the brain young” or that you should learn a new language in order to “boost your brain power”, though claiming to draw on scientific research on languages and brains, in fact misrepresent actual findings to go on feeding current neuromyths. In my academic courses, in one of the assignments that became most popular among students, I had them search for wow! media headlines about multilingualism, retrieve the original studies quoted in those pieces, and assess matches between headline and content of the piece, on the one hand, and content of the piece and the studies, on the other. Expectedly, very few matches were found. And unfortunately, given that academic publications aren’t regularly made available outside of academia, very few of us are able to judge for ourselves spin cycles and hype of this kind. Simple repetition of appealing myths doesn’t turn them into facts.Keeping (somewhat) to the topic of what we like to believe, my next post departs from the adult world to check out how children look at their own multilingualism. ... Read more »

Beck, D. (2010) The Appeal of the Brain in the Popular Press. Perspectives on Psychological Science, 5(6), 762-766. DOI: 10.1177/1745691610388779  

  • March 25, 2017
  • 10:32 PM
  • 30 views

Is global warming causing the increase in prevlance of diabetes?

by Craig Payne in Its a Foot Captain, But Not as You Know It

Is global warming causing the increase in the prevalence of diabetes?... Read more »

  • March 25, 2017
  • 02:39 PM
  • 42 views

Shaking dinosaur hips and messing with their heads

by Piter Boll in Earthling Nature

by Piter Kehoma Boll This week brought astonishing news regarding the phylogeny of dinosaurus, as you perhaps have heard or read. New anatomical evidences have completely rebuilt the basis of the dinosaur family tree and I’m here to explain a … Continue reading →... Read more »

  • March 25, 2017
  • 01:14 PM
  • 11 views

The multilingual scapegoat

by Madalena Cruz-Ferreira in Being Multilingual

P { margin-bottom: 0.08in; } Scapegoating has historically been instrumental in alleviating consciences. The fact that scapegoating, as historically, has had no effect whatsoever on what caused those consciences to become burdened in the first place doesn’t seem to deter its continued practice.Multilingualism has served as a handy goat candidate for a good while now. In typically recurrent scenarios, if a child presents with a (suspected) language-related disorder, and that child is multilingual, then the child’s multilingualism is to blame for the disorder. It happened in my family, too. A few weeks into one of my children’s first preschool experience, her teachers reported to me their concern about her behavioural issues. Among other things, she preferred to entertain herself on her own rather than seeking group play, she grabbed at the faces of both children and adults who addressed her, and she was disruptive at story time, when everyone sat on the floor around the reader. The teachers completed their report by sternly advising me that the burden, as they put it, of dealing with two languages from birth might well have started taking its toll on her. You may have guessed what was really going on: the specialist test that I requested at the next paediatric check-up showed that my girl had 40% deafness. If you can’t hear in an environment meant for typical hearing, if you need to have other people face you when they talk to you in order to lip-read and, likewise, if you can’t see their lowered faces when they’re reading to you, my child’s behaviour becomes no issue after all. Throughout my children’s early schooling years, other rounds of this Blame Multilingualism game only served to confirm that the multilingual scapegoat, like its predecessors, didn’t arise out of inherent goat properties but out of our propensity to explain what we don’t understand by means of what we understand even less. In the words of David L. Rosenhan’s report On being sane in insane places: “Whenever the ratio of what is known to what needs to be known approaches zero, we tend to invent ‘knowledge’ and assume that we understand more than we actually do. We seem unable to acknowledge that we simply don’t know.”The reason we don’t understand multilingualism is that we refuse to deal with it as multilingualism: we prefer to check it out as an indicator of (in)conformity to other linguistic behaviours, as is evident from the profuse academic and lay literature reporting findings about multilingualism through the bias of monolingual lenses. Taking other-than-multilingual as a norm expectedly results in assessments of multilingualism as ‘special’, whether special-bad or special-good. Special things demand explanations which depart from the ‘ordinary’ explanatory norms which made them special, and thus self-fulfil their special status. Add to this our readiness to explain things by means of causality, and we’re ready to conclude that some of us are special because we’re multilinguals.Blaming multilingualism for a (suspected) problem is equivalent in practice to diagnosing people with multilingualism. Multilingualism is a problem and must therefore be banished: that’s why so many of us, parents, educators, clinicians, advise monolingualism as a cure. Proclaiming that we’ve found an answer to a problem has an immediate effect, which is to stop asking questions, our own and especially others’: our quest is ended and we may sleep with a clear conscience. Anything, in other words, feels and looks better than simply acknowledging our ignorance. This is why typically developing multilingual children continue to be over-referred to specialist care, wasting precious time as well as human and financial resources. Not to speak of the stigma attached to those diagnosed as ‘special’, of course. As Rosenhan’s unsettling study crucially found, simply entering the special care circle is enough to confirm that special care was needed in the first place, and so that the special diagnosis was warranted: once a special label sticks to you, whatever you do will serve as proof that you deserved to be labelled.Mythologies typically generate their own evidence in this way. This is why scapegoating goes on saving both our faces P { margin-bottom: 0.08in; }and our prejudices. Is it so that we care more for upholding our ingrained beliefs than for the people who come to us for help? What seems to matter is to make the stray sheep return to the normality fold of our collective imaginary: what matters is conformity to an illusionary norm. As Thomas Szasz compellingly shows in The Manufacture of Madness, “Safety lies in similarity”.Believing that multilingualism is the problem further prevents us from accepting it as a norm in itself, blinding us to disordered multilingualism. As Annick De Houwer, Marc H. Bornstein and Diane L. Putnick argue in A bilingual-monolingual comparison of young children’s vocabulary size, if there are any concerns about bi-/multilingual children’s language development, “reasons other than their bilingualism should be investigated.”Next time, I’ll keep to matters of gathering knowledge about multilingualism.... Read more »

  • March 25, 2017
  • 01:06 PM
  • 11 views

Native multilinguals

by Madalena Cruz-Ferreira in Being Multilingual

P { margin-bottom: 0.08in; } Some of my language teaching students sometimes express out loud their heartfelt desire to become native speakers. I was quite baffled the first time I heard this: we’re all native speakers, surely, and we can’t become natives, if we take the word “native” to mean what I supposed it is meant to mean, ‘from birth’. But does it? It turned out that my students’ previous teacher training had included the mantra that “native” means ‘flawless’ in this collocation, and flawless, whatever we take this word to mean, is certainly something that all of us can at least aspire to become. This latter meaning of the word “native” has in fact been made quite explicit in the literature about “second” (or “foreign”) languages – with my profuse apologies for the scare quotes that will crop up all over this post: I’ve no idea what the scared words might mean, in this literature. This meaning explains, for example, why some of us think it a worthwhile endeavour to compare school language learners to “native speakers”, for purposes of language quality assessment. But there is a snag: if learning languages from birth entails flawless use of those languages, how come multilinguals across the board, including simultaneous multilinguals who learn more than one language from Day One, go on being compared to “native speakers”? The thing is that “native speaker” has yet a third meaning, ‘monolingual’, this time a covert one, which nevertheless heeds the overt, systematic practice of comparing any multilinguals to monolinguals. This meaning explains, for example, the virtual absence of acknowledgement that multilinguals can be “native” users of their languages. If we accept that multilingual proficiency should be assessed through comparison with “native” proficiency, then we’re saying that multilinguals and natives are two distinct kinds of language users, since we can’t compare a thing to itself.But there is another snag. If multilinguals aren’t native users of their languages, then they must be “non-native”, by the logic of the assumedly useful labels which populate research on language uses. However, they aren’t, because multilinguals get compared to non-natives, too. In addition, simultaneous multilinguals can’t be “non-native”, if their languages are there for them from Day One, which is one of the meanings of “native”. Multilinguals, in sum, appear to inhabit a Linguistic No Man’s Land.“Day One”, unfortunately, may not be what clinches the issue either. If the language(s) in which we’re brought up from birth happen to be imported languages, then those languages aren’t “ours”. And if we learn a new language in early childhood, though not exactly from Day One, how many days should we count to count as a native user of it? Can I, for example, claim French as native language, having lived with it from just before age 3? Or was I then already way past my native learning prime, as I must have been when I learned my other languages several years later? If you’re interested in the mysteries of “critical periods” which snipe at “native” language learning abilities, Carmen Muñoz and David Singleton’s state of the art discussion, A critical review of age-related research on L2 ultimate attainment, is a must-read. Scare-quoted terminological acrobatics about multilingualism would be hilarious, of course, if it didn’t appear in “serious” research, thereby proving that we’ve no idea what we’re talking about. Have a look in my article First language acquisition and teaching, to see what I mean. The muddle got compounded when researchers developed a preference for labelling the languages of a multilingual by means of numbers, possibly on the belief that identifying things by numbers makes them look scientifically unquestionable. There’s always some “L1” lurking in there somewhere, which means that there must be rankings of L2, ... Ln, where the numbers apparently serve the purpose of showing that languages either politely follow one another or should do so. But what do these numbers mean when, say, simultaneous multilinguals learn one or more new languages in school? Not much, it seems, because we prefer to stick to labels rather than acknowledge their undefinable uselessness. Since “L1” represents an inherently singular concept (in more than one sense of “singular”), the logic of cardinal and ordinal numbering requires that L1 = “first language”, whereby everyone must have a single “first” language, endowed with rights of primogeniture associated with other firstborns. If there’s no single chronological first language, no problem: we just assign one to children, for reasons of administrative expediency, and call it their “mother tongue”. Finally, by the logic that first = “best”, we end up talking about “dominant” and “balanced” languages, and about all the other hopeless labels which do no more than betray our hopeless beliefs that multilinguals are, in fact, funny monolinguals. This state of affairs may well explain why multilingualism goes on being blamed for anything that deviates from monolingualism, to which I’ll return some other day. Meanwhile, the next post, a guest post, goes back to where this post started, to report vivid encounters with “nativeness” from a language teacher who’s also had plenty of reasons to wonder about the meaning of this word.... Read more »

  • March 25, 2017
  • 12:40 PM
  • 12 views

Sign-speech multilinguals

by Madalena Cruz-Ferreira in Being Multilingual

P { margin-bottom: 0.08in; } Opinions and decisions about multilingualism involving sign languages suffer from the same resilient fantasies which have plagued multilingualism in general over the past 100 years or so. With sign languages, however, there’s the aggravating factor that fantasies about them join the chorus. Only the other week, for example, I had a couple of (speech-speech) multilingual friends wonder why all the fuss about sign languages among linguists like me, since these languages are but a set of universal gestural primitives, like rubbing your tummy to indicate you’re hungry, as they put it. Aren’t they?, they nevertheless asked at the end of their reasoning. No, I replied. This would be roughly equivalent to saying that spoken languages are but a set of universal groany primitives to indicate your mood, as I put it. I took this chance to dispel their other illusion, that sign languages are straightforward fingerspelling systems, which draws on the interesting assumption that all signers must be literate. Many sign languages do include fingerspelling components, but the fact that, say, BSL (British Sign Language) and ASL (American Sign Language) use two-handed and one-handed spelling, respectively, for the same printed language, should help reassess the presumed straightforwardness of fingerspelling. In addition, BSL and ASL are as mutually unintelligible as other sign languages around the world. My friends are well educated, cosmopolitan professionals. Their take reflects the overarching myth that sign languages really aren’t languages at all, which goes on shaping policies devised by other professionals, those who have been empowered to deal with language education and who therefore aren’t in the habit of asking questions at the end of their reasonings. In a book chapter discussing The British Sign Language community up to the early 1990s, Paddy Ladd gives a distressing review of the ignorance and associated prejudice which, among other rulings, sanctioned physical violence to ‘cure’ deaf children of their signing ‘compulsion’. Just like, as I reported elsewhere, multilingualism came to be beaten out of hearing schoolchildren, the hands of deaf schoolchildren were tied behind their backs in order to force them to use spoken language. Just like, as I also reported elsewhere, multilingualism came to be medicalised, the language of deaf people was “pathologised” (Ladd’s word). Small wonder, then, that sign-speech multilinguals came to be viewed as doubly ‘handicapped’. When sign languages finally became legitimised, as it were, as objects of linguistic enquiry, sign multilingualism turned out, unsurprisingly, to match speech multilingualism. It comes complete with mixes, as David Quinto-Pozos reports for LSM (Lengua de Señas Mexicana) and ASL in Sign language contact and interference, for example, and with a lingua franca, International Sign, which Anja Hiddinga and Onno Crasborn discuss in Signed languages and globalization. But sign multilingualism remained the business of signers, so hearing communities needn’t bother with the eccentricities of deaf communities. Dealing with sign-speech multilingualism, however, appears to invite regression to hand-tied Fantasy Land: sign languages may be languages after all, but they are less so than spoken ones and should therefore not take priority in (so-called) multilingual education. It may help to understand that we’re talking about difference here, not winner-takes-it-all competition of gradable merits. It is as useful to compare the contexts of use of distinct linguistic modes as it’s useful to compare multilinguals and monolinguals. Insisting on doing so fails to recognise one of the many paradoxes reflecting our perennial difficulty in defining what languages are: do we want to say that speech beats sign, hands down, because we’re persuaded that auditory resources rank higher than visual ones in linguistic sophistication? Or should we rank those resources the other way around, because we believe that spoken languages are subsidiary to spelt ones? Language is as independent of the modes we’ve found to represent it – whether natural, sense-bound ones like sight, hearing, touch, or artificial ones like print – as music is independent of the instruments (our voice included) through which we produce it. What’s more, our senses seldom serve us to the exclusion of other senses. Manual gestures, for example, are intrinsic to spoken interaction, where attention to both visual and sound clues necessarily assists (de)coding. There’s even evidence that adequate gesturing enhances learning, as Martha W. Alibali and colleagues showed for a speech-based maths class in Students learn more when their teacher has learned to gesture effectively. In this sense, speakers and signers alike are multimodal users of language, and so are all of us, speakers or signers, who are literate. There may be some overlap between gestural uses in spoken and signed interaction, as Trevor Johnston argued for pointing gestures in Towards a comparative semiotics of pointing actions in signed and spoken languages, but the fundamental issue is that signs and speech belong to two different linguistic modes, each with their rules, standards and practices. Precisely for this reason, sign-speech multilinguals can avail themselves of means of linguistic expression which monomodal interaction lacks, in that “distinct modalities allow for simultaneous production of two languages”, as Karen Emmorey and colleagues discuss in Bimodal bilingualism. This means that sign-speech multilinguals, like any language users, must draw on the whole of their linguistic resources in order to be able to develop as human beings. The Position Statement on Early Cognitive and Language Development and Education of Deaf and Hard of Hearing Children, adopted by the NAD (National Association of the Deaf, USA) in June this year, makes for as engrossing reading as Paddy Ladd’s chapter – with many thanks to Beppie van den Bogaerde, who brought this publication to my attention on Twitter, @HU_DeafStudies. The document examines the relationship between sign, speech and print modes, debunking the usual myths about minority languages causing delayed development of mainstream languages (why never the other way around, one wonders?), about the primacy of spoken languages over signed ones, about reading abilities presupposing “... Read more »

Alibali, M., Young, A., Crooks, N., Yeo, A., Wolfgram, M., Ledesma, I., Nathan, M., Breckinridge Church, R., & Knuth, E. (2013) Students learn more when their teacher has learned to gesture effectively. Gesture, 13(2), 210-233. DOI: 10.1075/gest.13.2.05ali  

  • March 25, 2017
  • 05:37 AM
  • 44 views

Including the "full intellectual range" in autism vision research

by Paul Whiteley in Questioning Answers

The paper by Alyse Brown and colleagues [1] (open-access available here) is probably not going to gain any significant media headlines (unlike other recent studies - see here and see here) but does cover a rather important question regarding the autism research landscape: how representative is autism research?Specifically looking at the collected research on visual processing (distinct from physical issues with the eyes that still require greater awareness) with autism in mind, the authors surveyed the research literature to determine "what extent the ASD with-ID [intellectual disability] population has been excluded from visual research." Intellectual or learning disability is one of the more frequently over-represented comorbidities that can accompany a diagnosis of autism or autism spectrum disorder (ASD). Their answer: "our searches indicate that 80% of the vision research associated with ASD is representative of less than 60% of the appropriate population, i.e., those with ASD without ID while the ASD with ID group who we argue currently represent 42% of the ASD population, have not been adequately considered."You may well quibble with the "recalculation of ASD prevalence figures, using the criteria of DSM-5" as a means of calculating that '~40% of those with autism have ID too' figure. For me however, the message is quite stark: autism research - specifically related to visual processing issues - is not yet representative of  'all autism'."Reluctance to test individuals who are below 80 in IQ is presumably a practical stance as the data collected from these individuals are often hard to obtain, and often close to floor level performance." The authors note however that the presence of ID alongside autism in the area of visual processing is not something that cannot be 'overcome' by researchers with some creative thinking and a few modification(s) to their experimental designs. Indeed, visual processing research lends itself well to quite a few alterations to methods [2]...How applicable might these results be to other areas of autism research? Well, we just don't know. I daresay that quite a lot of the 'psychology' based autism research in particular might show a bias towards autism without intellectual disability for just those reasons listed above. The problem then of grand, over-arching generalisations to 'all autism' on the basis of results from the more 'cognitively-able' becomes apparent. Of course, in these days of the plural 'autisms' (see here) and the realisation that 'heterogeneity means heterogeneity' when it comes to autism (see here) one could argue that even characterisations based on the presence of ID or not when it comes to autism are equally 'simplistic' and equally 'useless'. How many autisms might well have an ID element to them? Is ID a comorbidity or something rather more central to some of the autisms? These questions and related others are ones that autism research as a whole will eventually have to start looking at and taking into account.And going back to the issue of eye disorders being potentially over-represented and under-diagnosed in relation to autism, the paper by Mouridsen and colleagues [3] reiterates that intellectual ability when accompanying autism needs more health equality: "The rate of eye disorder was particularly high (24.5%) in those with a co-occurring profound or severe learning disability (IQ < 50)."----------[1] Brown AC. et al. Vision Research Literature May Not Represent the Full Intellectual Range of Autism Spectrum Disorder. Front Hum Neurosci. 2017 Feb 14;11:57.[2] Boot FH. et al. Delayed visual orienting responses in children with developmental and/or intellectual disabilities. J Intellect Disabil Res. 2013 Dec;57(12):1093-103.[3] Mouridsen SE. et al. Eye Disorders among Adult People Diagnosed with Infantile Autism in Childhood: A Longitudinal Case Control Study. Ophthalmic Epidemiol. 2017 Mar 15:1-4.----------Brown AC, Chouinard PA, & Crewther SG (2017). Vision Research Literature May Not Represent the Full Intellectual Range of Autism Spectrum Disorder. Frontiers in human neuroscience, 11 PMID: 28261072... Read more »

  • March 24, 2017
  • 07:58 AM
  • 58 views

Ammonium regulates mTOR signalling

by Joana Guedes in BHD Research Blog

mTORC1 and mTORC2 are two distinct mammalian TOR (target of rapamycin) complexes that regulate cell growth and metabolism. In cancer, genetic alterations lead to activation of mTOR signalling impacting tumour metabolism. Upregulated glutaminolysis is part of the metabolic reaction occurring in cancer that liberates high levels of ammonium, a toxic waste product. Although the importance of glutamine as a tumour nutrient is recognized, little is known about the potential effects of ammonium produced by glutaminolysis in tumours. In their new study, Merhi et al., 2017 identify ammonium as a dose-dependent regulator of mTORC2, mTORC1 and of proliferation in cancer cells.... Read more »

  • March 24, 2017
  • 07:00 AM
  • 49 views

Friday Fellow: Divergent Dinobryon

by Piter Boll in Earthling Nature

by Piter Kehoma Boll Let’s return once more to the troublesome and neglected protists. This time I’m bringing you another tiny but beautiful alga, more precisely a golden alga. Its name is Dinobryon divergens and as usual there is no common … Continue reading →... Read more »

  • March 24, 2017
  • 03:46 AM
  • 64 views

Autism and anxiety disorder: zooming in on the details

by Paul Whiteley in Questioning Answers

Although it is not necessarily new news that (a) autism rarely exists in some sort of diagnostic vacuum, and (b) that some of the comorbidity 'over-represented' when it comes to autism can actually be more disabling than autism itself, there are still more investigations to be done.The paper by Vicki Bitsika & Christopher Sharpley [1] represents an example of how autism science is starting to go past the whole 'is there a connection between...' bit when it comes to autism and various comorbidity, specifically focused on the issue of anxiety. Looking at parental responses on "the Social Responsiveness Scale (SRS) and the GAD subscale of the Child and Adolescent Symptom Inventory (CASI-4 GAD) about their sons" researchers reported some rather interesting trends when it came to the two based on a cohort of young males diagnosed with autism. The authors used the term 'high-functioning' to describe the particular 'type' of autism being looked at in their study but I'm rather less sure this is an appropriate description ('high- and low-functioning' tend to be very generalised terms).I should back-track slightly and point out that the reasoning behind this research was to "assist in treatment or avoidance of GAD [generalised anxiety disorder] by identifying ASD [autism spectrum disorder]-related behaviours as 'targets' for intervention with anxious children as well as for preventative treatments that could be implemented into daily routines before children become anxious." Of all the debates past and present in relation to autism, specifically on the topic of 'treatment' (or even 'cure'), I don't think anyone would be opposed to the idea that anxiety (whether symptoms or disorder) should be treated and potentially 'cured' in this context. Anxiety can be absolutely disabling including when tied into autism.Results: bearing in mind their focus on only two parameters (SRS scores and GAD scores) in this study, there are some interesting trends in need of further investigation. So: "For pre-adolescents, high levels of tension in social situations were associated with 3.5-times greater likelihood of having GAD; for adolescents, experiencing difficulty in changes in routine was associated with a 10-fold increase in risk of GAD." The pre-adolescents and adolescents bit in that sentence was due to the division of their cohort on the basis of age. The results suggest therefore that anxiety (or at least GAD) might express itself for various different reasons potentially linked to the age/maturity of the person.I know some people might be shrugging their shoulders at such a finding and saying 'we already knew that'. Well, I'm not one of them. Take for example the 'change in routines' as being a possible factor in the expression of GAD in adolescents. The recent work by Joyce and colleagues [2] looking at another important term relevant to this issue - intolerance of uncertainty - adds an additional layer to the Bitsika/Sharpley findings as per their conclusion that: "replicated previous findings based on parent report showing a significant positive relationship between RRB [restricted and repetitive behaviours] and anxiety." RRBs can, amongst other things, include responses to routine (and changes to said routines).As to the question of what such findings might mean in the context of intervention, the authors talk about how intervening in the symptoms of GAD (a kind of reactionary approach) might also benefit from also trying to focus intervention on certain autistic symptoms too. Outside of the [careful] use of some of the talking/behavioural therapies and perhaps the whiff of some effect from certain pharmacological interventions when it comes to RRBs and autism, there isn't a great deal on offer at the moment in autism science and practice in this area. Indeed, if the relationship between RRBs and anxiety is further confirmed (and I mean confirmed [3]), I'd perhaps suggest that moves to target RRBs in the context of autism could/should be a research priority if only to potentially reduce the effects of anxiety.And the inquiry continues [4]...----------[1] Bitsika V. & Sharpley CF. The association between parents' ratings of ASD symptoms and anxiety in a sample of high-functioning boys and adolescents with Autism Spectrum Disorder. Res Dev Disabil. 2017 Mar 1;63:38-45.[2] Joyce C. et al. Anxiety, Intolerance of Uncertainty and Restricted and Repetitive Behaviour: Insights Directly from Young People with ASD. J Autism Dev Disord. 2017 Feb 25.[3] Wang S. et al. Sex Differences in Diagnosis and Clinical Phenotypes of Chinese Children with Autism Spectrum Disorder. Neurosci Bull. 2017 Feb 25.[4] South M. et al. Symptom overlap on the srs-2 adult self-report between adults with asd and adults with high anxiety. Autism Res. 2017. March 7.----------Bitsika, V., & Sharpley, C. (2017). The association between parents’ ratings of ASD symptoms and anxiety in a sample of high-functioning boys and adolescents with Autism Spectrum Disorder Research in Developmental Disabilities, 63, 38-45 DOI: 10.1016/j.ridd.2017.02.010... Read more »

  • March 23, 2017
  • 04:02 AM
  • 81 views

Congenital cytomegalovirus (CMV) infection and autism continued

by Paul Whiteley in Questioning Answers

I wanted to briefly talk about the paper by Francesca Garofoli and colleagues [1] on congenital cytomegalovirus (CMV) infection and autism not because it contains any novel data (see here), but because it reminds us that the potential 'pathways' to a diagnosis of autism are multiple and not necessarily 'pre-programmed' as per the 'it's all genetic' arguments that frequently figure in various domains.Congenital CMV infection refers to the transmission of CMV - "a common virus that belongs to the herpes family of viruses" - from mother to foetus during pregnancy. The details are still under investigation as to how and why CMV affects a foetus (bearing in mind this is quite a common virus) but autism as a consequence of [some] congenital CMV infection has growing evidence-based support [2].Garofoli et al included 70 'proven' cases of CMV "congenitally-infected infants" in their study; specifically looking "to correlate congenital cytomegalovirus (CMV) infection with autism spectrum disorder (ASD) and to define its prevalence." They determined that 2 of their 70 strong cohort met criteria for an ASD at the age of 3 years. Two of 70 translated as 2.8% of their cohort and contrasts with [estimated] autism prevalence "in general Italian population (0.66-1.36%)." The figure of 2.8% is also not a million miles away from other estimates of autism suggested via congenital CMV infection [3].Although 2.8% of the cohort (2/70) might not sound like a lot I'm inclined to suggest that it does prompt quite a lot more additional investigation. Not least is the question: 'why was autism/ASD not diagnosed in the other 68 children?' and onward whether other factors (genetics(!), biology, infection timing, immunologic response, etc) might come into play [4] in relation to the congenital CMV infection - autism association? Taking also into account the estimated prevalence of ASD in Italy, these figures (estimates) do seem to be a little lower than that described in other geographical locations (see here and see here for examples). Indeed, bearing in mind the research evidence already looking at estimated ASD prevalence in Italy [5] it's not unfair to say that 'under-estimation' might be a familiar theme...----------[1] Garofoli F. et al. An Italian Prospective Experience on the Association Between Congenital Cytomegalovirus Infection and Autistic Spectrum Disorder. J Autism Dev Disord. 2017 Mar 3.[2] Ornoy A. et al. Prenatal factors associated with autism spectrum disorder (ASD). Reprod Toxicol. 2015 Aug 15;56:155-69.[3] Engman ML. et al. Prenatal acquired cytomegalovirus infection should be considered in children with autism. Acta Paediatr. 2015 Aug;104(8):792-5.[4] Lombardo MV. et al. Maternal immune activation dysregulation of the fetal brain transcriptome and relevance to the pathophysiology of autism spectrum disorder. Mol. Psychiatr. 2017. March 21.[5] Ferrante M. et al. Prevalence and age at diagnosis of Autism Spectrum Disorder in south Italy, 2004–2014. Eur J Public Health. 2015; 25 (suppl_3).----------Garofoli F, Lombardi G, Orcesi S, Pisoni C, Mazzucchelli I, Angelini M, Balottin U, & Stronati M (2017). An Italian Prospective Experience on the Association Between Congenital Cytomegalovirus Infection and Autistic Spectrum Disorder. Journal of autism and developmental disorders PMID: 28258350... Read more »

  • March 22, 2017
  • 12:55 PM
  • 84 views

Pollination Mystery Unlocked by Stirling Bee Researchers

by beredim in Strange Animals





Bees latch on to similarly-sized nectarless flowers to unpick pollen - like keys fitting into locks, according to a new study by researchers at the University of Stirling.

The research shows the right size of bee is needed to properly pollinate a flower. The bee fits tightly with the flower's anthers, to vibrate and release the pollen sealed within.



"We found that a pollinator's size, ... Read more »

  • March 22, 2017
  • 05:38 AM
  • 87 views

Break a leg!

by Jente Ottenburghs in Evolutionary Stories

What to do when your prey refuses to be swallowed? Eurasian Spoonbills (Platalea leucordia) in Hungary have a solution…... Read more »

  • March 22, 2017
  • 04:08 AM
  • 89 views

On genotype and environmental exposure patterns

by Paul Whiteley in Questioning Answers

I was rather interested to read the paper by Michela Traglia and colleagues [1] (open-access available here) concluding that: "maternal and fetal genetic make-up are important determinants of mid-gestational maternal circulating levels of some environmental organohalogens." Interested because, in these days of gene-environment interactions being applied to just about everything, the detail that is missing - which genes might potentially be linked to which environmental factors - has not yet been suitably addressed in the peer-reviewed science literature.So, based on data - "serum levels of a set of 21 organohalogens in a subset of 790 genotyped women and 764 children" - derived from participants included in the Early Markers for Autism (EMA) Project, researchers set about assessing how genetics might impact on environmental pollutant exposure profiles. Maternal blood samples were collected at around 15-20 weeks pregnancy. Children provided blood samples via the fabulous resource that is the newborn screening program, where: "Newborn blood spots were collected on filter paper 1-2 days after birth." Maternal samples were analysed for various environmental pollutants and both sets of samples were analysed for the genetic material they contained pertinent to whether "circulating mid-gestational levels of organohalogens would be driven by common maternal genetic determinants, and that these results could shed light on the observed associations between the organohalogens and ASD [autism spectrum disorder]."Results: yes, the authors "found evidence that a large proportion of maternal circulating levels of BB-153, BDE-47, -100, -153 [polybrominated congeners] and their sum was significantly controlled by common genetic factors." Those 'common genetic factors' typically referred to the presence of point mutations (SNPs) that litter everyone's genome and on occasion, can affect the function/production of specific biological processes. So: "Genome-wide association analyses identified significant maternal loci for p,p'-DDE... in the CYP2B6 gene and for BDE-28... near the SH3GL2 gene, both involved in xenobiotic and lipid metabolism." In other words, although the environmental pollutants measured are not great products in the first place (in terms of safety), a person's genetic make-up can influence how such products are eventually dealt with by the body and potentially onwards, what subsequent effects they might have.Additionally: "results suggest that the maternal circulating levels of some compounds were more highly influenced by fetal genetic factors than maternal genetics." This leads into another aspect of the current study whereby foetal genetic factors might also play a part in "controlling the toxicant disposition between mother and fetus." Specifically, authors noted that aspects of the individual genetics of a foetus (distinct from its mother) "contributed to the levels of BDE-100... and PCB187... near the potential metabolic genes LOXHD1 and PTPRD, previously implicated in neurodevelopment."And finally: "We confirmed that the serum levels of BDE-100, -153 and the total sum of PBDEs were significantly lower in mothers of ASD-affected children compared to mothers of control children." This is interesting in light of other discussions about PBDEs and autism in particular (see here). The authors do discuss various scenarios to account for their results not least that "transplacental transfer of organohalogens during pregnancy may be driven by the fetal genome expressed in placenta." Further analyses of the 'placentome' might therefore be indicated.To reiterate, this is interesting research. It tells us that many [adverse] environmental exposures, whilst typically to be avoided, don't act on the body in a uniform way as a function of differing genomes and differences in the ways that the body 'handles' such exposures. With autism in mind, this is not necessarily new news (remember paraoxonase gene variants and organophosphate metabolism [2] and air pollution and offspring autism?) but is a useful reminder. Such work also provides a template for looking at the myriad of other environmental factors put forward to influence autism risk and whether individual product safety is necessarily the only or most important factor when it comes to assessing relative risk profiles.I might finally also draw your attention to a recent interesting meta-analysis of the various environmental risk factors potentially linked to autism [3] (open-access) and another article talking about similar things [4] (open-access) (thanks Annabelle). Genes and environment, genes and environment...Music: Petula Clark sings the Beatles? Personally, I think it's better than the original...----------[1] Traglia M. et al. Independent Maternal and Fetal Genetic Effects on Mid-gestational Circulating Levels of Environmental Pollutants. G3 (Bethesda). 2017 Feb 24. pii: g3.117.039784.[2] D'Amelio M. et al. Paraoxonase gene variants are associated with autism in North America, but not in Italy: possible regional specificity in gene-environment interactions. Mol Psychiatry. 2005 Nov;10(11):1006-16.[3] Modabbernia A. et al. Environmental risk factors for autism: an evidence-based review of systematic reviews and meta-analyses. Molecular Autism. 2017; 8: 13.[4] Parker W. et al. The role of oxidative stress, inflammation and acetaminophen exposure from birth to early childhood in the induction of autism. Journal of International Medical Research. 2017. Jan 20.----------Traglia M, Croen LA, Lyall K, Windham GC, Kharrazi M, DeLorenze GN, Torres AR, & Weiss LA (2017). Independent Maternal and Fetal Genetic Effects on Mid-gestational Circulating Levels of Environmental Pollutants. G3 (Bethesda, Md.) PMID: 28235828... Read more »

  • March 21, 2017
  • 01:00 PM
  • 89 views

Study proposes fruition as a new attribute of information representation for works of contemporary art

by SciELO in SciELO in Perspective | Press Releases

It discusses information and art starting from the books of artists, from the collection of the Núcleo de Arte Contemporânea da Paraíba (NAC/UFPB), analyzing the performance of CI through the representation of information, in a collaborative working relationship between professionals. The representation of information could help in the treatment and organization of information, softening the complexity of these objects in the face of their possibilities of abstraction and fruition. … Read More →... Read more »

  • March 21, 2017
  • 10:04 AM
  • 134 views

The Weirdest Animals on Earth: 12 Amazing Facts About Platypuses

by Miss Behavior in The Scorpion and the Frog

What IS that? A photo by Stefan Kraft at Wikimedia Commons.1. Platypuses are so strange, that when British scientists first encountered one, they thought it was a joke: A Governor of New South Wales, Australia, sent a platypus pelt and sketch to British scientists in 1798. Even in their first published scientific description of the species, biologists thought that this duck-beaked, beaver-bodied, web-footed specimen may be some Frankenstein-like creation stitched together as a hoax. But this is only the beginning of their oddities…2. Platypuses are egg-laying mammals. Mammals are animals that have a backbone, are warm-blooded, and females produce milk for their young. Most females that nurse their young also carry their developing babies in their bodies and give birth to live young… But platypuses don’t play by those rules. Platypuses are monotremes, egg-laying mammals that include the platypus and four species of echidna. Most female mammals have two functional ovaries, but female platypuses, like most female birds, only have a functional left ovary. Once a year, a female platypus may produce a clutch of two or three small, leathery eggs (similar to reptile eggs), that develop in her uterus for 28 days. Because female platypuses don’t even have a vagina, when the eggs are ready, she lays them through her cloaca, an opening that serves for reproduction, peeing and pooping. (In fact, monotreme comes from the Greek for “one hole”). She then curls around them and incubates them for another 10 days until they hatch. 3. Platypuses sweat milk! Not only do female platypuses not have vaginas, they don’t have nipples either! Instead, lactating mothers ooze milk from pores in their skin, which pools in grooves on their bellies so the babies can lap it up. …And they’re not even embarrassed about it! 4. Adult platypuses are toothless. Baby platypuses (that is the actual technical term for them, by the way… not “puggles”, which would be way more fun) are born with teeth but they lose them around the time that they leave the breeding burrow. In their place are rigid-edged keratinized pads that they use as grinding plates. When they catch their prey (worms, bugs, shrimp, and even crayfish), they store it in their cheek pouches and carry it to the surface, where they use gravel to crush it in their toothless maw.5. The platypus “duck bill” is a sensory organ used to detect electric fields. Muscles and neurons use electrical impulses to function, and these impulses can be detected by electroreceptors. Although common in shark and ray species, electroreception is rare in mammals, only having been discovered in monotremes and the Guiana dolphin. Platypuses have rows of around 40,000 electroreceptors on their highly sensitive bill, which they wave back and forth in the water, much like a hammerhead shark, to determine the location of their prey. It’s a good thing this sense is so sensitive, since they close their eyes, nose and ears every time they dive. 6. Platypuses don’t use their tails like beavers do. Whereas beavers use their large, flat, leathery tails for swimming and slapping the water to send signals, platypuses don’t use their tails for any of that. Platypuses have large, flat tails for storing fat in case of a food shortage. Unlike beaver tails, platypus tails are covered in fur, which the mothers use to snuggle with their incubating eggs.A platypus ankle spur. Photo by E.Lonnon at Wikimedia Commons.7. Male platypuses have venomous ankle spurs. Their venom is strong enough to kill small animals and to create excruciating pain in humans. Since only males have it and they produce more venom during the breeding season, we think its main function may be to compete for mates and breeding territories.8. Platypuses are knuckle-walkers with a reptilian gait. Although they are well-built for swimming with their webbed feet and legs on the sides of their bodies, these traits make it quite awkward to get around on dry land. To walk, they pull in their webbing and walk on their knuckles, exposing their claws. Like reptiles and salamanders, platypuses flex their spines from side-to-side, supported by their sprawling legs. 9. Platypuses have unusually low body temperatures. As unusual as they are, platypuses are still mammals, which are defined, in part, by their ability to generate most of their own body heat with their metabolism. Platypuses do this as well, but whereas most mammals maintain body temperatures between 37-40 degrees C (99-104 degrees F), platypuses are happy with a body temperature of 32 degrees C (90 degrees F). This lower metabolism reduces the amount of calories they need to eat.10. They have no stomach. Stomachs are specialized protein-digesting chambers of digestive tracts that contain protein-digesting enzymes and acids to activate them. Not all animals have them, but most carnivores do. The most common exceptions to this rule are fish… and platypuses. Why? We don’t know for sure, but many of these animals consume diets high in calcium carbonate, which is a natural antacid. If their own diet would constantly neutralize their stomach acid, then the stomach really isn’t going to do them any good anyway.11. They have 10 sex chromosomes! Most mammals have two sex chromosomes, one from each parent. An individual that has two X chromosomes is usually female and an individual that has one X and one Y chromosome is usually male. Thus, female mammals pass along an X chromosome to each offspring and males can pass along an X or a Y. But platypuses are not content to be normal in any way…They have 10 sex chromosomes: 5 from mom and 5 from dad. All 5 chromosomes from mom are Xs, whereas a male sperm either contains 5 Xs or 5 Ys. Birds also have two sex chromosomes, but in birds, individuals with two of the same type are usually male and individuals with different chromosomes are usually female. Their system is called ZW, where the mammalian system is XY. The platypus X chromosome is more similar than the X chromosome of other mammals to the bird Z chromosome.12. The platypus genome is as much of a hodgepodge as its body. Only 80% of the platypus’ genes are like other mammals. Some of their genes have only previously been found in birds, reptiles, fish, or amphibians.To learn about more weird animals, go here.References: ... Read more »

Scheich, H., Langner, G., Tidemann, C., Coles, R., & Guppy, A. (1986) Electroreception and electrolocation in platypus. Nature, 319(6052), 401-402. DOI: 10.1038/319401a0  

Warren, W., Hillier, L., Marshall Graves, J., Birney, E., Ponting, C., Grützner, F., Belov, K., Miller, W., Clarke, L., Chinwalla, A.... (2008) Genome analysis of the platypus reveals unique signatures of evolution. Nature, 453(7192), 175-183. DOI: 10.1038/nature06936  

  • March 21, 2017
  • 03:57 AM
  • 115 views

PACE trial recovery data and chronic fatigue syndrome - a reply

by Paul Whiteley in Questioning Answers

I'd encourage readers interested in the background to the response paper by Michael Sharpe and colleagues [1] to have a look at a previous blogging occasion when the topic of the PACE trial, chronic fatigue syndrome (CFS) and 'recovery' were discussed (see here).Suffice to say that this latest paper is a reply to one published by Carolyn Wilshire and colleagues [2] who concluded that: "The claim that patients [with CFS] can recover as a result of CBT [cognitive behaviour therapy] and GET [graded exercise therapy] is not justified by the data, and is highly misleading to clinicians and patients considering these treatments." Said discussions linking back to some quite extensive debates on how one should (and shouldn't) treat/manage conditions like CFS (see here).I wanted to highlight the latest Sharpe paper because (a) I anticipated a reply from these authors following the Wilshire paper criticism of their recovery paper [3], and (b) although the debates in this area have been quite extensive already, the use of the scientific peer-reviewed medium to discuss and even argue is an important avenue. The authors have a right to scientific reply.So how did Sharpe et al respond? Well the words 'recovery', 'threshold' and ''no generally agreed measure of recovery" when it comes to CFS form the crux of the response to the Wilshire paper. They address the issue of recovery thresholds that have been a real source of discussion in relation to the PACE trial secondary analysis concluding that: "No participant met our full criteria for recovery at baseline." They point out that whilst "13% of participants met the recovery criterion of being within the normal range... for physical functioning when entering the trial" physical functioning was but one measure they used to determine recovery.They also approach the topic of 'changing thresholds' when it came to the definition of recovery in the PACE trial. To quote: "We changed these thresholds for our detailed analysis plan because after careful consideration and consultation, we concluded that they were simply too stringent to capture clinically meaningful recovery." They also report that elements of their assessment - the PACE walking test - are "not comparable with data collected in other studies" as a function of their reliance on personal motivation/ability over and above the use of encouragement as in other studies.Finally, authors also talk about 'what other studies have found regarding recovery' when it comes to CFS. They note that their findings in relation to the use of standard medical care (SMC) for CFS in the PACE trial were similar to other reports [4]. They also point to research suggesting that the use of CBT in independent study for CFS show similar rates of recovery [5] to theirs originally reported. In other words, they make a case for their findings fitting in with some of the other literature on this topic.A quick trawl of PubMed with the terms 'chronic fatigue syndrome' and 'recovery' reveals that there is indeed quite a bit more to do in this area of science. To quote from one paper (a critical review) [4]: "Estimates of recovery ranged from 0 to 66 % in intervention studies and 2.6 to 62 % in naturalistic studies." What this tells us is that (a) how recovery is reported in relation to CFS is still in need of some clarification [6] and perhaps more importantly, agreed uniformity is still required in its assessment; (b) some of the measures used to form judgements of recovery when it comes to CFS are not necessarily fit for purpose [7] (bearing in mind not everyone agrees with this); and (c) further efforts need to go into looking at many more aspects of CFS recovery outside of just a reliance on the fatigue parameter (see here and see here for examples). In short, science does not really know what recovery looks like in relation to CFS [8] despite it seemingly happening for all manner of reasons...Where do we go from here? This is a difficult question to answer. It is doubtful that the response from Sharpe and colleagues is going to change too many opinions about PACE given the strength of feeling on the topic and the various goings-on that have occurred around debate in this area (see here). Still today, other comments on the PACE trial continue to emerge in the peer-reviewed domain [9] from notable CFS researchers and there are even calls to retract the original recovery paper (see here). Yes, there are lessons to be learned from the PACE trial (e.g. stick to your "original protocol thresholds", make your data 'open-access' and think about how to do this in the planning/recruitment stages of your trial, be mindful that short-term gains don't necessarily translate into long-term ones, work with the ME/CFS community (rather than labelling elements of them 'vexatious' or worse when they ask questions or request data) but I can't see how these factors will immediately and positively affect the lives of people living with CFS/ME here and now. That recommendations on the use of CBT for CFS have already altered in some parts of the world (see here) - "The strength of evidence on global improvement is downgraded from moderate to low when considering CBT separately from other counseling and behavioral interventions" - and are potentially likely to change here in Blighty perhaps signifies that science and medicine is moving on when it comes to this topic. Science should be doubling its efforts to expand its research boundaries when it comes to managing CFS outside of just a reliance on the [outdated?] psychosomatic model and indeed, it is...And on the topic of other CFS research avenues, I've already talked about a few interesting avenues on this blog (see here and see here and see here) mindful that when we talk about CFS/ME, we're probably not talking about just one entity (see here). Also alongside, that there seems to be an awful lot of 'over-represented' comorbidity accompanying quite a lot of CFS/ME (see here for example) to also contend with...Music: Lush Life (even if you don't know the song title, you might rec... Read more »

M Sharpe, T Chalder, AL Johnson, KA Goldsmith, & PD White. (2017) Do more people recover from chronic fatigue syndrome with cognitive behaviour therapy or graded exercise therapy than with other treatments?. Fatigue: Biomedicine, Health , 1-5. info:/10.1080/21641846.2017.1288629

  • March 20, 2017
  • 04:31 PM
  • 118 views

Why ear plugs are great for clubbing and concerts

by Richard Kunert in Brain's Idea

I enjoy clubbing and pop/rock concerts exclusively with my ear plugs in. Does that mean I miss out? No, I enjoy the music exactly as it is meant to be. Picture by Melianis at fi.wikipedia (CC BY 2.5) Since 2004 the urban dictionary includes the term ‘deaf rave’ to describe a ‘rave, or party, organised […]... Read more »

Huang J, Gamble D, Sarnlertsophon K, Wang X, & Hsiao S. (2013) Integration of auditory and tactile inputs in musical meter perception. Advances in experimental medicine and biology, 453-61. PMID: 23716252  

Russo FA, Ammirante P, & Fels DI. (2012) Vibrotactile discrimination of musical timbre. Journal of experimental psychology. Human perception and performance, 38(4), 822-6. PMID: 22708743  

Zhao F, Manchaiah VK, French D, & Price SM. (2010) Music exposure and hearing disorders: an overview. International journal of audiology, 49(1), 54-64. PMID: 20001447  

  • March 20, 2017
  • 01:00 PM
  • 76 views

Research analyzes use of TRS in organizational studies

by SciELO in SciELO in Perspective | Press Releases

Bibliometric research analyzes the use of Social Representation Theory (SRT) in Organizational Studies (OS). We investigated 90 papers published in journals and scientific events from 2001 to 2014. The results indicate that the use of SRT in OS is incipient, superficial and presents theoretical and methodological inconsistencies. … Read More →... Read more »

  • March 20, 2017
  • 11:25 AM
  • 114 views

Opioids, Benzos and Risk for Overdose

by William Yates, M.D. in Brain Posts

The evolving epidemic of opioid overdose and overdose deaths is receiving increased public and research attention.Opioids overdoses and overdose deaths are often unintentional or accidental. It has been known that concurrent use of opioids with alcohol or benzodiazepines (i.e. Valium or Xanax) increases risk for overdose toxicity.A recent study published in the British Medical Journal confirmed the association of concurrent benzodiazepine prescription with opioid overdose.This research team examined confidential medical database records from over 500,000 patients in the U.S.Those that were enrolled in a medical plan including pharmaceutical benefits between 2001 and 2013 were included in the analysis.The key findings from the study included the following:The percentage of opioid users concurrently using a benzodiazepine rose from 9% of opioid users in 2001 to 17% of opioid users in 2013Chronic users of opioids nearly doubled their risk of opioid overdose if they took a concurrent benzodiazepine medication (4/100 persons/year to 7-8/100 person years)If the association is causal, the authors estimate emergency room visits and inpatient admissions could be reduced by 15% by stopping concurrent prescriptionsThis association of risk seems reasonable given the toxicities of opioids and benzodiazepines. Both at higher doses decrease respiratory drive potentially contributing to hypoxia and death.The authors note several take home messages for clinicians. Chronic users of benzodiazepines should be prescribed opioids cautiously if at all. Opioid prescriptions should be for short periods of time and low doses for chronic benzodiazepine patients.Likewise, if chronic opioids are necessary they should rarely be combined with intermittent or long-term benzodiazepine prescriptions.Readers with more interest in this topic can access the free full-text manuscript by clicking on the PMID link in the citation below.Photo of NCAA men's basketball tournament in Tulsa, OK is from my files.Follow me on Twitter WRY999Sun EC, Dixit A, Humphreys K, Darnall BD, Baker LC, & Mackey S (2017). Association between concurrent use of prescription opioids and benzodiazepines and overdose: retrospective analysis. BMJ (Clinical research ed.), 356 PMID: 28292769... Read more »

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