In a previous post on this blog I talked about an important paper by Vannucchi and colleagues  summarising the state of the peer-reviewed research (up to 2014) on bipolar disorder and Asperger syndrome (AS). Today, I'm adding to the conversation on this important topic by introducing two papers to the discussions: the first by Xenia Borue and colleagues  and the second by Ahmad Abu-Akel and colleagues  covering the longitudinal course of bipolar disorder (BD) in relation to autism and the appearance of autistic and other traits in relation to cases of BD respectively.Bipolar disorder (BD) previously known as manic depression is a condition affecting mood and specifically how it can 'swing' between extremes of depression and mania. There are a couple of different 'types' of BD reflective of how such mood swings can sometimes centre more on one aspect of BD over the other. As per the Vannucchi findings, the experience of BD may not be uncommon to the autism spectrum - "BD prevalence in adults with AS ranges from 6% to 21.4% of the cases" - but importantly: "is often characterized by atypical presentation, making its correct identification particularly difficult." Keep that in mind for now.The papers by Borue and Abu-Akel put a little more scientific flesh on to the discussions about autism and BD. Specifically, how in these days of increasing recognition that autism rarely appears in some sort of diagnostic vacuum (see here), comorbidity might have some pretty important effects on clinical presentation.To discuss the Borue findings first... well, based on a cohort of some 360 youths diagnosed with various types of BD who were followed for around 9 years, authors "compared youth with and without ASD [autism spectrum disorder] on clinical presentation, percentage of time with mood symptomatology, and psychosocial functioning." Approximately 8% of their cohort "met DSM-IV criteria for Asperger disorder or pervasive developmental disorder-NOS (referred to here as ASD)" which is an important detail. Further: "Compared to youth with BD, the clinical presentation of youth with BD+ASD more frequently involved distractibility, racing thoughts, depressed mood, social withdrawal, and low reactivity of negative mood states." The 'distractibility' side of things tallies with the observation that comorbid "attention-deficit/hyperactivity" (akin to ADHD) was more frequent in this group too and might be important . Insofar as longitudinal course (at least over about 9 years), authors note: "Significant amelioration of clinical symptoms occurred over time, suggesting that early recognition and treatment of mood disorders in youth with ASD may improve clinical outcomes."The Abu-Akel group set out to "determine the expression of autistic and positive schizotypal traits in a large sample of adults with bipolar I disorder (BD-I), and the effect of co-occurring autistic and positive schizotypal traits on global functioning in BD-I." BD-I focuses more on the manic side of clinical presentation. Bearing in mind autistic and schizotypal traits were self-assessed, authors reported that nearly 50% of their BD cohort (~800 people recruited via the Bipolar Disorder Research Network) "showed clinically significant levels of autistic traits." Around a quarter of their group also showed potentially important schizotypal traits too. Interestingly: "In the worst episode of mania, the high autistic, high positive schizotypal group had better global functioning compared to the other groups" with the requirement for quite a bit more study in this area.What could these collective results mean?Well, first and foremost all the chatter about traits and behaviours 'overlapping' shines through in these results. ESSENCE may indeed extend quite a bit further than just in childhood (see here) and this has some important implications for preferential screening services when an autism diagnosis is suspected or given. Second, I'm struck by how important traits outside of the autism spectrum might be to the presentation of something like BD in those reaching clinical thresholds for autism. I'm yet more convinced that the increasingly important association being made between autism and ADHD for example (see here) is really, really important. Third, the idea that autistic and certain schizotypal traits might actually be useful when it comes to 'global functioning' in cases of BD-I is an eye-opener. This needs further investigation. Finally, treatment for BD exists and with no medical or clinical advice given or intended, should not be withheld on the basis of a comorbid autism diagnosis.Timely and accurate diagnosis of BD when co-occurring alongside autism (or the presence of autistic traits) continues to be a priority. Not least because of the potentially far-reaching and sometimes extreme effects that BD can have (see here for example) potentially overlapping with some distressing figures noted alongside autism (see here). Yes, the presentation of BD might be slightly different when autism/autistic traits are included in the diagnostic mix, but clinicians and other health professionals need to be sensitive to such subtleties. Once again, screening is the first step of the process...---------- Vannucchi G. et al. Bipolar disorder in adults with Asperger׳s Syndrome: a systematic review. J Affect Disord. 2014 Oct;168:151-60. Borue X. et al. Longitudinal Course of Bipolar Disorder in Youth With High-Functioning Autism Spectrum Disorder. Journal of the American Academy of Child & Adolescent Psychiatry. 2016. Oct 4. Abu-Akel A. et al. Autistic and Schizotypal Traits and Global Functioning in Bipolar I Disorder. Journal of Affective Disorders. 2016. Oct 3. Wang HR. et al. Prevalence and correlates of bipolar spectrum disorder comorbid with ADHD features in nonclinical young adults. J Affect Disord. 2016 Sep 28;207:175-180.----------Borue, X., Mazefsky, C., Rooks, B., Strober, M., Keller, M., Hower, H., Yen, S., Gill, M., Diler, R., Axelson, D., Goldstein, B., Gol... Read more »
Borue, X., Mazefsky, C., Rooks, B., Strober, M., Keller, M., Hower, H., Yen, S., Gill, M., Diler, R., Axelson, D.... (2016) Longitudinal Course of Bipolar Disorder in Youth With High-Functioning Autism Spectrum Disorder. Journal of the American Academy of Child . DOI: 10.1016/j.jaac.2016.08.011
Abu-Akel, A., Clark, J., Perry, A., Wood, S., Forty, L., Craddock, N., Jones, I., Gordon-Smith, K., & Jones, L. (2016) Autistic and Schizotypal Traits and Global Functioning in Bipolar I Disorder. Journal of Affective Disorders. DOI: 10.1016/j.jad.2016.09.059
People with persistent complaints 6 to 12 months after an ankle sprain walk differently than those without persistent complaints.... Read more »
Kros, W., Keijsers, N., van Ochten, J., Bierma-Zeinstra, S., & van Middelkoop, M. (2016) Center of pressure during stance and gait in subjects with or without persistent complaints after a lateral ankle sprain. Gait , 24-29. DOI: 10.1016/j.gaitpost.2016.04.022
There are plenty of reasons it's important to maintain a healthy weight, and now you can add one more to the list: It may be good for your brain. Researchers have found that having a higher body mass index, or BMI, can negatively impact cognitive functioning in older adults.
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Bourassa, K., & Sbarra, D. (2016) Body mass and cognitive decline are indirectly associated via inflammation among aging adults. Brain, Behavior, and Immunity. DOI: 10.1016/j.bbi.2016.09.023
Neu5Gc, a non-human sialic acid sugar molecule common in red meat that increases the risk of tumor formation in humans, is also prevalent in pig organs, with concentrations increasing as the organs are cooked, a study has found. The research suggests that Neu5Gc may pose a significant health hazard among those who regularly consume organ meats from pigs.
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Ji, S., Wang, F., Chen, Y., Yang, C., Zhang, P., Zhang, X., Troy, F., & Wang, B. (2016) Developmental changes in the level of free and conjugated sialic acids, Neu5Ac, Neu5Gc and KDN in different organs of pig: a LC-MS/MS quantitative analyses. Glycoconjugate Journal. DOI: 10.1007/s10719-016-9724-9
fMRI researchers should care about (and report) the size of the effects that they study, according to a new Neuroimage paper from NIMH researchers Gang Chen and colleagues. It's called Is the statistic value all we should care about in neuroimaging?. The authors include Robert W. Cox, creator of the popular fMRI analysis software AFNI.
Chen et al. explain the purpose of their paper:
Here we address an important issue that has been embedded within the neuroimaging community for a long tim... Read more »
Chen G, Taylor PA, & Cox RW. (2016) Is the Statistic Value All We Should Care about in Neuroimaging?. NeuroImage. PMID: 27729277
A fairly quick post for your reading delight today as I bring the paper by Miller and colleagues  to your attention suggesting that: "Early intervention targeting language and motor skills may improve later achievement in this population."'This population' referred to a small cohort (N=26) of children diagnosed with an autism spectrum disorder (ASD) who were examined "at the approximate ages of two, four, and ten" years with regards to their academic achievement and the variables that might be important to 'successful' achievements.Including some familiar names when it comes to the concept of 'outcome' in relation to autism ('optimal outcome' that is), researchers determined a few potentially important relationships from their collected data: "Preschool verbal abilities significantly predicted school-age reading comprehension" and "early motor functioning predicted later math skills."I'm not entirely surprised that infancy verbal (talking) abilities might play a role in later reading comprehension but I was rather more intrigued by the observation potentially linking motor skills to later maths abilities. Yes, I get that children learn to count on their fingers (and toes) and no doubt this and other scenarios might influence the connection between the two, but it strikes me that this connection requires quite a bit more study . Indeed, welcoming the idea that motor skills are an important issue with regards to autism (see here) and that maths ability is 'as varied as the label of autism is itself' (see here) the idea that the archetypal all-rounder that is the occupational therapist (OT) might have a key role here is rather interesting (see here).I'm also minded to suggest that a certain sport/discipline that I'm particularly fond of on this blog (the martial arts) might have some rather far-reaching 'mathematical' effects if one considers it's application to autism and motor functioning...To close, Marvel are going full-strength with their next Wolverine film instalment titled 'Logan'...---------- Miller LE. et al. Preschool predictors of school-age academic achievement in autism spectrum disorder. Clin Neuropsychol. 2016 Oct 5:1-22. Pitchford NJ. et al. Fine Motor Skills Predict Maths Ability Better than They Predict Reading Ability in the Early Primary School Years. Front Psychol. 2016 May 30;7:783.----------Miller LE, Burke JD, Troyb E, Knoch K, Herlihy LE, & Fein DA (2016). Preschool predictors of school-age academic achievement in autism spectrum disorder. The Clinical neuropsychologist, 1-22 PMID: 27705180... Read more »
Miller LE, Burke JD, Troyb E, Knoch K, Herlihy LE, & Fein DA. (2016) Preschool predictors of school-age academic achievement in autism spectrum disorder. The Clinical neuropsychologist, 1-22. PMID: 27705180
Pathogen epitopes are fragments of bacterial or viral proteins. Attached to the surface structure of cells, they prompt the body's immune system to mount a response against foreign substances. Researchers have determined that nearly a third of all existing human epitopes consist of two different fragments. Known as 'spliced epitopes', these types of epitopes have long been regarded as rare. The fact that they are so highly prevalent might, among other things, explain why the immune system is so highly flexible.
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Liepe, J., Marino, F., Sidney, J., Jeko, A., Bunting, D., Sette, A., Kloetzel, P., Stumpf, M., Heck, A., & Mishto, M. (2016) A large fraction of HLA class I ligands are proteasome-generated spliced peptides. Science, 354(6310), 354-358. DOI: 10.1126/science.aaf4384
Patients that present with a spontaneous pneumothorax (SP) without a known medical history of lung disease are usually diagnosed as primary spontaneous pneumothorax - a pneumothorax that occurs without underlying diseases. However, underlying diffuse cystic lung diseases such as Birt-Hogg-Dube syndrome (BHD), lymphangioleiomyomatosis (LAM) and pulmonary Langerhans cell histiocytosis (PLCH) may have a spontaneous pneumothorax as their first symptom. In their new study, Gupta et al. (2016) evaluate the cost-effectiveness of high resolution computed tomographic (HRCT) chest imaging for early diagnosis of LAM, BHD, and PLCH in patients presenting with an apparent primary SP. In their analysis the authors show that HRCT image screening for BHD, LAM and PLCH in patients with apparent primary SP is cost-effective and suggest that clinicians should consider performing a screening HRCT in these patients.... Read more »
Gupta N, Langenderfer D, McCormack FX, Schauer DP, & Eckman MH. (2016) Chest Computed Tomographic Image Screening for Cystic Lung Diseases in Patients with Spontaneous Pneumothorax is Cost-effective. Annals of the American Thoracic Society. PMID: 27737563
I'm actually getting a little bored of talking about the various peer-reviewed research looking at a possible connection between asthma and autism on this blog. It's not that it isn't an interesting topic but rather that the data is coming in thick and fast suggesting that behaviour and physiology are not completely separate anymore.I did however want to direct you to the paper by Alessandro Tonacci and colleagues  who, following a systematic review "according to the PRISMA guidelines" suggested that "Autism Spectrum Disorder and asthma could be associated conditions, as evidenced by the higher prevalence of asthma in autistic children with respect to typically developed controls." I might add that this is not the first time that this authorship group have examined the coincidence of allergic disease with autism (see here).The idea that asthma and autism might be connected is an important finding because not so long ago I talked about another paper  - a meta-analysis - that came up with a slightly different conclusion to that listed by Tonacci (see here). OK, a systematic review and a meta-analysis whilst related are not necessarily one and the same and so one has to be a little careful. That being said, I did raise a few 'issues' with that previous meta-analysis by Zheng and colleagues  around what they did and did not seemingly include in their paper. A meta-analysis or systematic review is only as good as the number and quality of the studies it includes.The strength of the Tonacci review is that it followed those PRISMA guidance - the Preferred Reporting Items for Systematic reviews and Meta-Analyses - and also that "Methods for study selection and inclusion criteria were specified in advance and documented in PROSPERO protocol #CRD42014012851." In other words, much like when study protocols for clinical trials are pre-registered to avoid any 'massaging' of results or changing/switching outcomes, so their aims and objectives were on record for all to see.Where next for the suggestion of a possible link between asthma and autism? Well, how about taking into account a role for comorbidity as per the increasingly strong evidence coming out about how asthma and attention-deficit hyperactivity disorder (ADHD) may be linked (see here) and what that means for the over-representation of ADHD in autism or vice-versa (see here). I might once again suggest that immune function (i.e. inflammation or inflammatory processes) could be a common variable requiring further study too (see here for example). Such research may wish to take into account overlapping genetics/epigenetics as being important as well as the more functional biochemistry of immune system processes.Given also the specific focus on "allergic asthma" by Tonacci et al I'm also wondering whether the various research on allergy symptoms affecting autism presentation might be important for some (see here). Indeed, with no medical advice given or intended, the idea of treating allergic disease in cases of ADHD for example (see here) is perhaps an area ripe for further investigation when it comes to autistic presentation too...To close: Guardians of the Galaxy is back (and the soundtrack will be as cool as ever I guess).---------- Tonacci A. et al. A systematic review of the association between allergic asthma and autism. Minerva Pediatr. 2016 Oct 5. Zheng Z. et al. Association between Asthma and Autism Spectrum Disorder: A Meta-Analysis. PLoS One. 2016 Jun 3;11(6):e0156662.----------Tonacci A, Billeci L, Ruta L, Tartarisco G, Pioggia G, & Gangemi S (2016). A systematic review of the association between allergic asthma and autism. Minerva pediatrica PMID: 27706122... Read more »
Tonacci A, Billeci L, Ruta L, Tartarisco G, Pioggia G, & Gangemi S. (2016) A systematic review of the association between allergic asthma and autism. Minerva pediatrica. PMID: 27706122
There are three kinds of glial cells in the brain, oligodendrocyte, astrocyte and microglia. Oligodendrocytes myelinate neuronal axons to increase conduction velocity of neuronal impulses. A Japanese research team found a characteristic feature of oligodendrocytes that selectively myelinate a particular set of neuronal axons.
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Osanai, Y., Shimizu, T., Mori, T., Yoshimura, Y., Hatanaka, N., Nambu, A., Kimori, Y., Koyama, S., Kobayashi, K., & Ikenaka, K. (2016) Rabies virus-mediated oligodendrocyte labeling reveals a single oligodendrocyte myelinates axons from distinct brain regions. Glia. DOI: 10.1002/glia.23076
A lack of scrutiny of articles published in peer-reviewed journals on the basis of a belief that pre-publication peer-review provides sufficient scrutiny, may well add to the relatively high number of articles in which results are presented that cannot be replicated. … Read More →... Read more »
A quote to begin: "... in this small trial of children with non-syndromic ASD [autism spectrum disorder] and language impairment, treatment with high-dose folinic acid for 12 weeks resulted in improvement in verbal communication as compared with placebo, particularly in those participants who were positive for FRAAs [folate receptor-α autoantibody]."Those were the findings reported by Richard Frye and colleagues  (open-access) continuing a research theme from this group looking at how folinic acid - a reduced form or vitamer of folate - may "markedly" improve symptoms in some children diagnosed with ASD (see here). Some media reporting about these latest results are available (see here for example) but if you're sticking with my interpretation there are a few important points to note.So:This was a gold-standard "double-blind, randomized placebo-controlled" study meaning that as well as pitting folinic acid against a placebo, both researchers and participants were blind to 'who got what' during the 12 weeks of study. The aim was to compare a "target dose" of folinic acid "(2 mg kg−1 per day)" with said placebo formulation. It also appears that the authors went to some lengths to ensure that folinic acid and placebo capsules were "indistinguishable by sight and feel" as well as odour and taste.Participants (~7 years old) (N=48) were allocated to the folinic acid (n=23) or placebo group (n=25). All had a diagnosis of ASD and importantly, "Reconfirmation of the diagnosis using the lifetime version of the Autism Diagnostic Interview-Revised by an independent research reliable rater was requested from all participants." Participants were also required to have "documentation of language impairment" accompanying their autism as well as being free from current antipsychotic medication use alongside various other inclusion/exclusion criteria."Verbal communication was the primary outcome" we are told, offering a rather refreshing prospect insofar as the focus being on symptoms rather than syndromes. That's not to say that various behavioural schemes pertinent to the presentation of autism and other general 'adaptive behaviours' weren't also included, but this was a study looking specifically at what happened to verbal communication.Results: well, first and foremost folinic acid seemed to be pretty safe and well tolerated as we are told that "no serious adverse effects" were recorded for the folinic acid group when blinding was broken. First, do no harm and all that. As per the opening sentence of this post, there were some significant group improvements noted for the group taking folinic acid in relation to verbal communication ("an important core ASD symptom") compared with the placebo group.Going back to the whole 'positive for FRAAs' there were also some results to be seen. "This study suggests that FRAAs predict response to high-dose folinic acid treatment. This is consistent with the notion that children with ASD and FRAAs may represent a distinct subgroup." Without turning this post into some grand explanation of what FRAAs are (bearing in mind I'm barely getting my head around this myself), this ties into other findings (see here) and how these autoantibodies work to impair folate transport and 'block' or 'bind' to the folate receptor. One explanation is that folinic acid is able to 'bypass the FRα [folate receptor-α] when it is blocked and/or dysfunctional' particularly at higher doses. The use of the term "distinct subgroup" when it comes to autism is music to many ears in these days of the more plural 'autisms' and recognition that certain inborn errors of metabolism seem to be associated with 'some types' of autism  (more on this paper to come soon).Of course there is more to do in this area as the authors themselves identify the small participant numbers as one limitation and the future requirement to "determine the optimal folinic acid dose". Although no adverse effects were reported during the 12-week period, I'd also suggest that longer-term follow-up is needed to make sure that this effect extends a little longer too. Given the folate connection evident in this line of research, I'd for example, also be interested to see a little more work done on whether everyone's favourite scrabble gene - methylenetetrahydrofolate reductase (MTHFR) - potentially linked to some autism (see here) might also be an important player with regards to folinic acid use and response. Finally, minus any sweeping generalisations, the idea that FRAAs might also extend across labels to schizophrenia (see here) for example, is also potentially worthy of further investigation insofar as the 'links' that still remain when it comes to the autism and schizophrenia spectrums (see here) (remembering too the important work of Mildred Creak).Having said all that, these are important results as they stand. Not least because under rigorous methodological conditions, folinic acid has seemingly passed yet another scientific hurdle with regards to its potential relevance to at least some autism. We will no doubt see more on this topic in the peer-reviewed literature in times to come...---------- Frye RE. et al. Folinic acid improves verbal communication in children with autism and language impairment: a randomized double-blind placebo-controlled trial. Molecular Psychiatry. 2016. Oct 18. Simons A. et al. Can psychiatric childhood disorders be due to inborn errors of metabolism? European Child & Adolescent Psychiatry. 2016. Sept 30.----------Frye, R., Slattery, J., Delhey, L., Furgerson, B., Strickland, T., Tippett, M., Sailey, A., Wynne, R., Rose, S., Melnyk, S., Jill James, S., Sequeira, J., & Quadros, E. (2016). Folinic acid improves verbal communication in children with autism and language impairment: a randomized double-blind placebo-controlled trial Molecular Psychiatry DOI: 10.1038/mp.... Read more »
Frye, R., Slattery, J., Delhey, L., Furgerson, B., Strickland, T., Tippett, M., Sailey, A., Wynne, R., Rose, S., Melnyk, S.... (2016) Folinic acid improves verbal communication in children with autism and language impairment: a randomized double-blind placebo-controlled trial. Molecular Psychiatry. DOI: 10.1038/mp.2016.168
In 1962, the Nobel Prize of Medicine was given to Watson, Crick and Wilkins, for their finding of the double-helical structure of the DNA molecule. But who were the scientists overshadowed by the names of Watson and Crick?... Read more »
Leslie Pray. (2008) Discovery of DNA structure and function: Watson and Crick. Nature Education, 1(1). info:other/
The best time to start disaster preparation for your pet is now.Recently, like many people in this part of the world, we heard there was a big storm on the way. The third of three windstorms was said to be the most powerful. Since we live in an area with many beautiful trees and the power lines are above ground, it does not take much to knock out the power.In the end, we were lucky. The storm was not as strong as predicted, and it changed track and went further north. But it’s a reminder that we all need to be prepared for emergencies. And pets are an important part of our emergency preparedness.Planning starts with thinking about the kinds of emergencies you might face. Maybe you live in an area that is prone to floods or forest fires, or has the potential for big earthquakes. It’s helpful to think about smaller events too, that might impact you without affecting others: house fires, job losses, illnesses. These could all have an impact on your ability to care for your pet.You could come to arrangements with friends and family about how you will care for each other’s pets if something happens. It helps to talk about these things in advance.For me, with an incoming storm I wanted to be sure I had enough pet food and cat litter, and to charge up my cellphone. A bad storm last year knocked the power out for more than a day, and I can tell you that by day 2 the novelty was really wearing off. It was long enough that once the power came back, local stores had to stay closed to throw out ruined food. Also some roads were blocked with fallen trees, making travel more difficult for a short while. In this part of the world, the big risk we are meant to be prepared for is an earthquake. The official advice is to have enough supplies that you can manage on your own for at least 72 hours, preferably longer.That means food and water supplies for your pets as well as yourself, flashlights and spare batteries, and a radio so that you know what’s happening in the world. (A wind-up and/or solar-powered one that you can use to charge a cellphone seems like a good idea).Don’t forget to include some of your dog or cat’s favourite treats.A harness and leash would be handy so you don't run out of the house without them. A towel or blanket could be useful as a temporary bed for your dog or cat. Bowls for food and water, washing up liquid and some garbage bags would all be useful too.Having some cash in small notes is sensible in case of power being out at ATMs. This is a habit you can get into, or you can keep a small amount at home.What about copies of important documents, not just your own but also your pets’ vaccination records? Keep them in a plastic wallet or container that will keep them dry, and add them to your ‘grab bag’ that you will grab and take with you in an emergency.Identification for your pet is sometimes overlooked (tattoo, microchip, collar tag). As well as making sure your pet has id, ensure the people who keep the microchip/tattoo records have an up-to-date address and phone number for you.Helping your pet to be well-socialized and to be calm and well-behaved in ordinary life pays off in an emergency too. After the M9 earthquake in Fukushima, those who had trained and socialized their pets were more likely to be able to take them with them when they evacuated (Yamazaki 2015).Training your cat or dog to go in a carrier is useful in ordinary life, since it means you can take them to the vet. In an emergency, it’s easy to see that it might make the difference to being able to take them with you.Heath and Linnabary (2015) also say that having a good starting point for animals is part of emergency planning. While they are thinking about the broader societal level, we can apply this to our individual situations too. If your dog or cat is fearful or has other struggles in ordinary life, finding ways to solve those issues is worthwhile (if you need help from a certified trainer or behaviourist, this could be the moment to make that call).This post is not a guide to how to prepare for emergencies; rather it’s intended to encourage you to think about the kinds of events you might have to prepare for, and get started. It’s not a solo activity; discuss it with your family and friends. And you might be kind enough to also consider neighbours who are seniors or who might need a little help for other reasons.You can also put a regular date in your diary to review your plans and update your supplies (even bottled water has a sell-by date). Pick a date that you will remember, either because it’s meaningful to you or because it’s the date your city carries out earthquake drills (thus you will be reminded by the media). For me, that's tomorrow: ShakeOut BC is on 20th October.You can find more information about emergency planning for pets in this ASPCA guide.ReferencesHeath SE, & Linnabary RD (2015). Challenges of Managing Animals in Disasters in the U.S. Animals : an open access journal from MDPI, 5 (2), 173-92 PMID: 26479228Yamazaki, S. (2015). A Survey of Companion-Animal Owners Affected by the East Japan Great Earthquake in Iwate and Fukushima Prefectures, Japan Anthrozoös, 28 (2), 291-304 DOI: 10.1080/08927936.2015.11435403Photo: Josh Powell (Shutterstock.com)... 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Heath SE, & Linnabary RD. (2015) Challenges of Managing Animals in Disasters in the U.S. Animals : an open access journal from MDPI, 5(2), 173-92. PMID: 26479228
Yamazaki, S. (2015) A Survey of Companion-Animal Owners Affected by the East Japan Great Earthquake in Iwate and Fukushima Prefectures, Japan. Anthrozoös, 28(2), 291-304. DOI: 10.1080/08927936.2015.11435403
Patients with chronic ankle instability who received a 4-week supervised rehabilitation program consisting of therapeutic exercise, joint mobilization, and neural mobilizations had greater clinical improvements compared with patients who were treated with therapeutic exercise alone.... Read more »
Plaza-Manzano, G., Vergara-Vila, M., Val-Otero, S., Rivera-Prieto, C., Pecos-Martin, D., Gallego-Izquierdo, T., Ferragut-Garcías, A., & Romero-Franco, N. (2016) Manual therapy in joint and nerve structures combined with exercises in the treatment of recurrent ankle sprains: A randomized, controlled trial. Manual Therapy, 141-149. DOI: 10.1016/j.math.2016.08.006
"In this study, we again show that acetaminophen use is associated with ASD [autism spectrum disorder]."That was one of the results reported by Stephen Schultz & Georgianna Gould  (open-access available here) as part of their survey of the US "National Database for Autism Research (NDAR) of the National Institute of Mental Health (NIMH)" looking at "whether ASD is associated with acetaminophen use." Acetaminophen by the way, is another name for paracetamol, the over-the-counter pain relief medication that is going through some turbulent times at the moment (see here for example).Shultz & Gould - one of whom has some research form in this area  - eventually relied on information for 118 children diagnosed with an ASD and 79 'non-ASD' children with an average age of about 11 years old. The sorts of data they looked at surrounded the parental choice of medication to treat fevers (I think) including whether paracetamol, ibuprofen or aspirin were used. I have to say that the authors could have made the methodology behind their analysis a little bit clearer in terms of how the questions were posed and to whom rather than just referring to another study with regards to participant selection for example. I had to go fishing for various details which is guaranteed to furrow my brow...Results: well, I'm slightly puzzled it has to be said. When it came to questions about paracetamol use (I use the term paracetamol 'cos that's what us Limeys are used to) between the ASD and non-ASD groups I didn't see too much difference overall. Take for example the questions about 'only using paracetamol' for fever or 'first choice' use for fever. The percentage figures for the ASD and non-ASD group were 15% and 12% respectively for 'only use this' and 35% and 46% respectively for 'first choice'. Given the participant numbers, I'm not sure that these stats are so wildly different. Yes, I appreciate that when it came to the question about 'rarely or never using' paracetamol to treat fever, 17% of those with ASD reported positive to this question compared with only 3% of controls, but does this really tell us much about very different patterns of paracetamol use?Further, the authors report results based on "age-adjusted models for levels of fever medication use". They observe that using "acetaminophen as a first choice was 83% less likely in children with ASD... while use of acetaminophen if other medication doesn’t bring down fever was 82% less likely in children with ASD." They interpret this to mean that compared with their previous results  findings were reversed in that "older children with ASD compared to control children were significantly less likely to use acetaminophen for fever; whereas, in our 2008 study, younger children with ASD compared to control children were significantly more likely to use acetaminophen at 12-18 months of age and after the MMR vaccination." The mention of immunisation in that last sentence was based on their 2008 paper suggesting that "acetaminophen use after measles-mumps-rubella vaccination was associated with autistic disorder" but I have to say that I'm left a little wanting in terms of these recent findings by Shultz & Gould.I do think there is a 'where next?' discussion to be had when it comes to the idea that paracetamol use might be linked to 'some' autism. Given the growing research interest in paracetamol use and a 'hyperactive phenotype' of autism (see here), this stalwart of pain relief is deserving of much further inspection in relation to autism. Shultz & Gould do offer one possible research direction based on some speculation about the how the endocannabinoid system might fit into this (something mentioned by other authors too). I am interested in the hypothetical situation they conclude their paper with implicating the endocannabinoid system and how paracetamol might affect 'endocannabinoid tone' but to what extent is perhaps another question.Just before I finish on this topic I'm minded to bring to your attention another detail from the Shultz / Gould paper with regards to the sentence: "children with ASD vs. non-ASD children are significantly more likely to show an increase in sociability when they have a fever." I've always thought the observations on behaviour and fever when it comes to [some] autism to be quite important (see here). Speculation that "this increase [in sociability] is due to anandamide activation of the endocannabinoid system in ASD children" is also ripe for further scientific investigation...It's been a while but here is some music to close: Mrs Robinson.---------- Schultz ST. & Gould GG. Acetaminophen Use for Fever in Children Associated with Autism Spectrum Disorder. Autism Open Access. 2016 Apr;6(2). pii: 170. Schultz ST. et al. Acetaminophen (paracetamol) use, measles-mumps-rubella vaccination, and autistic disorder: the results of a parent survey. Autism. 2008 May;12(3):293-307.----------Schultz ST, & Gould GG (2016). Acetaminophen Use for Fever in Children Associated with Autism Spectrum Disorder. Autism-open access, 6 (2) PMID: 27695658... Read more »
Schultz ST, & Gould GG. (2016) Acetaminophen Use for Fever in Children Associated with Autism Spectrum Disorder. Autism-open access, 6(2). PMID: 27695658
Zika Virus (ZIKV) was first isolated in 1947 from a sentinel monkey in Uganda and associated with human infection in 1954 when neutralizing antibodies were detected in the sera of residents in India, with antibodies also being found in residents from various African countries. ZIKV is mosquitoe-borne Flavivirus that is predominantly transmitted via Aedes Agypti, although sexual transmission (female to male, male to female, male to male) and transmission via blood transfusion has also been reported.the induction of apoptosis is a hallmark of ZIKV infection of foetal brain cells. Here the ZIKV virus autophagy is compared to the induction of autophagy in persistently classical swine fever virus (CSFV) infected cells and a model is introduced in which the inhibition of autophagic flux by ZIKV might contribute to the development of microcephaly. ... Read more »
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Cugola FR, Fernandes IR, Russo FB, Freitas BC, Dias JL, Guimarães KP, Benazzato C, Almeida N, Pignatari GC, Romero S.... (2016) The Brazilian Zika virus strain causes birth defects in experimental models. Nature, 534(7606), 267-71. PMID: 27279226
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We discuss properties of type III bursts that change the sign of their drift rate from negative to positive and vice versa. Moreover, these bursts may change the sign of their drift rates more than once. These particular type III bursts were observed simultaneously by the radio telescopes UTR-2, URAN-2, [...]... Read more »
V. Melnik et al. (2015) Decameter type III bursts with changing frequency drift-rate signs . Solar Physics. info:/
'The times they are a changin'' said a Nobel prize winner and that's also a sentiment that seems true when it comes to chronic fatigue syndrome / myalgic encephalomyeltis (CFS/ME) too (see here for example).Anyone who has followed the tos-and-fros of the PACE trial - the one that suggested that CBT (cognitive behavioural therapy) and GET (graded exercise therapy) might provide some significant relief of symptoms associated with CFS/ME - will probably have heard the quite open claims being made that "the study was bad science." Scientific dirty laundry continues to be aired in public as a result of the focus on the wrongs and rights of PACE and with it, precious money that might well have been used for CFS/ME science has instead seemingly been used in legal disputes.Outside of the methodological points potentially associated with the PACE trial/results, at the heart of the issue on whether CBT for example, might influence the progression of CFS/ME is the continued idea in some quarters that ME/CFS is part of a spectrum of conditions primarily centred in the domain of the biopsychosocial (BPS) model. Here, the suggestion is that a biological agent or agents act to trigger the condition but thereafter psychological and sociological factors play a major part in 'maintaining' the condition. For many people who suffer (yes, suffer) with ME/CFS the application of the BPS model to their symptoms has been likened to charges of malingering and subsequently many patients feel let down by medicine and indeed, that their symptoms have been trivialised.The paper by Keith Geraghty & Aneez Esmail  puts some scientific flesh on to the idea that continued use of the BPS model applied to CFS/ME might be detrimental to many patients and particularly their interactions with healthcare providers. Including reference to the quite extensive literature suggesting that all-manner of biological factors may be at work on the various experiences of CFS/ME (see here for example), the authors question "whether or not the BPS model generates ‘harms’ for CFS patients." The conclusion: yes, applying the logic of the BPS model during healthcare consultation is probably not doing much for quite a few patients with ME/CFS who are often in real distress and don't really want to be told it's 'all psychological' and treated as such.This is an important piece of work. Irrespective of your personal viewpoint of what ME/CFS is (and isn't) it tells us that healthcare interactions are important to people diagnosed with the condition and that "an over-emphasis on the 'psycho' (and only then with regard to alleged causation, rather than impact), at the expense of 'bio' and 'social' aspects of their impairments" has done little to either treat or manage or improve symptoms or quality of life for many people. It also tells us to respect the concept that CFS/ME is a heterogeneous condition and perhaps offer some viable alternatives to the BPS model. Not least is the idea that screening for conditions known to influence fatigue (see here) might be a good starting point and then taking things from there.I do however think it is important that we don't minimise the psychological effects that ME/CFS can have on a person. Sometimes being bed-bound with only limited contact with the 'outside world' trapped in a spiral of fatigue and rest, fatigue and rest is unlikely to do anyone any good. Indeed, when researchers talk about depression and other psychiatric features being potentially over-represented in cases of CFS/ME, I'm not surprised given how severe fatigue and other symptoms can sometimes be. A good physician should be screening for such accompanying issues and offering the appropriate treatment for them, mindful that these are not necessarily a core part of CFS/ME .I get the impression that the BPS model (in its current form ) is coming to the end of its reign when applied to a label like CFS/ME on the basis of more research resources being pumped into looking at the biology/biological course of the condition and less emphasis on the psychological 'treatment' of the condition (see here). This perhaps follows a more general trend where psychogenic explanations for physical illness are starting to receive some critical commentary  including critically looking at the idea that "psychogenic illnesses are believed to be more responsive to psychological interventions than comparable "organic" illnesses". This is of course, little consolation for those patients with ME/CFS who've had to face the BPS model even in light of contrary indication  and perhaps not had the best experience of it. Indeed, I wonder if there will come a point where a formal apology will be issued about the way science and medicine has treated many people with ME/CFS and the sometimes needless suffering that the BPS model in particular, has had on many aspects including the doctor-patient relationship.---------- Geraghty KJ. & Esmail A. Chronic fatigue syndrome: is the biopsychosocial model responsible for patient dissatisfaction and harm? Br J Gen Pract. 2016 Aug;66(649):437-8. Taylor AK. et al. 'It's personal to me': A qualitative study of depression in young people with CFS/ME. Clin Child Psychol Psychiatry. 2016 Oct 14. pii: 1359104516672507. Maes M. & Twisk FN. Chronic fatigue syndrome: Harvey and Wessely's (bio)psychosocial model versus a bio(psychosocial) model based on inflammatory and oxidative and nitrosative stress pathways. BMC Med. 2010 Jun 15;8:35. Wilshire CE. & Ward T. Psychogenic Explanations of Physical Illness: Time to Examine the Evidence. Perspect Psychol Sci. 2016 Sep;11(5):606-631. Twisk FN. & Maes M. A review on cognitive behavorial therapy (CBT) and graded exercise therapy (GET) in myalgic encephalomyelitis (ME) / chronic fatigue syndrome (CFS): CBT/GET is not only ineffective and not evidence-based, but also potentially harmful for many patients with ME/CFS. Neuro Endocrinol Lett. 2009;30(3):284-99.----------... Read more »
Geraghty KJ, & Esmail A. (2016) Chronic fatigue syndrome: is the biopsychosocial model responsible for patient dissatisfaction and harm?. The British journal of general practice : the journal of the Royal College of General Practitioners, 66(649), 437-8. PMID: 27481982
Bladder cancer is the seventh most common cancer in males worldwide. Every year, about 20,000 people in Japan are diagnosed with bladder cancer, of whom around 8,000--mostly men--succumb to the disease. Bladder cancers can be grouped into two types: non-muscle-invasive cancers, which have a five-year survival rate of 90 percent, and muscle-invasive cancers, which have poor prognoses.
... Read more »
Matsumoto, R., Tsuda, M., Yoshida, K., Tanino, M., Kimura, T., Nishihara, H., Abe, T., Shinohara, N., Nonomura, K., & Tanaka, S. (2016) Aldo-keto reductase 1C1 induced by interleukin-1β mediates the invasive potential and drug resistance of metastatic bladder cancer cells. Scientific Reports, 34625. DOI: 10.1038/srep34625
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