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  • August 6, 2014
  • 04:39 AM

Gastrointestinal response to A1 vs A2 milk

by Paul Whiteley in Questioning Answers

I want to talk about the findings from Ho and colleagues [1] today, and in particular their observation of: "differences in gastrointestinal responses in some adult humans consuming milk containing beta-casein of either the A1 or the A2 beta-casein type". If you're wondering why such a paper finds it's way on to a blog predominantly about autism research, well stay with me on this rather long blogging entry...Start your engines... @ Wikipedia Before progressing, I am going to put a sort of COI (conflict of interest) statement into this blog post. As part of my day job, I have, down the years, been party to some conversations on A2 milk and how one might scientifically test some of the claims / assumptions made about this milk with specific populations in mind. That also our lab has been looking at analytical ways of differentiating A1 and A2 milk from each other is another COI, allowing for the fact that I am neither a consumer of, nor advocate for, anything to do with any of the white stuff.In case you're not up to speed with A1 and A2 milk, well, it all boils down to type of cow and type of milk produced. Anyone with a handle on autism research history will have probably heard about the opioid-excess hypothesis [2]. The long-and-short-of-it is that casein, the protein found in milk and dairy products, is eventually metabolised into it's constituent amino acids. Along the way, short chains of amino acids called peptides are formed. Some of these peptides look (chemically) similar to compounds like morphine and are hence referred to as the casomorphins (casein derived morphine-like). The opioid-excess hypothesis suggested that these exogenously derived peptides mimic some of our own naturally occurring morphine-like compounds that we all have, and disrupt typical functioning in this area to such an extent that it may correlate with some of the signs and symptoms called autism. I talked about something similar quite recently.Granted, such a model looks a little simplistic these days knowing what we think we know about the very plural autisms and the ESSENCE of cormorbidity. Still, such a hypothesis did seem to fit in well with the suggested effectiveness of a casein-free (and gluten-free) diet for some on the autism spectrum, and also some work looking at the opioid receptor blocker that is naltrexone (see here) and autism. It is with the structure of those peptides in mind that we come to the differences suggested for A1 and A2 milk. Y'see not every cow or other mammal produces the same kind of casein protein in their milk and hence peptide formulations can vary also. For A2 casein, the idea is that beta-casomorphin fragment 1-7 (BC 1-7), a peptide formed during digestion is not the same as the BC1-7 from A1 milk (see here) particularly when it comes to a single amino acid change (proline over histidine) [3].After such a long-winded explanation, we come back to the Ho paper and some interesting findings...First things first, this was a double-blind, randomised cross-over study looking at "gastrointestinal effects" in adults under conditions of either A1 or A2 milk consumption. Two weeks of either A1 or A2 milk consumption (with an appropriate washout period in between) were completed.The very informative Bristol Stool Chart was used to grade poop (stool) consistency alongside other more physiological measures such as faecal calprotectin.Results: "The A1 beta-casein milk led to significantly higher stool consistency values". That and a correlation between stool consistency and reports of abdominal pain for participants when on the A1 milk compared with when on A2 milk. Ergo, it didn't seem that A2 milk did anything over and above A1 milk, rather that consumption didn't seem to be linked to the symptoms noted when drinking A1 milk. Appreciating the authors' call for further study in this area, I was intrigued by these results. Not so many moons ago, I came across the paper by Barnett and colleagues [4] talking about greater gastrointestinal (GI) transit time in rats fed A1 milk over A2 milk (see here for some additional commentary from one of the study authors). One might very well overlap those rodent reports with the more recent Ho results in terms of how longer transit time from A1 milk might mean greater discomfort bearing in mind some of the literature on longer transit time and "pain and distension" [5] in certain conditions. Interestingly, the authors ask that research not only focus on confirmation of their results but: "confirmation in a larger study of participants with perceived intolerance to ordinary A1 beta-casein-containing milk" which begs the question: who and what ailments are being reported?That all being said, not all the literature on A2 milk is so directional. Take for example the paper by Crowley and colleagues [6] (open-access) looking at the question of milk consumption correlating with the functional bowel issue constipation. They concluded that: "that removal of CMP [cow's milk protein] from the diet of children with CFC [chronic functional constipation] significantly increased the number of bowel motions and improved constipation". Their results however did not show any significant effect based on casein type when looking at A1 and A2 milk. Constipation, by the way, is also something talked about with some autism in mind (see here) and particularly the findings from Afzal and colleagues [7] which concluded: "Multivariate regression analysis showed consumption of milk to be the strongest predictor of constipation in the autistic group".I am quite interested in this whole area of different milks from different animals potentially possessing different qualities which might impact on physiology particularly if eventually applied to conditions like autism, or at least some comorbidity. I think back to the post I did on milk derived opioid peptides and methylation status (see here) as also being important, as might be the work on something like the use of camel milk (see here) bearing in mind ... Read more »

  • August 5, 2014
  • 01:28 PM

Weight loss Stalled? Kick those Hunger Cravings!

by Gabriel in Lunatic Laboratories

Trying to drop the weight, but find yourself picking up more of it? Is your diet failing because you are so hungry you could eat a horse?  Well a new […]... Read more »

Li SS, Kendall CW, de Souza RJ, Jayalath VH, Cozma AI, Ha V, Mirrahimi A, Chiavaroli L, Augustin LS, Blanco Mejia S.... (2014) Dietary pulses, satiety and food intake: A systematic review and meta-analysis of acute feeding trials. Obesity (Silver Spring, Md.), 22(8), 1773-80. PMID: 24820437  

  • August 5, 2014
  • 10:51 AM

Kids Name the Darnedest Animals

by Elizabeth Preston in Inkfish

Here’s an experiment that’s easy to do on your own. Grab the nearest elementary- or middle-school-age kid, sit her down in a quiet place, and ask her to name everything she can think of that’s alive. The results might tell you a lot about your young subject’s life. The wilder the animals, the more domestic […]The post Kids Name the Darnedest Animals appeared first on Inkfish.... Read more »

  • August 5, 2014
  • 04:05 AM

Bipolar disorder is frequent in adult Asperger syndrome

by Paul Whiteley in Questioning Answers

"BD [bipolar disorder] in AS [Asperger syndrome] patients is frequent, usually it onsets during adolescence and is often characterized by atypical presentation, making its correct identification particularly difficult".Maybe I'm better suited as a brunette? @ WikipediaThat was the primary finding reported by Vannucchi and colleagues [1] based on their systematic review of the relevant peer-reviewed research literature in this area. They found that the prevalence of BD ranged between 6 - 20% depending on the studies included for review. They also reported that "BD assumes peculiar features which might shape its under-recognition or misdiagnosis" in cases of AS. In short, this is an area which perhaps requires a little more investigation.Bipolar disorder, previously called manic depression, is concerned with mood and how it can 'swing' between extremes of depression and mania. Although discussions about the 'causes' of BD parallel discussions on the causes of lots of conditions which manifest psychiatric symptoms, research like that from Faedda and colleagues [2] talking about "generalized anxiety disorders" as risk factors for BD might be important. I've mentioned BD a few times on this blog: be it in relation to the genetic 'common ground' of psychiatry (see here) or the interesting work coming out of Johns Hopkins on gastrointestinal (GI) inflammation and immune activation in cases of BD (see here). Suffice to say that there may be quite a bit more to BD [3] than what just goes on the old grey-pinkish matter.Asperger syndrome probably needs little introduction to regular readers of this blog. In case you don't know, here is the UK National Autistic Society (NAS) description of the condition. As per the growing acceptance that comorbidity, some medical comorbidity, might be elevated when a diagnosis on the autism spectrum is received (see here), there is also a realisation that the presence of autism or AS might also elevate the risk of psychiatric comorbidity too. The paper by Rosenberg and colleagues [4] (open-access here) corroborates this view, and indeed highlights how BD represents one such comorbid psychiatric diagnosis. At the risk of going off at a tangent, I was also intrigued by the finding by Rosenberg et al that: "Autistic regression was associated with lower risk of any comorbidity" which might imply different factors or weightings (genetic, environment) being involved in different types of autism...The comment in the Vannucchi review about "atypical presentation" of BD in cases of AS got me thinking quite a bit. The case report detailed by Frazier and colleagues [5] (open-access) offers some insight into how this atypical presentation might manifest; in particular: "Bipolar disorder should be entertained as a possible diagnosis when there is deterioration in cognition, language, behavior, or activity; when there is a clear pattern of fluctuation or cyclicity in activity, behavior, and interests (with "good times" and "bad times"); and when observed behavior indicates a mood problem". They go on to mention: "His affective [mood] disorder exacerbated the underlying symptoms of Asperger’s [syndrome]" and that: "Once comorbid bipolar disorder was diagnosed and appropriate treatment occurred, Abraham gradually began to recover and his self-injury, aggression, and intense pressured obsessiveness disappeared". Self-injury and aggression eh?I'm not necessarily saying that everyone with AS who has BD will fit into the description provided by Frazier et al in terms of presentation or intervention (which, by the way, was made up of "oral clonazepam... lithium... and risperidone"). But this and other reports do offer some good starting points to looking at the issue of BD as comorbid to cases of AS or other autism spectrum diagnoses. Oh and if one is to assume that something like immune function might be related to cases of BD, maybe, just maybe, one might consider looking at some of the correlates of immune activation as per reports like the one from Emily Severance and colleagues [6] on food potentially being a factor. Food and psychiatry... now where have I heard about that before?Music to close. When You Were Young by The Killers.----------[1] Vannucchi G. et al. Bipolar disorder in adults with Asperger׳s Syndrome: A systematic review. J Affect Disord. 2014 Jul 8;168C:151-160.[2] Faedda GL. et al. Clinical risk factors for bipolar disorders: A systematic review of prospective studies. J Affect Disord. 2014. July 18.[3] Rege S. & Hodgkinson SJ. Immune dysregulation and autoimmunity in bipolar disorder: Synthesis of the evidence and its clinical application. Aust N Z J Psychiatry. 2013 Dec;47(12):1136-51.[4] Rosenberg RE. et al. Parent report of community psychiatric comorbid diagnoses in autism spectrum disorders. Autism Res Treat. 2011;2011:405849.[5] Frazier JA. et al. Treating a child with Asperger's disorder and comorbid bipolar disorder. Am J Psychiatry. 2002 Jan;159(1):13-21[6] Severance EG. et al. Immune activation by casein dietary antigens in bipolar disorder. Bipolar Disord. 2010 Dec;12(8):834-42.----------Vannucchi G, Masi G, Toni C, Dell׳Osso L, Erfurth A, & Perugi G (2014). Bipolar disorder in adults with Asperger׳s Syndrome: A systematic review. Journal of affective disorders, 168C, 151-160 PMID: 25046741... Read more »

Vannucchi G, Masi G, Toni C, Dell׳Osso L, Erfurth A, & Perugi G. (2014) Bipolar disorder in adults with Asperger׳s Syndrome: A systematic review. Journal of affective disorders, 151-160. PMID: 25046741  

  • August 4, 2014
  • 02:02 PM

Want a Larger Brain: How About an Implant?

by Gabriel in Lunatic Laboratories

Feel like you could use some extra grey matter? Maybe get a dash of genius added to all those cobwebs in the brain? Well then science might just have the […]... Read more »

Hemmer, K., Zhang, M., van Wüllen, T., Sakalem, M., Tapia, N., Baumuratov, A., Kaltschmidt, C., Kaltschmidt, B., Schöler, H., Zhang, W.... (2014) Induced Neural Stem Cells Achieve Long-Term Survival and Functional Integration in the Adult Mouse Brain. Stem Cell Reports. DOI: 10.1016/j.stemcr.2014.06.017  

  • August 4, 2014
  • 10:45 AM

Who said beer is just for drinking?

by Sarah Wilson in The 'Scope

An alternative use for beer that will "get under your skin"!... Read more »

Chen, W., Becker, T., Qian, F., & Ring, J. (2014) Beer and beer compounds: physiological effects on skin health. Journal of the European Academy of Dermatology and Venereology, 28(2), 142-150. DOI: 10.1111/jdv.12204  

  • August 4, 2014
  • 07:31 AM

‘‘Transit amplification in the cerebellum evolved via a heterochronic shift in NeuroD1 expression’’

by Thomas Butts in the Node

They are a mouthful, paper titles, sometimes. This is exactly the sort of title that would have made me ignore it in the days when I worked on the evolution of Hox genes. But I now find myself frequently justifying to people who work on evolution why the nervous system deserves attention, and of justifying […]... Read more »

  • August 4, 2014
  • 04:10 AM

Stopping gliadin peptides in their tracks?

by Paul Whiteley in Questioning Answers

A micropost if you will, to bring to your attention the paper by Marco Sarno and colleagues [1] and their suggestion of "a novel effect of probiotics in the prevention of undigested gliadin peptides toxic effects".Knitting on't Moors @ Wikipedia The probiotic in question is something called Lactobacillus paracasei CBA L74, which if I'm not mistaken is connected with a certain '57 varieties' company. The authors (which included one Alessio Fasano) indicated that said probiotic appeared to inhibit two gliadin peptides, P31-43 and P57-68, entrance in Caco2 cells, a model of the intestinal barrier [2]. Given that the entrance of such gliadin peptides into the gut mucosa (well the lamina propria) is part of the autoimmune condition known as coeliac (celiac) disease (see here), one might reasonably assume that use of Lactobacillus paracasei CBA L74 (LP CBA L74) might hold some potential as a possible treatment strategy outside of the standard gluten-free diet. At the very least, assuming some further investigations are indicated, it might be added to the list of other compounds being tested with coeliac disease in mind (see here).I note that this is not the first time that LP CBA L74 has come under the peer-reviewed research spotlight as per the paper by Elena Zagato and colleagues [3] (open-access here). On that occasion the authors reported that: "fermented products of Lactobacillus paracasei CBA L74 act via the inhibition of proinflammatory cytokine release" and "could protect against colitis and against an enteric pathogen infection". With those statements in mind, I wonder whether coeliac disease might just be the tip of the iceberg when it comes to the applications for LP CBA L74 as per the work of a distant relation?Speaking of tracks, here's Smokey and the Tracks of My Tears.----------[1] Sarno M. et al. Lactobacillus paracasei CBA L74 interferes with gliadin peptides entrance in Caco-2 cells. Int J Food Sci Nutr. 2014 Jul 17:1-7.[2] Sambuy Y. et al. The Caco-2 cell line as a model of the intestinal barrier: influence of cell and culture-related factors on Caco-2 cell functional characteristics. Cell Biol Toxicol. 2005 Jan;21(1):1-26.----------Sarno M, Lania G, Cuomo M, Nigro F, Passannanti F, Budelli A, Fasano F, Troncone R, Auricchio S, Barone MV, Nigro R, & Nanayakkara M (2014). Lactobacillus paracasei CBA L74 interferes with gliadin peptides entrance in Caco-2 cells. International journal of food sciences and nutrition, 1-7 PMID: 25030417... Read more »

Sarno M, Lania G, Cuomo M, Nigro F, Passannanti F, Budelli A, Fasano F, Troncone R, Auricchio S, Barone MV.... (2014) Lactobacillus paracasei CBA L74 interferes with gliadin peptides entrance in Caco-2 cells. International journal of food sciences and nutrition, 1-7. PMID: 25030417  

  • August 3, 2014
  • 07:12 PM

Ebola: Role of the Glycoprotein in viral entry and ER stress

by thelonevirologist in Virology Tidbits

Ebola viruses (EBOV) are the causative agent of severe hemorrhagic fever in humans with a high mortality rate, with a case fatality rate of up to 90%, with Ebola Zaire the most pathogenic.The role of viral Glycoprotein in viral entry and induction of apoptosis are discussed.... Read more »

Ito H, Watanabe S, Sanchez A, Whitt MA, & Kawaoka Y. (1999) Mutational analysis of the putative fusion domain of Ebola virus glycoprotein. Journal of virology, 73(10), 8907-12. PMID: 10482652  

Matsuyama, S., Ujike, M., Morikawa, S., Tashiro, M., & Taguchi, F. (2005) Protease-mediated enhancement of severe acute respiratory syndrome coronavirus infection. Proceedings of the National Academy of Sciences, 102(35), 12543-12547. DOI: 10.1073/pnas.0503203102  

Schornberg K, Matsuyama S, Kabsch K, Delos S, Bouton A, & White J. (2006) Role of endosomal cathepsins in entry mediated by the Ebola virus glycoprotein. Journal of virology, 80(8), 4174-8. PMID: 16571833  

Marzi A, Reinheckel T, & Feldmann H. (2012) Cathepsin B . PLoS neglected tropical diseases, 6(12). PMID: 23236527  

Carette JE, Raaben M, Wong AC, Herbert AS, Obernosterer G, Mulherkar N, Kuehne AI, Kranzusch PJ, Griffin AM, Ruthel G.... (2011) Ebola virus entry requires the cholesterol transporter Niemann-Pick C1. Nature, 477(7364), 340-3. PMID: 21866103  

Miller EH, Obernosterer G, Raaben M, Herbert AS, Deffieu MS, Krishnan A, Ndungo E, Sandesara RG, Carette JE, Kuehne AI.... (2012) Ebola virus entry requires the host-programmed recognition of an intracellular receptor. The EMBO journal, 31(8), 1947-60. PMID: 22395071  

Aleksandrowicz P, Marzi A, Biedenkopf N, Beimforde N, Becker S, Hoenen T, Feldmann H, & Schnittler HJ. (2011) Ebola virus enters host cells by macropinocytosis and clathrin-mediated endocytosis. The Journal of infectious diseases. PMID: 21987776  

Bröcker C, Kuhlee A, Gatsogiannis C, Balderhaar HJ, Hönscher C, Engelbrecht-Vandré S, Ungermann C, & Raunser S. (2012) Molecular architecture of the multisubunit homotypic fusion and vacuole protein sorting (HOPS) tethering complex. Proceedings of the National Academy of Sciences of the United States of America, 109(6), 1991-6. PMID: 22308417  

Lamb CA, Yoshimori T, & Tooze SA. (2013) The autophagosome: origins unknown, biogenesis complex. Nature reviews. Molecular cell biology, 14(12), 759-74. PMID: 24201109  

Ao X, Zou L, & Wu Y. (2014) Regulation of autophagy by the Rab GTPase network. Cell death and differentiation, 21(3), 348-58. PMID: 24440914  

Takáts S, Pircs K, Nagy P, Varga Á, Kárpáti M, Hegedűs K, Kramer H, Kovács AL, Sass M, & Juhász G. (2014) Interaction of the HOPS complex with Syntaxin 17 mediates autophagosome clearance in Drosophila. Molecular biology of the cell, 25(8), 1338-54. PMID: 24554766  

Olejnik J, Alonso J, Schmidt KM, Yan Z, Wang W, Marzi A, Ebihara H, Yang J, Patterson JL, Ryabchikova E.... (2013) Ebola virus does not block apoptotic signaling pathways. Journal of virology, 87(10), 5384-96. PMID: 23468487  

McElroy AK, Erickson BR, Flietstra TD, Rollin PE, Nichol ST, Towner JS, & Spiropoulou CF. (2014) Ebola hemorrhagic Fever: novel biomarker correlates of clinical outcome. The Journal of infectious diseases, 210(4), 558-66. PMID: 24526742  

  • August 3, 2014
  • 04:11 PM

The Alondra Oubré Academic Fraud Exposed

by nooffensebut in The Unsilenced Science

Two respected authors, Alondra Oubré and Massimo Pigliucci, are implicated in the academic fraud of taking false information from Wikipedia and falsely attributing it to a research database in order to fulminate against the conclusions of Nicholas Wade’s book, A Troublesome Inheritance, and the science of the warrior gene, monoamine oxidase A.... Read more »

Alia-Klein N, Goldstein RZ, Tomasi D, Woicik PA, Moeller SJ, Williams B, Craig IW, Telang F, Biegon A, Wang GJ.... (2009) Neural mechanisms of anger regulation as a function of genetic risk for violence. Emotion (Washington, D.C.), 9(3), 385-96. PMID: 19485616  

Buckholtz JW, Callicott JH, Kolachana B, Hariri AR, Goldberg TE, Genderson M, Egan MF, Mattay VS, Weinberger DR, & Meyer-Lindenberg A. (2008) Genetic variation in MAOA modulates ventromedial prefrontal circuitry mediating individual differences in human personality. Molecular psychiatry, 13(3), 313-24. PMID: 17519928  

Cerasa A, Cherubini A, Quattrone A, Gioia MC, Magariello A, Muglia M, Manna I, Assogna F, Caltagirone C, & Spalletta G. (2010) Morphological correlates of MAO A VNTR polymorphism: new evidence from cortical thickness measurement. Behavioural brain research, 211(1), 118-24. PMID: 20303364  

Fergusson DM, Boden JM, Horwood LJ, Miller A, & Kennedy MA. (2012) Moderating role of the MAOA genotype in antisocial behaviour. The British journal of psychiatry : the journal of mental science, 200(2), 116-23. PMID: 22297589  

Gilad Y, Rosenberg S, Przeworski M, Lancet D, & Skorecki K. (2002) Evidence for positive selection and population structure at the human MAO-A gene. Proceedings of the National Academy of Sciences of the United States of America, 99(2), 862-7. PMID: 11805333  

Huang YY, Cate SP, Battistuzzi C, Oquendo MA, Brent D, & Mann JJ. (2004) An association between a functional polymorphism in the monoamine oxidase a gene promoter, impulsive traits and early abuse experiences. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 29(8), 1498-505. PMID: 15150530  

Koen L, Kinnear C, Corfield V, Emsley R, Jordaan E, Keyter N, Moolman-Smook J, Stein D, & Niehaus D. (2004) Violence in male patients with schizophrenia: risk markers in a South African population. Australian and New Zealand Journal of Psychiatry, 38(4), 254-259. DOI: 10.1111/j.1440-1614.2004.01338.x  

Kunugi H, Ishida S, Kato T, Tatsumi M, Sakai T, Hattori M, Hirose T, & Nanko S. (1999) A functional polymorphism in the promoter region of monoamine oxidase-A gene and mood disorders. Molecular psychiatry, 4(4), 393-5. PMID: 10483059  

Lei H, Zhang X, Di X, Rao H, Ming Q, Zhang J, Guo X, Jiang Y, Gao Y, Yi J.... (2014) A Functional Polymorphism of the MAOA Gene Modulates Spontaneous Brain Activity in Pons. BioMed research international, 243280. PMID: 24971323  

Philibert RA, Gunter TD, Beach SR, Brody GH, & Madan A. (2008) MAOA methylation is associated with nicotine and alcohol dependence in women. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 147B(5), 565-70. PMID: 18454435  

Williams RB, Marchuk DA, Gadde KM, Barefoot JC, Grichnik K, Helms MJ, Kuhn CM, Lewis JG, Schanberg SM, Stafford-Smith M.... (2003) Serotonin-related gene polymorphisms and central nervous system serotonin function. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 28(3), 533-41. PMID: 12629534  

Wong CC, Caspi A, Williams B, Craig IW, Houts R, Ambler A, Moffitt TE, & Mill J. (2010) A longitudinal study of epigenetic variation in twins. Epigenetics : official journal of the DNA Methylation Society, 5(6), 516-26. PMID: 20505345  

Yu YW, Tsai SJ, Hong CJ, Chen TJ, Chen MC, & Yang CW. (2005) Association study of a monoamine oxidase a gene promoter polymorphism with major depressive disorder and antidepressant response. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 30(9), 1719-23. PMID: 15956990  

  • August 3, 2014
  • 02:37 PM

Is Fat making you… Fat?

by Gabriel in Lunatic Laboratories

Fast food, let’s face it, it’s not the best for you. Yet Mcdonalds and Pizza hut are known practically world wide [although menu options differ]. With the rise of our […]... Read more »

  • August 2, 2014
  • 01:53 PM

At risk for Cancer? Try Spicy Food!

by Gabriel in Lunatic Laboratories

Like spicy food? Well next time you eat some you should hug that chili pepper, because he might just save your life. This is an interesting find, researchers have found that […]... Read more »

de Jong PR, Takahashi N, Harris AR, Lee J, Bertin S, Jeffries J, Jung M, Duong J, Triano AI, Lee J.... (2014) Ion channel TRPV1-dependent activation of PTP1B suppresses EGFR-associated intestinal tumorigenesis. The Journal of clinical investigation. PMID: 25083990  

  • August 1, 2014
  • 01:12 PM

Possible treatment and Prevention for Parkinson’s

by Gabriel in Lunatic Laboratories

Parkinson’s disease affects neurons in a particular brain region, when it develops brain cells have their mitochondrial activity cease and then the cells die. But now researchers have shown that supplying D-lactate […]... Read more »

  • August 1, 2014
  • 09:35 AM

Fly Life: Why fruit flies are a good model organism for research

by Bethany Christmann in Fly on the Wall

What makes Drosophila melanogaster (fruit flies) a good model organism for research? A general overview of fruit flies and some important papers demonstrating their relevance to human health.... Read more »

Valente EM, Salvi S, Ialongo T, Marongiu R, Elia AE, Caputo V, Romito L, Albanese A, Dallapiccola B, & Bentivoglio AR. (2004) PINK1 mutations are associated with sporadic early-onset parkinsonism. Annals of neurology, 56(3), 336-41. PMID: 15349860  

Adams MD, Celniker SE, Holt RA, Evans CA, Gocayne JD, Amanatides PG, Scherer SE, Li PW, Hoskins RA, Galle RF.... (2000) The genome sequence of Drosophila melanogaster. Science (New York, N.Y.), 287(5461), 2185-95. PMID: 10731132  

Lloyd TE, & Taylor JP. (2010) Flightless flies: Drosophila models of neuromuscular disease. Annals of the New York Academy of Sciences. PMID: 20329357  

  • August 1, 2014
  • 08:00 AM

The Friday Five for 8/1/2014

by Bill Sullivan in The 'Scope

Five of the coolest science news stories of the week! Friends & DNA, Alzheimer’s, a satanic gecko, fist bumps, and political brains... Read more »

Christakis, N., & Fowler, J. (2014) Friendship and natural selection. Proceedings of the National Academy of Sciences, 111(Supplement_3), 10796-10801. DOI: 10.1073/pnas.1400825111  

  • August 1, 2014
  • 07:18 AM


by Amy Swanston in Antisense Science

Tumours are incredibly heterogeneic- that is that they have different properties including morphology (how they look), metabolism (the processes they use to generate energy), proliferation (how fast they grow, divide and replicate themselves) and potential to metastasise (where a tumour moves to another part of the body). But why is this so?

Many people are under the assumption that a cancer will arise from a single mutation in the DNA, but this is not actually the case. For a cancer to develop we must first have that single mutation, or “hit”, which may make a cell more likely to receive further mutations. But in a final tumour mass what we actually find is that different populations of cells have entirely different mutations. The “clonal evolution” theory explains that this is because the initial few mutations have a cascading effect, allowing further DNA damage, and as these damaged cancerous cells replicate themselves their daughter cells will in turn develop further mutations.... Read more »

Lo, Y., Corbetta, N., Chamberlain, P., Rai, V., Sargent, I., Redman, C., & Wainscoat, J. (1997) Presence of fetal DNA in maternal plasma and serum. The Lancet, 350(9076), 485-487. DOI: 10.1016/S0140-6736(97)02174-0  

De Mattos-Arruda L, Weigelt B, Cortes J, Won HH, Ng CK, Nuciforo P, Bidard FC, Aura C, Saura C, Peg V.... (2014) Capturing Intra-Tumor Genetic Heterogeneity by De Novo Mutation Profiling of Circulating Cell-Free Tumor DNA: A Proof-of-Principle. Annals of oncology : official journal of the European Society for Medical Oncology / ESMO. PMID: 25009010  

Pantel K, & Alix-Panabières C. (2013) Real-time liquid biopsy in cancer patients: fact or fiction?. Cancer research, 73(21), 6384-8. PMID: 24145355  

  • August 1, 2014
  • 06:26 AM

Investing in cancer research pays off

by Lizzie Perdeaux in BHD Research Blog

In the UK, a significant amount of medical research funding – an estimated £2.9 billion in 2012/13 – comes from the public purse through taxes and charitable donations, or from the Wellcome Trust, so it is important to see whether … Continue reading →... Read more »

  • August 1, 2014
  • 03:46 AM

Restricted and repetitive behaviours disappeared? More optimal outcome and autism

by Paul Whiteley in Questioning Answers

Today I'm bringing to your attention the paper by Eva Troyb and colleagues [1] and the quite dramatic assertion: "Reports of current behavior indicated that RRB's [restricted and repetitive behaviors] had almost totally disappeared in the OO [optimal outcomes] group". RRBs just in case you might not know include quite an array of behaviours, some of which might not be considered 'disabling' such as the presence of certain circumscribed interests. Others, such as an insistence of sameness and the presence of often rigid routines, can have a rather more profound effect on quality of life.Where's my hat? @ Wikipedia For those who might not know, optimal outcome in relation to cases of autism spectrum disorder (ASD) refers to the idea that for some (emphasis on some) diagnosed as being on the autism spectrum, the label of autism or ASD is not as immutable as was once thought. The latest Troyb paper adds to a growing body of literature in this area coincidentally talked about in this piece appearing recently in the New York Times.I've covered this emerging area of work for some time on this blog and so present a brief history so far...beginning with the concept of differing developmental trajectories being present across the very heterogeneous autism spectrum (see here),then there was the publication of the paper by Deborah Fein and colleagues [2] first discussing optimal outcome and autism (see here),further research on the nature of optimal outcome followed and how it might impact on some of the psychology associated with autism (see here),optimal outcome, by any other name, was described by other independent research groups (see here),and then focus shifted to a possible role for intervention as being associated with optimal outcome (see here).I might add that whilst I have indicated the Fein paper was the first to describe optimal outcome in respect of ASD, there have been some rumblings down the ages in the autism research peer-reviewed literature about remission of core symptoms. Take for example the paper by Gajzago & Prior [3] from 1974 reporting on 2 children "thought to be classical cases of Kanner syndrome" who went on to be "functioning adequately both intellectually and socially and are progressing normally at local schools". Mention of the word 'recovery' in the title of that paper, sandwiched in between quotation marks, hints at how delicate a subject symptom remission was even in those times.I will, as I always seem to do on this topic, reiterate that when talking about optimal outcome and autism we are not talking about some universal concept occurring across the entire autism spectrum. For the majority of those diagnosed as being on the autism spectrum, their strengths and difficulties are a lifelong feature albeit fluctuating and changing/adapting as a consequence of factors like maturation, the presence of comorbidity and the environment they find themselves in. The group which do seem to fit into the concept of optimal outcome however, represent an important part of that autism spectrum insofar as increasing our knowledge about just how heterogeneous a condition autism really is [4] and how, far from being a singular condition, autism is perhaps better reflected in the description of the more plural autisms (see here). ----------[1] Troyb E. et al. Restricted and Repetitive Behaviors in Individuals with a History of ASDs Who Have Achieved Optimal Outcomes. J Autism Dev Disord. 2014 Jul 17. [Epub ahead of print][2] Fein D. et al. Optimal outcome in individuals with a history of autism. J Child Psychol Psychiatry. 2013 Feb;54(2):195-205.[3] Gajzago C & Prior M. Two Cases of "Recovery" in Kanner Syndrome. Arch Gen Psychiatry. 1974;31(2):264-268.[4] Kohane IS. An Autism Case History to Review the Systematic Analysis of Large-Scale Data to Refine the Diagnosis and Treatment of Neuropsychiatric Disorders. Biol Psychiatry. 2014 Jun 12. pii: S0006-3223(14)00422-3. ----------Troyb E, Orinstein A, Tyson K, Eigsti IM, Naigles L, & Fein D (2014). Restricted and Repetitive Behaviors in Individuals with a History of ASDs Who Have Achieved Optimal Outcomes. Journal of autism and developmental disorders PMID: 25030967... Read more »

  • August 1, 2014
  • 03:11 AM

Floating Fried Eggs

by beredim in Strange Animals

Fried Egg JellyfishCotylorhiza tuberculataThe common name says it all. This weird-looking jellyfish literally looks like a fried egg! Scientifically known as Cotylorhiza tuberculata, it is one of the two jellyfish species that resemble a fried egg. The other one is Phacellophora camtschatica. Not surprisingly, it also goes by the same name.They may look tasty, but you probably don't want to have one for breakfast! However, you can have a lot of fun with C. tuberculata. This jellyfish has a mild sting that causes very little - if any - pain to humans. One of my best childhood memories is me and my friends grabbing them with our bare hands and wearing them like hats to other unsuspecting kids! To be honest, it's something I continue to do. Give it a try if you ever happen to come across one. Just avoid doing it to strangers, I don't think they will appreciate it!Now, let's learn a few things about these two strange, egg-like creatures:Credit: Rosario Beach Marine Laboratory(CC BY-NC-SA 2.0)Kingdom: AnimaliaPhylum: CnidariaClass: ScyphozoaOrder: SemaeostomeaeFamily: PhacellophoridaeGenus: PhacellophoraSpecies: Phacellophora camtschaticaCommon Name(s): Fried egg jellyfish or egg-yolk jellyfishP. camtschatica is a massive jellyfish, with a bell up to 60 cm (23 in) in diameter and sixteen clusters of up to a few dozen tentacles, each measuring up to 6 m (~20 ft) long. In the past, the species was part of the family Ulmaridae, but is now listed as the sole member of the family Phacellophoridae.This cool-water jellyfish can be found in all major oceans, occurring in depths ranging from 0 to 168 m. Its diet is mainly comprised of other smaller jellyfish and gelatinous zooplankton, that get trapped in its tentacles. It spends much of its life motionless or slowly pulsing the bell while drifting. The egg-yolk jellyfish has a very weak sting. Many small crustaceans take advantage of this - like the larva of the Cancer gracilis crab - and regularly ride on its bell and even steal food from its oral arms and tentacles!Fried egg jellyfish, Enoshima Aquarium, Japan.Much of our knowledge on the species' life cycle comes from the Monterey Bay and other public aquariums, which have had much success in breeding the species. Fertilized eggs develop into ciliated planula larvae which swim, then settle and metamorphose into scyphistoma polyps. Mature scyphistoma have 30 to 44 tentacles and reproduce asexually by side budding as well as strobilating to produce ephyra which develop into mature jellyfish. In captivity, it takes about 9 months for an ephyra to grow into a mature medusa.By T.Friedrich CC-BY-2.5Kingdom: AnimaliaPhylum: CnidariaClass: ScyphozoaOrder: RhizostomeaeFamily: CepheidaeGenus: CotylorhizaSpecies: Cotylorhiza tuberculataCommon Name(s): Mediterranean jelly, Fried egg jellyfishC. tuberculata is a species of jellyfish commonly found in aggregations in the Mediterranean, Aegean and Adriatic Sea. As aforementioned, it has a sting with little to no effect on humans. The scientific name Cotylorhiza is derived by the greek words “κοντύλι,” meaning cup, and “ρίζα,” meaning root.A typical adult measures 17 to 20 centimeters wide, though they can reach 50 centimeters across. They have a smooth, elevated dome that is surrounded by a gutter-like ring. The marginal lappets are elongated and subrectangular. Each mouth-arm bifurcates near its base and branches several times. In addition to some larger appendages there are many short, club-shaped ones that bear disk-like ends.Mediterranean jelly, somewhere in GreeceThese jellies primarily feed on zooplankton and reproduce asexually. Larva attach themselves to a hard ocean surface and grow in a polyp colony that looks like a stack of saucers. The tiny babies are then released from capsules, like spaceships and drift away.Phacellophora camtschatica: References & Further Reading- Reum, J., Hunsicker, M., & Paulsen, C. (2010). Species Composition and Relative Abundance of Large Medusae in Puget Sound, Washington Northwest Science, 84 (2), 131-140 DOI: 10.3955/046.084.0202- Widmer, C. (2006). Life cycle of Phacellophora camtschatica (Cnidaria: Scyphozoa) Invertebrate Biology, 125 (2), 83-90 DOI: 10.1111/j.1744-7410.2006.00043.x- ... Read more »

  • July 31, 2014
  • 05:26 PM

Functional Neuroimaging’s Neymar Problem

by Neuroskeptic in Neuroskeptic_Discover

As a “World Cup tie in post” this one’s a bit late, but here’s a story that’s been getting a lot of attention: According to scientists, Neymar uses instinct and not his brain when playing football Yes, if you believe the headlines, research has shown that legendary Brazilian forward Neymar da Silva Santos is so […]The post Functional Neuroimaging’s Neymar Problem appeared first on Neuroskeptic.... Read more »

Eiichi Naito, & Satoshi Hirose. (2014) Efficient foot motor control by Neymar’s brain. Front. Hum. Neurosci. info:/

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