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  • September 15, 2014
  • 12:58 PM

The Genetic Roots of Schizophrenia

by Gabriel in Lunatic Laboratories

I have a friend who lost an eye — not in a war zone like you might suspect given my background — but to his brother. Yes, you read that correctly, his brother tried to kill him and in the process he lost his eye. I’ve told this story before, but whenever new schizophrenia research comes out I feel the need to tell it again. While he has forgiven his brother (partly because not long after, he was diagnosed as schizophrenic), he will not be able to see him again until he is released from prison. A tragedy that could’ve been avoided had he been diagnosed sooner.... Read more »

avier Arnedo, M.S.; Dragan M. Svrakic, M.D., Ph.D.; Coral del Val, Ph.D.; Rocío Romero-Zaliz, Ph.D.; Helena Hernández-Cuervo, M.D.; Molecular Genetics of Schizophrenia Consortium; Ayman H. Fanous, M.D.; Michele T. Pato, M.D.; Carlos N. Pato, M.D., Ph.D. (2014) Uncovering the Hidden Risk Architecture of the Schizophrenias: Confirmation in Three Independent Genome-Wide Association Studies. The American Journal of Psychiatry. info:/10.1176/appi.ajp.2014.14040435

  • September 15, 2014
  • 08:00 AM

Sweating Is The Pits

by Mark E. Lasbury in The 'Scope

New research is delving into the possible negative aspects of antiperspirants and deodorants. A 2014 study indicates that bacterial fauna is altered by the use of antiperspirants and can lead to overgrowth of bacteria that actually produce more foul smelling chemicals. On a more important note, research is showing that aluminum from antiperspirants may contribute to breast cancer growth, including promotion of estrogen hormone production, altered iron metabolism, and increased oxygen radical formation. However, no definitive proof shows that antiperspirants cause breast cancer, and a 2013 study showed no difference in aluminum levels from normal to diseased tissue.... Read more »

Callewaert C, Hutapea P, Van de Wiele T, & Boon N. (2014) Deodorants and antiperspirants affect the axillary bacterial community. Archives of dermatological research. PMID: 25077920  

  • September 15, 2014
  • 04:47 AM

Zinc and copper and autism

by Paul Whiteley in Questioning Answers

The paper by Li and colleagues [1] looking at serum copper (Cu) and zinc (Zn) levels in a group of participants diagnosed with an autism spectrum disorder (ASD) is the source material for today's post. Highlighting how "mean serum Zn levels and Zn/Cu ratio were significantly lower in children with ASD compared with normal cases... whereas serum Cu levels were significantly higher" the continued focus on the metallome in autism carries on at a pace. I should at this point out that I'm not in favour of the use of the word 'normal' in this or any context (anyone who feels that they are normal, please make themselves known to the population at large)."Bring me... the bore worms!"Anyhow... I've talked zinc and autism / other conditions on this blog quite a few times (see here and see here). Alongside other more recent data [2] there is a growing realisation that zinc deficiency present in at least some diagnosed on the autism spectrum might have quite a few implications. With this thought in mind, I might also draw your attention to the recent paper by Chaves-Kirsten and colleagues [3] talking about how zinc might also show some connection to the protein kinase of the hour, mTOR (see here) and in particular reducing mTOR levels in a rodent model of autism. This follows other work in this area [4].The Li paper alongside looking at individual levels of zinc and copper and how they seemed to correlate with presented symptoms according to the Childhood Autism Rating Scale (CARS) also talks about the zinc/copper ratio which is something that has been previously discussed in the peer-reviewed literature with reference to autism and various other conditions as per the excellent review by Osredkar & Sustar [5] (open-access). The paper by Faber and colleagues [6] for example, indicated that a low Zn/Cu ratio may "indicate decrement in metallothionein system functioning". They also talked about how issues with this ratio "may be a biomarker of heavy metal, particularly mercury, toxicity in children with ASDs" as per the various biological uses of metallothionein [7]. I know this moves discussions into some quite uncomfortable realms but science is science (see here) and one should not be afraid to have scientific discourse on any topic. Importantly too, the Faber results also seemed to show more than a passing similarity to those presented by Li et al. Same goes for the paper by Russo and colleagues [8].The other interesting point recorded by Li and colleagues was their use of the good 'ole ROC curve as a means to indicate an "auxiliary diagnosis of autism". More frequently linked to a certain Egyptian-Saudi autism research group (see here), ROC curves - "a fundamental tool for diagnostic test evaluation" - basically plots the true positive rate against the false positive rate for a test. Li et al projected the cut-off value for the Zn/Cu ratio to be 0.665 for a diagnosis, with "a sensitivity of 90.0% and a specificity of 91.7%". Bearing in mind the relatively small participants included for analysis (n=60), those aren't bad figures for sensitivity and specificity remembering my recent discussions on the observation-based classifier (OBC) from Wall and colleagues [9] (see here) and what they got.There's little more for me to say about the Li data that I haven't already said here and in other posts on this topic. If you want to read a little more about the possible role of zinc and copper in cases of autism, the report by Bjorklund [10] covers quite a bit of the literature on possible links. The next question is what might we be able to do about any issues in this area? [11]So then, The Last of the Famous International Playboys? (not me of course..)----------[1] Li SO. et al. Serum copper and zinc levels in individuals with autism spectrum disorders. Neuroreport. 2014 Aug 26.[2] Grabrucker S. et al. Zinc deficiency dysregulates the synaptic ProSAP/Shank scaffold and might contribute to autism spectrum disorders. Brain. 2014 Jan;137(Pt 1):137-52.[3] Chaves-Kirsten GP. et al. Prenatal zinc prevents mTOR disturbance in a rat model of autism induced by prenatal lipopolysaccharide. Brain, Behavior & Immunity. 2014; 40: e11-e12.[4] McClung JP. et al. Effect of supplemental dietary zinc on the mTOR signaling pathway in skeletal muscle from post-absorptive mice. FASEB J. 2006; 20 (Meeting Abstract Supplement) A627.[5] Osredkar J. & Sustar N. Copper and Zinc, Biological Role and Significance of Copper/ZincImbalance. Journal of Clinical Toxicology. 2011; S3.[6] Faber S. et al. The plasma zinc/serum copper ratio as a biomarker in children with autism spectrum disorders. Biomarkers. 2009 May;14(3):171-80.[7] Coyle P. et al. Metallothionein: the multipurpose protein. Cell Mol Life Sci. 2002 Apr;59(4):627-47.[8] Russo AJ. et al. Plasma copper and zinc concentration in individuals with autism correlate with selected symptom severity. Nutr Metab Insights. 2012 Feb 28;5:41-7.[9] Duda M. et al. Testing the accuracy of an observation-based classifier for rapid detection of autism risk. Transl Psychiatry. 2014 Aug 12;4:e424.[10] Bjorklund G. The role of zinc and copper in autism spectrum disorders. Acta Neurobiol Exp (Wars). 2013;73(2):225-36.[11] Russo AJ. & Devito R. Analysis of Copper and Zinc Plasma Concentration and the Efficacy of Zinc Therapy in Individuals with Asperger's Syndrome, Pervasive Developmental Disorder Not Otherwise Specified (PDD-NOS) and Autism. Biomark Insights. 2011;6:127-33.----------... Read more »

  • September 15, 2014
  • 12:05 AM

Acute Gains in Motion After Single Bout of Stretching Predicts Short-Term Gains

by Jane McDevitt in Sports Medicine Research (SMR): In the Lab & In the Field

Acute changes in flexibility after either static or PNF stretching predict the gains in flexibility after a 7-day stretching program.... Read more »

  • September 14, 2014
  • 02:24 PM

Biospleen Helps Clean Blood to Prevent Sepsis

by Gabriel in Lunatic Laboratories

When a patient has sepsis Things can go downhill fast. A life-threatening condition in which bacteria or fungi multiply in a patient's blood -- sepsis is often too fast for antibiotics to help. But that's all about to change with the introduction of a new device -- inspired by the human spleen -- that may radically transform the way doctors treat sepsis.... Read more »

Kang JH, Super M, Yung CW, Cooper RM, Domansky K, Graveline AR, Mammoto T, Berthet JB, Tobin H, Cartwright MJ.... (2014) An extracorporeal blood-cleansing device for sepsis therapy. Nature medicine. PMID: 25216635  

  • September 14, 2014
  • 01:00 AM

Telepathy is Almost Here

by Viputheshwar Sitaraman in Draw Science

Telepathy is under works; it's just super clunky right now. Non-invasive technology enables brain-to-brain communication by converting words into binary and from binary into pulses of light and back.... Read more »

Grau C, Ginhoux R, Riera A, Nguyen TL, Chauvat H, Berg M, Amengual JL, Pascual-Leone A, & Ruffini G. (2014) Conscious Brain-to-Brain Communication in Humans Using Non-Invasive Technologies. PloS one, 9(8). PMID: 25137064  

  • September 13, 2014
  • 01:13 PM

Need a Kidney? Lab Grown Kidneys Coming Soon!

by Gabriel in Lunatic Laboratories

Stem cells offered the promise of having a patents own organ grown to replace a failing or damaged one. Unfortunately the road to that future has been paved with seemingly insurmountable challenges. Thankfully now we are one step closer, researchers have addressed a major challenge in the quest to build replacement kidneys in the lab. Working with human-sized pig kidneys, the scientists developed the most successful method to date to keep blood vessels in the new organs open and flowing with blood.... Read more »

In Kap Ko,, Mehran Abolbashari,, Jennifer Huling,, Cheil Kim,, Sayed-Hadi Mirmalek-Sani,, Mahmoudreza Moradi,, Giuseppe Orlando,, John D. Jackson,, Tamer Aboushwareb,, Shay Soker,.... (2014) Enhanced re-endothelialization of acellular kidney scaffolds for whole organ engineering via antibody conjugation of vasculatures. Technology . info:/10.1142/S2339547814500228

  • September 12, 2014
  • 09:52 PM

The Re-emergence of the Minimal Running Shoe

by Craig Payne in Running Research Junkie

The Re-emergence of the Minimal Running Shoe ... Read more »

Davis IS. (2014) The Re-emergence of the Minimal Running Shoe. The Journal of orthopaedic and sports physical therapy, 1-19. PMID: 25211531  

  • September 12, 2014
  • 03:44 PM

Inflammation of the Brain and Memory Problems

by Gabriel in Lunatic Laboratories

Neurological disorders typically involve memory issues. Most of the problems are attributed to plaques that build up in the brain (which are typically prions), yet some causes are unknown. New research however sheds some light on at least one cause of memory problems. As it turns out brain inflammation can rapidly disrupt our ability to retrieve complex memories of similar but distinct experiences.... Read more »

  • September 12, 2014
  • 11:47 AM

Insulin, growth hormone and risk of schizophrenia?

by Paul Whiteley in Questioning Answers

"Overall, the present findings suggest that metabolic and hormonal disturbances such as effects on insulin and growth hormone may represent a vulnerability factor to develop mental disorders". That was the conclusion reported by van Beveren and colleagues [1] (open-access) looking at "disruption of insulin and growth factor signaling pathways as an increased risk factor for schizophrenia"."Years ago you served my father in the Clone Wars"Drawing on data derived from participants taking part in the Genetic Risk and Outcome of Psychoses (GROUP) study [2] researchers looked at blood serum samples "to measure the levels of 184 molecules in serum from 112 schizophrenia patients, 133 siblings and 87 unrelated controls". Multiplex immunoassay was the analytical weapon of choice.The results indicated that "10 proteins were present at significantly different levels between schizophrenia patients and controls" which can be seen here. The insulin synthesis pathway showed more than a passing connection to group differences as per the appearance of insulin and precursor molecules such as proinsulin and C-peptide (connecting peptide). Some of these pathway molecules were also reported to be altered in the sibling group(s) too. Growth hormone also featured as a potentially distinguishing marker, as did adiponectin among others.The authors conclude (again) their findings for "the presence of a molecular endophenotype involving disruption of insulin and growth factor signaling pathways as an increased risk factor for schizophrenia". Perhaps even more interesting is their view of the body of work [3] suggesting that "antipsychotic drugs are known to increase peripheral glucose levels" and how, in light of their findings, "these effects may be intrinsically related to the therapeutic mechanism of action by increasing the peripheral blood glucose levels and thereby increasing glucose availability in the brain".As the authors point out, there is still quite a bit more to do in this area including examining larger samples sizes and importantly, looking at blood glucose levels as a measure of insulin resistance to further complement their findings. I note however that issues with insulin function being potentially related to mood and other psychiatric conditions are nothing new as per the various literature in this area. Anderson and colleagues [4] for example, talked about a diagnosis of diabetes doubling the odds of comorbid depression. Bearing in mind, the possible interfering effect of medication, Verma and colleagues [5] found that in drug-naive (unmedicated) patients with first-episode psychosis there was a significantly increased likelihood of diabetes to be present compared with age and sex-matched asymptomatic control participants. I don't doubt however, that any relationship is going to be complicated.Finally, and bearing in mind the prime directive of this blog (no medical or clinical advice given or intended), there is the question of how this research might translate into therapeutic intervention. A final quote from the authors on this and the possibility of: "novel disease prevention approaches, which could involve nutrition modification, stress reduction and pharmaco-therapeutic interventions, including the application of well-tolerated drugs that combat insulin resistance". Alongside the dietary aspect (which is something very favourable to this blog for lots of reasons), I am wondering whether we could also learn something from times gone by [6]? Perhaps even the appliance of prophylactic psychiatry [7]?Music to close and Andrea Bocelli sings Funiculì, Funiculà...----------[1] van Beveren NJM. et al. Evidence for disturbed insulin and growth hormone signaling as potential risk factors in the development of schizophrenia. Translational Psychiatry. 2014; 4: e430.[2] Korver N. et al. Genetic Risk and Outcome of Psychosis (GROUP), a multi-site longitudinal cohort study focused on gene-environment interaction: objectives, sample characteristics, recruitment and assessment methods. Int J Methods Psychiatr Res. 2012 Sep;21(3):205-21.[3] Wirshing DA. et al. The effects of novel antipsychotics on glucose and lipid levels. J Clin Psychiatry. 2002 Oct;63(10):856-65.[4] Anderson RJ. et al. The prevalence of comorbid depression in adults with diabetes: a meta-analysis. Diabetes Care. 2001 Jun;24(6):1069-78.[5] Verma SK. et al. Metabolic risk factors in drug-naive patients with first-episode psychosis. J Clin Psychiatry. 2009 Jul;70(7):997-1000.[6] Anderson K. et al. Salsalate, an old, inexpensive drug with potential new indications: a review of the evidence from 3 recent studies. Am Health Drug Benefits. 2014 Jun;7(4):231-5.[7] Sawa A. & Seidman LJ. Is Prophylactic Psychiatry around the Corner? Combating Adolescent Oxidative Stress for Adult Psychosis and Schizophrenia. Neuron. 2014; 83: 991-993.----------van Beveren NJ, Schwarz E, Noll R, Guest PC, Meijer C, de Haan L, & Bahn S (2014). Evidence for disturbed insulin and growth hormone signaling as potential risk factors in the development of schizophrenia. Translational psychiatry, 4 PMID: 25158005... Read more »

  • September 12, 2014
  • 09:15 AM

The Friday Five for 09/12/2014

by Bill Sullivan in The 'Scope

Get caught up quick on the hottest science news from this week!... Read more »

Denoeud, F., Carretero-Paulet, L., Dereeper, A., Droc, G., Guyot, R., Pietrella, M., Zheng, C., Alberti, A., Anthony, F., Aprea, G.... (2014) The coffee genome provides insight into the convergent evolution of caffeine biosynthesis. Science, 345(6201), 1181-1184. DOI: 10.1126/science.1255274  

  • September 11, 2014
  • 08:21 PM

"Barefoot Running and Hip Kinematics: Good News for the Knee?"; what about "Bad News for the Ankle"?

by Craig Payne in Running Research Junkie

"Barefoot Running and Hip Kinematics: Good News for the Knee?"; what about "Bad News for the Ankle"?... Read more »

McCarthy C, Fleming N, Donne B, & Blanksby B. (2014) Barefoot Running and Hip Kinematics: Good News for the Knee?. Medicine and science in sports and exercise. PMID: 25207927  

  • September 11, 2014
  • 12:45 PM

The Origami Brain and a new marker for Schizophrenia

by Gabriel in Lunatic Laboratories

Anyone who has seen pictures or models of the human brain (like the one above) is aware that the outside layer, or cortex, of the brain is folded in an intricate pattern of “hills”, called gyri, and “valleys”, called sulci which give the brain it’s distinctive look. It turns out that the patterns of cortical folding are largely consistent across healthy humans, broadly speaking. However, disturbances in cortical folding patterns suggest deeper disturbances in brain structure and function.... Read more »

Nanda P, Tandon N, Mathew IT, Giakoumatos CI, Abhishekh HA, Clementz BA, Pearlson GD, Sweeney J, Tamminga CA, & Keshavan MS. (2014) Local gyrification index in probands with psychotic disorders and their first-degree relatives. Biological psychiatry, 76(6), 447-55. PMID: 24369266  

  • September 11, 2014
  • 09:55 AM

Treating autism in the first year of life

by Paul Whiteley in Questioning Answers

I had been waiting y'know. Waiting a while for the paper by Sally Rogers and colleagues [1] to finally appear quite a few days after the media headlines about 'reducing', 'reversing' and even 'eliminating' the signs and symptoms of autism in early infancy had appeared. Personally, I prefer the New Scientist headline: 'Early autism intervention speeds infant development' given the text of the paper. I should perhaps also add the words 'for some' to that sentence as you will hopefully see...I'm sure most people have already read about the study ins and outs: take an intervention called 'Infant Start' (IS), a relation of the Early Start Denver Model (ESDM), and apply it with a small (very small) group of "symptomatic" young infants (n=7, aged between 6-15 months old) showing signs and symptoms of autism. Plot baseline measures and progress of those children under IS using various psychometric tools including something like the Autism Observation Scale for Infants (AOSI) and old reliable: the ADOS (the Autism Diagnostic Observation Schedule) compared against four comparison groups. One of those control groups included those with similar early autism symptoms as judged by "elevated AOSI scores and clinician concerns" but who did not receive IS; a so-called "declined referral (DR) group" (n=4). Record results and report outcome based on said 12-week program and added extra sessions a few months down the line.The headline conclusion: "At 36 months, the treated group had much lower rates of both ASD [autism spectrum disorder] and DQs [developmental quotients] under 70 than a similarly symptomatic group who did not enroll in the treatment study". Further: "the pilot study outcomes are promising". I should add that when it came to the "final visit" and "based on standardized assessments and clinical judgement" 2 of the 7 children in the IS group did eventually receive a diagnosis of ASD/PDD-NOS (pervasive developmental disorder not otherwise specified). This compared with 3 of the 4 children in the DR group who met criteria for ASD/PDD-NOS (the other child "presented with intellectual disability"). Insofar as DQ - specifically "overall DQ at or below 70 at 36 months" - well, one child in the IS group fell into this category compared with 3 children in the DR group (note to authors, you've called this the 'DE' group... sorry to be pedantic). You can um-and-ah about the links between ASD and PDD-NOS for example, but suffice to say that any effect from IS was not universal across all participants included in the trial. If you'd like a few more details about the trial and results, I'll refer you to the press release from UC Davis (see here).Of course this is not the first time that this type of very early intervention has been discussed in the peer-reviewed domain. Take for example another paper by Rogers and colleagues [2] (open-access) talking about the use of ESDM with a cohort of 14-24 month old toddlers "at risk for autism spectrum disorders". The results on that occasions were slightly less dramatic than the more recent ones with the caveat that "both younger child age at the start of intervention and a greater number of intervention hours were positively related to the degree of improvement in children's behavior for most variables". I talked about this in a previous post (see here). Indeed it appears that age at start of intervention might be an important variable after all.So, where next with this research? Well, aside from some discussions reiterating how useful it would be to have something to aid early diagnosis (see here) bearing in mind that it has not been conclusively proven that all autism is present from birth (see here), discussions have turned to why such early intervention might have had the effect that it had. Brain plasticity has been mentioned, and how critical periods in early development might be particularly amenable to such intensive intervention. Of course, without the all-important "testing the treatment’s efficacy" under more controlled conditions and with larger groups, one cannot discount some role for chance in the recent findings. Not buying that as an answer? How about differing developmental trajectories then?----------[1] Rogers SJ. et al. Autism Treatment in the First Year of Life: A Pilot Study of Infant Start, a Parent-Implemented Intervention for Symptomatic Infants. Journal of Autism and Developmental Disorders. 2014. 12 September.[2] Rogers SJ. et al. Effects of a brief Early Start Denver model (ESDM)-based parent intervention on toddlers at risk for autism spectrum disorders: a randomized controlled trial. J Am Acad Child Adolesc Psychiatry. 2012 Oct;51(10):1052-65.----------S. J. Rogers, L. Vismara, A. L. Wagner, C. McCormick, G. Young, & S. Ozonoff (2014). Autism Treatment in the First Year of Life: A Pilot Study of Infant Start, a Parent-Implemented Intervention for Symptomatic Infants Journal of Autism and Developmental Disorders : 10.1007/s10803-014-2202-y... Read more »

S. J. Rogers, L. Vismara, A. L. Wagner, C. McCormick, G. Young, & S. Ozonoff. (2014) Autism Treatment in the First Year of Life: A Pilot Study of Infant Start, a Parent-Implemented Intervention for Symptomatic Infants. Journal of Autism and Developmental Disorders. info:/10.1007/s10803-014-2202-y

  • September 11, 2014
  • 04:42 AM

Omega-3 fatty acids rescues Fragile X phenotypes in Fmr1-Ko mice

by Paul Whiteley in Questioning Answers

"These results demonstrate that n-3 PUFAs dietary supplementation, although not a panacea, has a considerable therapeutic value for FXS [Fragile X syndrome] and potentially for ASD [autism spectrum disorder], suggesting a major mediating role of neuroinflammatory mechanisms".A view @ Wikipedia That was the conclusion reached by Susanna Pietropaolo and colleagues [1] who "evaluated the impact of n-3 PUFA dietary supplementation in a mouse model of fragile X syndrome (FXS), i.e., a major developmental disease and the most frequent monogenic cause of ASD". Looking at the Fmr1-KO mouse model of FXS, a mouse specifically bred to mimic the silencing of the FMR1 gene noted in FXS (see here) with onwards adverse effects for the production of FMRP, researchers looked at what happened when diets were "enriched or not with n-3 PUFAs from weaning until adulthood when they were tested for multiple FXS-like behaviors". The results seemed to indicate that "n-3 PUFA supplementation rescued most of the behavioral abnormalities displayed by Fmr1-KO mice, including alterations in emotionality, social interaction and non-spatial memory, although not their deficits in social recognition and spatial memory". Neuroinflammatory imbalances noted in the knock-out mice were also positively affected by omega-3 supplementation.I don't need to remind you that the Pietropaolo study was a study of mice and one needs to be quite careful about extrapolating animal results when it comes to humans. That being said, given the quite extensive work that has been done on FXS and the detailing of it's molecular background, one might assume that the current results are treated with a little less scepticism than in relation to other more idiopathic 'types' of autism. Still, proper trials with people are indicated as per other research.Omega-3 fatty acids have been discussed before on this blog with autism in mind (see here). The collected literature on their usefulness as supplements for autism is rather mixed at present [2] despite some emerging evidence on their involvement in various biological processes in cases of autism (see here). That being said, I'm not getting too down on omega-3 fatty acids in light of some associations being made with specific skills over and above any condition-specific relationship and some new light being shed on their use in other conditions [3]. I'm yet to find anything like an experimental trial of fatty acids in real people with FXS but did chance(!) upon the study by Lachance and colleagues [4] (open-access) talking about the use of fenretinide (N-(4-hydroxyphenyl) retinamide (4HPR)) in the test-tube and effects "associated with the normalization of arachidonic acid/docosahexaenoic acid ratio in macrophages". The effect talked about translates as a down-regulation in the "production of arachidonic acid (AA), a pro-inflammatory omega-6 polyunsaturated fatty acid, and to increase levels of omega-3 polyunsaturated docosahexaenoic acid (DHA), which has an anti-inflammatory effect". Mmm... possibly some new targets to replace quite a few disappointments when it comes to FXS therapeutics (see here).Music to close. Fontella Bass and Rescue Me.----------[1] Pietropaolo S. et al. Dietary supplementation of omega-3 fatty acids rescues fragile X phenotypes in Fmr1-Ko mice. Psychoneuroendocrinology. 2014 Jul 9;49C:119-129.[2] James S. et al. Omega-3 fatty acids supplementation for autism spectrum disorders (ASD). Cochrane Database Syst Rev. 2011 Nov 9;(11):CD007992.[3] Hawkey E. & Nigg JT. Omega-3 fatty acid and ADHD: Blood level analysis and meta-analytic extension of supplementation trials. Clin Psychol Rev. 2014 Jun 2;34(6):496-505.[4] Lachance C. et al. Fenretinide corrects the imbalance between omega-6 to omega-3 polyunsaturated fatty acids and inhibits macrophage inflammatory mediators via the ERK pathway. PLoS One. 2013 Sep 12;8(9):e74875.----------Pietropaolo S, Goubran MG, Joffre C, Aubert A, Lemaire-Mayo V, Crusio WE, & Layé S (2014). Dietary supplementation of omega-3 fatty acids rescues fragile X phenotypes in Fmr1-Ko mice. Psychoneuroendocrinology, 49C, 119-129 PMID: 25080404... Read more »

Pietropaolo S, Goubran MG, Joffre C, Aubert A, Lemaire-Mayo V, Crusio WE, & Layé S. (2014) Dietary supplementation of omega-3 fatty acids rescues fragile X phenotypes in Fmr1-Ko mice. Psychoneuroendocrinology, 119-129. PMID: 25080404  

  • September 10, 2014
  • 08:26 PM

Patellofemoral Joint Stress during Running with Alterations in Foot Strike Pattern

by Craig Payne in Running Research Junkie

Patellofemoral Joint Stress during Running with Alterations in Foot Strike Pattern... Read more »

  • September 10, 2014
  • 06:00 PM

Anecdotes and the Appearance of Improvement

by Rogue Medic in Rogue Medic

We like to give treatments that produce results that we can see and logically attribute to the treatments we gave.

We like to give IV (IntaVenous) furosemide (Lasix – frusemide in Commonwealth countries) for CHF (Congestive Heart Failure).

1. The patient had CHF.
2. I gave IV furosemide.
3. The patient produced urine.... Read more »

  • September 10, 2014
  • 02:26 PM

Multiple Sclerosis and Myelin loss

by Gabriel in Lunatic Laboratories

Multiple sclerosis (MS) is an unpredictable, often disabling disease of the central nervous system that disrupts the flow of information within the brain, and between the brain and body. The exact cause is unknown, however people with multiple sclerosis lose myelin in the gray matter of their brains and the loss is closely correlated with the severity of the disease, according to a new magnetic resonance imaging (MRI) study.... Read more »

Vasily L. Yarnykh, James D. Bowen, Alexey Samsonov, Pavle Repovic, Angeli Mayadev, Peiqing Qian, Beena Gangadharan, Bart P. Keogh, Kenneth R. Maravilla, & Lily K. Jung Henson. (2014) Fast Whole-Brain Three-dimensional Macromolecular Proton Fraction Mapping in Multiple Sclerosis. Radiological Society of North America . info:/10.1148/radiol.14140528

  • September 10, 2014
  • 09:36 AM

Video Tip of the Week: #Docker, shipping containers for software and data

by Mary in OpenHelix

Breaking into the zeitgeist recently, Docker popped into my sphere from several disparate sources. Seems to me that this is a potential problem-solver for some of the reproducibility and sharing dramas that we have been wrestling with in genomics. Sharing of data sets and versions of analysis software is being tackled in a number of […]... Read more »

  • September 10, 2014
  • 08:00 AM

Return of Results from Next-gen Sequencing

by Daniel Koboldt in Massgenomics

The rapid adoption of next-gen exome and genome sequencing for clinical use (i.e. with patient DNA) raises some difficult questions about the return of results to patients and their families. In contrast to traditional genetic testing, which usually checks for variants in specific genes, high-throughput sequencing has the potential to reveal a number of secondary […]... Read more »

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