Nodding syndrome.Ever heard of it? Well, up until a few days ago I hadn't. That is before coming across articles on the topic by Richard Idro and colleagues* (open-access) and Angelina Kakooza-Mwesige and colleagues** (open-access). Whilst not specifically my line of expertise or interest, I was intrigued to read about how nodding and other symptoms of the epileptic variety, at least in some cases, seemed to be precipitated by food and showed a potential nutritional angle.Curving spacetime @ Wikipedia Granted, the hows and whys of nodding syndrome are still a mystery, but the first thought that went through my mind was whether any specific types of food(s) might be implicated. Y'know in a similar vein to Marios Hadjivassiliou and the notion of gluten ataxia*** for example? Just speculating...With all that talk of food and behaviour in mind there are a few things that piqued my attention towards the paper by Herbert & Buckley**** seemingly part of a string of articles looking at the topic of dietary intervention published in the Journal of Child Neurology. The first thing was the title of the paper: "Autism and Dietary Therapy" simply because I have some research interest in this area. Perhaps I might have mentioned it before...Next was the authorship list, focused on at least one of the authors, Dr Martha Herbert (no disrespect intended to Dr Buckley). Alongside an already distinguished career in autism research, Dr Herbert is also making some waves with her new book: 'The Autism Revolution' co-authored with Karen Weintraub who wrote that very interesting Nature article on autism prevalence a few years back.Finally, a sentence from the paper abstract: "Over the course of several years following her initial diagnosis, the child’s Childhood Autism Rating Scale score decreased from 49 to 17, representing a change from severe autism to nonautistic, and her intelligence quotient increased 70 points".Such a dramatic description of change in presentation might once have been received with a very, very sceptical eye. Indeed I assume that still might be the case in some quarters. The publication of the Deborah Fein study (see here and here) on optimal outcome in relation to autism in conjunction with the rising tide of research looking at the potential benefits of early intervention for cases of autism, have perhaps made such observations slightly more 'acceptable', at least to some elements of the autism research community. Indeed I was also very taken by the recent BBC interview of Kristine and Jacob Barnet which discussed similar changes to symptom presentation in a young man now tipped for some absolutely amazing things. The fact that said changes detailed in the Herbert & Buckley paper seemed to occur at the same time that a "gluten-free casein-free ketogenic diet" was being followed is... interesting.Now round about this time, some people might be thinking what does this study actually show? A case study of a girl / young woman with autism where comorbid epilepsy was controlled both by anti-seizure medication and a ketogenic diet (yes, such a diet has been linked to the control of cases of epilepsy). Said dietary intervention originating in the gluten- and casein-free (GFCF) dietary domain. As time went on, seizures dissipated and over time her clinical scores on the CARS reduced indicative of quite a change in her autism presentation.One of course might say, a single case study, it means very little in the grand methodological scheme of things. That is unless you think back to the mantra 'if you've met one person with autism, you've met one person with autism' highlighting the power of the N=1 where autism is concerned (see here). That and the interesting viewpoint expressed by people like Gary Mesibov on the issue of evidence-based medicine when applied to a extremely heterogeneous condition like autism, sorry the autisms.I am interested in the coincidental factors reported in this paper. I have questions: did the (almost) resolution of the epileptic symptoms carry any influence on the presentation of autism? In particular, I'm thinking back to that very interesting piece of research which suggested one particular type of autism (and epilepsy) might be related to a metabolic issue with the branched-chain amino acids (see here). Is this a potential model for that epilepsy-autism relationship for some people on the spectrum? What about the "resolution of morbid obesity" also reported; could this similarly have had any effect on symptom presentation?I have questions about the role of the diet adopted in this case. A ketogenic diet, as well as finding some value in cases of epilepsy or seizure disorders, has also been looked at with autistic behaviours in mind. Yep, at least one trial***** albeit preliminary, suggested that this might be an option for some people on the spectrum bearing in mind I'm not making any recommendations. Down the years I've also heard anecdotal reports about how the GFCF diet might have aided in the reduction/amelioration of certain signs and symptoms linked to autism. The paper by Stephen Genuis (see this post) is one example. Just before you say something along the lines of 'there is no methodologically sound experimental evidence for dietary effect'; well, yes and no (see here) accepting the need for much more rigorous experimental study and that the evidence is not all one-way (see here).If anyone has alternative explanations for the change in symptoms outside of just healthier eating, any placebo effect or just the research attention paid to the participant in question, please feel free to post them in the comments section. That being said, no mumbo-jumbo please like I've being reading today which has been roundly answered by psychiatry. Going back to the Fein study and the promise of more details to come, I'll be interested to see whether they report any of their optimal outcomers were following such a dietary intervention alongside other interventions.A... Read more »
Herbert, M., & Buckley, J. (2013) Autism and Dietary Therapy: Case Report and Review of the Literature. Journal of Child Neurology. DOI: 10.1177/0883073813488668
Medieval alchemists devoted their lives to the pursuit of the infamous Philosopher's Stone, an elusive substance that was thought to convert base metals into valuable gold. Needless to say, nobody ever discovered the Philosopher’s Stone. Well, perhaps some alchemist did get lucky but was wise enough to keep the discovery secret. Instead of publishing the discovery and receiving the Nobel Prize for Alchemy, the lucky alchemist probably just walked around in junkyards, surreptitiously collected scraps of metal and brought them to home to create a Scrooge-McDuck-style money bin. Today, we view the Philosopher’s Stone as just a myth that occasionally resurfaces in the titles of popular fantasy novels, but cell biologists have discovered their own version of the Philosopher’s Stone: The conversion of fibroblast cells into precious heart cells (cardiomyocytes) or brain cells (neurons).... Read more »
Nam, Y., Song, K., Luo, X., Daniel, E., Lambeth, K., West, K., Hill, J., DiMaio, J., Baker, L., Bassel-Duby, R.... (2013) Reprogramming of human fibroblasts toward a cardiac fate. Proceedings of the National Academy of Sciences, 110(14), 5588-5593. DOI: 10.1073/pnas.1301019110
Researchers have found that blood of youngsters can rejuvenate the heart of the old ones - at least in mice.
Previously, researchers found that the blood from the young mice could rejuvenate the brain of the older mice. (Nature, doi:10.1038/nature10357).
In the new study, researchers worked on two mice; one was 2-month-old and the other was 23-month-old having cardiac hypertrophy - a condition in which the heart muscle thickens leading to heart failure. Researchers surgically joined the circulatory system of the two mice that caused the blood to flow around each other’s bodies.
Researchers found that the heart of the older mouse reverted back to almost the same size as that of the younger animal and the heart of the younger animal remained unaffected even after circulating the blood from the older mice.
“After 4 weeks of exposure to the circulation of young mice, cardiac hypertrophy in old mice dramatically regressed, accompanied by reduced cardiomyocyte size and molecular remodeling,” Researchers wrote.
Researchers found that a protein, GDF11, was present in huge amount in the young mice. This protein is important in cell development and healing, and now researchers have found its role in the betterment of hearts. They are think that this protein in low levels could help the people with cardiac hypertrophy. However, further researches are needed on this.
Loffredo, F., Steinhauser, M., Jay, S., Gannon, J., Pancoast, J., Yalamanchi, P., Sinha, M., Dall’Osso, C., Khong, D., Shadrach, J., Miller, C., Singer, B., Stewart, A., Psychogios, N., Gerszten, R., Hartigan, A., Kim, M., Serwold, T., Wagers, A., & Lee, R. (2013). Growth Differentiation Factor 11 Is a Circulating Factor that Reverses Age-Related Cardiac Hypertrophy Cell, 153 (4), 828-839 DOI: 10.1016/j.cell.2013.04.015... Read more »
Loffredo, F., Steinhauser, M., Jay, S., Gannon, J., Pancoast, J., Yalamanchi, P., Sinha, M., Dall’Osso, C., Khong, D., Shadrach, J.... (2013) Growth Differentiation Factor 11 Is a Circulating Factor that Reverses Age-Related Cardiac Hypertrophy. Cell, 153(4), 828-839. DOI: 10.1016/j.cell.2013.04.015
For over a decade, cardiologists have been conducting trials in patients using cells extracted from the bone marrow and infusing them into the blood vessels of the heart in patients who have suffered a heart attack. This type of a procedure is not without risks.... Read more »
Surder, D., Manka, R., Lo Cicero, V., Moccetti, T., Rufibach, K., Soncin, S., Turchetto, L., Radrizzani, M., Astori, G., Schwitter, J.... (2013) Intracoronary Injection of Bone Marrow Derived Mononuclear Cells, Early or Late after Acute Myocardial Infarction: Effects on Global Left Ventricular Function Four months results of the SWISS-AMI trial. Circulation. DOI: 10.1161/CIRCULATIONAHA.112.001035
Rehman, J. (2013) Bone Marrow Tinctures for Cardiovascular Disease: Lost in Translation. Circulation. DOI: 10.1161/CIRCULATIONAHA.113.002775
Right and Left Insula Cortex Highlighted in TealBiomarker research in brain disorders including schizophrenia and mood disorders is an important pathway to early identification and prevention.In a previous post, I reviewed a summary of current biomarker research in schizophrenia. This summary suggested that accelerated brain gray matter volume decline during childhood and adolescence is a candidate biomarker in schizophrenia.In this post, I will look at a similar imaging biomarker study in bipolar and unipolar mood disorder. Heather Whalley and colleagues from the Division of Psychiatry at the University of Edinburgh recently published a fMRI activation study in a group of asymptomatic high-risk mood disorder subjects.The key elements of the design of their study included the following:Study subjects: 98 case subjects were identified between the ages of 16-25 with a first degree relative identified as having a diagnosis of bipolar I. Control subjects were identified as a matched age group with no first degree relative with bipolar disorder.Clinical assessment: Cases and control were interviewed at baseline and two years later for presence of a mood disorder using a structured interview of DSM-IV diagnoses (SCID)Imaging protocol: fMRI imaging was completed for cases and controls using the Hayling sentence completion test. This test provides a sentence with the last word missing and subjects are expected to think of a word to complete the sentence while being scanned.Statistical analysis: 18 case subjects developed major depression disorder (MDD) during the follow-up period and were compared to a group of cases who did not develop MDD and controls who did not develop MDD. Groups were also compared on baseline psychometric scores on cyclothymia, neuroticism and extraversion. Potential confounding variables (alcohol and drug use frequency) were also examined.The key results from this study included:fMRI results: High-risk mood disorder subjects who developed MDD in the follow-up period demonstrated increased bilateral insula activation with the sentence completion task compared to high-risk subjects not developing MDD and healthy controls. Receiver operating characteristic analysis showed the area under the curve for identifying those developing MDD was 0.77 and 0.73 for the right and left insulaPsychometric tests: High-risk individuals who developed MDD in follow-up showed higher baseline scores on cyclothymia and depression on the Temperament and Personality Measures (TEMPS-A) score and higher scores on the neuroticism and extraversion subscale of the NEO-Five Factor Inventory. The authors note the insula is known to be a "part of a network of regions that plays a key role in the regulation of emotion, including emotional processing, response inhibition, and in the experience of emotion".Psychometric measures of cyclothymia, neuroticism and extraversion correlated with increased insula hyperactivity supporting the validity of these measures as additional biomarkers for depression risk. Since these measures are relatively inexpensive to obtain, they may hold clinical utility in identifying high-risk adolescents for close monitoring.Due to cost, fMRI is not yet practical for use in clinical populations. However, this study supports the promise of fMRI in future studies that might identify mechanisms and potential treatments to prevent depression in those at highest risk.Readers with more interest in this subject can access the free full-text manuscript by clicking on the PMID link in the citation below.The image of the bilateral insula cortex is an iPad screen shot from the Brain Tutor app.Whalley HC, Sussmann JE, Romaniuk L, Stewart T, Papmeyer M, Sprooten E, Hackett S, Hall J, Lawrie SM, & McIntosh AM (2013). Prediction of depression in individuals at high familial risk of mood disorders using functional magnetic resonance imaging. PloS one, 8 (3) PMID: 23483904... Read more »
Whalley HC, Sussmann JE, Romaniuk L, Stewart T, Papmeyer M, Sprooten E, Hackett S, Hall J, Lawrie SM, & McIntosh AM. (2013) Prediction of depression in individuals at high familial risk of mood disorders using functional magnetic resonance imaging. PloS one, 8(3). PMID: 23483904
"There's no mystical energy field that controls my destiny". So said a very sceptical Han Solo.Regular readers might know that I'm a bit of fan of the whole gut-brain axis; indeed other kinds of axes too. I know that to some it might sound a bit daft that what goes on in our deepest, darkest bowels might actually have some important effects on the operations of the grey-pinkish matter floating around in skull central - and vice-versa - but nonetheless it interests me. The gastrointestinal (GI) tract is not quite the mystical energy field that Captain Solo was referring to, but make no mistake, we are still very much in the infancy of looking at the connection between the two systems*.Black dog @ Wikipedia I've tended to discuss/speculate on the gut-brain relationship with regards to cases of autism spectrum disorder (ASD) on this blog. In this post I'm branching out to look at the paper by Mary Rogers and colleagues** (open-access) on a potentially new dimension to the gut-brain conversation with depression and Clostridium difficile infection in mind.The Rogers paper is open-access and has also attracted some media attention as a result (see here and here for the press release). The long-and-short of it was that based on two studies - a sort of scientific BOGOF - looking at the rates of C.diff infection (CDI) in participants with and without depression and the potential effects of antidepressant medication use and hospital-acquired CDI, some interesting correlations were noted. Note that word 'correlations'...Primary among the findings was the suggestion that the chances of CDI were higher in those presenting with depression: "After adjusting for demographic characteristics, comorbidities and frequency of medical visits, there was a 36% increase in the odds of developing CDI for individuals with major depression compared with those without major depression" (CI: 1-06-1.74, p=0.016). Indeed when it came to the label of "emotional, nervous or psychiatric problems", the CDI risk was found to be even higher (OR: 1.47). Certainly some interesting data, made all the more credible by the fact that the total sample size numbered in the thousands. When it came to medication use, there were some equally interesting associations (not) made. So for example, laboratory confirmed CDI (via stool testing) seemed not to correlate with the majority of medicines participants were also taking at the time of testing. The exceptions were mirtazapine (OR: 2.14) and fluoxetine (OR: 1.92) which were individually associated with an approximate doubling of CDI risk and also carrying some dose-related associations.Authors also reported that polypharmacy - if I can use that word with less than 5 meds being taken - might also impact on CDI risk, as per the "significant interaction between mirtazapine and trazodone" where "the odds of a positive C. difficile test were 5.72 times greater" bearing in mind the small participant numbers who were prescribed these two drugs combined. As per the press on this paper: "People who have been prescribed these types of anti-depressants need to keep taking them unless otherwise advised by their physician"; a viewpoint that I can only echo at this stage.You can perhaps see why I might be interested in this line of research. There is of course the chicken-and-egg question about which came first: microbial changes which place a person at greater risk of CDI and perhaps depression, or depression leading to changes to the gut microbiota and onwards elevated CDI risk. I'm not going to speculate too much on what came first because I dare say the clinical picture is going to be much more complicated than such a simple question. I've talked before about the possibility of a bi-directional relationship between gut bacteria and behaviour (at least in mice) and my viewpoint has changed very little in the intervening years. Bear also in mind that the hows and whys of depression (in all its forms) are likely to be numerous; perhaps even related to our earliest years****It's interesting that the authors discuss quite a few important overlapping pieces of research in their summary of their findings related to things like the presence of bowel disease in cases of depression*** and that magical word 'inflammation'*****. To quote: "It is possible that there is a lifelong liaison between the gut microbiota and neurologic response to external stimuli" which certainly does seem to link in with at least some of the current research literature.Alongside the tentative associations made by Rogers et al on the issue of depression and CDI, I find my mind wandering back to the question of whether such an association might be something which could be translated into therapeutic options. Y'know whether treating the CDI actually had any quantifiable impact on the presentation of depression or vice-versa. Indeed whether one of the more unusual methods suggested to help combat CDI - yep, the fecal transplant - might also impact on depression via changes to the gut microbiota as per the very preliminary reports from other conditions such as chronic fatigue syndrome (CFS)? That and possibility that gut bacteria might, just might, be in cahoots with other more barrier-related issues******, makes for some interesting suggestions for further scientific inquiry*******.To end, y'know I prefer Constantiople over Istanbul....----------* Collins SM. & Bercik P. Gut microbiota: intestinal bacteria influence brain activity in healthy humans. Nature Reviews Gastroenterology and Hepatology. May 2013.** Rogers MAM. et al. Depression, antidepressant medications, and risk of Clostridium difficileinfection. BMC Medicine 2013; 11: 121.*** Graff LA. et al. Depression and anxiety in inflammatory bowel disease: a review of comorbidity and management. Inflamm Bowel Dis. 2009; 15: 1105-1118.**** Parboosing R. et al. Gestational influenza and bipolar disorder in adult offspring. JAMA Psychiatry. May 2013.***** Vogelzangs N. et al. Association of depressive disorders, depression characteristics and antidepressant medication with inflammation. Transl Psychiatry. 2012; 2: e79.****** Maes M. et al. Increased IgA and IgM responses against gut commensals in chronic depression: further evidence for increased bacterial translocation or leaky gut. J Affect Disord. 2012; 141: 55-62.******* Hughes PA. et al. Immune activation in irritable bowel syndrome: can neuroimmune interactions explain symptoms? Am J Gastroenterol. May 2013----------... Read more »
Rogers, M., Greene, M., Young, V., Saint, S., Langa, K., Kao, J., & Aronoff, D. (2013) Depression, antidepressant medications, and risk of Clostridium difficile infection. BMC Medicine, 11(1), 121. DOI: 10.1186/1741-7015-11-121
Take Home Message: The Wii Balance Board is an acceptable substitute for measuring the center of pressure during single leg stance balance tests.
While a laboratory grade force plate is the gold standard for both testing and training balance, these force plates are limited to research laboratories. Due to the importance of balance testing and training during the rehabilitation process, a cost effective, widely available and portable force plate is desirable. Therefore, Huurnink and colleagues compared a laboratory grade, in-floor force plate to the Wii Balance Board (WBB).... Read more »
Huurnink A, Fransz DP, Kingma I, & van Dieën JH. (2013) Comparison of a laboratory grade force platform with a Nintendo Wii Balance Board on measurement of postural control in single-leg stance balance tasks. Journal of Biomechanics, 46(7), 1392-5. PMID: 23528845
....public health advocates have called for deworming as a cost-effective strategy to reduce risk of contracting HIV in regions endemic for S. haematobium and HIV... Read more »
Ndeffo Mbah, M., Kjetland, E., Atkins, K., Poolman, E., Orenstein, E., Meyers, L., Townsend, J., & Galvani, A. (2013) Cost-effectiveness of a community-based intervention for reducing the transmission of Schistosoma haematobium and HIV in Africa. Proceedings of the National Academy of Sciences, 110(19), 7952-7957. DOI: 10.1073/pnas.1221396110
Heart failure (also known as congestive heart failure) is one of the most common and debilitating conditions associated with ageing. At present, there is no real cure for the condition and treatments focus on improving the symptoms and preventing the progression of the disease. Today, a new study was published by researchers at Harvard Stem Cell Institute (HSCI) that sheds new light on the condition and proposes a potential new treatment option.Read More... Read more »
Loffredo, F., Steinhauser, M., Jay, S., Gannon, J., Pancoast, J., Yalamanchi, P., Sinha, M., Dall’Osso, C., Khong, D., Shadrach, J.... (2013) Growth Differentiation Factor 11 Is a Circulating Factor that Reverses Age-Related Cardiac Hypertrophy. Cell, 153(4), 828-839. DOI: 10.1016/j.cell.2013.04.015
by Andrea in Science of Eating Disorders
The idea of including dance and movement in interventions for eating disorders may seem somewhat controversial; generally, exercise and physical activity are discouraged for individuals recovering from eating disorders. Including dance in therapeutic interventions might raise a few eyebrows given the links between appearance-oriented athletic endeavors such as ballet and gymnastics and the development of eating disorders.
However, some therapists and scholars interested in alternative therapies for eating disorders have suggested that certain forms of movement therapy may help individuals with eating disorders connect to their bodies in a different, more positive way.
In 2011, two such scholars from Portugal, Padrão & Coimbra, published a 6-month pilot intervention for individuals hospitalized for anorexia nervosa (AN) based around body movement.
Data consisted of observations of free movement and conversations that came up during and after the sessions. Their sample size consisted of only 7 young women hospitalized for anorexia.
I’ll admit that despite years of dance training and a keen interest in the potential of dance therapy in mental health treatment, I was skeptical of this study from the start. …
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... Read more »
Padrão, M., & Coimbra, J. (2011) The Anorectic Dance: Towards a New Understanding of Inner-Experience Through Psychotherapeutic Movement. American Journal of Dance Therapy, 33(2), 131-147. DOI: 10.1007/s10465-011-9113-7
Stem cells drawn from amniotic fluid show promise for tissue engineering, but it’s important to know what they can and cannot do. A new study by researchers at Rice University and Texas Children’s Hospital has shown that these stem cells can communicate with mature heart cells and form electrical couplings with each other similar to those found in heart tissue. But these electrical connections alone do not prompt amniotic cells to become cardiac cells.... Read more »
MIKE WILLIAMS. (2013) Heart cells change stem cell behavior. Rice University News. info:/
Prefrontal Cortex Highlighted in RedIdentifying valid biomarkers for psychosis and schizophrenia is an active focus in brain research.Tyronne Cannon, Ph.D. from Yale University recently presented a summary of research on this topic at the William K. Warren Neuroscience Symposium in Tulsa, Oklahoma. Here are my notes from his presentation along with related free full-text research references.Biomarker research in psychosis is important because current treatment for psychosis with the antipsychotic drugs is limited by:discovery by serendipity without a specific molecular mechanismabsence of effect on psychosis negative symptoms (anergia, anhedonia and amotivation)poor tolerability of antipsychotic drugs with significant compliance issuesno evidence that antipsychotic drugs modify the progression of the diseaseBiomarker research in psychosis is promising because an extended prodrome period is present in childhood and adolescence. Biomarker research can be divided into markers with a progressively deviant pattern and those with a stable deviant pattern.Two studies are available to summarize current findings: The North American Prodrome Longitudinal Study, parts I and II (NAPLS I and NAPLS II). These studies have identified three biomarker candidate categories:Hormonal disruption involving the hypothalamic-pituitary-adrenal (HPA) axisEvent related potential abnormalities including the p300 marker and an NMDA synapse-related marker identified in a negativity mismatch taskBrain magnetic resonance imaging (MRI) showing a greater cortical gray matter volume decline (primarily in bilateral frontal cortex regions) in high-risk individuals who later convert to psychosisThe first two biomarkers appear to be of the stable deviant type while the gray matter deficit biomarker appears to be a progressive deviant markerAn important potential confounding issue in gray matter deficits is the role of antipsychotic drug exposure in producing gray matter changes. Research to date supports an independent contribution of psychosis progression risk with frontal gray matter reductionProgress in understanding the MRI biomarker changes in psychosis/schizophrenia require a better understanding of the mechanism of this change. At least three avenues of research for a mechanism are promising:Disruption of neuroplasticity: fetal hypoxia environments produce impairment in brain neuroplasticity possibly through disruption of the BDNF systemDisruption of brain inflammation: risk for progression to psychosis is linked to increase blood inflammation using a multiplex composite variable. This variable is associated with 35% of the variance in brain gray matter volumesHPA-Glutamate pathways: The glutamate pathway is known to be involved in psychosis with the psychotic effect produce by PCP and ketamine. It is possible glutamate disruption effects gray matter reduction through effects on the microgliaAlthough not discussed in this lecture, other promising targets for understanding psychosis mechanism and risk include: neuropsychologic deficits, brain white matter abnormalities and fMRI activation abnormalities and resting connectivity deficits.Further identification of biomarkers in psychosis will be key in designing prevention strategies and in smart drug development through understanding the mechanism of risk and progression of the disease.Readers with more interest in this topic are directed to the free full-text citations below.Image of the frontal cortex noted to be a biomarker of psychosis risk above is from a iPad screen shot from the Sun D, van Erp TG, Thompson PM, Bearden CE, Daley M, Kushan L, Hardt ME, Nuechterlein KH, Toga AW, & Cannon TD (2009). Elucidating a magnetic resonance imaging-based neuroanatomic biomarker for psychosis: classification analysis using probabilistic brain atlas and machine learning algorithms. Biological psychiatry, 66 (11), 1055-60 PMID: 19729150... Read more »
Sun D, van Erp TG, Thompson PM, Bearden CE, Daley M, Kushan L, Hardt ME, Nuechterlein KH, Toga AW, & Cannon TD. (2009) Elucidating a magnetic resonance imaging-based neuroanatomic biomarker for psychosis: classification analysis using probabilistic brain atlas and machine learning algorithms. Biological psychiatry, 66(11), 1055-60. PMID: 19729150
Seidman LJ, Giuliano AJ, Meyer EC, Addington J, Cadenhead KS, Cannon TD, McGlashan TH, Perkins DO, Tsuang MT, Walker EF.... (2010) Neuropsychology of the prodrome to psychosis in the NAPLS consortium: relationship to family history and conversion to psychosis. Archives of general psychiatry, 67(6), 578-88. PMID: 20530007
Gee DG, Karlsgodt KH, van Erp TG, Bearden CE, Lieberman MD, Belger A, Perkins DO, Olvet DM, Cornblatt BA, Constable T.... (2012) Altered age-related trajectories of amygdala-prefrontal circuitry in adolescents at clinical high risk for psychosis: a preliminary study. Schizophrenia research, 134(1), 1-9. PMID: 22056201
NC3Rs-funded PhD student Kamar Ameen-Ali, Department of Psychology, Durham University, takes us on a trip to the House of Commons SET for BRITAIN event, where she presented her research recently to MPs and VIPs.... Read more »
Ameen-Ali, K., Eacott, M., & Easton, A. (2012) A new behavioural apparatus to reduce animal numbers in multiple types of spontaneous object recognition paradigms in rats. Journal of Neuroscience Methods, 211(1), 66-76. DOI: 10.1016/j.jneumeth.2012.08.006
In spite of the evidence to the contrary and a lack of rationality in the claim, we continue to be told that increasing the number of people with a title, such as paramedic, will result in better care.
Here is more evidence that dividing the skills among more people leads to less skilled care.
The authors begin by referring to other studies that demonstrate the high failure rate of doctors performing procedures on children.
How is that relevant to EMS? We have a low frequency of use of critical skills – and that is with our adult patients. With children, our absence of experience is even more of a problem. When we do use our infrequently used skills, we often use them inappropriately.,... Read more »
Mittiga, M., Geis, G., Kerrey, B., & Rinderknecht, A. (2013) The Spectrum and Frequency of Critical Procedures Performed in a Pediatric Emergency Department: Implications of a Provider-Level View. Annals of Emergency Medicine, 61(3), 263-270. DOI: 10.1016/j.annemergmed.2012.06.021
Blaivas M. (2010) Inadequate needle thoracostomy rate in the prehospital setting for presumed pneumothorax: an ultrasound study. Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine, 29(9), 1285-9. PMID: 20733183
Tanz RR, & Charrow J. (1993) Black clouds. Work load, sleep, and resident reputation. American journal of diseases of children (1960), 147(5), 579-84. PMID: 8488808
Meyr, A., Gonzalez, O., & Mayer, A. (2011) Quantification and Perception of On-call Podiatric Surgical Resident Workload. The Journal of Foot and Ankle Surgery, 50(5), 535-536. DOI: 10.1053/j.jfas.2011.04.035
When you think of drum circles taking place in the United States, visions of hippies, Birkenstocks and the vibrant green lawns of private colleges may appear. The bacteria Bacillus anthracis, or anthrax, does not often materialize alongside the skunky mix of patchouli and ganja hovering above the crowd in one’s visions of (ar)rhythmic drumming events.
... Read more »
Centers for Disease Control and Prevention (CDC). (2010) Gastrointestinal anthrax after an animal-hide drumming event - New Hampshire and Massachusetts, 2009. MMWR. Morbidity and mortality weekly report, 59(28), 872-7. PMID: 20651643
Like Mother, like baby! Photo from freedigitalphotos.net.Moms give us so much more than we ever give them credit for. Biologically speaking, we all have a mom and a dad (unless you’re a flatworm or some other species that can reproduce without sex) that provide us with one of each chromosome type (our chromosomes contain our genes, commonly thought of as our “biological blueprints”). So it makes sense that we tend to think of ourselves as being half-our-mom and half-our-dad. But not so! All of us are slightly more-our-mom and slightly less-our dad.Our genes are encoded in our DNA, which is coiled and tightly packed into dense little chromosomes. Most of our cells contain 23 different pairs of chromosomes (for a total of 46), and one from each pair comes from each parent. One of those pairs is the sex chromosomes. Individuals with two X sex chromosomes are genetically females and individuals with an X and a Y sex chromosome are genetically male. Because genetic males are the only ones with Y chromosomes, all Y chromosomes are inherited from dad. But compared to X chromosomes, Y chromosomes are piddly little things that don’t contain as many genes. So if you’re a guy, you already have more genes from mom than from dad.In addition to our 46 chromosomes that we keep in the nucleus of each cell, we also have a tiny set of genes in another cell structure, the mitochondria. This mitochondrial DNA is only inherited from the mother, so regardless of whether you are XX or XY, you have a few more genes from mom than from dad.Wait! My genes are where?? Your genes are lined up on the doubled-stranded DNA, which is tightly coiled and packed into chromosomes. You have 23 different pairs of chromosomes, where one of each pair came from mom and the other came from dad. A copy of each of these 23 pairs of chromosomes (46 chromosomes in total) is in the nucleus of every cell you have (except for sperm or egg cells, which only have one of each pair, or 23 chromosomes in total). Get it? Figure adapted from an image by KES47 at Wikimedia.But we are not simply a product of our genes. If we were, identical twins would be, well… identical. But they’re not. The slight differences between twins results from differences in how our environment interacts with our genes. (By environment, I’m not just talking about temperature and air quality, but rather all external influences). Our environment plays a big role in shaping the individuals we become, and our mothers have more effect on our environment than our fathers do. When we are developing in the womb, our moms’ bodies single-handedly provide us with nutrients, hormones, and antibodies (and sometimes pathogens). During this time, her circumstances and decisions will determine what kind of setting we are born into. After we’re born, the social interaction, nutrition, and antibodies (through breast feeding and/or vaccines) she provides will all influence our gene activity and thus how we develop. Collectively, the traits that we develop due to these factors and all mom’s other nongenetic influences are called maternal effects.Mom gives us more genes, and has more input in determining how active each gene is. In the end, we are who we are in large part because of our moms.So Mom, this is for you: Happy (early) Mother’s Day! Want to know more? Check these out:1. BERNARDO, J. (1996). Maternal Effects in Animal Ecology Integrative and Comparative Biology, 36 (2), 83-105 DOI: 10.1093/icb/36.2.832. Wolf, J., & Wade, M.J. (2009). What are maternal effects (and what are they not)? Phil. Trans. R. Soc. B, 364, 1107-1115 ... Read more »
epression together with pain, but not pain alone, may increase activity in the immune system and inflammation. These are the important findings of a new study just published in the journal “Pain Medicine”.... Read more »
Kim Kristiansen, M.D. (2013) Pain and Depression Linked to the Immune System. Picture of Pain Blog. info:/
Humans are relatively weak when it comes to oxygen utilization. We can’t go very long without breathing, while other animals can make much better use of the oxygen they take in and can therefore go longer between breaths. The reasons for these differences are starting to be understood. These include special proteins in the brain to prevent hypoxic damage, and alternate gas exchange pathways, like plastron respiration in ticks. Mycobacterium tuberculosis can survive 50 years in hypoxic conditions, a dormancy that includes respiration and metabolism. Now that’s holding your breath!... Read more »
Gengenbacher, M., & Kaufmann, S. (2012) Mycobacterium tuberculosis: success through dormancy. FEMS Microbiology Reviews, 36(3), 514-532. DOI: 10.1111/j.1574-6976.2012.00331.x
Fielden, L., Knolhoff, L., Villarreal, S., & Ryan, P. (2011) Underwater survival in the dog tick Dermacentor variabilis (Acari:Ixodidae). Journal of Insect Physiology, 57(1), 21-26. DOI: 10.1016/j.jinsphys.2010.08.009
Williams, T., Zavanelli, M., Miller, M., Goldbeck, R., Morledge, M., Casper, D., Pabst, D., McLellan, W., Cantin, L., & Kliger, D. (2008) Running, swimming and diving modifies neuroprotecting globins in the mammalian brain. Proceedings of the Royal Society B: Biological Sciences, 275(1636), 751-758. DOI: 10.1098/rspb.2007.1484
Behavioural Risk Factors for Running Injury... Read more »
Nielsen, R., Buist, I., Parner, E., Nohr, E., Sorensen, H., Lind, M., & Rasmussen, S. (2013) Predictors of Running-Related Injuries Among 930 Novice Runners: A 1-Year Prospective Follow-up Study. Orthopaedic Journal of Sports Medicine, 1(1). DOI: 10.1177/2325967113487316
Shocker alert: medicines might have more effects than those listed on the patient information leaflet.I like being surprised. I particularly like being surprised about medicines and health, and how many of the medicines which even reside in the typical household medicines cabinet* might carry the potential to do so much more than that listed on the package insert. Leaking? @ Wikipedia Take for example the recent paper I bumped into by Sommansson and colleagues** continuing their scientific journey through the potential gastrointestinal effects of melatonin***. Melatonin - as many people with a connection to the autism spectrum disorders (ASD) or more generally neurodevelopmental disorders**** might know - is almost becoming the treatment of choice for issues with sleep disturbance*****. That's not to say it's for everyone, and also not necessarily the only potential option bearing in mind my caveat about not giving medical or any other advice.I've talked about melatonin with autism in mind quite a few times on this blog (see here for example). Not only because the source material for melatonin (in the body) is tryptophan, one of those truly remarkable aromatic amino acids, but also because outside of the traditional sleep-wake link, melatonin might be quite the molecular 'handyman'****** (or handywoman). Indeed it is with the ethos of that last study by Boga and colleagues in mind that I head into the two Sommansson reports.The first thing to note about the the Sommansson reports is that they are both studies on rats. I know that in recent times, there has been some chatter about using rodents to model conditions like autism (see here) focused in particular on the dangermouse that is the BTBR mouse model. In the current studies, the variable of rodent behaviour is not relevant given that the authors were looking at the physiological data pertaining to intestinal permeability (leaky gut) with melatonin as the primary variable.Ah yes, intestinal permeability aka leaky gut. The same leaky gut that a recent NHS Choices entry described as being expounded by "largely nutritionists and practitioners of complementary and alternative medicine". Just for the record I am neither of those two occupational options but I am a believer in the concept in relation to quite a few conditions. And you can perhaps understand why I'm so interested in the Sommansson reports whereby leaky gut - or gut hyperpermeability - seems to be positively affected (i.e. reduced) by the introduction of melatonin, at least in rats. Indeed how this might fall into line with other observations of leaky gut being defined in cases of ASD (see here) and very possibly in a mouse model of autism (see here). A part of the effect of melatonin administration in cases of autism?I'm not by the way falling hook, line and sinker for the author's observations that "melatonin reduces ethanol- and wine-induced increases in duodenal paracellular permeability partly via enteric neural pathways involving nicotinic receptors" being the same conditions as that found in cases of autism or any other condition. As far as I am aware children with autism are not knocking back copious amounts of alcohol, so one has to be careful about extrapolating such specific conclusions to the population with such tentative data. That and the fact that we currently know so little about gut barrier issues in cases of autism; assuming that people like this chap (yes, you Alessio Fasano with your zonulin et al) might shed some light on it in the near future. Oh and should I also mention the suggested link******* between melatonin being a modifier of toll-like receptor signalling too?But... if anything the Sommansson papers might lead us to ask some pertinent questions about responses to melatonin both in general and also with autism in mind. A simple-ish experiment: two groups, randomised to melatonin or placebo, looking at the traditional responses to melatonin in terms of sleep and quality of sleep, at the same time some before and after measures of the lactulose:mannitol ratio and whether there is any correlation between supplementation, response and gut permeability. All fairly noninvasive by all accounts but if you really wanted to go to town you might also want to look at other measures like glutathione for example******** which has also found a spot in autism research.But don't listen to my ramblings... listen instead to the these guys who are still going strong.----------* Berk M. et al. Aspirin: a review of its neurobiological properties and therapeutic potential for mental illness. BMC Medicine 2013; 11: 74.** Sommansson A. et al. Melatonin inhibits alcohol-induced increases in duodenal mucosal permeability in rats in vivo. Am J Physiol Gastrointest Liver Physiol. May 2013.*** Sommansson A. et al. Melatonin decreases duodenal epithelial paracellular permeability via a nicotinic receptor-dependent pathway in rats in vivo. J Pineal Res. 2013; 54: 282-291.**** Gringras P. et al. Melatonin for sleep problems in children with neurodevelopmental disorders: randomised double masked placebo controlled trial. BMJ. 2012; 345: e6664.***** Malow BA. et al. A practice pathway for the identification, evaluation, and management of insomnia in children and adolescents with autism spectrum disorders. Pediatrics. 2012; 130: S106-S124.****** Boga JA. et al. Beneficial actions of melatonin in the management of viral infections: a new use for this "molecular handyman"? Rev Med Virol. 2012; 22: 323-338.******* Kang JW. et al. Melatonin protects liver against ischemia and reperfusion injury through inhibition of toll-like receptor signaling pathway. J Pineal Res. 2011; 50: 403-411.******** Swiderska-Kołacz G. et al. The effect of melatonin on glutathione and glutathione transferase and glutathione peroxidase activities in the mouse liver and kidney in vivo. Neuro Endocrinol Lett. 2006 ; 27: 365-368.----------... Read more »
Sommansson A, Wan Saudi WS, Nylander O, & Sjöblom M. (2013) Melatonin inhibits alcohol-induced increases in duodenal mucosal permeability in rats in vivo. American journal of physiology. Gastrointestinal and liver physiology. PMID: 23639810
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