Researchers have reported that the oral administration of lactic acid microbes, having symbiotic relationship with body, can help in increasing the healing process of wounds and social fitness.
Researchers have found that wound healing process can be increased by over two times by adding lactic acid microbes, obtained from human milk, in drinking water. They reported that the microbe Lactobacillus reuteri increases wound healing process by enhancing the activity of neuropeptide hormone oxytocin. As a mechanism, they are of the opinion that the anagen-inducing and anti-inflammatory properties of L. reuteri are the most probable explanations of the increased wound healing process.
This finding is also interesting from the social point of view, i.e. microbial symbionts can help in developing better social relations, as they can help in up-regulating the oxytocin activity and this chemical has been found to be involved in social recognition, pair bonding, anxiety, and maternal behaviors.
Recently, researchers have found that oxytocin can increase the placebo effect, so the microbes can also help in increasing the therapeutic performance. Moreover, the present study also explains the mechanism behind the increased placebo effect as a result of oxytocin.
Oxytocin increases as a result of administration of the symbiotic microbes. You can work on the effect of the microbial symbionts on delivery process, i.e. at the time of birth.
As mentioned above that oxytocin enhances placebo effect, you can work on the same study while considering microbes instead of oxytocin to increase placebo effect.
Poutahidis T et al. (2013). Microbial Symbionts Accelerate Wound Healing via the Neuropeptide Hormone Oxytocin. PLoS ONE DOI: 10.1371/journal.pone.0078898... Read more »
Poutahidis T et al. (2013) Microbial Symbionts Accelerate Wound Healing via the Neuropeptide Hormone Oxytocin. PLoS ONE. DOI: 10.1371/journal.pone.0078898
This week my blog is about Cystic Fibrosis as it is a condition which can cause devastation in families and is a topic of continuous research to improve the quality of life and life expectancy of suffers.
Cystic Fibrosis (CF) is a genetic multi-organ disorder which is usually characterised by mucus clogging up the lungs causing a persistent cough and recurrent chest infections. These chest infections occur throughout a patient’s life and cause lung complications meaning a transplant is often needed. The current life expectancy for CF suffers being born now is 40 years old, but this is continuously increasing with on-going research and new treatments.
... Read more »
McKiernan PJ, Cunningham O, Greene CM, & Cryan SA. (2013) Targeting miRNA-based medicines to cystic fibrosis airway epithelial cells using nanotechnology. International journal of nanomedicine, 3907-15. PMID: 24143095
Photo: Mila Atkovska / ShutterstockCan dogs be trained to alert diabetics when their blood sugar levels fall too low or too high? A new study by Nicola Rooney (University of Bristol) et al investigates the success of just such a program. Medical Detection Dogs is a charity in the UK that trains dogs to detect disease. For example, they are investigating whether it is possible to train dogs to help with the early diagnosis of cancer, such as detecting prostate cancer from urine samples. They have bedbug detection dogs, who raise money to support the charity, which is reliant on public donations. And they also have medical alert dogs, trained to alert diabetics when their blood sugar becomes dangerously low.Type 1 diabetes is a serious medical condition in which the pancreas is not able to produce enough insulin. Consequently, there is not enough insulin to get sugar into the cells. The symptoms include increased thirst, hunger, fatigue and blurred vision, as well as many complications that can be life-threatening. People with type 1 diabetes have to monitor their blood sugar levels frequently to ensure they don’t suffer from blood sugar that is too low or too high.The charity has trained a number of dogs to alert when their owner is at risk of becoming hypoglycaemic (low blood sugar). Many of them are also able to detect hyperglycaemia (high blood sugar), though this is not trained until after the hypoglycaemia detection training is complete. The dogs wear a high-visibility red jacket that identifies them as medical alert dogs. While the most common breed is Labrador Retriever, other breeds include Golden Retriever, Poodle, Labradoodle, Cocker Spaniel, and a Yorkshire Terrier. Dogs that are trained by the charity typically go their owner at about eighteen months of age.Seventeen owners of hypoglycaemia alert dogs took part in the research. Nine of the dogs had completed their training, while the remainder were at an advanced stage. Nine of the dogs (a different subset) were trained by the charity and placed with their owners, while the other dogs already lived with their owners and were subsequently trained. The alert behaviour might involve jumping up, licking, nudging, barking and/or staring.The study asked clients to record occasions when the dog alerted them and whether or not this was accurate. They answered a questionnaire about their experiences, provided data from blood samples, and allowed the researchers to access their medical records so that pre- and post-dog results could be compared. The full dataset was available for ten clients.All of the people said since they got the dog there was a reduction in at least one of low blood sugar, becoming unconscious, or having to call a paramedic. The majority agreed that “The dog has enhanced my quality of life” and “I am totally satisfied with my dog.” This shows the dogs have made a big difference to their owners' lives.Comparing blood tests to alert episodes showed that almost all of the dogs successfully identified when blood sugar was out of the normal range. In almost all cases, there was a significant change in glucose levels after they acquired the dog. The people who have these dogs all have what is known as “brittle” diabetes, in other words it is unstable. The researchers say “their present Quality of Life and Wellbeing are comparable to other populations of non-dog users living with Type I diabetes. This suggests that the benefits of alert-dog ownership reported here have improved the clients’ life quality to levels comparable to the general Type I diabetes population.” This is a huge achievement, and it is beneficial to the individual as well as to society since it will result in lower emergency medical costs.Most of the owners showed high levels of trust in their dog (remember that some dogs had not quite completed their training yet). Some liked the attention their dogs brought, while others were less keen on it.The data showed there were differences in the dogs’ detection abilities, and future research is needed to investigate the reasons for this, such as whether some dogs are naturally better at it than others, and whether record-keeping is also a factor. The researchers also suggest that differences in training may play a role. Future research could investigate any differences between dogs raised by the charity and those that were raised by their owners. There may also be differences in owners’ abilities when it comes to on-going training and rewarding successful alerts, so future research could usefully focus on the relationship between client and dog.This study shows the dogs have made a big difference to the lives of their owners. Medical Detection Dogs now also trains dogs for other medical alerts, including narcolepsy and nut allergy. Have you seen a medical assistance dog at work?ReferenceRooney NJ, Morant S, & Guest C (2013). Investigation into the value of trained glycaemia alert dogs to clients with type I diabetes. PloS one, 8 (8) PMID: 23950905... Read more »
Rooney NJ, Morant S, & Guest C. (2013) Investigation into the value of trained glycaemia alert dogs to clients with type I diabetes. PloS one, 8(8). PMID: 23950905
Regression as part of the presentation of autism is still a topic which has the ability to create discussion and fuel controversy. I've talked about it a few times on this blog (see here and here) and how, after a bit of a laboured start, modern day autism research has finally come around to acknowledging that regression can occur in cases of autism.Fire @ Wikipedia The cause(s) of regression associated with autism has been where a lot of the debate has been had over the years. I've talked for example, about how vitamin B12 deficiency has been associated with cases of Childhood Disintegrative Disorder (CDD) (see here). This being one of the less 'controversial' theories put forward for regression in autism or in an autistic-like presentation as per other papers analysing factors such as thimerosal (thiomersal) exposure* and that-which-should-not-be-mentioned**.What I take from the collection of literature on this topic is that (a) autism is probably better defined as the autisms insofar as the regression being present or not for example, and (b) there probably isn't just one factor influencing regression where and when it occurs in relation to those autisms. Oh and (c) getting to the bottom of the causes of regression in cases of autism is a mighty difficult task.For today's post I'm talking about the paper by Ori Scott and colleagues*** describing a case report of a child where anti-N-methyl-D-Aspartate (NMDA) receptor encephalitis was suspected "as the cause of autistic regression".From the top, anti-N-Methyl-D-Aspartate (NMDA) receptor encephalitis is an autoimmune condition whereby a person generates antibodies against self, in particular, antibodies that target NMDA receptors in the brain. As per the paper by Florance and colleagues**** (open-access here) the presentation of the anti-NMDA receptor encephalitis in children and adolescents is not wholly dissimilar from that in adults including behaviour and personality changes albeit including "temper tantrums, behavioral change, agitation, aggression, and progressive speech deterioration as initial symptoms". For those more interested in the adult presentation of the condition, the book 'Brain on Fire' by Susannah Cahalan is probably a good starting point.Scott and colleagues chart the clinical course of a young boy following "an upper respiratory tract infection" into what would eventually "fit the diagnostic criteria for autistic spectrum disorder". Said anti-NMDA receptor antibodies were detected in cerebrospinal fluid (CSF) and treatment with "intravenous immunoglobulins and steroids" brought about a resolution of some of the behavioural issues. I might add that this is not the first time that anti-NMDA receptor encephalitis has been mentioned with autism in mind***** including that cross-over with CDD.Taking into account the Scott paper and the writings of Cahalan, I get the impression that luck played a big role in the resolution of both cases. As per the Grauniad (sorry, Guardian) write-up of her book "Cahalan is never in any doubt about the extent of her luck: the luck in finding a sensitive doctor who listened to her, and took her case on its own merits". One can perhaps see that other medics might have not offered a similar diagnosis to the one she was eventually given and upon which treatment was commenced.The Scott paper also brings into sharp focus how, when presented with cases of "autistic regression", it may be worthwhile undertaking some pretty detailed medical examination to determine whether the source of the regression might just fall into the jurisdiction of something like anti-NMDA receptor encephalitis. This accepting that getting a sample of CSF is not the nicest of procedures although as per other case studies, a full medical work-up is indicated****** (open-access).That there also may be a medical reason for such a regression to occur is another lesson for autism research as and when it is confronted by children presenting with a fairly rapid regression into autism or autistic-like symptoms. It for example, strikes me that there is a growing respect for anti-NMDA receptor encephalitis when it comes to the presentation of something like delerium******* or even some cases of schizophrenia******** (open-access here) even without seizures being present. So when such a regression occurs in younger children, are they any less deserving of such medical consideration too? Exactly how the Scott report might play into the blanket 'autism is a lifelong condition' is another consideration.Finally, I have to point out that the Scott paper was a case report and before anyone gets too carried away, does not necessarily mean that every case of regression in autism is due to this factor. That being said, the use of something like IVIg as the chosen treatment method for anti-NMDA receptor encephalitis is not necessarily a stranger to autism research (see here). The use of steroids as immunosuppressive agents, indicated for certain autoimmune conditions, might also offer some clues about certain parts of those autisms (see here) too bearing in mind my caveat on this blog about not giving medical or clinical advice.Some music to close this post I think. Oasis and Don't Look Back in Anger. "Please [Mr McGee], don't make me angry, you wouldn't like me when I'm angry" (he says hiding behind the sofa).----------* Kern JK. et al. Thimerosal exposure and the role of sulfation chemistry and thiol availability in autism. Int J Environ Res Public Health. 2013 Aug 20;10(8):3771-800.** Richler J. et al. Is there a 'regressive phenotype' of Autism Spectrum Disorder associated with the measles-mumps-rubella vaccine? A CPEA Study. J Autism Dev Disord. 2006 Apr;36(3):299-316.*** Scott O. et al. Anti-N-Methyl-D-Aspartate (NMDA) Receptor Encephalitis: An Unusual Cause of Autistic Regression in a Toddler. J Child Neurol. 2013 Oct 3. [Epub ahead of print]**** Florance NR. et al. Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis in children and adolescents. Ann Neurol. 2009 Jul;66(1):11-8.***** Creten C. et al. Anti-NMDA-receptor encephalitis: a new axis-III disorder in the differential diagnosis of childhood disintegrative disorder, early onset schizophrenia and late onset autism. Tijdschr Psychiatr. 2012;54(5):475-9.****** Chapman MR. & Vause HE. Anti-NMDA Receptor Encephalitis: Diagnosis, Psychiatric Presentation, and Treatment. Am J Psychaitry. 2011; 168: 245-251.******* Punja M. et al. Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis: an etiology worth considering in the differential diagnosis of delirium. Clin Toxicol (Phila). 2013 Sep;51(8):794-7.******** Tsutsui K. et al. Anti-NMDA-receptor antibody detected in encephalitis, schizophrenia, and narcolepsy with psychotic features. BMC Psych... Read more »
Scott O, Richer L, Forbes K, Sonnenberg L, Currie A, Eliyashevska M, Goez HR. (2013) Anti-N-Methyl-D-Aspartate (NMDA) Receptor Encephalitis: An Unusual Cause of Autistic Regression in a Toddler. Journal of Child Neurology. DOI: 10.1177/0883073813501875
Aerobic performance was not impacted by hydration status among 10 well-trained male cyclists during a 25 km time trial.... Read more »
Wall BA, Watson G, Peiffer JJ, Abbiss CR, Siegel R, & Laursen PB. (2013) Current hydration guidelines are erroneous: dehydration does not impair exercise performance in the heat. British Journal of Sports Medicine. PMID: 24055782
Opinion paper on Blastocystis in 'Trends in Parasitology' free for download all of November 2013.... Read more »
Scanlan PD, & Stensvold CR. (2013) Blastocystis: getting to grips with our guileful guest. Trends in parasitology. PMID: 24080063
This study found that motivation and an academic profile (SAT scores and high school GPA) are poor predictors of neurocognitive and postural control scores in collegiate athletes; however, they are related.... Read more »
Trinidad KJ, Schmidt JD, Register-Mihalik JK, Groff D, Goto S, & Guskiewicz KM. (2013) Predicting Clinical Concussion Measures at Baseline Based on Motivation and Academic Profile. Clinical Journal of Sport Medicine. PMID: 24071664
Scientists have shed new light on RCAN1 and suggest that inhibiting this protein may provide successful treatments for atherosclerosis.
Atherosclerosis is a disease which involves narrowing of the arteries due to a build-up of cholesterol and other fatty substances. As a major cause of stroke, heart attack and other cardiovascular diseases, atherosclerosis is a big problem both in the UK and worldwide.
... Read more »
Méndez-Barbero N, Esteban V, Villahoz S, Escolano A, Urso K, Alfranca A, Rodríguez C, Sánchez SA, Osawa T, Andrés V, Martínez-González J, Minami T, Redondo JM, Campanero MR. (2013) A major role for RCAN1 in atherosclerosis progression. EMBO Mol Med. DOI: 10.1002/emmm.201302842
A decade ago, Helen Mayberg first tried to treat a person with depression through deep brain stimulation (DBS) of the brain region called area 25. She and other groups, some targeting different brain regions, have subsequently used DBS to treat depression in more than 200 people. Between 40% and 60% of these patients demonstrated significant improvements, she says. The prospect that this experimental procedure can bring recovery for people who had given up hope has “reinvigorated the field” of depression treatment, says Husseini Manji, former director of the National Institute of Mental Health’s Mood and Anxiety Disorders Program and head of therapeutic neuroscience at Janssen Pharmaceuticals. And it has given researchers a powerful way to pursue an old but largely untested hypothesis: that much depression results not from an imbalance in the soup of neurochemicals that bathes the brain, but from disrupted neural “circuits.”... Read more »
Risk factors for achilles tendon pain in runners... Read more »
T. Hein, P. Janssen, U. Wagner-Fritz, G. Haupt, S. Grau. (2013) Prospective analysis of intrinsic and extrinsic risk factors on the development of Achilles tendon pain in runners. Scandinavian Journal of Medicine . DOI: 10.1111/sms.12137
Charles CoxNew data from a preclinical study led by Charles Cox, M.D., from The University of Texas Health Science Center at Houston (UTHealth) Medical School reveals that a stem cell therapy previously known to reduce inflammation in the critical time window after traumatic brain injury, also promotes lasting cognitive improvement.Cellular damage in the brain after traumatic injury can cause severe, ongoing neurological impairment and inflammation.As of now, few treatment options are available for this problem. About half of patients with severe head injuries need surgery to remove or repair ruptured blood vessels or bruised brain tissue.Read More... Read more »
Supinder S. Bedi, Robert Hetz, Chelsea Thomas, Philippa Smith, Alex B. Olsen, Stephen Williams, Hasen Xue, Kevin Aroom, Karen Uray, Jason Hamilton, Robert W. Mays, Charles S. Cox, Jr. (2013) Intravenous Multipotent Adult Progenitor Cell Therapy Attenuates Activated Microglial/Macrophage Response and Improves Spatial Learning After Traumatic Brain Injury. Stem Cells Translational Medicine. info:/
More elaborate statistical training is important for clinicians so that they can do research, and elaborate/interpret the medical findings better, according to a recent study.
Researchers, in the present study, worked on the statistical techniques used in one of the most prestigious journals, Journal of the American Medical Association (JAMA), and found that the frequency and complexity of statistical reporting have increased in the past two decades. However, researchers have reported that very few internal medicine residents (... Read more »
Arnold LD, Braganza M, Salih R, Colditz GA. (2013) Statistical Trends in the Journal of the American Medical Association and Implications for Training across the Continuum of Medical Education. PLoS ONE. DOI: 10.1371/journal.pone.0077301
An article a few weeks back on the SFARI site alerted me to the fact that the paper by Shruti Garg and colleagues* looking at the prevalence of autism spectrum disorder (ASD) in cases of neurofibromatosis type 1 (NF1) here in Blighty was on its way. The SFARI entry talked about NF1 in the context of "higher prevalence and severity of autism traits in RASopathies compared to unaffected siblings" as per the findings by Adviento and colleagues**.Café au lait spots @ Wikipedia I'm not going to claim to be an expert on the RASopathies because I'm not. From what I gather from the accumulated literature on these developmental syndromes is that we are dealing with a group of conditions which are marked by "mutations in Ras/mitogen-activated protein kinase (Ras/MAPK) pathway genes" which is involved in cell signalling. Quite a good overview of the Ras/MAPK pathway can be found in this article by Jarell and colleagues*** (open-access) with melanoma in mind, hinting at the connection with cancer (see here).Neurofibromatosis type 1 (NF1), one of the RASopathy family of conditions, is a genetic condition characterised by the presence of coffee coloured patches on the skin called café au lait spots. There are certain criteria for the minimum number of such spots to be present on the skin as part of the diagnosis of NF1. Neurofibromas (little bumps under the skin) are also generally noted in later development, alongside other potential symptoms such as scoliosis and tumours on the optic nerve (optic nerve glioma) among other things.There is also a connection between NF1 and cognitive and behavioural functions. Although not a universal connection, NF1 is associated with some degree of learning disability for some; as per the paper by Lorenzo and colleagues**** "young children with NF1 have significantly poorer intellectual functioning, expressive language, and visual perception". Other research has detailed an overlap in cases of NF1 with the symptoms of conditions such as ADHD*****.OK so after all that, what was found?The paper by Garg et al reports a "high prevalence of ASD in NF1" based on a survey of an NF1 registry based on first a screen for possible autistic traits (using the SRS) and then further assessment of a random sample of the group screening positive for a potential ASD. Indeed: "The population prevalence estimate is 24.9% ASD (95% confidence interval 13.1%–42.1%) and 20.8% broad ASD (95% confidence interval 10.0%–38.1%); a total of 45.7% showing some ASD spectrum phenotype". These figures are pretty astounding in terms of the presentation of autism in cases of NF1.This is not the first time that neurofibromatosis has been linked to autism. I note that Prof. Gillberg (he of the ESSENCE suggestion) discussed "the simultaneous occurrence of neurofibromatosis and childhood psychosis" back in the early 1980s******. For those slightly mystified as to why I'm referencing a paper on childhood psychosis, I might point you to some of the history of autism research and times perhaps less scientifically enlightened. The paper by Mbarek and colleagues******* carries an even more startling revelation in that "Neurofibromatosis type 1 (NF1) is increased about 150-fold in autistic patients" and their linking back to the severity of presentation in autism.Right up to date, there is also another paper by Garg and colleagues******** from earlier this year (2013) including Prof. Jonathan Green on the authorship list, noting "a high prevalence of ASD symptoms associated with NF1 as well as substantial co-occurrence with ADHD symptoms". That also NF1 was "a potentially important single-gene cause for autism symptoms" brings us full circle as to the latest paper by Garg and colleagues. I should also tip my hat to the paper by Walsh and colleagues which very much supported the previous Garg findings (see here*********).This is an interesting area of autism research, of that there is no doubt. I'm minded to suggest that the results pointing towards an association between NF1 and autism not only offer some potentially interesting insights into how genes and biochemical pathways might intersect across the conditions, but also provide further evidence that our use of the singular term 'autism' is becoming more and more outdated as time goes on, to eventually be replaced by the 'autisms'. As part of those autisms, the NF1 connection might eventually offer new targets for intervention for some (yes, even a potential role for things like mTOR inhibitors as per some connection**********) and given that skin connection, might even fit into that emerging skin-brain axis that I've talked about on a previous post (see here).In short, some really quite interesting findings.---------* Garg S. et al. Neurofibromatosis Type 1 and Autism Spectrum Disorder. Pediatrics. November 2013.** Adviento B. et al. Autism traits in the RASopathies. J Med Genet. 2013 Oct 7. doi: 10.1136/jmedgenet-2013-101951.*** Jarell AD. et al. The RAS/mitogen activated protein (MAP) kinase pathway in melanoma biology and therapeutics. Biologics. 2007 December; 1(4): 407–414.**** Lorenzo J. et al. Cognitive Features that Distinguish Preschool-Age Children with Neurofibromatosis Type 1 from Their Peers: A Matched Case-Control Study. J Pediatr. 2013 Aug 1. pii: S0022-3476(13)00797-X.***** Mautner VF. et al. Treatment of ADHD in neurofibromatosis type 1. Dev Med Child Neurol. 2002 Mar;44(3):164-70.****** Gillberg C. & Forsell C. Childhood psychosis and neurofibromatosis--more than a coincidence? J Autism Dev Disord. 1984 Mar;14(1):1-8.******* Mbarek O. et al. Association study of the NF1 gene and autistic disorder. Am J Med Genet. 1999 Dec 15;88(6):729-32.******** Garg S. et al. Autism and other psychiatric comorbidity in neurofibromatosis type 1: evidence from a population-based study. Dev Med Child Neurol. 2013 Feb;55(2):139-45.********* Walsh KS. et al. Symptomatology of autism spectrum disorder in a population with neurofibromatosis type 1. Dev Med Child Neurol. 2013 Feb;55(2):131-8.********** Liu N. et al. Mammalian target of rapamycin inhibitor abrogates abnormal osteoclastogenesis in neurofibromatosis type 1. Chin Med J (Engl). 2013 Jan;126(1):101-7.----------... Read more »
Shruti Garg, Jonathan Green, Kathy Leadbitter, Richard Emsley, Annukka Lehtonen, D. Gareth Evans, MD, Susan M. Huson, MD, FRCP. (2013) Neurofibromatosis Type 1 and Autism Spectrum Disorder. Pediatrics. info:/
A new study by Taiwanese researchers reveals how nanotechnology may be used to provide new strategies for regenerative medicine, including better tools to improve or restore damaged tissues. Published in the journal Science and Technology of Advanced Materials, the study summarizes the current state of knowledge on nanotechnology* with application to stem cell biology.Stem cells are considered an important potential source for repairing damaged human tissues. Researchers have found that the adhesion, growth, and differentiation of stem cells are likely controlled by their surrounding microenvironment, which contains both chemical and physical cues.These cues include the “nanotopography” of the complex extracellular matrix or architecture that forms a network for human tissues.Read More... Read more »
King-Chuen Wu, Ching-Li Tseng, Chi-Chang Wu, Feng-Chen Kao, Yuan-Kun Tu, Edmund C So, Yang-Kao Wang. (2013) Nanotechnology in the regulation of stem cell behavior. Science and Technology of Advanced Materials. DOI: 10.1088/1468-6996/14/5/054401
South Africa is known to have a major burden of HIV infection cases. As Pieter Fourie put it in 2006: “AIDS is killing South Africans at a rate equivalent to one September 11th attack every three days”. The situation still is as serious as this: life expectancy should have reached 64 years by now, but with the HIV pandemic it has regressed to about 47 years.... Read more »
Hontelez JA, Lurie MN, Bärnighausen T, Bakker R, Baltussen R, Tanser F, Hallett TB, Newell ML, & de Vlas SJ. (2013) Elimination of HIV in South Africa through Expanded Access to Antiretroviral Therapy: A Model Comparison Study. PLoS medicine, 10(10). PMID: 24167449
Ford N, & Hirnschall G. (2013) Modelling the Strategic Use of Antiretroviral Therapy for the Treatment and Prevention of HIV. PLoS medicine, 10(10). PMID: 24167450
Granich RM, Gilks CF, Dye C, De Cock KM, & Williams BG. (2009) Universal voluntary HIV testing with immediate antiretroviral therapy as a strategy for elimination of HIV transmission: a mathematical model. Lancet, 373(9657), 48-57. PMID: 19038438
In this randomized controlled study, researchers found that the inclusion of platelet-rich plasma for huge rotator cuff decreased retear rate and resulted in a slight increase in cross-sectional area of the supraspinatus a year following surgery.... Read more »
Jo CH, Shin JS, Lee YG, Shin WH, Kim H, Lee SY, Yoon KS, & Shin S. (2013) Platelet-rich plasma for arthroscopic repair of large to massive rotator cuff tears: a randomized, single-blind, parallel-group trial. The American Journal of Sports Medicine, 41(10), 2240-8. PMID: 23921338
A post about a selection of papers related to Blastocystis research emerging in October 2013.... Read more »
Maas L, Dorigo-Zetsma JW, de Groot CJ, Bouter S, Plötz FB, & van Ewijk BE. (2013) Detection of intestinal protozoa in paediatric patients with gastrointestinal symptoms by multiplex real-time PCR. Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases. PMID: 24131443
In the eternal search for the various potential factors (yes, there are probably going to be several) to account for the quite staggering increases in diagnosed cases of the autism spectrum conditions, no stone is seemingly being left unturned. Accepting the important and oft-cited sentence "correlation is not the same as causation" and accepting that the reasons for the increase in the autisms (plural) might differ from location to location, country to country and people to people, retrospective reviews of registries and case notes have featured quite a bit in this search for reasons.The paper by Suzanne Bolton and colleagues* follows in this methodological tradition, suggesting: "an observation of increased rates of ASD [autism spectrum disorder] among a migrant population derived particularly from children born to mothers originating in Sub-Saharan Africa" based on a review of some 366 children presenting at a child development service in Ireland (Éire).Based on those 366 case reports, autism or rather an ASD, was diagnosed in 131 and speech and language issues in 132 children. This in itself is interesting data based on the proportion of children coming to use the child development services - I assume because someone, somewhere had observed something worthy of the referral - and those eventually diagnosed with autism. Even more interesting in light of further genetic connections being made between autism and language impairment**.No mind, when looking at those born to mothers born themselves in Africa "a higher proportion of the African cohort 13/18 (72.2 %) presented with moderate/severe cognitive disability compared to the Irish group 9/55(16.3 %)". In other words, the presentation of autism and intellectual (learning) disability towards the more severe end of the spectrum seemed to be more pronounced in the migrant population than those born to mothers themselves born in Ireland.This is not the first time such a finding has been reported. I hark back to my post on the work of Cecilia Magnusson and colleagues*** who also reported a similar trend in their registry-based study following on from similar suggestions from other work.So, what might one surmise from this growing body of work. Well, if I were to use the paper by Rai and colleagues**** as my starting point (see a previous post here) I might say that we should be looking at factors such as socio-economic status (SES) among those families arrived from Africa compared to Irish families to see if they could account for the differences raised by Bolton et al. Rai concluded that "Lower, not higher, socioeconomic status was associated with an increased risk of ASD" and without making any sweeping generalisations, one has to wonder whether demographic disparities might exist on the basis of indigenous and naturalised status.That all being said, Ireland has some pretty comprehensive measures when it comes to the screening and diagnosis of autism (see here) no matter what side of the border you are on. If we are talking about children presenting with "a more severely affected" type of autism, it's highly likely that if not parents, nursery or school or other services would pick up on the need for a referral for assessment even if not knowing that it might be autism. Language and cultural differences about autism (see here) may impact on this process but I'd hazard a guess that not as much as one might first think.Other potential explanators please. Well, without getting too bogged down in the debate about different ethnicities and different genetics, one has to wonder whether the risk of autism might be somehow reduced or elevated among different peoples. At the moment, we can't say for sure because worldwide, not everyone has access to the same screening, assessment and diagnostic resources that we perhaps take for granted in the modern Western world (see here). Autism research is also not exactly thriving in some parts of the world. Throw in again those language and cultural issues - even in our supposedly developed world***** - and the big question mark on this area still remains.Then to environment. Lots of potential factors here including the stress of moving to and integrating into a new country, the introduction of a very new environment and climate - Ireland vs. Sub-Saharan Africa, mmm? - new foods, new microbes/infections, etc. Take your pick of what might be important or not. With my current interest in all things sunshine and vitamin D, I'm minded to suggest that this might be a factor worth considering given all the research attention that has been paid to vitamin D and autism. That and the whole solar intensity and ADHD link (no, really).... Likewise, I'm sure lessons can be learned from other research highlighting a similar pattern of risk in relation to other conditions such as schizophrenia and its link to immigration status******.Whatever the reasons for the disparity being highlighted by the studies by Bolton and others, from a practical point of view it is perhaps more important that measures are put in place to accommodate this potentially heightened risk of offspring autism in immigrant populations. This might mean additional screening and assessments being offered to communities (language-appropriate) as well as providing any advice and education that may be required about autism and raising a child with autism.And while we're on the topic, I'll also throw the paper by Lehti and colleagues******* (open-access) into the mix and their suggestion that "In Finland, children who are born to immigrant mothers with or without an immigrant partner, have an increased risk of childhood autism".----------* Bolton S. et al. Autism in a recently arrived immigrant population. Eur J Pediatr. 2013 Oct 2.** Bartlett CW. et al. A Genome Scan for Loci Shared by Autism Spectrum Disorder and Language Impairment. Am J Psychiatry. 2013.*** Magnusson C. et al. Migration and autism-spectrum disorder: population-based study. British Journal of Psychiatry. February 2012. DOI: 10.1192/bjp.bp.111.095125**** Rai D. et al. Parental socioeconomic status and risk of offspring autism spectrum disorders in a Swedish population-based study. J Am Acad Child Adolesc Psychiatry. 2012 May;51(5):467-476.e6.***** Zuckerman KE. et al. Pediatrician Identification of Latino Children at Risk for Autism Spectrum Disorder. Pediatrics. 2013; 132: 445-453.****** Cooper B. Immigration and schizophrenia: the social causation hypothesis revisited. Br J Psychiatry. 2005; 186: 361-363.******* Lehti V. et al. The risk of childhood autism among second-generation migrants in Finland: a case--control study. BMC Pediatrics 2013, 13:171----------Bolton S, McDonald D, Curtis E, Kelly S, Gallagher L. (2013). Autism in a recently arrived immigrant population Eur J Pediatr... Read more »
Researchers from Boston University School of Medicine (BUSM) and Boston Medical Center (BMC) announced yesterday that they have developed the first known disease-specific induced pluripotent stem cell (iPSC) lines from a patient with familial transthyretin amyloidosis. They hope that their findings may lead to new treatments for genetic diseases such as familial amyloidosis.Familial transthyretin amyloidosis (ATTR) is a lethal, autosomal dominant protein-folding disorder caused by one of more than 100 distinct mutations in the transthyretin (TTR) gene. In ATTR, protein secreted from the liver aggregates and forms fibrils in target organs, chiefly the heart and peripheral nervous system, highlighting the need for a model capable of duplicating the multisystem complexity of this clinically variable disease.Read More... Read more »
Amy Leung, Shirley K. Nah, Whitney Reid, Atsushi Ebata, Clarissa M. Koch, Stefano Monti, Joseph C. Genereux, R. Luke Wiseman, Benjamin Wolozin, Lawreen H. Connors, John L. Berk, David C. Seldin, Gustavo Mostoslavsky, Darrell N. Kotton, George J. Murphys. (2013) Induced Pluripotent Stem Cell Modeling of Multisystemic, Hereditary Transthyretin Amyloidosis. Stem Cell Reports. DOI: 10.1016/j.stemcr.2013.10.003
Harvard Stem Cell Institute (HSCI) researchers have a new model for how the kidney repairs itself, a model that adds to a growing body of evidence that mature cells are far more plastic than it was previousy thought.After injury, mature kidney cells dedifferentiate into more primordial versions of themselves, and then differentiate into the cell types needing replacement in the damaged tissue. This finding conflicts with a previously held theory that the kidney has scattered stem cell populations that respond to injury. The research appears online inPNAS Early Edition.HSCI Kidney Diseases Program Leader Benjamin Humphreys, MD, PhD, a Harvard Medical School assistant professor at Brigham and Women's Hospital, was suspicious of the kidney stem cell repair model because his previous work suggested that all kidney cells have the capacity to divide after injury. He and his colleagues decided to test conventional wisdom by genetically tagging mature kidney cells in mice that do not express stem cell markers; the hypothesis being that the mature cells should do nothing or die after injury. The results showed that not only do these fully differentiated cells multiply, but they can multiply several times as they help to repair the kidney.Read More... Read more »
Kusaba T, Lalli M, Kramann R, Kobayashi A, & Humphreys BD. (2013) Differentiated kidney epithelial cells repair injured proximal tubule. Proceedings of the National Academy of Sciences of the United States of America. PMID: 24127583
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