'Everything is awesome' (that's awesome not 'awsome') went the very catchy tune accompanying the LEGO movie not so long ago. Given the popularity of those colourful interlocking plastic bricks down the years, it was perhaps unsurprising that the film did so well and with the promise of more to come.Aside from helping to influence generations of would-be engineers and dreamers (a double-decker couch?), LEGO has also found something of a following in relation to labels like autism (see here). Perhaps also why games such as Minecraft have 'taken off' with autism in mind, is the very 'systemising-based' principles behind LEGO and how, minus sweeping generalisations, autism and systemising have some research history (see here).A recent paper by Helen Peckett and colleagues  adds to the small but emerging peer-reviewed research base looking at LEGO and autism, and specifically the idea that: "findings are supportive of previous Lego Therapy studies and have implications for strengths-based service provision." Peckett et al actually explored "mothers' experience of implementing Lego Therapy at home within the family" within the context of paediatric autism. Rather than assessing the intervention in a clinical trial manner (i.e. randomised, placebo-controlled, etc. study) the onus was on what mums of children with autism actually thought about the use of LEGO therapy. I know to some people this might seem like 'fluffy science' but in the context of a heterogeneous label like autism, I do think there is place for such research. More so when such intervention is designed to be carried out in the home environment with parents and siblings as intervention deliverers.Suffice to say that much of the maternal discussions about LEGO therapy were quite positive in line with previous findings  and not just in the short-term . As per the title of the paper, family relationships were a winner following the intervention, probably as a consequence of the greater involvement between mother and child (and siblings) in line with other reported findings (see here). There were however some fairly down-to-earth comments made about the intervention during the "interpretative phenomenological analysis" not least about "the impact of the intervention in the wider context." In other words, whilst LEGO therapy (or just playing with LEGO in a more structured way) may indeed have some value in terms of social skills such as sharing and turn-taking for example, how does this translate outside of the LEGO therapy context?Similar questions could probably be asked about the use of Minecraft and related platforms too, bearing in mind how such 'gaming' probably does little to address important issues such as the promotion of physical activity for example  and the benefits that sports can potentially bring to some of the autism spectrum. That screen time might also have a negative side in terms of self-reported inattention in other groups  is something else to consider, as are other reports in the peer-reviewed literature .By saying all that I'm not trying to poo-poo LEGO or Minecraft; I'm just saying that outside of being recreational activities, one has to be a little guarded about turning every play and leisure activity into 'therapy'. I might also mention how addictive LEGO and/or Minecraft can be; something which I assume can be as much of an issue for parents of children on the autism spectrum as it is for everyone else when it comes to getting children on to other tasks. Oh, and LEGO certainly isn't cheap either...---------- Peckett H. et al. Maternal experience of Lego Therapy in families with children with autism spectrum conditions: What is the impact on family relationships? Autism. 2016 Feb 5. pii: 1362361315621054.  Owens G. et al. LEGO therapy and the social use of language programme: an evaluation of two social skills interventions for children with high functioning autism and Asperger Syndrome. J Autism Dev Disord. 2008 Nov;38(10):1944-57. Legoff DB. & Sherman M. Long-term outcome of social skills intervention based on interactive LEGO play. Autism. 2006 Jul;10(4):317-29.  Bremer E. et al. A systematic review of the behavioural outcomes following exercise interventions for children and youth with autism spectrum disorder. Autism. 2016 Jan 28. pii: 1362361315616002. Montagni I. et al. Association of screen time with self-perceived attention problems and hyperactivity levels in French students: a cross-sectional study. BMJ Open. 2016; 6:e009089. MacMullin JA. et al. Plugged in: Electronics use in youth and young adults with autism spectrum disorder. Autism. 2016 Jan;20(1):45-54.----------Peckett H, MacCallum F, & Knibbs J (2016). Maternal experience of Lego Therapy in families with children with autism spectrum conditions: What is the impact on family relationships? Autism : the international journal of research and practice PMID: 26851230... Read more »
Peckett H, MacCallum F, & Knibbs J. (2016) Maternal experience of Lego Therapy in families with children with autism spectrum conditions: What is the impact on family relationships?. Autism : the international journal of research and practice. PMID: 26851230
The February entry in the "This Month in Blastocystis Research" blog post series is all on Blastocystis and chronic urticaria (hives).... Read more »
Armentia A, Méndez J, Gómez A, Sanchís E, Fernández A, de la Fuente R, & Sánchez P. (1993) Urticaria by Blastocystis hominis. Successful treatment with paromomycin. Allergologia et immunopathologia, 21(4), 149-51. PMID: 8237719
Casero, R., Mongi, F., Sánchez, A., & Ramírez, J. (2015) Blastocystis and urticaria: Examination of subtypes and morphotypes in an unusual clinical manifestation. Acta Tropica, 156-161. DOI: 10.1016/j.actatropica.2015.05.004
Kolkhir P, Balakirski G, Merk HF, Olisova O, & Maurer M. (2016) Chronic spontaneous urticaria and internal parasites - a systematic review. Allergy, 71(3), 308-22. PMID: 26648083
Lepczyńska M, Chen WC, & Dzika E. (2016) Mysterious chronic urticaria caused by Blastocystis spp.?. International journal of dermatology, 55(3), 259-66. PMID: 26469206
Vogelberg C, Stensvold CR, Monecke S, Ditzen A, Stopsack K, Heinrich-Gräfe U, & Pöhlmann C. (2010) Blastocystis sp. subtype 2 detection during recurrence of gastrointestinal and urticarial symptoms. Parasitology international, 59(3), 469-71. PMID: 20363362
Cognitive impairment following a traumatic brain injury (TBI) is common, often adversely affecting quality of life for those 1.7 million Americans who experience a TBI each year. Researchers have identified complex brain connectivity patterns in individuals with chronic phases of traumatic brain injury which may explain long term higher order cognitive function deficits.
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Han, K., Chapman, S., & Krawczyk, D. (2016) Disrupted Intrinsic Connectivity among Default, Dorsal Attention, and Frontoparietal Control Networks in Individuals with Chronic Traumatic Brain Injury. Journal of the International Neuropsychological Society, 22(02), 263-279. DOI: 10.1017/S1355617715001393
One of the main reasons we study how bacteria and fungi work is to minimize their negative effects on our health. These effects usually stem from being munched on (in other words, an infection) and/or being damaged by a toxic substance (being poisoned). While poisonings due to bacteria and fungi predominantly occur either in association with infections (e.g. diphtheria and tetanus) or via eating contaminated food (e.g. botulinum toxin and aflatoxins) or a misidentified mushroom (e.g. amatoxins), it's also possible to become sick after breathing in harmful gases or aerosols produced by these groups of organisms.Our cells can acquire energy by taking electrons from certain bits of organic carbon and transferring them via a series of steps to oxygen, producing water as a byproduct. Sulfur-reducing bacteria do something similar, but instead of oxygen they dump their electrons on sulfate and other electron-deficient forms of sulfur, producing hydrogen sulfide. It's a poisonous (to human cells), corrosive, flammable, AND explosive gas. Hydrogen sulfide lacks colour but is nevertheless detectable at very, very low concentrations because of its potent rotten egg odour. However, our noses quickly adjust to the smell, rendering it odourless.There's an old saying in toxicology, which is the dose makes the poison. Hydrogen sulfide is no exception. It's present in our bodies in very small amounts, where it helps ensure our nerves and blood vessels work properly. Being exposed to low concentrations of the gas isn't too much of a problem, since we're equipped with enzymes able to detoxify limited amounts of it. However, at high concentrations, the gas is a lethal fast-acting poison. It acts much like hydrogen cyanide to prevent our cells from extracting energy from organic carbon using oxygen. Due to its effects on the central nervous system, it quickly knocks people unconscious. Thereafter, death typically occurs as a result of the gas suppressing the region of the brain where breathing is controlled (central respiratory arrest).Hydrogen sulfide is heavier than air, so it can accumulate in low-lying places with poor airflow. The gas tends to show up wherever you have sulfur-reducing bacteria, lots of organic carbon and sulfur (for the bacteria to live off of), no oxygen (otherwise other bacteria would take over), and warm conditions (>20 °C) (to ensure appreciable bacterial growth). These conditions can be found in outhouses, sewers, septic tanks, and manure pits, particularly in the summertime. People can be fatally poisoned by hydrogen sulfide if they enter these confined and poorly ventilated spaces without their own separate air supply.The harmful nature of hydrogen sulfide was reported as early as 1700 by the Italian physician Bernardo Ramazzini, who noted cases of poisoning among those employed to clean bacteria-filled cesspits and latrines. During the 18th and 19th centuries, a number of people working in the sewers of Paris died when they were exposed to hydrogen sulfide. Victor Hugo described how dangerous the situation was in Les Misérables (1862), even mentioning sulphuretted hydrogen (an old way of saying hydrogen sulfide) by name.A section of the sewers beneath Paris (Source)Another airborne poison worth mentioning is clouds of fungal spores. Many of the fungi hiding out as networks of threads inside plants and soils reproduce by creating mushrooms, which serve to spread their spores (seeds) around. In the case of puffballs and earthstars, pushing on them causes a large number of spores (we're talking billions to trillions) to be shot into the air through a central hole. It looks a bit like smoke. The push can happen via falling raindrops or a trampling foot. Puffballs and earthstars often grow in dense groups, so a lot of spores can end up in the air all at once.Animals who breathe in a bunch of fungal spores can end up with a nasty lung-based illness known as hypersensitivity pneumonitis. Essentially, the spores trick the immune system into overreacting, causing a damaging inflammation deep within the lungs. Lycoperdonosis is a form of hypersensitivity pneumonitis specifically caused by inhaling spores from puffballs of the genus Lycoperdon.White blood cells (indicating inflammation) and a fungal spore (arrow) from the lung of a dog (Source)In one particularly unfortunate case, a group of eight apparently sober teenagers decided it would be a good idea to inhale the spores squeezed from some puffballs they had acquired. After a couple of days, they started to cough, had trouble breathing, ran a fever, and felt generally crappy. Things got so bad that five of the teens were hospitalized, two of them needing to be intubated to help them breathe. Their inflamed lungs were treated with corticosteroids and they all eventually recovered from their illness.Lycoperdonosis has also been seen in people who snorted puffball spores as a folk remedy for a nosebleed. Both puffballs and earthstars have killed or seriously injured dogs who disturbed them and inhaled their spores as they ran about or dug holes.ReferencesAlenghat T et al. 2010. Lycoperdonosis in two dogs. Journal of Veterinary Diagnostic Investigation 22(6):1002-1005. [Full text]Nogué S, Pou R, Fernández J, Sanz-Gallén P. 2011. Fatal hydrogen sulphide poisoning in unconfined spaces. Occupational Medicine 61(3):212-214. [Full text]Policastro MA, Otten EJ. 2007. Case files of the University of Cincinnati fellowship in medical toxicology: Two patients with acute lethal occupational exposure to hydrogen sulfide. Journal of Medical Toxicology 3(2):73-81. [Full text]Whitney J, Beijerink N, Martin P, Talbot J, Barrs V. 2013. Hypersensitivity pneumonitis in a dog associated with Geastrum triplex spores. Medical Mycology Case Reports 2:122-124. [Full text]http://www.cdc.gov/mmwr/preview/mmwrhtml/00032029.htm... Read more »
Nogué S, Pou R, Fernández J, & Sanz-Gallén P. (2011) Fatal hydrogen sulphide poisoning in unconfined spaces. Occupational Medicine, 61(3), 212-214. PMID: 21467246
Whitney J, Beijerink N, Martin P, Talbot J, & Barrs V. (2013) Hypersensitivity pneumonitis in a dog associated with Geastrum triplex spores. Medical Mycology Case Reports, 122-124. DOI: 10.1016/j.mmcr.2013.05.002
Toxoplasma may no longer be responsible for mental disorders... Read more »
Fuller Torrey, E., Simmons, W., & Yolken, R. (2015) Is childhood cat ownership a risk factor for schizophrenia later in life?. Schizophrenia Research, 165(1), 1-2. DOI: 10.1016/j.schres.2015.03.036
Sugden, K., Moffitt, T., Pinto, L., Poulton, R., Williams, B., & Caspi, A. (2016) Is Toxoplasma Gondii Infection Related to Brain and Behavior Impairments in Humans? Evidence from a Population-Representative Birth Cohort. PLOS ONE, 11(2). DOI: 10.1371/journal.pone.0148435
"Having AD [atopic dermatitis] before age 2 years was associated with an increased hazard ratio (HR) for ASD [autism spectrum disorder] by 10% and that for ADHD [attention-deficit hyperactivity disorder] by 16%; such increases were particularly prominent among those with earlier-onset or more severe AD."So said the findings reported by Tzu-Chu Liao and colleagues  as yet again, the Taiwanese National Health Insurance Research Database (NHIRD) continues to give. Indeed, the idea of an association between conditions implicating immune function and behavioural-based diagnoses such as autism or ADHD has become something of a point-of-interest for researchers utilising the NHIRD (see here). The data - reporting on participant groups in the thousands, even hundreds of thousands - is stacking up pertinent to "a disordered immunologic response [that] may exert effects on neurodevelopment" (see here).This time around researchers "identified 387 262 children who had a diagnosis of atopic dermatitis (AD) before age 2 years, with 1:1 individualized matching to children without AD." The overall frequency of AD-exposed children who received a diagnosis of autism or ADHD don't necessarily look hugely different from non AD-exposed children (0.5% and 3.7% vs. 0.4% and 2.9% respectively). But when taking into account the numbers of participants, even small percentage differences can reveal potentially important correlations. The authors also report that: "HRs were especially higher for children with persistent AD and emerging atopic respiratory diseases in childhood." Emerging 'atopic respiratory disease' is something else that might be implicated in some autism (see here) and even more strongly, in some ADHD (see here).What does it all mean? Well, I think there is quite a strong case for more research attention to be directed to this area of investigation outside of just correlating conditions in large population numbers. That childhood atopic disease might also increase the risk of later episodes of psychotic experiences for example (see here) offers some important research directions too, onwards to the idea that immune function and psychiatry might not be unstrange bedfellows (see here). Screening for one or other condition (autism/ADHD and atopic diseases) might also be more widely implicated as a result of these and other findings and then there are the tantalising implications of what treatment of one might do for the other as per discussions about work from Harumi Jyonouchi recently (see here). Before getting too excited about these findings, I might however add that to talk about autism or ADHD and atopic disease being potentially linked does not necessarily mean that it is applicable to every single person...---------- Liao TC. et al. Comorbidity of Atopic Disorders with Autism Spectrum Disorder and Attention Deficit/Hyperactivity Disorder. J Pediatr. 2016 Feb 1. pii: S0022-3476(15)01653-4.----------Liao TC, Lien YT, Wang S, Huang SL, & Chen CY (2016). Comorbidity of Atopic Disorders with Autism Spectrum Disorder and Attention Deficit/Hyperactivity Disorder. The Journal of pediatrics PMID: 26846570... Read more »
Liao TC, Lien YT, Wang S, Huang SL, & Chen CY. (2016) Comorbidity of Atopic Disorders with Autism Spectrum Disorder and Attention Deficit/Hyperactivity Disorder. The Journal of pediatrics. PMID: 26846570
There’s no pain like nerve pain. Whether it is because of a chronic illness or related to an injury, it may be obvious, but nerve pain hurts. That may change soon though, as a specific molecule involved in maintaining pain after a nerve injury has been identified and blocked in mice by researchers. These results reveal a promising therapeutic strategy for treating neuropathic pain.
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Zhang, F., Morioka, N., Harano, S., Nakamura, Y., Liu, K., Nishibori, M., Hisaoka-Nakashima, K., & Nakata, Y. (2016) Perineural expression of high-mobility group box-1 contributes to long-lasting mechanical hypersensitivity via matrix metalloprotease-9 up-regulation in mice with painful peripheral neuropathy. Journal of Neurochemistry, 136(4), 837-850. DOI: 10.1111/jnc.13434
By Maranda CardielHow cool would it be if you could regenerate your own body parts? Just imagine: you are chopping up some carrots for dinner, but whoops! You accidentally cut off your thumb! No worries, it’ll grow back in a few weeks, good as new and fully functional. No need to take a trip to the hospital and pay all of those annoying medical costs. That all sounds pretty nifty, but that can’t actually happen, right? Tissue regeneration on that large of a scale is something you can only find in science fiction. …Or so you may think. Nature has actually found a way to regenerate full limbs and other body parts after they have been completely amputated. However, among animals with spines, this unique ability is only found in salamanders. But how does it work, and why can’t we do it too? A cartoon illustrating examples of the three different methods of tissue regeneration in animals. A.) An adult hydra being cut into two pieces and regenerating into two separate hydras. B.) Part of a human liver being cut off and the remaining liver regenerating via cell division. C.) A salamander’s arm being amputated and undergoing epimorphosis to regenerate an entire new arm. Source: Maranda CardielThere are actually three ways that animals can regenerate tissues. Some animals, such as hydras, can use the tissues they already have to regenerate themselves after being cut in two, resulting in two separate hydras. Mammals, including humans, have the ability to regenerate their livers by having the liver cells divide into more liver cells. This is how liver transplants work – a portion of liver from a live donor will grow into a fully-functioning liver in the recipient. The third method is called epimorphosis, which is the ability to change existing cells of specific types so that they can re-grow as different cell types, and this is what salamanders are able to do.When the limb of a salamander is cut off, only the outermost layer of skin moves to cover the wound. This single layer forms a special skin cap known as the epithelial cap, and the nerves at the amputation site shrink back from the wound. Then the cells beneath the cap dedifferentiate, losing their specific characteristics so all of the different types of cells become the same and detach from each other.A cartoon illustrating the process of a salamander regenerating its arm. A.) The limb is amputated. B.) The outermost layer of the skin begins to cover the wound. C.) This single layer of skin creates an epithelial cap and the blastema forms underneath it. D.) The cells of the blastema begin to differentiate into bone, nerves, etc. E.) The cells continue to divide and differentiate until the limb is fully formed. Source: Maranda CardielNow the amputated limb has a mass of indistinguishable cells under the cap, and this mass is called the regeneration blastema. A blastema is simply a clump of cells that is able to grow into an organ or body part. Over the course of several weeks, this blastema divides into more cells and the cells begin to differentiate - or turn into multiple types - again, forming different cell types such as bone, muscle, cartilage, nerves, and skin. Eventually, the salamander will have a brand new limb.The salamander’s body can even tell what body part it’s supposed to re-grow; if it’s amputated at the wrist it will grow a new hand, and if its entire hind leg is amputated it will grow a new hind leg. And it’s not only limbs that salamanders can regenerate – they can even grow back their tails, retinas, spinal cords, and parts of their hearts and brains! As you can see, the process of epimorphosis is much more complicated than simply having a single cell type divide a lot. It also requires certain chemicals and patterns of immune signaling to work properly. But why can’t people do this too? One of the reasons is because when our tissues are damaged, all of our skin grows to cover and heal the wound, which forms scars. In salamanders, only the outermost layer of skin does this, which prevents the scarring that would stop tissue regeneration. The salamander’s immune system is also regulated differently than our own, which allows them to regenerate whole body parts. Unfortunately we are not salamanders, so when you cut off your finger it’s not going to grow back. But researchers are continuing to study salamanders and their astounding regenerative abilities in the hopes of finding a way to apply it to people. Who knows, maybe someday we’ll be able to grow back our own limbs too. Sources:Gilbert, Scott F. Developmental Biology 6th Edition. Ncbi.nlm.nih.gov. National Center for Biotechnology Information, 2000.Godwin, J., Pinto, A., & Rosenthal, N. (2013). Macrophages are required for adult salamander limb regeneration Proceedings of the National Academy of Sciences, 110 (23), 9415-9420 DOI: 10.1073/pnas.1300290110 ... Read more »
Godwin, J., Pinto, A., & Rosenthal, N. (2013) Macrophages are required for adult salamander limb regeneration. Proceedings of the National Academy of Sciences, 110(23), 9415-9420. DOI: 10.1073/pnas.1300290110
With a title like "“Schizophrenia” does not exist", the opinion piece by Jim van Os  (open-access) was bound to attract some attention and comment (indeed, several). As per other examples where diagnostic labels have been questioned (see here) the response to such viewpoints typically falls into one of two categories: (a) the person or persons making the suggestion just want to make a name for themselves (and how better than to stir up a bit of controversy) or (b) the person or persons making the claim have a valid point.In the case of the viewpoint posited by van Os, and without trying to offend too many people, I'm tending towards the latter option because I think he has a point. Read onwards and I'll try and explain why.The crux of the suggestion is that in these days of increasing pluralisation of diagnostic labels (see here for another example) and realisation that individual behavioural or psychiatric labels rarely occur unaccompanied (see here) the idea that there is a discrete condition called schizophrenia is fast losing 'evidence-based' backing. His descriptions of how DSM-5 classifies schizophrenia and the various diagnostic classifications that patients may 'move in and out of', harks back to some of the reasons why the RDoC (Research Domain Criteria) initiative was first suggested and continues to gather momentum.As per other entries on this blog acknowledging the idea of the more plural 'schizophrenias' (see here) and even a 'bipolar - schizoaffective - schizophrenia spectrum' (see here), van Os suggests a more wide-ranging term to supplant schizophrenia: psychosis spectrum syndrome. This label, it is suggested, takes account of the "extreme heterogeneity, both between and within people, in psychopathology, treatment response, and outcome." van Os also suggests that the creation of such a spectrum is a way to "forget about “devastating” schizophrenia as the only category that matters and start doing justice to the broad and heterogeneous psychosis spectrum syndrome that really exists."I don't believe we're going to see a dramatic migration towards psychosis spectrum syndrome as a replacement for the singular schizophrenia term very quickly. Much like what goes on behind other conditions/labels, change is often a slow process in medicine and convincing people who might have their own reasons for sticking with the label schizophrenia (e.g. identity, management options, etc.) will prove difficult. That we already have a similarly worded term, [unspecified] schizophrenia spectrum disorder in the current manifestation of DSM is an additional point of complication to make.Still, I can see the benefits of taking a wider approach to the categorisation of symptoms in this area of psychiatry. Indeed, if one considers the data on schizophrenia spectrum disorder appearing alongside 22q11.2 deletion syndrome for example (see here) you get a flavour for how many routes there may be taking someone towards clinically significant symptoms. That 'treatment response' may also guide the appreciation of a wider spectrum definition encompassing schizophrenia (see here for example), one could foresee a time when a specific place on the psychosis spectrum is given to patients and the trial-and-error of symptom management potentially becomes a thing of the past with the right patient work-up. That is also assuming some accuracy in [some of] the management options put forward ...That all being said, in agreement with this article by Allen Frances on a related topic, I think we also have to be a little careful not to be too broad in our brush strokes on spectrum generalisations.Music: War and Low Rider.---------- Os van J. "Schizophrenia" does not exist. BMJ. 2016 Feb 2;352:i375. Jauhar S. et al. Cognitive-behavioural therapy for the symptoms of schizophrenia: systematic review and meta-analysis with examination of potential bias. Br J Psychiatry. 2014 Jan;204(1):20-9.----------Os, J. (2016). “Schizophrenia” does not exist BMJ DOI: 10.1136/bmj.i375... Read more »
A newly developed “Smart Cup” can detect disease-causing agents such as herpes simplex virus type 2 (HSV-2) with the help of smartphone camera.
Sensors and Actuators B: Chemical
Many novel ways of detecting infectious diseases have been developed. Among those methods are nucleic-acid amplification-based diagnostics that are sensitive, rapid, and specific on one side, but expensive, and requiring extensive procedure and trained personnel on the other side. That is why; such procedures are not available in many of those areas where infectious diseases can easily spread.
Recently, researchers have introduced a simple and inexpensive device, a smart cup that can detect pathogens in a rapid manner. This cup uses smartphone camera and its flashlight. Actually, the cup takes help of water-triggered exothermic chemical reaction to produce heat for nucleic acid-based, isothermal amplification. The amplification temperature is maintained at 60°C -65°C with the help of a phase-change material (PCM). Flashlight on the camera is used to activate the fluorescent dye, and the smartphone camera records real-time fluorescence emission during the process of amplification. The smartphone also checks multiple amplification reactors and analyze the obtained information.
Researchers have already used the cup in the diagnosis of HSV-2, which is responsible for genital herpes. Interestingly, this cup can be used anywhere, i.e. at home, in the clinic, or in the field, and in areas where sophisticated laboratories are not available.
Liao, S., Peng, J., Mauk, M., Awasthi, S., Song, J., Friedman, H., Bau, H., & Liu, C. (2016). Smart cup: A minimally-instrumented, smartphone-based point-of-care molecular diagnostic device Sensors and Actuators B: Chemical, 229, 232-238 DOI: 10.1016/j.snb.2016.01.073... Read more »
Liao, S., Peng, J., Mauk, M., Awasthi, S., Song, J., Friedman, H., Bau, H., & Liu, C. (2016) Smart cup: A minimally-instrumented, smartphone-based point-of-care molecular diagnostic device. Sensors and Actuators B: Chemical, 232-238. DOI: 10.1016/j.snb.2016.01.073
In a new paper, neurologists Elias D. Granadillo and Mario F. Mendez describe two patients in whom brain disorders led to an unusual symptom: "intractable joking."
Patient #1 was
A 69-year-old right-handed man presented for a neuropsychiatric evaluation because of a 5-year history of compulsive joking... On interview, the patient reported feeling generally joyful, but his compulsive need to make jokes and create humor had become an issue of contention with his wife. He would wake her u... Read more »
Life literally inside the world wide web, it’s an interesting idea. One that has tantalized sci-fi fans since before the framework for the internet was even finished. While the idea of a seemingly eternal disembodied life through the unfiltered and raw computer consciousness that we all share a connection with, maybe we are shooting for a goal that isn’t really possible — maybe we are asking the wrong questions.
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Nicolau, D., Lard, M., Korten, T., van Delft, F., Persson, M., Bengtsson, E., Månsson, A., Diez, S., Linke, H., & Nicolau, D. (2016) Parallel computation with molecular-motor-propelled agents in nanofabricated networks. Proceedings of the National Academy of Sciences, 201510825. DOI: 10.1073/pnas.1510825113
Morsella, E., Godwin, C., Jantz, T., Krieger, S., & Gazzaley, A. (2015) Homing in on Consciousness in the Nervous System: An Action-Based Synthesis. Behavioral and Brain Sciences, 1-106. DOI: 10.1017/S0140525X15000643
Alcock, J., Maley, C., & Aktipis, C. (2014) Is eating behavior manipulated by the gastrointestinal microbiota? Evolutionary pressures and potential mechanisms. BioEssays, 36(10), 940-949. DOI: 10.1002/bies.201400071
I'm pretty sure that the paper by Maria Dominguez-Bello and colleagues  speaks for itself when describing the results of "a pilot study in which infants delivered by C-section [Caesarean section] were exposed to maternal vaginal fluids at birth." If you need a graphic, some coverage of the research in the New York Times helpfully provides a visual aid (see here).The long-and-short of it is that following some concerns that infants delivered via C-section might be missing out on some valuable exposure to their mother's microbial passengers  as a function of their by-passing the birth canal and beyond, the use of a "vaginal microbial transfer" might be an option. Detailing results based on a small number of births - 11 born by C-section (planned or elective) and 7 via the more traditional route - researchers report what happened when 4 of the C-section infants were swabbed with previously collected gauze containing mum's bacterial passengers. Swabbing by the way, was done on various parts of the infant's body.The authors concluded that: "Similarly to vaginally delivered babies, the gut, oral and skin bacterial communities of these newborns [swabbed C-section infants] during the first 30 d[ays] of life was enriched in vaginal bacteria—which were underrepresented in unexposed C-section–delivered infants." That being said, the results appeared to show that whilst swabbing was good at delivering a microbial transplant for C-section infants, it was no substitute for the real thing (a vaginal birth) bacterially-speaking. I might also add that important variables such as breastfeeding (or not) can also influence the constitution of our gut bacteria (see here).There is some media chatter about this study and onwards what the longer-term effects might be in terms of health and well-being in the context of how our bacterial masters may show various health/disease links . I'd be interested to see how this cohort and other larger ones fare as a result. I do however, have a word of caution to add to proceedings alongside others it seems (see here).Accepting that a vaginal microbial transfer is not the same as the more 'popular' talking point that is a faecal microbiota transplant, and that the bacteria that colonise the gut may not necessarily be the same as that colonising other parts of the body, I'm minded to direct readers to a post not-so-long-ago covering weight gain following poo(p) transplant (see here). I don't think the specific 'obesogenic' bacteria were isolated in the case report by by Neha Alang and Colleen Kelly  or indeed, whether other elements such as the gut virome may have exerted some effect on patient weight gain following "receiving stool from a healthy but overweight donor." But one question might be to ask whether a similar 'process' could potentially be pertinent to the swabbing of C-section infants?OK, I appreciate that there has been some research discussion about how C-section babies *might* be slightly more prone to obesity in later life (see here). But if one assumes that outside of the typical risk factors linked to obesity, there may be a microbial link too, is it not inconceivable that an early-days microbial transplant from a mum who is herself overweight or obese at the time of birth might potentially 'transmit' the basis of such weight problems to offspring too? Indeed, with all the chatter about microbes and mood these days (see here for example) one could potentially stretch the 'bacterial association' even further...I'll leave you with those thoughts and some (new) music from the Leppard (hopefully really not a "nuclear waste of time").---------- Dominguez-Bello MG. et al. Partial restoration of the microbiota of cesarean-born infants via vaginal microbial transfer. Nature Medicine. 2016. Feb 2. Biasucci G. et al. Cesarean delivery may affect the early biodiversity of intestinal bacteria. J Nutr. 2008 Sep;138(9):1796S-1800S. Alang N. & Kelly CR. Weight Gain After Fecal Microbiota Transplantation. Open Forum Infect Dis. 2015; 2: 1.----------Dominguez-Bello MG, De Jesus-Laboy KM, Shen N, Cox LM, Amir A, Gonzalez A, Bokulich NA, Song SJ, Hoashi M, Rivera-Vinas JI, Mendez K, Knight R, & Clemente JC (2016). Partial restoration of the microbiota of cesarean-born infants via vaginal microbial transfer. Nature medicine PMID: 26828196... Read more »
Dominguez-Bello MG, De Jesus-Laboy KM, Shen N, Cox LM, Amir A, Gonzalez A, Bokulich NA, Song SJ, Hoashi M, Rivera-Vinas JI.... (2016) Partial restoration of the microbiota of cesarean-born infants via vaginal microbial transfer. Nature medicine. PMID: 26828196
The majority of BHD patients develop pulmonary cysts and approximately 1 in 3 will suffer a pneumothorax. Although BHD pulmonary cysts have defining characteristics compared to other cystic lung diseases (as discussed in recent reviews), the underlying pathogenesis is not yet clearly understood. A recent review from Kennedy, Khabibullin & Henske (2016) summarises the current understanding of BHD pulmonary pathology relative to the stretch hypothesis for cyst formation.... Read more »
Kennedy JC, Khabibullin D, & Henske EP. (2016) Mechanisms of Pulmonary Cyst Pathogenesis in Birt-Hogg-Dube Syndrome: The Stretch Hypothesis. Seminars in cell . PMID: 26877139
I probably don't need to provide most readers with too much background information on the topic of wandering/elopement and autism given the multitude of news reports that have been, and continue to be, generated on this worrying behaviour. The article titled: 'The Life and Death of Avonte Oquendo' pretty much sums up the very saddest outcome of wandering, and how in some respects, autism can potentially be a life-limiting condition.I do however think it is important to discuss the findings reported by Bridget Kiely and colleagues  (open-access) and how science continues to contribute to questions such as "the prevalence and correlates of wandering in a nationally representative sample of school-age children in the United States with developmental conditions." I might add that I've seen very little in the peer-reviewed domain about wandering behaviour and autism here in Blighty (UK) or indeed, in other countries outside of the USA. Another important research inequality methinks...The Kiely paper, which has itself received some press attention (see here), starts with the idea that as a result of the increasing numbers of people being diagnosed with an autism spectrum disorder (ASD) (see here) the likelihood that issues such as wandering or elopement will happen is going to increase. You can um-and-ah about the reasons for the increase in cases (bearing in mind findings such as the one by Russell and colleagues  talked about recently) but by mass action, increasing numbers of people with autism = increasing numbers of wandering/elopement episodes."Data were obtained from the 2011 Survey of Pathways to Diagnosis and Services (“Pathways”), a cross sectional, nationally representative survey of the parents and guardians of children with special health care needs (CSHCN) ages 6–17 with a current or past parent-reported diagnosis of ASD, ID [intellectual disability], and/or DD [developmental delay]." In all some 4000 parents and guardians of children with ASD, ID and/or DD were surveyed from a total population of some 7500. A proportion of those 4000 parents/guardians provided some data on their children incorporating elements from "the Children’s Social Behavior Questionnaire (CSBQ)." The issue of wandering/elopement "was assessed based on four questions about the child’s history of wandering from various locations within the previous twelve months" and data was divided according to diagnosis.Results: "Among all children with a current developmental condition (ASD, ID, and/or DD), the overall rate of elopement within the previous 12 months was 26.7%." Readers should bear in mind the emphasis on elopement within 'the previous 12 months'. Further: "Compared to the ID/DD-only group, the odds of elopement were higher for the ASD-only group... and the ASD+ID/DD-group." This is based on participant groupings including: "492 had ASD-only; 924 had ASD plus ID and/or DD; and 2,085 had ID and/or DD without ASD."The authors also observed that "children who were between the ages of 6 and 11 were more likely to have eloped than those that were 12–17 at the time of the Pathways interview" but there was little to see when it came to factors such as "household income, sex, or race/ethnicity." Elopement behaviour, it appears, crosses socio-economic differences. They did however report some associations between wandering behaviour and some of the clinical data reported using the CSBQ among other things. So; "wanderers were more likely than non-wanderers to show sudden mood changes...; to over-react to everything and everyone...; to get angry quickly...; not to realize when there is danger...; to have difficulty distinguishing between strangers and familiar people...; to be disobedient...; to panic in new situations or if change occurs...; to remain clammed up in new situations or if change occurs...; and to get lost easily." At this point I'm also going to introduce a new measure that also covers the topic of 'disappearing behaviour'  that might figure in future work in this area.There is little more for me to say on this topic outside of the presented results. As I've indicated in previous posts (see here), in amongst all the 'differences' that divide people when it comes to the label of autism, moves to reduce the potentially devastating consequences of elopement/wandering when it occurs alongside autism seemingly unites everyone. Statistics that point to accidental death potentially including wandering as being contributory to early mortality in autism (see here) provide a stark message that investment in technology in particular, is an important area to minimise the potential adverse effects of wandering. Teaching skills such as those related to pedestrian safety  could also be a good idea. I might liekwise add that the involvement of water in several cases of death following wandering in relation to autism should also persuade policy-makers to provide something like free swimming classes to those on the autism spectrum?---------- Kiely B. et al. Prevalence and Correlates of Elopement in a Nationally Representative Sample of Children with Developmental Disabilities in the United States. PLoS ONE. 2016; 11(2): e0148337. Russell G. et al. Changes in diagnosis rates and behavioural traits of autism spectrum disorder over time. British Journal of Psychiatry Open. 2015; 1: 110-115. Tyrer P. et al. The Problem Behaviour Checklist: short scale to assess challenging behaviours. British Journal of Psychiatry Open. 2016; 2: 45-49. Harriage B. et al. An Evaluation of a Parent Implemented In Situ Pedestrian Safety Skills Intervention for Individuals with Autism. J Autism Dev Disord. 2016 Feb 10.----------Kiely, B., Migdal, T., Vettam, S., & Adesman, A. (2016). Prevalence and Correlates of Elopement in a Nationally Representative Sample of Children with Developmental Disabilities in the United States PLOS ONE, 11 (2) DOI: 10.1371/journal.pone.0148337... Read more »
Kiely, B., Migdal, T., Vettam, S., & Adesman, A. (2016) Prevalence and Correlates of Elopement in a Nationally Representative Sample of Children with Developmental Disabilities in the United States. PLOS ONE, 11(2). DOI: 10.1371/journal.pone.0148337
Surprisingly complex interactions between neurotransmitter receptors and other key proteins help explain the brain’s ability to process information with lightning speed, according to a new study. Scientists at McGill University, working with collaborators at the universities of Oxford and Liverpool, combined experimental techniques to examine fast-acting protein macromolecules, known as AMPA receptors, which are a major player in brain signaling.
... Read more »
Dawe, G., Musgaard, M., Aurousseau, M., Nayeem, N., Green, T., Biggin, P., & Bowie, D. (2016) Distinct Structural Pathways Coordinate the Activation of AMPA Receptor-Auxiliary Subunit Complexes. Neuron. DOI: 10.1016/j.neuron.2016.01.038
Curries, macaroons, piña coladas...where would we be without the captivating culinary contributions of the coconut?... Read more »
Mulford JS, Oberli H, & Tovosia S. (2001) Coconut palm-related injuries in the Pacific Islands. ANZ Journal of Surgery, 71(1), 32-34. PMID: 11167595
Sekar N, Veetil SK, & Neerathilingam M. (2013) Tender coconut water an economical growth medium for the production of recombinant proteins in Escherichia coli. BMC Biotechnology, 70. PMID: 24004578
Rubella rash @ NHS Choices"Rubella might still cause autism, even in vaccinated populations."That was one of the points raised in the '2015 reappraisal' document published by Jill Hutton  (open-access) covering a topic that has quite a long history with autism in mind (see here).Rubella, also called german measles, a previously common childhood disease characterised by a rash, high temperature and cold-like symptoms, has in many parts of the world almost been entirely eradicated as a consequence of vaccination and other health measures. Here in Blighty (UK), our public health agency has even recently announced that it will soon halt screening for rubella in pregnant women as a result of the decline of the disease (see here). That screening was carried out following some potentially pretty serious complications to the unborn child known to be associated with maternal contraction of the disease. Sounds familiar doesn't it?Anyhow, Hutton takes readers through the main points of the research linking rubella or rather congenital rubella syndrome (CRS) and autism down the years. Stella Chess, the first person to talk about rubella (CRS) and autism  (at least in the peer-reviewed domain) gets a pretty big shout-out throughout the article, alongside the overlap between CRS and autism from various different perspectives (behavioural, physiological, genetic). Drawing also on literature around the topic of vaccination and autism (see here), discussions also turn to the quite important group of children with autism who do not seem to display the appropriate immunological response to rubella infection/vaccination as per that discussed by Libbey and colleagues  for example. The idea being that antibody titers normally showing whether a vaccination has 'worked' in terms of conferring protection against a disease, were lower or none existent in some children on the autism spectrum and potentially indicates some type of immune dysfunction. Similar things have been talked about in other research papers (see here).Hutton also discusses an important feature of the literature intersecting with migration and autism (see here) and how some: "Foreign born mothers (from the developing world, without vaccinations) are less likely to be immune or again more likely to be susceptible to rubella" and what potential effect this might have on cases of CRS and autism. During the times I've discussed the topic of autism and migration, I've tended to labour the point about how different foods, different exposures and in particular, different levels of vitamin D *might* be part and parcel of the effect noted in cases (see here). The Hutton discussions have been food for thought for me particularly in light of other findings ."The thought that vaccination has wiped out rubella is falsely reassuring and has managed to wipe out most rubella research, but unfortunately rubella lingers." I was also interested in this statement and how, on the back of those previous findings about how a certain kind of immune system might react, or rather not react, to vaccination (assuming complete vaccine coverage), there may be quite a bit more scope for further research with at least some autism in mind. I know this has the potential to take us back into some quite heated discussions but if we are learning anything about the plural autisms (see here) it is that exposure to viral infection in particular, seems to have some important links to at least some types of autism (see here and see here).---------- Hutton J. Does Rubella Cause Autism: A 2015 Reappraisal? Front. Hum. Neurosci. 2016. 1 Feb. Chess S. Autism in children with congenital rubella. J Autism Child Schizophr. 1971 Jan-Mar;1(1):33-47. Libbey JE. et al. Are there altered antibody responses to measles, mumps, or rubella viruses in autism? J Neurovirol. 2007 Jun;13(3):252-9. Bahta L. & Ashkir A. Addressing MMR Vaccine Resistance in Minnesota's Somali Community. Minn Med. 2015 Oct;98(10):33-6.----------Hutton, J. (2016). Does Rubella Cause Autism: A 2015 Reappraisal? Frontiers in Human Neuroscience, 10 DOI: 10.3389/fnhum.2016.00025... Read more »
Scientists at the University of Michigan have found evidence that some carbon nanomaterials can enter into immune cell membranes, seemingly going undetected by the cell's built-in mechanisms for engulfing and disposing of foreign material, and then escape through some unidentified pathway.
... Read more »
Russ KA, Elvati P, Parsonage TL, Dews A, Jarvis JA, Ray M, Schneider B, Smith PJ, Williamson PT, Violi A.... (2016) C60 fullerene localization and membrane interactions in RAW 264.7 immortalized mouse macrophages. Nanoscale, 8(7), 4134-44. PMID: 26866469
Among adolescent ice hockey players, early pubertal stage is associated with longer concussion recovery in males. Young players should be discouraged from “playing-up.”... Read more »
Kriz, P., Stein, C., Kent, J., Ruggieri, D., Dolan, E., O'Brien, M., & Meehan, W. (2016) Physical Maturity and Concussion Symptom Duration among Adolescent Ice Hockey Players. The Journal of Pediatrics. DOI: 10.1016/j.jpeds.2015.12.006
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