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  • June 20, 2016
  • 09:12 AM
  • 222 views

Mosquitoes Don’t Like Parasites Either (A Guest Post)

by Miss Behavior in The Scorpion and the Frog

By Maranda CardielA photograph of Culex pipiens, the species of mosquito that the researchers used in their experiment. Source: David Barillet-Portal at Wikimedia Commons.Everybody hates mosquitoes. They are annoying, persistent, and make us itch like crazy. Sometimes there are so many of them that we are afraid to go outside unless we want to risk getting covered in spots and scratching ourselves all over for the next week. And if that wasn’t enough, they can also carry dangerous diseases with the potential to kill us. However, just like us, mosquitoes don’t like to be bugged by parasites that can make them sick either. Research shows that they may even avoid interacting with hosts that might pass along parasites to them. A group of researchers - Fabrice Lalubin, Pierre Bize, Juan van Rooyen, and Philippe Christe from the University of Lausanne in Switzerland and Olivier Glaizot from the Lausanne Museum of Zoology – wanted to see if mosquitoes would show a preference for feasting upon birds that were infected with malaria (a blood parasite) or uninfected birds. Mosquitoes find animals to snack on by sensing odors and carbon dioxide in the air that animals give off, along with using their senses of vision, hearing, and touch. In order to figure out if mosquitoes use these senses to specifically choose their unlucky victims, the researchers did an experiment with mosquitoes, malaria, and great tits (a type of bird with a funny name).For their experiment, the researchers collected mosquito eggs that they hatched and raised in a lab. Only female mosquitoes suck blood, so only female mosquitoes were used in the experiment. The mosquitoes had never been exposed to birds before and were starved of sugar for one day to make sure that they would be hungry. The researchers also caught wild adult great tits, and they took small blood samples from each bird to test for malaria before and after the experiment.Next it was time to see if the mosquitoes would find some birds to be more appealing than others. A special Y-shaped wind tunnel allowed the mosquitoes to choose between the odors of two birds: one that was infected with the malaria parasite and one that was not. But don’t worry, the mosquitoes could not directly contact the birds. The researchers set up the lab so that it was completely dark to mimic the natural settings of when mosquitoes feed in the wild. This also meant that the mosquitoes were blind and could only choose a bird based on the chemicals in the air. Randomly-chosen pairs of birds and new mosquitoes were used for each round of the test.A cartoon depicting the experiment setup. A hungry female mosquito hones in on the odors of a healthy great tit and a great tit infected with malaria parasites. Source: Maranda CardielThe results of the study showed that the mosquitoes had a strong preference for birds that were not infected with the malaria parasite. This was true even when the researchers took into account the body sizes and sexes of the birds. Previous studies with different kinds of birds, mosquitoes, and malaria or malaria-like parasites have found similar results. The researchers think that this may be because the malaria parasite somehow causes changes in the chemical processes in the birds’ bodies that the mosquitoes can pick up on. Infection with malaria might change what the birds smell like to the mosquitoes or how much carbon dioxide the birds give off. There is also evidence that birds who are more susceptible to malaria infections have a different odor than birds with stronger immune systems. But why should mosquitoes be picky and choose to bite healthy birds? They certainly don’t seem like they care whose blood they suck when they are swarming around us!Previous research has shown that mosquitoes infected with malaria parasites have problems developing their eggs and can have trouble sucking up blood from their victims. Female mosquitoes use blood to nourish their eggs, so if they don’t drink as much blood, they will not be able to lay as many eggs. This means that female mosquitoes carrying malaria parasites are less likely to produce as many healthy offspring. Thus, it makes sense for female mosquitoes to want to avoid feeding on birds that are infected with malaria.This probably has not changed your thoughts about mosquitoes. They are still a nuisance that we all squish - or at least attempt to squish - upon sight. It might be ironic, but mosquitoes don’t like to have parasites bothering them either. Even though we hate them, maybe now you can find some solace in mosquitoes finding you attractive. It might be a sign that you are actually healthier than your peers. Source:Lalubin, F., Bize, P., van Rooyen, J., Christe, P., & Glaizot, O. (2012). Potential evidence of parasite avoidance in an avian malarial vector Animal Behaviour, 84 (3), 539-545 DOI: 10.1016/j.anbehav.2012.06.004 ... Read more »

Lalubin, F., Bize, P., van Rooyen, J., Christe, P., & Glaizot, O. (2012) Potential evidence of parasite avoidance in an avian malarial vector. Animal Behaviour, 84(3), 539-545. DOI: 10.1016/j.anbehav.2012.06.004  

  • June 20, 2016
  • 04:30 AM
  • 193 views

Athletes Are Open to Genetic Testing and Are Willing to Share Results

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

Despite a number of concerns many athletes responded with substantial interest and little resistance to the idea of genetic testing for the purpose of risk assessment for prolonged concussion recovery and late onset Alzheimer’s disease.... Read more »

  • June 20, 2016
  • 02:49 AM
  • 182 views

Lactobacillus reuteri rescuing [mouse] social behaviours: relevance to autism?

by Paul Whiteley in Questioning Answers

Continuing a recent 'probiotic theme' on this blog I've decided to talk a little about the study results reported by Shelly Buffington and colleagues [1] on how a "single species of gut bacteria can reverse autism-related social behavior in mice." I say 'talk about' but my conversations on this topic should be viewed in light of what others have also said about this study (see here for example) including the lead author (see here).To summarise the findings: authors started from the idea that maternal obesity during pregnancy might have some implications for offspring in terms of their risk of "neurodevelopmental disorders including autism spectrum disorder (ASD)." It's something that has been covered before on this blog (see here) including the idea that inflammation or response to inflammation in-utero might be an important part of any risk mechanism (see here).Conversations then progressed towards the possibility that the gut microbiome might play a role in that elevated risk of offspring autism following pregnancy obesity. To test this theory out, researchers fed female mice a high fat or 'normal diet' for 8 weeks, paired them for mating and gave all their offspring a regular diet. They studied social behaviour of offspring mice and observed that "MHFD [maternal high-fat diet] offspring had impaired sociability and showed no preference for social novelty."To examine whether those mouse social behaviours were linked to the gut microbiome, researchers looked at the "bacterial composition and community structure in the feces" of offspring mice to ascertain any differences. They did find differences; indeed in one write-up of the study the authors note: "We found a clear difference in the microbiota of the two maternal diet groups." Could such bacterial differences account for the social differences noted between the groups? Quite possibly as Buffington et al reported that "co-housing one MRD [maternal regular diet] with three MHFD offspring was sufficient to rescue both the social behaviors and microbiota phylogenetic profile of MHFD offspring." Further, researchers transplanted the faecal microbiota from the MRD and MHFD offspring into germ-free mice providing "causal evidence that an imbalanced microbial ecology in the mice born to mothers on a high-fat diet is responsible for their social deficits."Then came a big question: what was it about the maternal high-fat diet offspring microbiome that might be 'responsible' for the social issues observed? The answer or at least one answer: "L. reuteri [Lactobacillus reuteri] was the most drastically reduced (>9-fold) in the MHFD microbiota population, compared to the MRD microbiota." Subsequent addition of L. reuteri to the drinking water of MHFD offspring was instigated and: "Remarkably, treatment with L. reuteri significantly improved sociability and preference for social novelty in MHFD offspring."As if all that wasn't enough researchers also looked at the old gut-brain axis and subsequently noted that: "L. reuteri treatment restores oxytocin levels, VTA [ventral tegmental area] plasticity and social behaviors." Oxytocin has something of an interesting possible connection to [some] autism (see here).And rest.As you can perhaps appreciate, this piece of research is fairly comprehensive both in terms of the methodologies used and also the findings in relation to maternal pregnancy obesity, offspring social behaviour, gut microbiome and the gut-brain axis. Certainly quite compelling evidence for some kind of effect including the concept of foetal programming allied to the idea of possible intervention.Of course you'd be right to question whether the processes described in this mouse model would necessarily map on to the human experience and indeed the very heterogeneous autism spectrum characterised by [variable] issues with social affect for example. Similar questioning is asked of all animal studies trying to model the complexities of autism (see here). But added to other research where mouse modelling of autism 'deficits' has been to some degree 'changed' as the result of the addition of a particular bacterial species (see here) there is some reason for potential excitement. More so when one considers other research on the gut microbiome in relation to specific preparations potentially modifying the risk of 'neurospychiatric disorder' (see here) for example, and potentially affecting mood and/or behaviour (see here). Don't even get me started on toddler temperament being linked to the inner workings of the gut (see here) minus any hype.But just before sales of Lactobacillus reuteri increase markedly there is further research to be done. Not least is the translation of elements of the Buffington research into studies of humans. Set within the idea that mapping exactly what kinds of wee beasties are residing in the gut is now fairly commonplace and has already stretched into autism research (see here) I would have thought that looking for the presence or absence of L. reuteri in certain groups (and sub-groups) on the autism spectrum and beyond should be fairly easy to do. If and when issues are found with this particular species, supplementing could be indicated bearing in mind some of the potential effects [2] noted already on this bacterium might already show indication in some cases of autism (see here). One might also see a way to look at this and other bacteria in conjunction with levels of oxytocin and possibly other important compounds too as part of that gut-brain axis. Given also that the Buffington study was a study of offspring of obese mice in terms of their sociability, does this also mean that kids born to overweight or obese mums are less likely to have age-appropriate social skills outside of any talk of autism?There is still a research journey to be travelled in this area of investigation and, I might add, potentially linking various areas together including the idea that not all fats in a high-fat diet are necessarily the one and the same (see here)...----------[1] Buffington SA. et al. Microbial Reconstitution Reverses Maternal Diet Induced Social and Synaptic Deficits in Offspring. Cell.2016; 165: 1762-1775.[2] Coccolrullo P. et al. Lactobacillus reuteri (DSM 17938) in Infants with Functional Chronic Constipation: A Double-Blind, Randomized, Placebo-Controlled Study. J Peds. 2010; 157: 598-602.----------... Read more »

  • June 18, 2016
  • 04:25 PM
  • 235 views

Mothers with diabetes more likely to have anti-fetal brain autoantibodies

by Dr. Jekyll in Lunatic Laboratories

Mothers of children with autism and were diagnosed with metabolic conditions during pregnancy, particularly gestational and type 2 diabetes, were more likely to have anti-fetal brain autoantibodies in their blood compared to healthy women of children with autism. The presence of these anti-fetal brain autoantibodies has been previously found to be specific to some mothers of children with autism and rare among mothers of children without autism.

... Read more »

  • June 18, 2016
  • 12:05 PM
  • 245 views

A Step Closer To Artificial Human Beings?

by Agnese Mariotti in United Academics

Scientists propose the creation of a synthetic human genome as a follow-up of the Human Genome Project... Read more »

Boeke, J., Church, G., Hessel, A., Kelley, N., Arkin, A., Cai, Y., Carlson, R., Chakravarti, A., Cornish, V., Holt, L.... (2016) The Genome Project-Write. Science. DOI: 10.1126/science.aaf6850  

  • June 18, 2016
  • 04:57 AM
  • 207 views

A study to watch... probiotics for autism

by Paul Whiteley in Questioning Answers

Happy as a pig in...Assuming that I'm still around as and when published, I'd like to think that the final product of the study protocol from Elisa Santocchi and colleagues [1] will eventually find it's way on to this blog when the peer-reviewed results are finally in.Alongside it's ClinicalTrials.gov entry (see here), authors describe an interesting double-blind, placebo-controlled study where the aim is to "determine the effects of supplementation with a probiotic mixture (Vivomixx®) in ASD [autism spectrum disorder] children not only on specific GI [gastrointestinal] symptoms, but also on the core deficits of the disorder, on cognitive and language development, and on brain function and connectivity."Detailing how researchers *might* be able to put a little scientific flesh on the to the bones of the whole 'gut-brain' relationship with autism in mind (see here), the focus will be on how manipulation of the gut microbiome *might* have various impacts for at least some on the autism spectrum. Indeed with mention of words like 'inflammation' and 'leaky gut', I'd be quite interested to read their eventual findings given other (mouse) research in this area (see here for example) and some more recent investigation [2] on a possible role for Lactobacillus reuteri currently garnering media headlines - blog post to follow soon.You will of course have picked up all the *might* parts of this post as the various subgroups ("Group 1) GI symptoms and probiotics, Group 2) GI Symptoms and placebo, Group 3) Non-GI symptoms and probiotics, Group 4) Non-GI symptoms and placebo") are followed over the 6-month study period. It is entirely conceivable that the Santocchi trial will reveal no effect from probiotic use on the facets of autism under study. Indeed, I'll be the first one to question whether, despite all the gut bacteria findings in relation to autism, we can actually 'change' the constitution of the gut microbiome long-term by such methods. Even some of our strongest antibiotics seem to only have a time-limited effect when it comes to autism and the deepest, darkest recesses of the gut (see here) and there is also the possibility of a 'critical window' for such supplementation use to also contend with.But studies such as this do fill a rather large research gap for at least some on the autism spectrum and perhaps even beyond (see here). "We will watch your career with great interest" to coin a phrase...----------[1] Santocchi E. et al. Gut to brain interaction in Autism Spectrum Disorders: a randomized controlled trial on the role of probiotics on clinical, biochemical and neurophysiological parameters. BMC Psychiatry. 2016 Jun 4;16(1):183.[2] Buffington SA. et al. Microbial Reconstitution Reverses Maternal Diet Induced Social and Synaptic Deficits in Offspring. Cell.2016; 165: 1762-1775.----------Santocchi E, Guiducci L, Fulceri F, Billeci L, Buzzigoli E, Apicella F, Calderoni S, Grossi E, Morales MA, & Muratori F (2016). Gut to brain interaction in Autism Spectrum Disorders: a randomized controlled trial on the role of probiotics on clinical, biochemical and neurophysiological parameters. BMC psychiatry, 16 (1) PMID: 27260271... Read more »

  • June 17, 2016
  • 05:49 AM
  • 280 views

FLCN activates mTORC1 by maintaining lysosomal leucine level

by Joana Guedes in BHD Research Blog

The intracellular amino acid pool within the lysosome has been shown to activate the mTORC1 signaling pathway (Zoncu et al., 2011; Jewell et al., 2013). However, how the sequester of the signaling molecules within the lysosome occurs remains poorly understood. New research from Wu et al. (2016) shows that the suppression of FLCN, a tumour suppressor gene associated with the Birt-Hogg-Dubé (BHD) syndrome, controls mTORC1 activity by modulating the lysosomal leucine levels. FLCN exerts this new function by regulating the accumulation of the amino acid transporter PAT1 on the lysosome surface.... Read more »

  • June 17, 2016
  • 03:06 AM
  • 216 views

Epilepsy begets autism?

by Paul Whiteley in Questioning Answers

"Individuals with epilepsy are at increased risk of ASD [autism spectrum disorder], especially if epilepsy appears in childhood. Further, ASD is more common in the siblings and offspring of individuals with epilepsy, suggesting shared etiology."That was the research bottom-line from Heléne Sundelin and colleagues [1] reporting results based on examination of the "Swedish Patient Register" with regards to the "risk of autism spectrum disorder (ASD) in individuals with epilepsy and in their first-degree relatives." Including one Jonas F. Ludvigsson, PhD on the authorship list (yes, he of 'gluten and autism: probably not coeliac disease but...' fame), researchers identified some 85,000 individuals diagnosed with epilepsy "as well as all their siblings (n = 80,511) and offspring (n = 98,534)." With some nifty statistical analysis including matching cases 5:1 with control participant data, they were able to conclude that around 1.6% of those with epilepsy were diagnosed with an ASD compared with 0.2% of controls. Those percentages are seemingly quite small both in real terms and also in differences between the groups but given the huge participant numbers included for study came out with a hazard ratio (HR) around 10.49 "confidence interval [CI] 9.55–11.53)." To put that HR of 10.49 in context, other work by Ludvigsson on epilepsy coinciding with coeliac disease for example, with a participant number in the tens of thousands came out with a HR of 1.42.When also looking at what happened to siblings and offspring of those diagnosed with epilepsy, the authors also observed something of a potentially increased risk of autism being also diagnosed, although quite a bit less than risk to those themselves diagnosed with epilepsy. The results did however suggest that: "The risk in the offspring was particularly high in mothers with epilepsy." And just for good measure, the Sundelin results also noted that risk of epilepsy was "also associated with a prior diagnosis of ASD" confirming what many others have reported over the years (see here).Although making some headlines I wasn't particularly shocked by the bi-directional associations reported by Sundelin and colleagues. Quite a few times on this blog I've talked about autistic features being potentially over-represented in cases of epilepsy (see here and see here) so to see some of those features crossing diagnostic thresholds into an actual autism diagnosis is perhaps not unsurprising. Continuing that line of thought I do wonder what might happen if the broader autism phenotype (BAP) was also analysed with epilepsy in mind (even the new DSM-5 categorisation of social communication disorder?)Insofar as the hows and whys of the association between epilepsy and autism, well, we're still in guessing mode at the current time. I've talked about some of the various genetic syndromes that tend to include autism and epilepsy together as a diagnostic package (see here) as evidence for the more plural 'autisms'. Such syndromes suggest that mechanisms linking the two conditions are likely to be multiple and not necessarily the same for everyone. The issue of GABA and autism might also show some connection in some cases as per what is starting to be known about this neurotransmitter (see here) and where it might fit with some autism (see here) on top of epilepsy. Assuming also that epilepsy in pregnant mothers for example is being managed by medication, it is also not outside of the realms of possibility that certain preparations could also exert an effect on offspring autism risk (see here). I say this with no scaremongering intended.I might also (speculatively) advance the idea that another research area might also be a connecting feature for some autism and some epilepsy: diet. Don't just click away yet as I will first bring your attention to the increasing peer-reviewed literature talking about the use of a ketogenic diet and autism (see here); said dietary intervention more typically indicated in 'some' cases of epilepsy. It's still early days but it strikes me that quite a bit more research is required in this area. Allied to the use of a ketogenic diet (see here) and also perhaps linking back to that other important research area frequently examined by Dr Ludvigsson (coeliac disease) I'm also inclined to ask whether some autism and some epilepsy might show a more specific connection to dietary gluten too. No, I'm not saying that a gluten-free diet nor a ketogenic diet is some sort of 'cure-all' for autism and epilepsy (please don't mess with epilepsy) but rather there may be overlapping genetics or biology potentially linked to facets of gluten metabolism that might be important for some on the autism spectrum with epilepsy. Certainly much more research on this and other less-traditional areas is indicated [2].There are many questions that remain unanswered in this area of research. With regards to the here and now, well, the Sundelin and other data perhaps suggest that as and when epilepsy is diagnosed, preferential screening for autism could and should be offered particularly in infancy; and perhaps even offered family wide.----------[1] Sundelin HEK. et al. Autism and epilepsy: A population-based nationwide cohort study. Neurology. 2016. June 15.[2] Frye RE. et al. A review of traditional and novel treatments for seizures in autism spectrum disorder: findings from a systematic review and expert panel. Front Public Health. 2013 Sep 13;1:31.----------... Read more »

Sundelin, H., Larsson, H., Lichtenstein, P., Almqvist, C., Hultman, C., Tomson, T., & Ludvigsson, J. (2016) Autism and epilepsy. Neurology, 10. DOI: 10.1212/WNL.0000000000002836  

  • June 16, 2016
  • 03:52 PM
  • 299 views

Postpartum depression least severe form of depression in mothers

by Dr. Jekyll in Lunatic Laboratories

Postpartum depression--a household term since actress Brooke Shields went public in 2005 about her struggle with it--is indeed serious. But depression that begins before or during pregnancy is often more severe because it lasts longer and usually goes undetected until the doctor screens for it after the birth of the baby.

... Read more »

  • June 16, 2016
  • 03:01 AM
  • 203 views

Prevalence of learning disability and autism in Western Australia

by Paul Whiteley in Questioning Answers

"The prevalence of ID [intellectual disability] in WA [Western Australia] has increased over the past 10 years compared with previous estimates... This increase is associated in a large part with an increased prevalence of ASDs [autism spectrum disorder] for whom 70% had comorbid ID or an unknown level of ID."Those were some of the findings reported by Jenny Bourke and colleagues [1] (open-access available here). Drawing on data derived from the Intellectual Disability Exploring Answers (IDEA) database, a resource designed to 'provide high-quality complete and population-based information on Western Australians with an intellectual disability', authors set about looking at cases of ID for those born between 1983 and 2010. Intellectual disability (ID) - sometimes called learning disability here in Blighty - is typically diagnosed when IQ is assessed as being below 70 where a score of between 55-69 denotes mild ID, a score of between 40-54 denotes moderate ID and a score below 40 denotes severe ID. Authors were also able to cross-reference cases with information in other databases in terms of race, gender and location of birth.Results: covering a total of nearly 750,000 live births during the period of inspection, some 10,000 infants "were identified with an ID by 2010." This equated to a total prevalence of ID of 17 per 1,000 live births. Most cases of ID were defined as being mild or moderate in terms of IQ scores (where available) and when compared to previous data from this authorship group [2] authors reported "an overall increase in prevalence of ID of 19% from 1999 to 2010."Insofar as the possible causes of ID, various factors are reported to be potentially contributory including ID accompanying Down's syndrome, ID linked to various other genetic/chromosomal issues, birth defects and infection(s). Increasing preterm birth and survival rates are also suggested to be another contributory factor. The authors also add: "It is also possible that a proportion of the observed increase in mild or moderate ID may be attributable to un-diagnosed Fetal Alcohol Syndrome."The link between autism and ID is also discussed by Bourke et al. On the basis of other research (see here) suggesting that approximately 30-40% of cases of autism will also include a degree of ID, I was pretty interested to see the authors of this latest research suggesting something a little bit different. To quote: "Of the 2307 [diagnosed with an ASD], 675 (29.3%) definitely did not have an ID." I've underlined the word 'not' because the implication is that up to 70% of those with autism did have some level of ID. I say this bearing in mind that Bourke did include children diagnosed with an ASD where "children with an autism diagnosis but an unknown level of ID were classified within the comorbid ASD and ID group." But how far will the true figure of autism and ID combined fall by excluding such unknowns?There is just one more detail of the results that I want to draw your attention to with regards to ID: "The prevalence for Aboriginal children was 39.0/1000 compared with 15.7/1000 for non-Aboriginal children." The idea of disparities in rates of ID among Indigenous Australians and other groups is not necessarily a new one as per other research [3] and strengthen calls for a lot more research focus on this and other groups [4] from a variety of different clinical perspectives.In terms of what to make of these combined findings, I'd like to think there are some important issues requiring further study. The idea that autism and ID can and do frequently co-exist is paramount to discussions. We can talk and discuss about the hows and whys until the cows come home but the link remains strong and indeed, among different populations, might be more variable [5] than previously suggested. Also, for many years in autism research circles, there have been discussions upon discussions about how the quite spectacular rise in autism cases (including that in Australia) might have been at the expense of diagnostic switching from categories such as ID. The Bourke data seem to suggest that not everywhere in the world is necessarily experiencing a corresponding 'drop' in cases of ID supportive of this diagnostic switching argument. Indeed, I'm minded to suggest that one has to be quite careful about explaining away any 'real increase' in autism cases solely using the ID switching argument (see here)...----------[1] Bourke J. et al. Population-Based Prevalence of Intellectual Disability and Autism Spectrum Disorders in Western Australia: A Comparison With Previous Estimates. Medicine (Baltimore). 2016 May;95(21):e3737.[2] Leonard H. et al. Prevalence of intellectual disability in Western Australia. Paediatr Perinat Epidemiol. 2003 Jan;17(1):58-67.[3] Leonard H. et al. Autism and intellectual disability are differentially related to sociodemographic background at birth. PLoS One. 2011 Mar 30;6(3):e17875.[4] Bennett M. & Hodgson V. The missing voices of Indigenous Australians with autism in research. Autism. 2016 May 25. pii: 1362361316643696.[5] Postorino V. et al. Intellectual disability in Autism Spectrum Disorder: Investigation of prevalence in an Italian sample of children and adolescents. Research in Developmental Disabilities. 2016; 48: 193-201.----------Bourke J, de Klerk N, Smith T, & Leonard H (2016). Population-Based Prevalence of Intellectual Disability and Autism Spectrum Disorders in Western Australia: A Comparison With Previous Estimates. Medicine, 95 (21) PMID: 27227936... Read more »

  • June 15, 2016
  • 10:18 AM
  • 274 views

Weird stuff found in recreational drugs: Meth edition

by Rosin Cerate in Rosin Cerate

As Breaking Bad has taught us, the clandestine manufacture of methamphetamine is a very dangerous undertaking. It involves the use of many harmful substances, which depending on the synthesis method include highly corrosive acids and bases, cancer-causing benzene, brain-damaging mercury and lead, jaw-wrecking phosphorus, and blood-breaking sodium cyanide. Blending these various substances together can produce noxious fumes, making gas masks and chemical suits a necessity if you want to avoid getting seriously hurt.Meth cooks, at least those involved in small scale operations, tend not to be trained chemists. If they don't follow the correct recipe, either because they lack the necessary knowledge or skill, or they just don't care, the aforementioned harmful substances can end up in the final product. Lead is a particularly dangerous meth contaminant. A batch of meth responsible for an outbreak of acute lead poisoning in Oregon in 1988 was found to contain >60 percent lead by weight, which is insane! If meth is synthesized using crushed tablets of pseudoephedrine, granules from the tablets can make their way into the veins of intravenous users, causing skin irritation and the increased likelihood of nasty bacterial infections. Meth can also be contaminated with organic compounds closely related to something called alpha-benzyl-N-methylphenethylamine, which when tested in mice proved to be more potent inducers of seizures compared to meth.In addition to the nasty stuff inadvertently introduced into a batch of meth during its manufacture, an interesting collection of substances are used to dilute meth prior to selling it (got to maximize those profits). These cutting agents are known to include sugars such as lactose and mannitol (cheap way to add bulk), methylsulfonylmethane (physically resembles meth, improving the perceived quality of the drug), mild stimulants such as caffeine and ephedrine (mimic the effects of meth), and sidewalk chalk (used to provide a splash of colour). ReferencesBurton BT. 1991. Heavy metal and organic contaminants associated with illicit methamphetamine production. NIDA Research Monograph 115:47-59. [Full text]Cole C, Jones L, McVeigh J, Kicman A, Syed Q, Bellis M. 2011. Adulterants in illicit drugs: A review of empirical evidence. Drug Testing and Analysis 3(2):89-96. [First page]Poulsen EJ, Mannis MJ, Chang SD. 1996. Keratitis in methamphetamine abusers. Cornea 15(5):477-482.Strathdee SA et al. 2008. The color of meth: Is it related to adverse health outcomes? An exploratory study in Tijuana, Mexico. American Journal on Addictions 17(2):111-115. [Full text]... Read more »

Cole C, Jones L, McVeigh J, Kicman A, Syed Q, & Bellis M. (2011) Adulterants in illicit drugs: A review of empirical evidence. Drug Testing and Analysis, 3(2), 89-96. PMID: 21322119  

  • June 15, 2016
  • 08:05 AM
  • 294 views

Tricky Little Buggers

by Mark Lasbury in As Many Exceptions As Rules

Evolution brings wisdom with age – and bacteria are ancient. Bacteria have evolved defenses ranging from evasion or inhibition of immune systems to protecting crucial functions from environmental injury. New studies have identified spring-loaded spikes that can be assembled and disassembled for puncturing other bacteria and delivering toxins, while other work is focused on using those same toxins to kill antibiotic resistant organisms, with E. coli have been engineered to produce toxins against MRSA organisms. More amazing, the engineered bacteria only produce the toxin when enough S. aureus is present, and then lyse themselves to allow the toxin to reach the target organisms. ... Read more »

Basler, M., Pilhofer, M., Henderson, G., Jensen, G., & Mekalanos, J. (2012) Type VI secretion requires a dynamic contractile phage tail-like structure. Nature, 483(7388), 182-186. DOI: 10.1038/nature10846  

Saeidi, N., Wong, C., Lo, T., Nguyen, H., Ling, H., Leong, S., Poh, C., & Chang, M. (2011) Engineering microbes to sense and eradicate Pseudomonas aeruginosa, a human pathogen. Molecular Systems Biology. DOI: 10.1038/msb.2011.55  

  • June 15, 2016
  • 04:30 AM
  • 222 views

Return to Sport and BMI are Associated with Quality of Life After an ACL Reconstruction

by Kyle Harris in Sports Medicine Research (SMR): In the Lab & In the Field

Lower overall quality of life after an anterior cruciate ligament (ACL) reconstruction was associated with higher body mass index (BMI) and not returning to sport.... Read more »

  • June 15, 2016
  • 03:10 AM
  • 183 views

The stability of an Asperger syndrome diagnosis continued

by Paul Whiteley in Questioning Answers

"The subsample that no longer fulfilled an autism spectrum disorder had full-time jobs or studies (10/11), independent living (100%), and reported having two or more friends (100%)."So said the paper by Adam Helles and colleagues [1] continuing a research theme from this authorship group on what happens to autism, or rather Asperger syndrome, in the longer-term (see here). Indeed, if you have the time, the thesis from Helles covering this area of study is well worth a read (see here).This time around the focus was on the often fuzzy concept called 'quality of life' (see here) in terms of "work, academic success, living situation, relationships, support system" for 50 males "with Asperger syndrome diagnosed in childhood and followed prospectively over two decades." Alongside those 'objective' measures of quality of life (QoL), Helles et al also sought some information about more 'subjective' reports of QoL with the use of the "Sense of Coherence and Short-Form Health Survey-36" schedules.As per the opening sentence to this post, I've initially focused in on those participants where diagnosis was not stable (i.e. the sub-group who did not continue to fulfil criteria for Asperger syndrome) as providing yet more evidence [2] on how objective outcomes were seemingly improved compared to those who still reached diagnostic thresholds. Allied to other work by other independent research groups (see here), these findings continue to demonstrate just how heterogeneous the autism spectrum is and that dogma about autism being a 'lifelong condition' might not necessarily be applicable to everyone who at one time or another met diagnostic thresholds. I know such a line of thought is not always received well by all, but I am of the opinion that remitting autism is at least as likely and important as remitting schizophrenia or remitting depression for example. As to the mechanisms, well, I don't want to speculate too much at this time but 'autisms' (plural) is a word that springs to mind as a first thought when it comes to such experiences (see here).When compared to this subgroup of those no longer meeting diagnostic criteria, those who remained within the diagnostic boundaries of Asperger syndrome did not appear to fare so well on those objective measures of QoL: "41% had full-time job or studies, 51% lived independently, and 33% reported two or more friends, and a significant minority had specialized employments, lived with support from the government, or had no friends." I say that bearing in mind the difference in participant numbers falling into one or other grouping.In terms of those subjective measures of QoL, we are also told that: "Stability of autism spectrum disorder diagnosis was associated with objective but not subjective quality of life" and that "psychiatric comorbidity was associated with subjective but not objective quality of life." This is perhaps not unexpected as per the growing body of research suggesting that various psychiatric comorbidity might be over-represented when a diagnosis of autism is received (see here) and how some of it can be truly disabling (see here). It's not then beyond the realms of possibility that one could have (and hold down) a job for example (objective QoL), but feel that one's subjective QoL is still poor as a result of said comorbidity and its impact on areas of life like employment. Indeed, I'd perhaps forward a research case for how what we term 'comorbidity' might actual be more central to the presentation of various types of autism (see here) outside of being just another add-on diagnosis.I don't want to come across as being too focused on outcomes around diagnostic instability when it comes to the autism spectrum because for the majority of people the diagnosis, whilst liable to fluctuation with regards to certain facets and skills, is very much a lifelong thing. That also definitions of long-term outcome and QoL say little about important concepts such as happiness and life satisfaction is another important point to make (see here). But the accumulating longitudinal work from Helles and others is providing something of an important window into autism in the long-term and how, wearing the cold, objective spectacles of science, the remittance of core symptoms might not be an unfavourable outcome for some...----------[1] Helles A. et al. Asperger syndrome in males over two decades: Quality of life in relation to diagnostic stability and psychiatric comorbidity. Autism. 2016 May 26. pii: 1362361316650090.[2] Gillberg IC. et al. Boys with Asperger Syndrome Grow Up: Psychiatric and Neurodevelopmental Disorders 20 Years After Initial Diagnosis. J Autism Dev Disord. 2016 Jan;46(1):74-82.----------Helles A, Gillberg IC, Gillberg C, & Billstedt E (2016). Asperger syndrome in males over two decades: Quality of life in relation to diagnostic stability and psychiatric comorbidity. Autism : the international journal of research and practice PMID: 27233289... Read more »

  • June 14, 2016
  • 03:16 PM
  • 307 views

Even when help is just a click away, stigma is still a roadblock

by Dr. Jekyll in Lunatic Laboratories

Stigma is a major barrier preventing people with mental health issues from getting the help they need. Even in a private and anonymous setting online, someone with greater self-stigma is less likely to take that first step to get information about mental health concerns and counseling.

... Read more »

Lannin, D., Vogel, D., Brenner, R., Abraham, W., & Heath, P. (2016) Does self-stigma reduce the probability of seeking mental health information?. Journal of Counseling Psychology, 63(3), 351-358. DOI: 10.1037/cou0000108  

  • June 14, 2016
  • 12:18 PM
  • 272 views

Nurturing the Gifted

by William Yates, M.D. in Brain Posts

My photo of Mozart No one denies the importance of public education. Raising graduation rates and academic ability in the general population are highly accepted education system goals. Additionally, identification of learning disorders and the barriers to academic progress are the focus of many.However, the study of the gifted is perhaps no less important but this topic receives less attention and research.Matthew Makel and colleagues at Duke University and Vanderbilt University recently published an important study of gifted populations.Using the Duke University Talent Identification Program they identified 259 U.S. adolescents designated as "profoundly gift" (top 0.01% or top score of 10,000 tested) using the following criteria:U.S. adolescents completing SAT before age 13 Achieving a score of 700 or better on the SAT-math Achieving a score of 630 or better on the SAT-verbal The research team then followed this profoundly gifted group using a validated web-based search strategy. The found the following results confirming the validity of early gifted status as a predictor of academic and occupational success:1. Thirty seven percent had gone on to receive a doctorate degree2. Academic tenure was achieved by 7.5%3. U.S. patents were held by 9%4. A significant number of the group held high level positions in major organizationsThe manuscript provides fascinating graphic showing the diverse disciplines of the graduate degrees from this cohort. STEM degrees predominate but many also achieved doctorates in arts and humanities as well as law.This current study confirmed a previous outcome analysis using the Study of Mathematically Precocious Youth cohort (see Kell et al citation below).The authors note "Profound intellectual talent, and its patterning, has cross-disciplinary and policy implications."Individual interest appears to play a key role in outcome. School systems need to provide a wide ranges of exposures to various academic disciplines. Early identification of profoundly gifted individuals is important. This group benefits by guidance and academic opportunity.This is an important study and highlights the need to develop gifted identification and nurturing the gifted programs.Follow the author on Twitter WRY999Photo of Mozart is a graphic design modification of a painting on the wall outside of the birthplace of Amadeus Mozart.Makel MC, Kell HJ, Lubinski D, Putallaz M, & Benbow CP (2016). When Lightning Strikes Twice: Profoundly Gifted, Profoundly Accomplished. Psychological science PMID: 27225220 Ke... Read more »

Kell HJ, Lubinski D, Benbow CP, & Steiger JH. (2013) Creativity and technical innovation: spatial ability's unique role. Psychological science, 24(9), 1831-6. PMID: 23846718  

  • June 14, 2016
  • 08:47 AM
  • 242 views

MaMaLoc: How To Change Cancer Surgeries With Magnets

by Rita dos Santos Silva in United Academics

A small magnetic device might transform breast cancer surgeries... Read more »

Anderson, R., Kimmick, G., McCoy, T., Hopkins, J., Levine, E., Miller, G., Ribisl, P., & Mihalko, S. (2011) A randomized trial of exercise on well-being and function following breast cancer surgery: the RESTORE trial. Journal of Cancer Survivorship, 6(2), 172-181. DOI: 10.1007/s11764-011-0208-4  

Lovrics, P., Cornacchi, S., Vora, R., Goldsmith, C., & Kahnamoui, K. (2011) Systematic review of radioguided surgery for non-palpable breast cancer. European Journal of Surgical Oncology (EJSO), 37(5), 388-397. DOI: 10.1016/j.ejso.2011.01.018  

  • June 14, 2016
  • 02:42 AM
  • 201 views

On fatty acid metabolism and autism and ADHD (again)

by Paul Whiteley in Questioning Answers

"Children with ADHD [attention-deficit hyperactivity disorder] and ASD [autism spectrum disorder] had low levels of EPA [eicosapentaenoic acid], DHA [docosahexaenoic acid] and AA [arachidonic acid] and high ratio of n-6/n-3 PUFAs [polyunsaturated fatty acid] and these correlated significantly with symptoms. Future research should further investigate abnormal fatty acid metabolism in these disorders."So said the research publication by Natalie Parletta and colleagues [1] (open-access available here) who completed assessments on erythrocytes in blood samples from "565 children aged 3-17 years with ADHD (n = 401), ASD (n = 85) or controls (n = 79)." Alongside fatty acid analyses (undertaken at "a commercial Pathology Laboratory") researchers also included various behavioural measures with their participant group looking at aspects such as attention and impulsivity and also autistic symptoms (via the CARS). Importantly we are told that: "Participants who had taken any nutritional supplement during the previous year were excluded" from the study.Results:  well as I've mentioned, compared to the asymptomatic (not autism nor ADHD) controls, group values for those with autism or ADHD were lower in terms of EPA and DHA among other things. In fact we are told that: "Children with ASD had lower DHA, EPA and AA and higher n-3/n-6 ratio than children with ADHD" suggesting that fatty acid metabolism might be even more irregular in this group compared to the others. EPA and DHA specifically fall under the banner of omega-3 fatty acids and are generally thought to be the 'good guys' when it comes to all-manner of health effects. I might particularly mention the word 'inflammation' when it comes to this class of fatty acids [2] which could be relevant to quite a bit of the autism spectrum as well (see here). When it however came to the overall ratio between omega 3 and omega 6 fatty acids (sometimes thought of the not-so-good guys), it was ADHD that beat autism that beat controls. The authors make a case for some interesting correlations between fatty acids levels and the various behavioural scores obtained but to be honest, I'm not all that impressed with the figures as they stand.I've used the word 'again' in the title of this post to denote how this is not the first time that unusual fatty acid metabolism has been described with both autism and ADHD in mind (see here and see here respectively). Minus any sweeping generalisations, the body of peer-reviewed evidence looking at fatty acids and autism or ADHD is pretty consistent in the the findings being reported that one for reason or another, there seems to be 'issues' with fatty acids and screening services should perhaps be preferentially offered as and when a diagnosis (or both) is received."This cross-sectional study is the largest of its kind, supporting previous work that showed low n-3 PUFA levels, particularly DHA, in children with neurodevelopmental disorders." Indeed.Then comes the question of whether supplementation as and when an atypical fatty acid profile is detected might be useful or not. The jury is still out on this side of things particularly when it comes to autism and the possible effects of supplementation (see here). For ADHD the evidence is a little stronger (see here) and continues to garner research attention [3] as a potentially cost-effective intervention option for some. I was also intrigued to read the authors' reasoning on a possible role for the trillions of wee beasties that call us home (the gut microbiota) and how: "Another explanation could involve the influence of gut microbiota on PUFA uptake and metabolism." In an unrelated post, I've talked about research suggesting a possible role for fatty acids in terms of gut bacteria and something like obesity (see here). One therefore wonders how deep the rabbit hole might go?For now however, we have more scientific evidence for a potential role for fatty acid metabolism and at least some autism and ADHD...----------[1] Parletta N. et al. Omega-3 and Omega-6 Polyunsaturated Fatty Acid Levels and Correlations with Symptoms in Children with Attention Deficit Hyperactivity Disorder, Autistic Spectrum Disorder and Typically Developing Controls. PLoS One. 2016 May 27;11(5):e0156432.[2] Simopoulos AP. Omega-3 fatty acids in inflammation and autoimmune diseases. J Am Coll Nutr. 2002 Dec;21(6):495-505.[3] Gow RV. et al. Current evidence and future directions for research with omega-3 fatty acids and attention deficit hyperactivity disorder. Curr Opin Clin Nutr Metab Care. 2015 Mar;18(2):133-8.----------Parletta N, Niyonsenga T, & Duff J (2016). Omega-3 and Omega-6 Polyunsaturated Fatty Acid Levels and Correlations with Symptoms in Children with Attention Deficit Hyperactivity Disorder, Autistic Spectrum Disorder and Typically Developing Controls. PloS one, 11 (5) PMID: 27232999... Read more »

  • June 13, 2016
  • 08:30 PM
  • 267 views

This Month in Blastocystis Research (MAY 2016)

by Christen Rune Stensvold in Blastocystis Parasite Blog

The May entry of "This Month in Blastocystis Research" focusses especially on the increasing interest in Blastocystis in a gut microbiota context. ... Read more »

Andersen LO, Bonde I, Nielsen HB, & Stensvold CR. (2015) A retrospective metagenomics approach to studying Blastocystis. FEMS microbiology ecology, 91(7). PMID: 26130823  

Stensvold CR, & Clark CG. (2016) Current status of Blastocystis: A personal view. Parasitology international. PMID: 27247124  

O'Brien Andersen L, Karim AB, Roager HM, Vigsnæs LK, Krogfelt KA, Licht TR, & Stensvold CR. (2016) Associations between common intestinal parasites and bacteria in humans as revealed by qPCR. European journal of clinical microbiology . PMID: 27230509  

Ramírez JD, Sánchez A, Hernández C, Flórez C, Bernal MC, Giraldo JC, Reyes P, López MC, García L, Cooper PJ.... (2016) Geographic distribution of human Blastocystis subtypes in South America. Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases, 32-5. PMID: 27034056  

  • June 13, 2016
  • 01:43 PM
  • 295 views

Experimental antibiotic treats deadly MRSA infection

by Dr. Jekyll in Lunatic Laboratories

The antibiotic arms race is on, while we are rushing to find new antibiotics, bacteria are working on finding ways around them. With that in mind, a new experimental antibiotic developed by a team of scientists successfully treats the deadly MRSA infection and restores the efficacy of a commonly prescribed antibiotic that has become ineffective against MRSA.

... Read more »

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