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  • February 18, 2015
  • 06:21 AM

Pathways of resistance: from mercury to methicillin

by socgenmicro in Microbe Post

In a climate of rising fear over the diminishing efficacy of antibiotics, microbiologists from the Universities of Nottingham and East Anglia have looked back at the bacteria-killing substances of the pre-antibiotic era: metals. Dr Jon Hobman and Dr Lisa Crossman’s … Continue reading →... Read more »

Hobman, JL., & Crossman, L. (2014) Bacterial antimicrobial metal ion resistance. Journal of Medical Microbiology. DOI: 10.1099/jmm.0.023036-0  

  • February 18, 2015
  • 05:02 AM

Fasting Fruit Flies: Improved Focus and Brain Power

by Pieter Carrière in United Academics

Fasting: solely a religious activity or is it also beneficial for focus and brain power? Research links fasting and hunger to formation of long-term memory.... Read more »

Hirano Y, Masuda T, Naganos S, Matsuno M, Ueno K, Miyashita T, Horiuchi J, & Saitoe M. (2013) Fasting launches CRTC to facilitate long-term memory formation in Drosophila. Science (New York, N.Y.), 339(6118), 443-6. PMID: 23349290  

Dubnau J. (2012) Neuroscience. Ode to the mushroom bodies. Science (New York, N.Y.), 335(6069), 664-5. PMID: 22323806  

Quinn, W., Harris, W., & Benzer, S. (1974) Conditioned Behavior in Drosophila melanogaster. Proceedings of the National Academy of Sciences, 71(3), 708-712. DOI: 10.1073/pnas.71.3.708  

  • February 18, 2015
  • 03:59 AM

Autism and the inter-pregnancy interval (again)

by Paul Whiteley in Questioning Answers

The paper from Maureen Durkin and colleagues [1] adds to something of a growing research evidence base suggesting that the temporal spacing between pregnancies / births - the inter-pregnancy interval (IPI) - may have something of an effect on the risk of receipt of a diagnosis of autism or autism spectrum disorder (ASD).We've been here before. In fact, a couple of times I've talked about the IPI in relation to autism risk (see here and see here) not including other, similar research findings in this area [2]. If I were to generalise from the collected data so far, it might be to say something like a short IPI (below 12 months) and a longer IPI (above about 5 years) seems to carry some elevated risk of offspring receipt of a diagnosis of autism or autism spectrum disorder (ASD). But remember risk is risk...Durkin et al looking through the records of almost 32,000 second-born children, reported that: "In adjusted analyses, both short (<12) and long (>84 month) IPIs were associated with a two-fold risk of ASD relative to IPIs of 24-47 months."I don't want to dwell too long on this topic outside of reiterating a suggestion made in the paper from Nina Gunnes and colleagues [3]: "A possible explanation is depletion of micronutrients in mothers with closely spaced pregnancies." That being said, there may be other factors influencing risk such as a heightened risk for preterm birth also being associated with a small IPI. The elevated risk associated with a longer IPI is slightly more difficult to explain away, assuming that is, that one doesn't include the variable of 'older mother' into proceedings (see here) and possibly some contribution from the young upstart discipline that is epigenetics (see here). More research is indicated although I might also throw into the research mix the idea that a longer IPI might also raise the risk of something like preeclampsia [4] and how this might also impact on offspring autism risk (see here).Patio Song to close (and some excellent interpretive dancing).----------[1] Durkin MS. et al. Inter-Pregnancy Intervals and the Risk of Autism Spectrum Disorder: Results of a Population-Based Study. J Autism Dev Disord. 2015 Feb 1.[2] Cheslack-Postava K. et al. Increased risk of autism spectrum disorders at short and long interpregnancy intervals in Finland. J Am Acad Child Adolesc Psychiatry. 2014 Oct;53(10):1074-81.e4.[3] Gunnes N. et al. Interpregnancy interval and risk of autistic disorder. Epidemiology. 2013 Nov;24(6):906-12.[4] Shachar BZ. & Lyell DJ. Interpregnancy interval and obstetrical complications. Obstet Gynecol Surv. 2012 Sep;67(9):584-96.----------Durkin MS, DuBois LA, & Maenner MJ (2015). Inter-Pregnancy Intervals and the Risk of Autism Spectrum Disorder: Results of a Population-Based Study. Journal of autism and developmental disorders PMID: 25636677... Read more »

  • February 17, 2015
  • 03:57 AM

Congenital rubella, autism and remote stroke

by Paul Whiteley in Questioning Answers

Case reports. I know they rank pretty low in the order of what counts as objective scientific evidence [1] despite their often interesting findings. That being said, when it comes to a diagnosis like autism, with all its associated heterogeneity and elevated risk of various comorbidity probably better encapsulated in a more 'plural autisms' understanding, case reports can offer something of an important view into the many and varied ways in which someone might arrive on the autism spectrum and their subsequent individual experiences. A focus on the N=1 if you like...The case report from Jill and George Hutton [2] (open-access) describing how the "diagnosis of congenital rubella was recognized more than ten years after the birth" of their male infant subject and how "congenital rubella is linked to both autism and ischemic brain injury" provides some rather interesting details for science and practice. The paper is open-access but a few pointers might be useful:The paper describes a boy delivered at 38 weeks to a "USA born physician at 30 years of age mostly working at a busy, urban, county hospital with a large immigrant population". Mum had been vaccinated against rubella at least once some decades earlier (possibly with a booster 7-8 years before giving birth). "She was non-immune to rubella at her first prenatal visit at 10 weeks gestation" but at delivery showed immunity to rubella suggesting intervening exposure. The authors reported the detail about 'large immigrant population' because of the issue of risk of transmission from those "emigrating from countries with absent or suboptimal national vaccination programs" [3].Her son "met all motor milestones, but was delayed in speech and exhibited social anxiety" during early infancy. He had a single seizure at 18 months (febrile seizure). He was eventually diagnosed with autism between 5-7 years old.An MRI was fortuitously offered at 10 years old with findings "most consistent with a remote stroke". The authors conclude that: "As causes of stroke were eliminated, the diagnosis of congenital rubella as a unifying diagnosis of autism and stroke became more probable."I was drawn to talk about this paper for various reasons.First is the continuing association between viral/bacterial exposures during pregnancy and offspring behavioural outcomes (see here). As per the research of people such as Stella Chess, mentioned in the Hutton article, discussing autism presenting in cases of congenital rubella [4] and reporting that "a high rate of autism and a high rate of recovery were observed" there is potentially so much more to see in this area of autism research. In-utero rubella exposure, by the way, is not the only infective agent linked to the presentation of autism for some (see here).Second were some of the details reported by the Huttons on their young participant and in particular, the idea that congenital rubella may 'unify' the findings of stroke + autism. Pediatric stroke has been looked at with infectious disease in mind before [5]. The research literature in the area of stroke and autism is however not exactly straight-forward. It would be easy to say that stroke had a deleterious effect on the brain which then 'lead' to autism as per other research in this area [6], but this perhaps rather simplifies an all-too-likely more complex relationship. Certainly, I would like to see a little more investigation done on this topic and in particular the delayed manifestations of congenital rubella [7] as and when appropriate to a diagnosis of autism or autism spectrum disorder [8]. If and when this connection is further established, one could also reasonably ask about intervention strategies and whether autistic symptoms could be ameliorated in any way in this group? Remember those words from Chess: "a high rate of recovery was observed"...Finally, the question is raised about the role of vaccination in preventing congenital rubella and possible knock-on effects for offspring development including autism-related outcomes. In a previous post on the talking point that is vaccination and autism (see here) I discussed some data which suggested that rubella vaccination may very well have "prevented hundreds, and perhaps thousands, of ASD [autism spectrum disorder] cases from 2001 through 2010 in the US." [9] The Hutton paper kinda overlaps with such discussions alongside detailing the issue of waning immunity [10]. I might add that analysis of the biology of individual responses (or not) to rubella vaccination [11] and even transmission from previous vaccinees [12] in light of other data is perhaps also implied in any future work in this area.What the Hutton paper serves to reiterate is that there may be many potential paths towards a diagnosis of autism or ASD. Receipt of said diagnosis should also perhaps be a starting point for further inquiry rather than an endpoint...Music: Blur - Out Of Time.----------[1] Nissen T. & Wynn R. The clinical case report: a review of its merits and limitations. BMC Res Notes. 2014 Apr 23;7:264.[2] Hutton J. & Hutton GJ. Congenital Rubella with Autism and Evidence of a Remote Stroke. J Vaccines Vaccin 2014, 5:6[3] Fang J. et al. Case report: congenital rubella syndrome: a rare but persistent concern in the United States. J Perinatol. 2013 Nov;33(11):899-902.[4] Chess S. Follow-up report on autism in congenital rubella. J Autism Child Schizophr. 1977 Mar;7(1):69-81.[5] Salih MA. et al. Infectious and inflammatory disorders of the circulatory system as risk factors for stroke in Saudi children. Saudi Med J. 2006 Mar;27 Suppl 1:S41-52.[6] Weir K. & Salisbury DM. Acute onset of autistic features following brain damage in a ten-year-old. J Autism Dev Disord. 1980 Jun;10(2):185-91.[7] Sever JL. et al. Delayed Manifestations of Congenital Rubella. Clin Infect Dis. 1985; 7 (Supplement 1): S164-S169.[8] Hwang SJ. & Chen YS. Congenital rubella syndrome with autistic disorder. J Chin Med Assoc. 2010 Feb;73(2):104-7.[9] Berger BE. et al. Congenital rubella syndrome and autism spectrum disorder prevented by rubella vaccination--United States, 2001-2010. BMC Public Health. 2011 May 19;11:340.[10] Just M. et al. Duration of immunity after rubella vaccination: a long-term study in Switzerland. Rev Infect Dis. 1985 Mar-Apr;7 Suppl 1:S91-4.[11] Kennedy RB. et al. Genetic polymorphisms associated with rubella virus-specific cellular immunity following MMR vaccination. Hum Genet. 2014 Nov;133(11):1407-17.[... Read more »

  • February 16, 2015
  • 06:00 PM

Why low-carb or fasting diets are good for your health

by Dr. Jekyll in Lunatic Laboratories

While most research regarding fat loss focuses on the risks of being overweight, a new study shows that fasting, low-carb diets, or high-intensity exercise have specific health benefits. Specifically, researchers have found that a compound produced by the body when dieting or fasting can block a part of the immune system involved in several inflammatory disorders such as type 2 diabetes, atherosclerosis, and Alzheimer’s disease.... Read more »

Youm, Y., Nguyen, K., Grant, R., Goldberg, E., Bodogai, M., Kim, D., D'Agostino, D., Planavsky, N., Lupfer, C., Kanneganti, T.... (2015) The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome–mediated inflammatory disease. Nature Medicine. DOI: 10.1038/nm.3804  

Coll, R., Robertson, A., Chae, J., Higgins, S., Muñoz-Planillo, R., Inserra, M., Vetter, I., Dungan, L., Monks, B., Stutz, A.... (2015) A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases. Nature Medicine. DOI: 10.1038/nm.3806  

  • February 16, 2015
  • 03:11 AM

Poo transplant and weight gain: a case study

by Paul Whiteley in Questioning Answers

The case report detailed by Neha Alang and Colleen Kelly [1] (open-access) reporting on "new-onset obesity after receiving stool from a healthy but overweight donor" has already garnered some significant press attention (see the BBC entry for example). Reporting on that seemingly most undesirable but in some cases life-saving of measures - the fecal microbiota transplant (FMT) - whereby some of those trillions of wee beasties which inhabit our deepest, darkest recesses are transferred from one person to another, the authors add a cautionary caveat to our current fascination with such a technique.The Alang/Kelly paper is open-access but a few pointers might be in order:Interesting viewing @ Paul Whiteley"A 32-year-old female with recurrent CDI [Clostridium difficile infection] underwent FMT". As per my previous mention of being a potentially 'life-saving' measure, FMT for CDI (recurrent CDI) is something which is now formally indicated, as per the directions from NICE here in Blighty. Such recommendations came on the back of quite a volume of science which suggested effectiveness particularly in hard to treat cases of CDI (see here).For this patient, quite a few avenues of treatment had been previously tried but with little success. "After extensive discussion, the patient elected to undergo fecal transplant. As per the patient’s request, her 16-year-old daughter was chosen as the stool donor." Said donor was, we are told: "∼140 pounds (BMI of 26.4), but it increased later to 170 pounds." BMI by the way, stands for body mass index and 140 pounds is equivalent to about 63 kilograms rising to about 77 kilograms in new (weight) currency. Results: well, FMT worked in that the mother: "improved and did not suffer a further CDI recurrence after FMT". But... "The patient presented again 16 months after FMT, and reported an unintentional weight gain of 34 pounds. She weighed 170 pounds and had become obese (BMI of 33)." Diet and exercise seemingly did very little to aid in weight loss and also after 3 years post FMT she "developed constipation and unexplained dyspeptic symptoms."The authors concluded that there was a link between her weight gain and FMT treatment and further instigated a policy: "to use nonobese donors for FMT."Repeating the fact that this is a single case report and so cannot really inform about any generalisable relationship between a poo(p) transplant and weight gain/loss and that correlation does not necessarily imply causation, this is an interesting paper. The first thoughts running through my mind when reading this paper was a comment from Dr Emily Deans a few years back about poo transplants and ensuring: "if you ever have a fecal transplant, make sure it is from a slender, non-asthmatic, happy person!" Although said in jest, it appears that Dr Deans may have been on the money with at least part of her prediction.Insofar as the possibility of a connection between the use of FMT and weight gain/loss, well, we have kinda seen evidence emerging that gut bacteria might be doing far more than just helping us digest our food or making the odd vitamin or two. I've covered something on the mouse - Akkermansia muciniphila weight study before on a sister blog (see here) and how in a mouse at least, certain types of bacteria might be implicated in energy homoeostasis. You could ask whether some profiling of the donor stool might be indicated in future attempts at FMT covering something like A. muciniphila and other potentially important species bearing in mind, the relationship is likely to be complex and not just limited to one type of gut bacteria being 'present or not'.The other intriguing point that also arises from the Alang/Kelly paper is the idea that weight gain/loss might not solely be driven by the classical 'food in, energy out' relationship which many people cling to as an explanation of our current obesity statistics. Again, I've talked about this idea before on this blog (see here) and how factors such as sleep and gut bacteria might come into play in some cases, albeit with a lot more research required including some genetic input into proceedings. Probiotics (to 'alter' gut bacteria) for weight management is still a relatively new area of investigation despite some intriguing initial results [2].More controlled studies are of course implied in this area. I might also advance the idea that a little more focus on other residents of the gastrointestinal (GI) tract might also be indicated in future work including the emerging idea of the gut virome and 'bacteriophages' (viruses attacking bacteria) as per what is being doing in other areas of interest to this blog [3]. That and further work on another of my preoccupations, gut barrier integrity bearing in mind things might not be entirely straight-forward [4].Then to some music: Shame Shame Shame (shame on you).----------[1] Alang N. & Kelly CR. Weight Gain After Fecal Microbiota Transplantation. Open Forum Infect Dis. 2015; 2: 1.[2] Sanchez M. et al. Effect of Lactobacillus rhamnosus CGMCC1.3724 supplementation on weight loss and maintenance in obese men and women. Br J Nutr. 2014 Apr 28;111(8):1507-19.[3] Yolken RH. et al. Metagenomic Sequencing Indicates That the Oropharyngeal Phageome of Individuals With Schizophrenia Differs From That of Controls. Schizophr Bull. 2015. Feb 9.[4] Kless C. et al. Diet-induced obesity causes metabolic impairment independent of alterations in gut barrier integrity. Molecular Nutrition & Food Research. 2015. Feb 10.----------Alang, N., & Kelly, C. (2015). Weight Gain After Fecal Microbiota Transplantation Open Forum Infectious Diseases, 2 (1) DOI: 10.1093/ofid/ofv004... Read more »

Alang, N., & Kelly, C. (2015) Weight Gain After Fecal Microbiota Transplantation. Open Forum Infectious Diseases, 2(1). DOI: 10.1093/ofid/ofv004  

  • February 15, 2015
  • 03:13 PM

The “successful aging” debate

by Dr. Jekyll in Lunatic Laboratories

We see it everyday in advertising, turn back the clock, reverse aging — look, feel, and be younger. With all these standards, how do you define aging, or more importantly successful aging. Scholars have long debated what successful aging is, how to measure it, and how to promote it. But researchers are now laying the groundwork for building consensus on the topic — while pointing out that the answer may differ among academics and the general public, as well as across populations and demographic groups.... Read more »

  • February 15, 2015
  • 12:44 PM

Stick Insect Genomes Reveal Natural Selection’s Role in Parallel Speciation

by Esra Durmaz in genome ecology evolution etc

Parallel evolution provides evidence for evolution by natural selection and can cause repeated divergence at specific genes. The parallel evolution of phenotypic traits under similar environmental pressures was estimated to cover almost half of same genomic regions. However, the genomic … Continue reading →... Read more »

Soria-Carrasco, V., Gompert, Z., Comeault, A., Farkas, T., Parchman, T., Johnston, J., Buerkle, C., Feder, J., Bast, J., Schwander, T.... (2014) Stick Insect Genomes Reveal Natural Selection's Role in Parallel Speciation. Science, 344(6185), 738-742. DOI: 10.1126/science.1252136  

  • February 15, 2015
  • 11:32 AM

Brain mosaicism and altered gene copy numbers could explain Alzheimer's

by EE Giorgi in CHIMERAS

© EEGI've tackled the problem of the missing heritability in the past, i.e. the fact that despite all the research on genetic studies and disease associations, we can explain only a small fraction of cancers and disorders. Today we know a lot more than what we knew back when the human genome project was completed, and in particular we know how much we don't know. I think we are only beginning to understand the complexity of human diseases and genetics. Back when I started working on disease associations, in 2004, we roughly thought that we could find a few "buttons" that would trigger cancer. Today we know that it's not about finding a few buttons. We thought DNA was more or less a keyboard, when in fact we have a whole orchestra: DNA, mRNA, proteome, epigenome, etc. Mutations can occur at any level, and besides genetic alterations there can be epigenetic alterations, proteins that don't fold correctly, an abnormal accumulation of proteins, and so many other ways that things can go wrong. To this add exercise, body mass, diet, and all kinds of other environmental exposures.Bottom line: we set out looking for a few "keys" to play on the DNA keyboard when in fact we should be looking for a whole symphony, and the symphony may very well change from person to person. Alzheimer's disease is among the many disorders that have baffled researchers. Recent studies have found that rather than genetic mutations in the DNA we should be looking at abnormal accumulation of misfolded proteins called amyloids. They can accumulate inside cells to a level where they become toxic and cause cell death. Amyloids have been associated with many diseases, not just Alzhemeir's, but in the case of Alzheimer's in particular they seem to be responsible for the progressive loss of neurons and brain connections. A gene called APP codes for a protein that is an amyloid precursor, and mutations in this gene have been associated with familial Alzheimer's (when the disease occurs before age 60). However, the vast majority of Alzheimer's cases occur much later in life and are not associated with those mutations. Do all these cases fall into yet another missing heritability mystery?As it turns out, genetic alterations come in many forms, not just mutations. The key, in the case of APP, could be not in what kind of gene allele one carries, but rather on how many copies we carry. Yes, we may have more than two copies in different parts of the brain.Remember when they taught us in school that we are born with one DNA and that DNA is identical throughout our cells and tissues? Forget that. Of all organs, the brain is one of the most plastic regions of our body, with numerous retrotransposons and mobile genetic elements that attest for its plasticity. Errors in chromosome segregation when cells divide can also produce cells with a gain or loss in chromosome numbers. This variability has been shown to be a common feature of the normal brain: our brains are genetic mosaics made of genetically distinct cell lines that have, over the years, accumulated somatic mutations [1].I've discussed retrotransposons a while back: these are genetic elements that can make copies of themselves and then reinsert in different parts of the DNA. They are particularly active in the brain and thanks to their activity the brain is in fact a somatic mosaic of genetically distinct neurons. Retrotransposons were first discovered in maize and explain why, for example, a single cob can have kernels of many different colors: the cob is in fact a mosaic and the repositioning of the retrotransposons causes the kernels to display different colors. So now you can think of the human brain as a cob and the neurons are kernels of different colors. ;-)There are multiple lines of evidence that seem to point at a correlation between number of copies of the APP gene in the brain and an increased risk of developing Alzheimer's. People with Down Syndrome, for example, have three copies of the APP gene and by age 65 they have a 75% chance of developing Alzheimer's. In a recent paper [2], a group of researchers from the Scripps Research Institute analyzed the nuclei of neurons harvested from the prefrontal cortex and cerebellum of postmortem brains, for a total of 134 samples (of which 47 from subjects with Alzheimer's) and concluded that the gene APP is mosaically amplified in brains affected by Alzheimer's. Some neurons had up to 12 copies of the APP gene. While their findings do not exclude the fact that the high APP gene dosage could be an effect of the disease, rather than the cause, even if it is an aftermath effect, it certainly plays a role in the progression of the disease.I find it fascinating that more and more evidence seems to indicate that the etiology of diseases goes beyond single mutations. Protein folding anomalies like the accumulation of amyloids and gene dosage add new pieces to an incredibly complicated puzzle.[1]Bushman DM, & Chun J (2013). The genomically mosaic brain: aneuploidy and more in neural diversity and disease. Seminars in cell & developmental biology, 24 (4), 357-69 PMID: 23466288[2]Bushman, D., Kaeser, G., Siddoway, B., Westra, J., Rivera, R., Rehen, S., Yung, Y., & Chun, J. (2015). Genomic mosaicism with increased amyloid precursor protein (APP) gene copy number in single neurons from sporadic Alzheimer's disease brains eLife, 4 DOI: 10.7554/eLife.05116... Read more »

  • February 14, 2015
  • 10:00 PM

Evolutionary non-commutativity suggests novel treatment strategies

by Dan Nichol in Evolutionary Games Group

In the Autumn of 2011 I received an email from Jacob Scott, now a good friend and better mentor, who was looking for an undergraduate to code an evolutionary simulation. Jake had just arrived in Oxford to start his DPhil in applied mathematics and by chance had dined at St Anne’s College with Peter Jeavons, […]... Read more »

Tan, L., Serene, S., Chao, H.X., & Gore, J. (2011) Hidden randomness between fitness landscapes limits reverse evolution. Physical Review Letters, 106(19), 198102. PMID: 21668204  

  • February 14, 2015
  • 06:36 PM

A very Sciencey Valentine’s day

by Dr. Jekyll in Lunatic Laboratories

Happy valentines day! Okay maybe it’s turned into more of a reason to spend money on chocolate and flowers than it is about showing affection — which is probably why some people hate it — but it can still be a somewhat special day. Unfortunately I’ve been struggling on what I could do for my wife on valentines day. So I thought I would work it out here and maybe even help a few of you who are stuck as well.... Read more »

  • February 14, 2015
  • 04:53 AM

Nutritional medicine as mainstream in psychiatry

by Paul Whiteley in Questioning Answers

Have you remembered? Flowers from the nearest petrol / gas station or something a little more amorous for February 14th?So as not to take up too much of your time today, I want to briefly draw your attention to the paper (personal view) from Jerome Sarris and colleagues [1] carrying the same title as that of this blog post: 'Nutritional medicine as mainstream in psychiatry' published in The Lancet Psychiatry.Aside from applauding the notion that nutrition is potentially of some importance to "both physical and mental health" alongside that is, the value of exercise (see here for example), the important word to come from the Sarris paper is 'mainstream', denoting 'current thought of the majority' and distinct from 'fringe' or 'pseudo' science. The kinda of words I've heard quite a bit down the years of my research interest in this whole gluten- and casein-free diet for [some] autism malarkey.Sarris already has some research form on, for example, the potentially beneficial role of multivitamins on mood and wellbeing [2] (open-access) so approaches this issue as a research insider rather than external commentator."Evidence is steadily growing for the relation between dietary quality (and potential nutritional deficiencies) and mental health, and for the select use of nutrient-based supplements to address deficiencies, or as monotherapies or augmentation therapies." I'd be minded to agree. I've covered this from a few angles on this blog, bearing in mind (a) no medical or clinical advice is given or intended and (b) the moves towards plurality in psychiatry (see here and see here) potentially also denotes the idea of best- and non-responders to various interventions:Vitamins and autism: double-blind, placebo-controlled RCT (December 2011)Psychosis, gluten and vitamin D (May 2012)Gliadin antibodies in schizophrenia replicated (January 2013)Folic-ing around in schizophrenia (March 2013)Vitamin-mineral mix for ADHD? (February 2014)Phenylalanine and schizophrenia: new directions for intervention? (April 2014)Vitamin D and depression / depressive symptoms (June 2014)Vitamin D and schizophrenia meta-analysed (August 2014)Omega-3 fatty acids and ADHD (September 2014)And with that, enjoy your day with some Hot Chocolate. Oh, and do be careful if...----------[1] Sarris J. et al. Nutritional medicine as mainstream in psychiatry. Lancet Psychiatry. 2015. January 25.[2] Sarris J. et al. Participant experiences from chronic administration of a multivitamin versus placebo on subjective health and wellbeing: a double-blind qualitative analysis of a randomised controlled trial. Nutr J. 2012 Dec 14;11:110.----------Jerome Sarris, Alan C Logan, Tasnime N Akbaraly, G Paul Amminger, Vicent Balanzá-Martínez, Marlene P Freeman, Joseph Hibbeln, Yutaka Matsuoka, David Mischoulon, Tetsuya Mizoue, Akiko Nanri, Daisuke Nishi, Drew Ramsey, Julia J Rucklidge, Almudena Sanchez-Villegas, Andrew Scholey, Kuan-Pin Su, & Felice N Jacka (2015). Nutritional medicine as mainstream in psychiatry Lancet Psychiatry : Read more »

Jerome Sarris, Alan C Logan, Tasnime N Akbaraly, G Paul Amminger, Vicent Balanzá-Martínez, Marlene P Freeman, Joseph Hibbeln, Yutaka Matsuoka, David Mischoulon, Tetsuya Mizoue.... (2015) Nutritional medicine as mainstream in psychiatry. Lancet Psychiatry. info:/

  • February 13, 2015
  • 11:00 PM

Evolutionrary game theory without interactions

by Artem Kaznatcheev in Evolutionary Games Group

When I am working on evolutionary game theory, I usually treat the models I build as heuristics to guide intuitions and push the imagination. But working on something as practical as cancer, and being in a department with many physics-trained colleagues puts pressure on me to think of moving more towards insilications or abductions. Now, […]... Read more »

  • February 13, 2015
  • 02:52 PM

HPV, DNA damage response, and autophagy: complex

by thelonevirologist in Virology Tidbits

Human Papillomavirus (HPV) are non-enveloped viruses with a small circular genome of about 8 kB in size that infect the epithelium of the skin or mucosal surfaces. Although most infections with HPV are benign, malignant tumours of the cervix or the oral cavity have been associated with the high-risk HPV types 16, 18, 31, and 58; indeed, HPV 16 and 18 alone cause two thirds of cervical cancers. In general, HPV infects undifferentiated cells in the basal layer of stratified epithelium and viral replication occurs in differentiated suprabasal epithelial cells that are prevented from exiting the cell cycle by the viral E6 and E7 proteins dependent on their ability to target the cellular Retinoblastoma (RB) and p53 proteins.
Here the implications of inducing the DDR response for autophagy are discussed and compared to HTLV-1 tax. Also, the differences between high and low risk HPV are explored and discussed.
... Read more »

Turnell, A., & Grand, R. (2012) DNA viruses and the cellular DNA-damage response. Journal of General Virology, 93(Pt_10), 2076-2097. DOI: 10.1099/vir.0.044412-0  

Anacker DC, Gautam D, Gillespie KA, Chappell WH, & Moody CA. (2014) Productive replication of human papillomavirus 31 requires DNA repair factor Nbs1. Journal of virology, 88(15), 8528-44. PMID: 24850735  

Jiang H, Martin V, Gomez-Manzano C, Johnson DG, Alonso M, White E, Xu J, McDonnell TJ, Shinojima N, & Fueyo J. (2010) The RB-E2F1 pathway regulates autophagy. Cancer research, 70(20), 7882-93. PMID: 20807803  

Fang HY, Chang CL, Hsu SH, Huang CY, Chiang SF, Chiou SH, Huang CH, Hsiao YT, Lin TY, Chiang IP.... (2010) ATPase family AAA domain-containing 3A is a novel anti-apoptotic factor in lung adenocarcinoma cells. Journal of cell science, 123(Pt 7), 1171-80. PMID: 20332122  

Pandey S, & Chandravati. (2012) Autophagy in cervical cancer: an emerging therapeutic target. Asian Pacific journal of cancer prevention : APJCP, 13(10), 4867-71. PMID: 23244072  

García-Zepeda SP, García-Villa E, Díaz-Chávez J, Hernández-Pando R, & Gariglio P. (2013) Resveratrol induces cell death in cervical cancer cells through apoptosis and autophagy. European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP), 22(6), 577-84. PMID: 23603746  

Shubassi G, Robert T, Vanoli F, Minucci S, & Foiani M. (2012) Acetylation: a novel link between double-strand break repair and autophagy. Cancer research, 72(6), 1332-5. PMID: 22422989  

Belgnaoui SM, Fryrear KA, Nyalwidhe JO, Guo X, & Semmes OJ. (2010) The viral oncoprotein tax sequesters DNA damage response factors by tethering MDC1 to chromatin. The Journal of biological chemistry, 285(43), 32897-905. PMID: 20729195  

Durkin SS, Guo X, Fryrear KA, Mihaylova VT, Gupta SK, Belgnaoui SM, Haoudi A, Kupfer GM, & Semmes OJ. (2008) HTLV-1 Tax oncoprotein subverts the cellular DNA damage response via binding to DNA-dependent protein kinase. The Journal of biological chemistry, 283(52), 36311-20. PMID: 18957425  

Mathew R, Karp CM, Beaudoin B, Vuong N, Chen G, Chen HY, Bray K, Reddy A, Bhanot G, Gelinas C.... (2009) Autophagy suppresses tumorigenesis through elimination of p62. Cell, 137(6), 1062-75. PMID: 19524509  

  • February 13, 2015
  • 12:35 PM

You Can Force Birds to Be Friends, but It Won't Stick

by Elizabeth Preston in Inkfish

As anyone who's made valentines for a whole elementary-school class knows, kids are often pushed into social groups not of their choosing. Scientists tried the same thing with wild birds and found it pretty easy to coax them into new cliques. The birds hung out with their new social circles even when they didn't have to. But once the experiment ended, those friendships dissolved faster than a candy conversation heart.

To create new social groups in birds, researchers essentially controlle... Read more »

  • February 13, 2015
  • 10:47 AM

The Tree of Earthworms

by Marc in Teaching Biology

Earthworm taxonomists describing what they do to a layperson is hilarious to watch. Laypeople often have a difficult time understanding the concept of a species – you will regularly hear statements that there are only 50 insect species, for example. Insect species often differ in colour and patterning, so it’s easy to then correct a layman’s misconceptions about […]
The post The Tree of Earthworms appeared first on Teaching Biology.
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Domínguez, J., Aira, M., Breinholt, J., Stojanovic, M., James, S., & Pérez-Losada, M. (2015) Underground evolution: New roots for the old tree of lumbricid earthworms. Molecular Phylogenetics and Evolution, 7-19. DOI: 10.1016/j.ympev.2014.10.024  

  • February 13, 2015
  • 07:52 AM

The lesser of two evils: e-cigarette exposure weakens anti-bacterial and anti-viral defenses

by Betty Zou in Eat, Read, Science

Electronic cigarettes, or e-cigarettes, are widely believed to be a healthier alternative to traditional cigarettes. While they undoubtedly cause less harm than traditional cigarettes, e-cigarettes are still hazardous to your health. A team of researchers led by Prof. Shyam Biswal at Johns Hopkins University has shown that exposure to e-cigarettes impairs your body’s ability to fight off bacterial and viral infections.... Read more »

Sussan, T., Gajghate, S., Thimmulappa, R., Ma, J., Kim, J., Sudini, K., Consolini, N., Cormier, S., Lomnicki, S., Hasan, F.... (2015) Exposure to Electronic Cigarettes Impairs Pulmonary Anti-Bacterial and Anti-Viral Defenses in a Mouse Model. PLOS ONE, 10(2). DOI: 10.1371/journal.pone.0116861  

  • February 13, 2015
  • 04:46 AM

Autism, CNVs and sensitivity to maternal infection?

by Paul Whiteley in Questioning Answers

An intriguing quote to begin today's post: "Our findings support a gene-environment interaction model of autism impairment, in that individuals with ASD-associated CNVs are more susceptible to the effects of maternal infection and febrile episodes in pregnancy on behavioral outcomes and suggest that these effects are specific to ASD [autism spectrum disorder] rather than to global neurodevelopment."The findings come from the paper by Varvara Mazina and colleagues [1] who sought to "explore the impact of ASD-associated copy number variants (CNVs) and prenatal maternal infection on clinical severity of ASD." Based on "data from the Simons Simplex Collection sample including 1971 children with a diagnosis of ASD aged 4 to 18 years" who underwent genetic screening for the presence of CNVs, researchers cross-referenced genetic information with parent reported maternal infection and/or febrile episodes during pregnancy alongside autism severity in cases. They found something of a potentially important relationship: "individuals with CNVs and history of maternal infection demonstrated increased rates of social communicative impairments and repetitive/restricted behaviors."Of course let us not forget that it is not beyond the realms of possibility that CNV load and maternal infection during pregnancy might just be a fluke finding when it comes to the presentation or severity of autistic traits. Indeed, outside of just looking at core autistic traits I'm taken to wonder whether other behaviours might show a similar relationship for example, based on some of the heightened comorbidity seemingly connected to autism such as attention-deficit hyperactivity disorder (ADHD) (see here).That being said, I do think there is more to see in this "gene-environment interaction model" specifically focused on what could bridge maternal infection and CNV load in cases of autism. CNVs and autism have something of a research history albeit rather complicated (see here). Maternal infections during pregnancy and autism have a similarly interesting history too (see here). In a previous post, I've covered CNV load and autism focused on behavioural presentation (see here) and the idea that some of the genes linked to cases of autism might also affect immune function  (see here and see here) including response to infection.Without also trying to speculate too much and bearing in mind the 'epigenetic' slant to the Mazina paper, I was wondering whether there may be additional merit in looking at something like the HERVs (human endogenous retroviruses) in future work in this area. I say this acknowledging the preliminary research forays that have already been taking into this area with autism (see here), ADHD (see here) and even myalgic encephalomyelits / chronic fatigue syndrome (ME/CFS) in mind (see here). HERVs by the way are perhaps best described as fossil viruses which we carry with us as badges of honour following our evolutionary war against such microscopic invaders (see here). The idea that HERVs could 'mediate' genetic variations for example, as per the findings reported by Shuvarikov and colleagues [2] is still quite a new one but interesting in light of the suggestion of 'reactivation' under certain circumstances including stress and/or infection [3]. The contribution of 'hypomethylation' to genomic instability [4] might also be important to such HERV research in light of the preliminary suggestions of methylation issues associated with cases of autism (see here).But enough of me speculating (on a blog in a very non-peer reviewed manner). The findings from Mazina et al stand as testament to our very limited understanding of how genes and environment [variably] interact when it comes to autism but offer something of a new area ripe for lots more investigation...Music: Ash and Girl from Mars.----------[1] Mazina V. et al. Epigenetics of Autism-related Impairment: Copy Number Variation and Maternal Infection. J Dev Behav Pediatr. 2015 Jan 27.[2] Shuvarikov A. et al. Recurrent HERV-H-mediated 3q13.2-q13.31 deletions cause a syndrome of hypotonia and motor, language, and cognitive delays. Hum Mutat. 2013 Oct;34(10):1415-23.[3] Schulz WA. et al. Methylation of endogenous human retroelements in health and disease. Curr Top Microbiol Immunol. 2006;310:211-50.[4] Li J. et al. Genomic hypomethylation in the human germline associates with selective structural mutability in the human genome. PLoS Genetics. 2012: 8: e1002692.----------Mazina V, Gerdts J, Trinh S, Ankenman K, Ward T, Dennis MY, Girirajan S, Eichler EE, & Bernier R (2015). Epigenetics of Autism-related Impairment: Copy Number Variation and Maternal Infection. Journal of developmental and behavioral pediatrics : JDBP PMID: 25629966... Read more »

Mazina V, Gerdts J, Trinh S, Ankenman K, Ward T, Dennis MY, Girirajan S, Eichler EE, & Bernier R. (2015) Epigenetics of Autism-related Impairment: Copy Number Variation and Maternal Infection. Journal of developmental and behavioral pediatrics : JDBP. PMID: 25629966  

  • February 12, 2015
  • 02:17 PM

February 12, 2015

by Erin Campbell in HighMag Blog

Biologists have to wear many hats, and one under-appreciated hat is that of marketing executive. You have to properly name whatever process/protein/structure you just identified so it will be easily remembered. Whoever coined the term “invadopodia” was spot-on….the term is informative, catchy, and ignites my imagination of what it’s like inside a cell. Today’s image is from a fascinating paper on invadopodia formation. Invadopodia are dynamic protrusions of plasma membrane that locally degrade a cell’s underlying extracellular matrix (ECM). A tumor cell’s invadopodia mediate the invasion of tissue and metastasis. A recent paper describes a study of invadopodia formation within the context of a highly-concentrated collagen matrix, to better mimic the ECM of cancerous tissue. This dense collagen network, Artym and colleagues found, triggers robust invadopodia formation and ECM degradation, in both cancerous and non-cancerous cell lines. This invadopodia formation did not require altered gene or protein expression, but did require phosphorylation of kindlin2, part of a complex integrin regulatory network. As seen in the images, the high-density fibrillary collagen (HDFC, top) network triggered the induction of many more invadopodia (yellow dots) than a gelatin-based matrix (bottom).  Artym, V., Swatkoski, S., Matsumoto, K., Campbell, C., Petrie, R., Dimitriadis, E., Li, X., Mueller, S., Bugge, T., Gucek, M., & Yamada, K. (2015). Dense fibrillar collagen is a potent inducer of invadopodia via a specific signaling network originally published in the Journal of Cell Biology, 208 (3), 331-350 DOI: 10.1083/jcb.201405099... Read more »

Artym, V., Swatkoski, S., Matsumoto, K., Campbell, C., Petrie, R., Dimitriadis, E., Li, X., Mueller, S., Bugge, T., Gucek, M.... (2015) Dense fibrillar collagen is a potent inducer of invadopodia via a specific signaling network. originally published in the Journal of Cell Biology, 208(3), 331-350. DOI: 10.1083/jcb.201405099  

  • February 12, 2015
  • 01:48 PM

Possible mechanism underpinning Alzheimer’s and Parkinson’s type diseases found

by Dr. Jekyll in Lunatic Laboratories

Neurodegenerative diseases have remained stubbornly increasing in prevalence for sometime now. Unfortunately longer life does not mean a better quality of life. Thankfully that could change sooner than you think, scientists have for the first time discovered a killing mechanism that could underpin a range of the most intractable neurodegenerative diseases such as Alzheimer’s, Parkinson’s and ALS.... Read more »

Minghai Zhou, Gregory Ottenberg, Gian Franco Sferrazza, Christopher Hubbs, Mohammad Fallahi, Gavin Rumbaugh, Alicia F. Brantley, & Corinne I. Lasmézas. (2015) Neuronal death induced by misfolded prion protein is due to NAD depletion and can be relieved in vitro and in vivo by NAD replenishment. Brain - A Journal of Neurology. info:/

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