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  • September 29, 2015
  • 05:26 AM

Herpes simplex virus (HSV) infection and cognitive ability

by Paul Whiteley in Questioning Answers

So: "our findings indicate that infection with HSV-1 [Herpes simplex virus] is associated with reduced cognitive functioning in healthy individuals."That was the conclusion reached in the study by Eyal Fruchter and colleagues [1] who based on a "representative, random sample of 612 soldiers before active duty in the Israeli military (Israeli defense force — IDF)" looked at cognitive functioning and language abilities as a function of HSV status ("62.2% HSV positive (n = 381) and 38.8% HSV negative (n = 231)").They observed some key differences between the HSV positive and negative groups whereby IQ scores were on average lower for the seropositive group compared with the seronegative group. This difference also stretched to language scores too and stayed pertinent as and when various psychopathology (anxiety, depression) were controlled for. The authors plant their findings within the context of schizophrenia and that their results indicate "that many research findings seemingly characteristic of schizophrenia are related to the association between HSV exposure and cognitive functioning in general, and are not illness specific."This is an interesting branch of research. I was unaware that HSV-1 seropositivity was potentially correlated to cognitive functions but a quick trawl through some of the other literature in this area does indeed reveal that this is not the first time that such an association has been made [2] (with appropriate caveats). Even some big names in schizophrenia research (Faith Dickerson & Robert Yolken) have discussed HSV-1 and cognitive functions, within the context of schizophrenia [3].There are some potentially pretty stark implications from such findings. That there may be a 'link' between cognitive and intellectual functions and infectious agents is a primary one (see here). That processes such as inflammation (and immune functions) might also play a role is another (see here). Whilst further research is required to put some scientific flesh on the bones of the potential biological / genetic processes involved in such a relationship, the tantalising question is whether 'treating' such viral infections (if treatment is available) might have a knock-on effect for intellectual functions?Music: Mumford & Sons - Ditmas.----------[1] Fruchter E. et al. The impact of Herpes simplex virus type 1 on cognitive impairments in young, healthy individuals — A historical prospective study. Schizophrenia Research. 2015. Sept 8.[2] Tarter KD. et al. Persistent viral pathogens and cognitive impairment across the life course in the third national health and nutrition examination survey. J Infect Dis. 2014 Mar;209(6):837-44.[3] Thomas P. et al. Exposure to herpes simplex virus, type 1 and reduced cognitive function. J Psychiatr Res. 2013 Nov;47(11):1680-5.----------Fruchter, E., Goldberg, S., Fenchel, D., Grotto, I., Ginat, K., & Weiser, M. (2015). The impact of Herpes simplex virus type 1 on cognitive impairments in young, healthy individuals — A historical prospective study Schizophrenia Research DOI: 10.1016/j.schres.2015.08.036... Read more »

  • September 28, 2015
  • 07:22 PM

Connecting Alzheimer’s disease and the immune system

by Dr. Jekyll in Lunatic Laboratories

The role of the immune system in Alzheimer’s disease is a hot topic, but exactly how the two are connected and what interventions could help lower risk remain a mystery. In a new study, researchers in the Ann Romney Center for Neurologic Diseases at Brigham and Women’s Hospital (BWH) investigate how genetic risk factors for Alzheimer’s disease may influence a key type of immune cell. Their results lay the groundwork for designing better therapeutic strategies and better prediction tools for risk of developing Alzheimer’s disease.... Read more »

Chan, G., White, C., Winn, P., Cimpean, M., Replogle, J., Glick, L., Cuerdon, N., Ryan, K., Johnson, K., Schneider, J.... (2015) CD33 modulates TREM2: convergence of Alzheimer loci. Nature Neuroscience. DOI: 10.1038/nn.4126  

  • September 28, 2015
  • 12:48 PM

What Animals Contageously Yawn?

by Miss Behavior in The Scorpion and the Frog

Does this sight make you want to yawn? A yawning Japanese macaque by Daisuke Tashiro at Wikimedia Commons.Do you think it would make other animals want to yawn? Many animals yawn spontaneously, but yawning in response to sensing or thinking about someone else doing it may be a completely different thing. Contagious yawning requires a sense of social connection and emotional empathy that not all species share. So far, scientists have found experimental evidence of contagious yawning in humans, chimpanzees, domestic dogs (who interestingly yawn when people yawn, but not when other dogs do), and an abnormally yawny genetic line of rats. However, there have also been reports of bonobos, baboons, wolves, and budgerigars (small social parrots, also called budgies or parakeets) yawning contagiously in the wild, so this phenomenon may be more widespread than previously thought. Andrew Gallup, Lexington Swartwood, Janine Militello and Serena Sackett from the State University of New York at Oneonta set out to experimentally test if budgerigars do in fact yawn contagiously. In one experiment, the researchers placed pairs of birds in separate adjacent cages with perches facing one another. They video recorded the birds both with an opaque barrier between them and without the opaque barrier. The researchers found that when the birds could see one another they were three times more likely to yawn within 5 minutes of the other bird yawning, although there was no difference in the overall number of spontaneous yawns. Images of a yawning budgie from Gallup et al., 2015.Next, the researchers decided to test if budgerigars contagiously yawn in response to videos of another budgerigar yawning. They played 10-minute videos of either yawning or non-yawning budgerigars on a laptop facing the birdcage. And who would have guessed that the budgies yawned twice as much in response to the yawning video than to the non-yawning video, showing that even our pet birds can get something out of watching TV! Budgerigars are now the first non-mammalian species to display contagious yawning. Contagious yawning is not just interesting in itself, but it may also indicate a sense of empathy. Although we often limit our thinking of empathy to our own species, it makes sense to find empathetic behavior among social species like budgerigars. Now if we could just find more of it amongst our own species… Want to know more? Check this out:Gallup, A., Swartwood, L., Militello, J., & Sackett, S. (2015). Experimental evidence of contagious yawning in budgerigars (Melopsittacus undulatus) Animal Cognition, 18 (5), 1051-1058 DOI: 10.1007/s10071-015-0873-1 ... Read more »

  • September 28, 2015
  • 03:11 AM

Autism traits in older adults with depressive disorders

by Paul Whiteley in Questioning Answers

"ASD [autism spectrum disorder] might be overlooked in older adults and especially within geriatric psychiatry when diagnosing and treating depression and anxiety in older patients one should be attentive to ASD."So concluded Hilde Geurts and colleagues [1] as a function of their results looking for the presence of autistic traits in older adults with and without depressive disorders participating in the Netherlands study of depression in older persons (NESDO) initiative. Based on the analysis of some 250 older adults (aged between 60-90 years) fulfilling DSM-IV depressive disorder criteria compared against 114 non-depressed older adults, researchers noted quite a few more autistic traits in the depressed older adults based on the use of the "abbreviated Autism Spectrum Quotient [AQ]." In more detail: "Of the older adults with a depressive disorder 31% showed elevated ASD characteristics, which is much higher than the observed 6% in the comparison group."I don't want to dwell too long on these results but there are some potentially important things to say about them. First is the emphasis on autistic traits over and above a diagnosis of autism. There is a difference; as I've discussed in other recent work (see here). Second is the authors' use of the AQ and how one has to be a little careful about what the AQ is actually measuring (see here). Third is the importance of the related finding reported by Geurts et al on how: "High ASD characteristics were associated with elevated depression and anxiety symptoms, and more comorbid anxiety disorders." As I've mentioned before on this blog, depression and anxiety can represent significant 'loading' when autism is diagnosed (see here and see here). These latest findings potentially further strengthen the links. Finally, is the intriguing prospect that autism screening in older adults might contribute to all those debates about the prevalence of autism and specifically adult autism (see here).No music to close today, just some rather peculiar news about the end of the world (again).----------[1] Geurts HM. et al. Autism characteristics in older adults with depressive disorders. The American Journal of Geriatric Psychiatry. 2015. Sept 3.----------Geurts, H., Stek, M., & Comijs, H. (2015). Autism characteristics in older adults with depressive disorders The American Journal of Geriatric Psychiatry DOI: 10.1016/j.jagp.2015.08.003... Read more »

  • September 27, 2015
  • 02:45 PM

Breaking the anxiety cycle

by Dr. Jekyll in Lunatic Laboratories

A woman who won’t drive long distances because she has panic attacks in the car. A man who has contamination fears so intense he cannot bring himself to use public bathrooms. A woman who can’t go to church because she fears enclosed spaces. All of these people have two things in common: they have an anxiety disorder. They’re also parents.... Read more »

  • September 26, 2015
  • 03:31 PM

Scientists discover new system for human genome editing

by Dr. Jekyll in Lunatic Laboratories

A team including the scientist who first harnessed the revolutionary CRISPR-Cas9 system for mammalian genome editing has now identified a different CRISPR system with the potential for even simpler and more precise genome engineering. In the study researchers describe the unexpected biological features of this new system and demonstrate that it can be engineered to edit the genomes of human cells.... Read more »

Zetsche, B., Gootenberg, J., Abudayyeh, O., Slaymaker, I., Makarova, K., Essletzbichler, P., Volz, S., Joung, J., van der Oost, J., Regev, A.... (2015) Cpf1 Is a Single RNA-Guided Endonuclease of a Class 2 CRISPR-Cas System. Cell. DOI: 10.1016/j.cell.2015.09.038  

  • September 26, 2015
  • 03:47 AM

T. gondii infection and autism?

by Paul Whiteley in Questioning Answers

I was interested to read the paper by Joseph Prandota and colleagues [1] who observed that: "latent chronic T. gondii [Toxoplasma gondii] infection have an important impact on triggering and development of ASD [autism spectrum disorders], at least in a subset of autistic children, and this requires some modification(s) of its diagnostic procedures and treatment regimens." Big words, I'm sure you'll agree.From the start I'll indicate that I'm interested in T. gondii on this blog. This parasitic protozoan is one of nature's survivors (and thrivers) with effects that may go far beyond your ordinary parasite. Aside from potentially making rats attracted to cats (or cat urine), I've been particularly interested in the collected research looking at a possible association between T. gondii and the presentation of schizophrenia (see here for example). The idea that infection with T. gondii under the right circumstances may be associated with a condition as complicated as schizophrenia is not without its critics, but in a world of increasing pluralisation of such labels (see here) I'd be minded to keep T. gondii on the research agenda (see here) for now.The Prandota findings, based on a small-ish group of children diagnosed with ASD living in Egypt, take things one step further when it comes to T. gondii and it's potentially wide-ranging effects. Working with the aim to "estimate the seroprevalence of chronic toxoplasmosis among autistic children" researchers set about assaying for "anti-T. gondii IgG antibody seroposivity" alongside a couple of other parameters including "serum levels of IFN-g and nitric oxide (NO) in T. gondii-positive and T. gondii-free patients." I might add that a positive anti-T. gondii IgG result indicates previous exposure to T. gondii. It does not necessarily mean current or on-going infection which can only be reliably ascertained via other tests (see here).Results: "11 (29.3%) out of the 46 autistic children... were positive for serum anti-T. gondii IgG antibodies as compared with 2 patients (4%) with toxoplasmosis found among 50 control children." Age was one of the parameters that seemed to play a role in infection history which kinda stands to reason (the older you are, the more likely that you have an exposure). Further: "Autistic children with toxoplasmosis had markedly increased both serum IFN-g and NO concentrations... as compared with the values obtained in patients without toxoplasmosis."I don't want to over-analyse the Prandota results at this stage in terms of what elevations of IFN-γ and NO might mean to T. gondii infection in autism, so I won't. The authors go into some detail about immune function, tryptophan metabolism and even glutathione gets a mention in relation to these issues, but I'd prefer to stick to the T. gondii estimates for now.As far as I can see, this is one of the first times that T. gondii infection has been discussed with autism in mind. That over a quarter of cases in the Prandota sample were found to have been in immunological contact with the protozoan is interesting and suggests that further independent investigations should be initiated in this area. I would, for example, be interested to know whether such findings are transferable to other geographical sites? Does cat ownership show any link to findings as per some discussions in schizophrenia (see here)? Are there any links with other 'autism-related' issues as suggested by Abdoli & Dalimi [2]? And, with some of my own research interests in mind (see here) could such findings further extend the observations of Emily Severance and colleagues [3] talking about T. gondii infection and "sensitivity to gluten" beyond schizophrenia (see here)? Well, it's not as if anti-gliadin antibodies (IgG) are strangers to [some] autism (see here).As for treating any on-going toxoplasmosis, well in the US at least, this might just have got a little bit more expensive...Questions (and answers) remain.Music: Artful Dodger - Movin' Too Fast.----------[1] Prandota J. et al. Increased Seroprevalence of Chronic Toxoplasmosis in Autistic Children: Special Reference to the Pathophysiology of IFN-γ and NO Overproduction. International Journal of Neurology Research. 2015; 3: 102-122.[2] Abdoli A. & Dalimi A. Are There any Relationships between Latent Toxoplasma gondii Infection, Testosterone Elevation, and Risk of Autism Spectrum Disorder? Front Behav Neurosci. 2014 Sep 24;8:339.[3] Severance EG. et al. Anti-gluten immune response following Toxoplasma gondii infection in mice. PLoS One. 2012;7(11):e50991.----------Joseph Prandota, Noha Abdel Fattah Elleboudy, Khadiga Ahmed Ismail, Osama Kamal Zaki, & Hanan Hussein Shehata (2015). Increased Seroprevalence of Chronic Toxoplasmosis in Autistic Children: Special Reference to the Pathophysiology of IFN-γ and NO Overproduction International Journal of Neurology Research, 1 (3), 102-122 : 10.17554/j.issn.2313-5611.2015.01.30... Read more »

Joseph Prandota, Noha Abdel Fattah Elleboudy, Khadiga Ahmed Ismail, Osama Kamal Zaki, & Hanan Hussein Shehata. (2015) Increased Seroprevalence of Chronic Toxoplasmosis in Autistic Children: Special Reference to the Pathophysiology of IFN-γ and NO Overproduction. International Journal of Neurology Research, 1(3), 102-122. info:/10.17554/j.issn.2313-5611.2015.01.30

  • September 25, 2015
  • 03:08 PM

It’s alive!! Study adds to evidence that viruses are alive

by Dr. Jekyll in Lunatic Laboratories

Classifying something as living isn’t as easy as it sounds, after all we are all atoms, so when do atoms go from nonliving to living? Despite the complexities of viruses, we have historically deemed them nonliving. However, a new analysis supports the hypothesis that viruses are living entities that share a long evolutionary history with cells. The study offers the first reliable method for tracing viral evolution back to a time when neither viruses nor cells existed in the forms recognized today.... Read more »

Arshan Nasir, & Gustavo Caetano-Anollés. (2015) A phylogenomic data-driven exploration of viral origins and evolution. Science Advances. info:/10.1126/sciadv.1500527

  • September 25, 2015
  • 06:00 AM

Northernmost Dinosaur Discovered in ‘Lost World’ of Animal Fossils in Alaska

by Blake de Pastino in Western Digs

Scientists exploring a remote riverbank on Alaska’s North Slope have made a surprising find — the discovery of the northernmost species of dinosaur ever found — and it’s just one of what may turn out to many more to come.
... Read more »

  • September 25, 2015
  • 04:30 AM

Baby teeth and autism research

by Paul Whiteley in Questioning Answers

"This report provides evidence that teeth can be useful biomarkers of early life exposure for use in epidemiologic case-control studies seeking to identify differential unbiased exposures during development between those with and without specific disorders such as autism."That was one of the conclusions reached in the paper by Raymond Palmer and colleagues [1] (open-access available here) who played science tooth fairy with 71 deciduous teeth (baby teeth) provided by children with autism from a "tooth repository consisting of 928 children’s deciduous teeth." As per other reports with autism in mind using these potentially important biological samples [2], there is quite a lot of information potentially available from baby teeth assuming one knows how to handle such samples.For Palmer et al the analytical methods of choice were "liquid chromatography tandem mass spectrometry and gas chromatography" echoing other autism biomarker research discussed on this blog (see here) and fairly commonly appearing in the peer-reviewed literature [3]. Levels of various compounds were assessed in the pulverised baby teeth samples including "acetaminophen [paracetamol], ARA [arachidonic acid], DEET [diethyl-m-toluamide], TCPy [3,5,6-trichloro-2-pyridinol], IMPy [2-isopropyl-6-methyl-4-pyrimidinol], and MEHP [mono-2-ethylhexyl phthalate]." Just in case you aren't an organic chemist, many of those compounds are metabolites of "pesticides, plastics, or medications" and were studied in light of previous work from this authorship group [4] and the suggestion that some of them might be relevant to autism risk and/or onset (see here for example) or at least serving up an interesting correlation.Consistent with that previous report, Palmer and colleagues "demonstrated that specific semivolatile organic chemicals relevant to autism etiology can be detected in deciduous teeth." Drawing on information from both US children with autism (a "collection of deciduous teeth through collaborative efforts with the Interactive Autism Network (IAN)") and Mexican children with autism, various results are presented. "Despite demographic differences in the two samples, there were similar rates of detection for all chemicals" was one of the primary findings. So, round about 40% of samples from both geographic groups were detected to have traces of acetaminophen (paracetamol) in them for example. This finding tallied to some degree with parent report about paracetamol use during pregnancy and infancy. Other results can be seen in some of the accompanying tables (see here for example).Importantly, Palmer and colleagues discuss what their findings do and do not mean. "While we have demonstrated that chemicals relevant to ASD [autism spectrum disorders] can be detected in deciduous teeth and are associated with mothers’ self-reported exposures, our results are limited in generalizability—largely due to the sample consisting entirely of children with ASD." In other words, the sole focus on baby teeth from children with autism does not necessarily mean that any compounds detected 'cause' autism given the snapshot view of their study and the lack of appropriate asymptomatic control samples analysed. Further work is indicated in this area to "include more diverse participants and neurotypical children as controls will allow case/control comparisons."The use of baby teeth represents an interesting addition to tissue analysis when it comes to autism. Given the availability of such teeth, the timing of their availability and the relatively non-invasive way that such samples can be collected, there are quite a few positives to the use of such as resource in autism research. Combined with other fairly non-invasively collected samples such as urine (see here), saliva samples (see here) and potentially even things like nail clippings [5], there is quite a bit of information potentially available for autism research. That being said, the word 'biomarker' with autism in mind, needs to be rather carefully used in light of things like plurality...Music: Maroon 5 - Sugar.----------[1] Palmer RF. et al. Organic Compounds Detected in Deciduous Teeth: A Replication Study from Children with Autism in Two Samples. J Environ Public Health. 2015;2015:862414.[2] Adams JB. et al. Mercury, lead, and zinc in baby teeth of children with autism versus controls. J Toxicol Environ Health A. 2007 Jun;70(12):1046-51.[3] Wang H. et al. Potential serum biomarkers from a metabolomics study of autism. J Psychiatry Neurosci. 2015 Sep 22;40(5):140009.[4] Camann DE. et al. Acetaminophen, pesticide, and diethylhexyl phthalate metabolites, anandamide, and fatty acids in deciduous molars: potential biomarkers of perinatal exposure. Journal of Exposure Science and Environmental Epidemiology. 2013; 23: 190–196.[5] Shu I. et al. Detection of Drugs in Nails: Three Year Experience. J Anal Toxicol. 2015 Oct;39(8):624-8.----------Palmer, R., Heilbrun, L., Camann, D., Yau, A., Schultz, S., Elisco, V., Tapia, B., Garza, N., & Miller, C. (2015). Organic Compounds Detected in Deciduous Teeth: A Replication Study from Children with Autism in Two Samples Journal of Environmental and Public Health, 2015, 1-9 DOI: 10.1155/2015/862414... Read more »

Palmer, R., Heilbrun, L., Camann, D., Yau, A., Schultz, S., Elisco, V., Tapia, B., Garza, N., & Miller, C. (2015) Organic Compounds Detected in Deciduous Teeth: A Replication Study from Children with Autism in Two Samples. Journal of Environmental and Public Health, 1-9. DOI: 10.1155/2015/862414  

  • September 24, 2015
  • 04:21 PM

What we know about fungi and cured meats

by Rosin Cerate in Rosin Cerate

I've been watching a lot of the food show Mind of a Chef on Netflix lately. In a couple of episodes, a chef visits a locale where meat is being cured. I've noticed there consistently appears to be fungi (mould) growing on the meat, whether it's skerpikjøt (mutton dried using the wind on the Faroe Islands), dry-aged beef, country ham, or dry-cured sausage. These fungi, having managed to grow to such an extent as to be visible to the naked eye, obviously influence the characteristics of the meat.Skerpikjøt, made by exposing sheep meat to wind and mould (Source)One thing fungi do particularly well is release all sorts of interesting substances into their surrounding environment. For fungi living on meat, these often include enzymes capable of breaking apart lipids and proteins. This tenderizes the meat while increasing levels of certain flavourful amino acids and free fatty acid derivatives. In less fun news, many of the fungi able to grow on food also synthesize and secrete mycotoxins (poisons made by fungi) and antibiotics. Food scientists who study cured meats are often on the lookout for these harmful substances.In addition to their production of meat-altering secretions, fungi growing on the outside of meats can form a protective coating of mycelium (a dense network of cell-filled filaments we usually see as moulds growing on bread, cheese, or fruit). This barrier limits exposure of the meat to oxygen and light, ensuring a stable colour and flavour while preventing meat fats from going rancid. It also can block the entrance of undesirable microbes (pathogens, agents of spoilage) into the meat.Let's focus in on a couple of meat products, starting with beef. Dry aging beef means hanging a recently slaughtered cow part in a refrigerator to cure for a couple of weeks. During this time, fungi will often grow on its surface, producing enzymes able to penetrate into the meat and break down its tougher components (e.g. collagen). There doesn't appear to be a whole lot of research out there on the fungi involved in the dry aging of beef, but one recent conference paper I came across reported finding Cochliobolus sativus and Mucor racemosus on subprimals dry aged for 3 weeks. Both of these fungi infect corn, and M. racemosus has also been isolated from Camembert cheese, so I'm speculating they were already present on cows brought in from farms for slaughtering and then found their way onto the hanging meat. Anyway, the big concern for the authors of the paper was whether or not fungi growing on the beef were producing mycotoxins, specifically aflatoxin. Fortunately, they didn't find a significant difference between aflatoxin levels in dry aged versus non-aged bits of beef. Further, levels of the toxin in all of the meat samples they looked at were well below the regulatory limit set by the US government. Whew.Note the fungi growing on this dry aged ribeye (Source)Other fungi known to be associated with dry aged beef include Thamnidium elegans, Mucor mucedo, and Chaetostylum fresenii. The first two appear as pale gray patches called 'whiskers' on the fatty parts of refrigerated red meats. This refers to their growth of tall specialized filaments (sporangiophores) sticking up into the air, at the tops of which spores are formed (in sporangia). Chaetostylum fresenii has also been found growing on refrigerated fish and can survive bouts of freezing below -20°C.Moving on to our next meat, dry-fermented sausages owe both their flavour and appearance to fungi. As with other cured meats, fungal growth can create enjoyable tastes and smells by bringing about the degradation of lipids and proteins. It also is used to add an aesthetically pleasing white or whitish grey coat to the surface of sausages. Producers will often use commercial starter cultures of particular fungi to ensure a consistent appearance and flavour. Two big players in the starter scene are Penicillium nalgiovense and Penicillium chrysogenum. Notably, both can produce the antibiotic penicillin, which is bad to have in a sausage since some folks are allergic to it and it could potentially lead to the development of harmful drug-resistant bacteria in our guts.Salami coated in what appears to be fungi (Source)Other sausage makers will just hang the sausages and allow them to become inoculated with whatever fungi are floating about in their production area. This is akin to spontaneously inoculated lambic and coolship beers where a specific community of microbes are already present in the brewery rafters and thus ensure a relatively consistent product. In one study I found on dry-fermented sausages produced in Colonia Caroya (a sausage-making hotbed in Córdoba, Argentina), their fungal inhabitants belonged to seven genera: Penicillium, Aspergillus, Mucor, Cladosporium, Scopulariopsis, Geotrichum, and Eurotium. These communities varied depending on whether the sausages were produced in the summer or winter. For example, Aspergillus ochraceus was found in most of the summer-made sausages but none of the winter-made ones, with this being explained by the higher temperatures in the ripening rooms during the summer. The presence of A. ochraceus wasn't good since it gave the sausages an unwanted yellowish gold colour and potentially contaminated them with mycotoxins.Ending off our meat tour, dry-cured ham is also typically rendered slightly fuzzy and appreciably more flavourful by the growth of fungi. The particular fungi that end up growing on the surface of a ham tend to be characteristic to the part of the world (e.g. Jinhua, China) where it is being produced, thus contributing to location-specific flavour profiles (meat terroirs, if you will). Hams are usually prepared by being covered in salt, which works its way into the meat, then dried for a while, and finally placed in a cellar for aging. The length of the whole process depends on the type being produced, but can take up to two years. Unlike dry-cured sausages, dry-cured ham usually isn't inoculated with a starter culture of fungi.Several species of Penicillium known to be capable of breaking apart fats are often residents of dry-cured ham. A concern with these fungi is that some of them produce ochratoxin A, which is capable of damaging the liver and kidneys of those who ingest it. The long aging times required for dry-cured ham can mean higher levels of the mycotoxin than might be found on other meats. One of the fungi responsible for contaminating ham with ochratoxin A is Penicillium nordicum, which has been found hanging out in pure table salt. P. nordicum produces ochratoxin A in order to increase its competitiveness in salt-rich habitats, which are fairly stressful places for organis... Read more »

  • September 24, 2015
  • 02:59 PM

Mexico City’s air pollution has detrimental impact on Alzheimer’s disease gene

by Dr. Jekyll in Lunatic Laboratories

A new study by researchers heightens concerns over the detrimental impact of air pollution on hippocampal metabolites as early markers of neurodegeneration in young urbanites carrying an allele 4 of the apolipoprotein E gene (APOE). This is associated with the risk for Alzheimer disease (AD) and a susceptibility marker for poor outcome in traumatic brain injury (TBI) recovery.... Read more »

  • September 24, 2015
  • 09:05 AM

Ice, Ice Baby: Bringing Frozen Viruses Back To “Life”

by Bill Sullivan in The 'Scope

It sounds like the beginning of a sci-fi/horror movie: scientists recently revived a 30,000 year old virus from Siberian ice. How...and WHY would they do this?!... Read more »

Legendre, M., Lartigue, A., Bertaux, L., Jeudy, S., Bartoli, J., Lescot, M., Alempic, J., Ramus, C., Bruley, C., Labadie, K.... (2015) In-depth study of , a new 30,000-y-old giant virus infecting . Proceedings of the National Academy of Sciences, 201510795. DOI: 10.1073/pnas.1510795112  

Legendre, M., Bartoli, J., Shmakova, L., Jeudy, S., Labadie, K., Adrait, A., Lescot, M., Poirot, O., Bertaux, L., Bruley, C.... (2014) Thirty-thousand-year-old distant relative of giant icosahedral DNA viruses with a pandoravirus morphology. Proceedings of the National Academy of Sciences, 111(11), 4274-4279. DOI: 10.1073/pnas.1320670111  

  • September 24, 2015
  • 04:28 AM

HERVs as a mechanism of genetic deletion formation: relevance to some autism?

by Paul Whiteley in Questioning Answers

My stark lack of knowledge in the area of genetics and specifically that linked to the human endogenous retroviruses (HERVs) that litter the genome is likely to shine through in this post so be ready with that pinch of salt.The starting point for today's post is the paper by Ines Quintela and colleagues [1] detailing a case report of "a 9-year-old female patient with autistic disorder, total absence of language, intellectual disability, anxiety disorder and disruptive, and compulsive eating behaviors." Following some genetic analysis of this young girl researchers reported on "the identification of a de novo recurrent 3q13.2-q13.31 deletion encompassing 25 genes." This in itself is interesting and adds to a growing tide of research suggesting that there may be lots of different genetic influences acting in different cases of autism; all pertinent to a more plural view of the label: the autisms.One sentence however took my specific interest in this paper insofar as: "a 3.4 Mb recurrently altered region at 3q13.2-q13.31 has been recently described and non-allelic homologous recombination (NAHR) mediated by flanking human endogenous retrovirus (HERV-H) elements has been suggested as the mechanism of deletion formation."As I indicated at the start of this post, the finer details of genetics are not really my forte so be warned. I was however really interested in the suggestion that the process of NAHR - when "highly similar portions of the genome wrongly recombine, deleting and sometimes duplicating a portion of the genome that lies between them" - might be linked to the presence of all/some of those fossil viruses that make us who we are [2].The long-and-short of it is the idea that some of those little variants that we ALL have in our genome might not be all due to just chance if described as de novo (as in not inherited from mum or dad). Take CNVs (copy number variants), small alterations to the genome characterised by gains and losses in segments of DNA (I think!), as the starting point. The idea is that the location of said CNVs in relation to HERVs and other transposable elements means that there may be some kind of relationship between the two. Preliminary research has suggested that HERVs flanking particular parts of the genome might be involved in the formation of CNVs [3]. Other research has noted this process as potentially being relevant in other case reports [4] similar to that described by Quintela and colleagues where behaviour and autism have been mentioned.Just to make the whole process even more complicated (and interesting) is the idea that CNVs when talked about with autism in mind might tend to be concentrated in 'hypomethylated' regions of the genome [5]. This brings in the potentially important process of DNA methylation (yes, epigenetics yet again) into proceedings, made further interesting by suggestions that hypomethylation of DNA = more genomic instability [6] and that certain HERVs might also to some degree be 'kept in check' by methylation means [7]. Add in some evidence of methylation issues associated with some autism (see here) and preliminary evidence of certain HERVs expression correlating with autism (see here) and comorbidity (see here), and there is the making of some potentially important hypotheses ripe for further testing.But please, don't take my word for it.Music: Purple Rain - Prince.----------[1] Quintela I. et al. Female patient with autistic disorder, intellectual disability, and co-morbid anxiety disorder: Expanding the phenotype associated with the recurrent 3q13.2-q13.31 microdeletion. Am J Med Genet A. 2015 Aug 29.[2] Nelson PN. et al. Demystified . . . Human endogenous retroviruses. Molecular Pathology. 2003;56(1):11-18.[3] Campbell IM. et al. Human endogenous retroviral elements promote genome instability via non-allelic homologous recombination. BMC Biol. 2014 Sep 23;12:74.[4] 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.[5] Li J. et al. Genomic hypomethylation in the human germline associates with selective structural mutability in the human genome. PLoS Genetics. 2012: 8: e1002692.[6] Wilson AS. et al. DNA hypomethylation and human diseases. Biochimica et Biophysica Acta. 2007; 1775: 138–162.[7] Lavie L. et al. CpG Methylation Directly Regulates Transcriptional Activity of the Human Endogenous Retrovirus Family HERV-K(HML-2). J. Virol. 2005; 79: 876-883----------Quintela I, Gomez-Guerrero L, Fernandez-Prieto M, Resches M, Barros F, & Carracedo A (2015). Female patient with autistic disorder, intellectual disability, and co-morbid anxiety disorder: Expanding the phenotype associated with the recurrent 3q13.2-q13.31 microdeletion. American journal of medical genetics. Part A PMID: 26332054... Read more »

  • September 23, 2015
  • 03:27 PM

What motivates ‘Facebook stalking’ after a romantic breakup?

by Dr. Jekyll in Lunatic Laboratories

Social networking makes it easy to monitor the status and activities of a former romantic partner, an often unhealthy use of social media known as interpersonal electronic surveillance (IES) or, more commonly, “Facebook stalking.” Psychological and relationship factors and how individuals cope with the termination of a romantic relationship can help predict their use of online surveillance, according to a new study.... Read more »

  • September 23, 2015
  • 02:10 PM

Phages fight back: how anti-CRISPRs interfere with the bacterial immune system

by Betty Zou in Eat, Read, Science

Bacteriophages encode anti-CRISPR genes that block the activity of the CRISPR-Cas system. In a paper published in Nature this week, researchers show that anti-CRISPRs inhibit CRISPR-Cas activity through distinct mechanisms. ... Read more »

Bondy-Denomy, J., Garcia, B., Strum, S., Du, M., Rollins, M., Hidalgo-Reyes, Y., Wiedenheft, B., Maxwell, K., & Davidson, A. (2015) Multiple mechanisms for CRISPR–Cas inhibition by anti-CRISPR proteins. Nature. DOI: 10.1038/nature15254  

  • September 23, 2015
  • 09:39 AM

Video Tip of the Week: UCSC Xena System for functional and cancer genomics

by Mary in OpenHelix

When we go out and do workshops, we get a lot of requests from researchers who would like some guidance on cancer genomics tools. Our particular mission has been to aim more broadly at tools that are of wide interest and not to focus on a particular disease or condition area. But certainly the cancer […]... Read more »

Cline, M., Craft, B., Swatloski, T., Goldman, M., Ma, S., Haussler, D., & Zhu, J. (2013) Exploring TCGA Pan-Cancer Data at the UCSC Cancer Genomics Browser. Scientific Reports. DOI: 10.1038/srep02652  

Cheng PF, Dummer R, & Levesque MP. (2015) Data mining The Cancer Genome Atlas in the era of precision cancer medicine. Swiss Med Wkly. info:/10.4414/smw.2015.14183

  • September 23, 2015
  • 08:51 AM

“Eppur (non) si muove”: why cellular movements may not be essential to the formation of Turing patterns in biology.

by D. Bullara in the Node

D. Bullara* and Y. De Decker *   When Catarina Vicente (Community Manager of “The Node”) proposed us to write a post about our recent paper on pattern formation in zebrafish [Bullara2015] we were very glad for the opportunity she was giving us to tell the background story about our work in this blog. We[...]

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The post “Eppur (non) si muove”: why cellular movements may not be essential to the formation of Turing patterns in biology. appeared first on the Node.
... Read more »

De Decker Y, Tsekouras GA, Provata A, Erneux T, & Nicolis G. (2004) Propagating waves in one-dimensional discrete networks of coupled units. Physical review. E, Statistical, nonlinear, and soft matter physics, 69(3 Pt 2), 36203. PMID: 15089388  

Hamada, H., Watanabe, M., Lau, H., Nishida, T., Hasegawa, T., Parichy, D., & Kondo, S. (2013) Involvement of Delta/Notch signaling in zebrafish adult pigment stripe patterning. Development, 141(2), 318-324. DOI: 10.1242/dev.099804  

Nakamasu, A., Takahashi, G., Kanbe, A., & Kondo, S. (2009) Interactions between zebrafish pigment cells responsible for the generation of Turing patterns. Proceedings of the National Academy of Sciences, 106(21), 8429-8434. DOI: 10.1073/pnas.0808622106  

Turing, A. (1952) The Chemical Basis of Morphogenesis. Philosophical Transactions of the Royal Society B: Biological Sciences, 237(641), 37-72. DOI: 10.1098/rstb.1952.0012  

  • September 23, 2015
  • 08:10 AM

Twins Versus Siblings, Where’s The Line?

by Mark Lasbury in As Many Exceptions As Rules

What makes two babies twins? Do they have to look similar; be born at the same time; be conceived at the same time? Twins of different races give us idea just how genetics can play out in siblings and how complex the control of skin pigmentation, hair and eye color and hair texture can be.... Read more »

Duffy DL, Montgomery GW, Chen W, Zhao ZZ, Le L, James MR, Hayward NK, Martin NG, & Sturm RA. (2007) A three-single-nucleotide polymorphism haplotype in intron 1 of OCA2 explains most human eye-color variation. American journal of human genetics, 80(2), 241-52. PMID: 17236130  

Maroñas, O., Phillips, C., Söchtig, J., Gomez-Tato, A., Cruz, R., Alvarez-Dios, J., de Cal, M., Ruiz, Y., Fondevila, M., Carracedo, �.... (2014) Development of a forensic skin colour predictive test. Forensic Science International: Genetics, 34-44. DOI: 10.1016/j.fsigen.2014.06.017  

  • September 23, 2015
  • 07:39 AM

What about Lignin?

by ragothamanyennamalli in Getting to know Structural Bioinformatics

Biofuel prodcution involves removing Lignin from the biomass, in fact efficient removal so that Lignin and its by-products do not inhibit the enzymatic process that follows. But, what happens to the Lignin? ... Read more »

Bourzac, K. (2015) Inner Workings: Paving with plants. Proceedings of the National Academy of Sciences, 112(38), 11743-11744. DOI: 10.1073/pnas.1509010112  

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