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  • October 3, 2014
  • 04:01 PM

Sleeping Brains Understand Words

by Neuroskeptic in Neuroskeptic_Discover

Have you ever heard someone describe a task as being so easy that they ‘could do it in their sleep’? A fascinating new study from a team of French neuroscientists shows that this statement may be literally true, far more often than you’d think: Inducing Task-Relevant Responses to Speech in the Sleeping Brain Sid Kouider […]The post Sleeping Brains Understand Words appeared first on Neuroskeptic.... Read more »

Kouider S, Andrillon T, Barbosa LS, Goupil L, & Bekinschtein TA. (2014) Inducing task-relevant responses to speech in the sleeping brain. Current Biology, 24(18), 2208-14. PMID: 25220055  

  • October 3, 2014
  • 11:00 AM

How the brain encodes massive spaces

by Sick Papes in Sick Papes

Rich, P., Liaw, H., & Lee, A. (2014). Large environments reveal the statistical structure governing hippocampal representations. Science, 345 (6198), 814-817 DOI: 10.1126/science.1255635

Have you ever felt lost and alone? If so, this experience probably involved your hippocampus, a seahorse-shaped structure in the middle of the brain. About 40 years ago, scientists with electrodes discovered that some neurons in the hippocampus fire each time an animal passes through a particular location in its environment. These neurons, called place cells, are thought to function as a cognitive map that enables navigation and spatial memory.

Place cells are typically studied by recording from the hippocampus of a rodent navigating through a laboratory maze. But in the real world, rats can cover a lot of ground. For example, many rats leave their filthy sewer bunkers every night to enter the cozy bedrooms of innocent sleeping children.

In a recent paper, esteemed neuroscientist Dr. Dylan Rich and colleagues investigated how place cells encode very large spaces. Specifically, they asked: how are new place cells recruited to the network as a rat explores a truly giant maze? Today, we huddle closely with Dr. Rich to whisper about his findings.... Read more »

  • October 3, 2014
  • 10:38 AM

Pediatric respiratory tract infections and antibiotics: overprescribing?

by Aurelie in Coffee break Science

Antimicrobial resistance is a serious threat to human health. As the WHO global report published in April 2014 highlighted, it is no longer a concern for the future but happening right now, in every part of the world. It threatens … Continue reading →... Read more »

  • October 3, 2014
  • 10:02 AM

How to Say “SOS” in Catfish

by Elizabeth Preston in Inkfish

It’s good to have a plan in case of emergency. If there’s a fire, take the stairs to the ground floor. If a bird tries to eat you, say “ERK ERK ERK” by grinding your spine bone against your shoulder bone until it drops you. That latter one will work best if you’re a certain […]The post How to Say “SOS” in Catfish appeared first on Inkfish.... Read more »

  • October 3, 2014
  • 08:40 AM

The Friday Five for 10/3/2014

by Bill Sullivan in The 'Scope

The coolest science of the week, including the physics of space battles, leeches eating worms, and how to get others to do your bidding!... Read more »

O'Shea TJ, Cryan PM, Cunningham AA, Fooks AR, Hayman DT, Luis AD, Peel AJ, Plowright RK, & Wood JL. (2014) Bat flight and zoonotic viruses. Emerging infectious diseases, 20(5), 741-5. PMID: 24750692  

  • October 3, 2014
  • 05:17 AM

Routine screening of lung resections taken during surgery for pneumothorax may help identify unrecognised cases of BHD

by Lizzie Perdeaux in BHD Research Blog

In many cases, early diagnosis means treatments are more effective, cost less and save more lives. Screening programmes aid early diagnosis and can be used to screen whole populations, such as the fetal anomaly screening given to all pregnant women … Continue reading →... Read more »

  • October 3, 2014
  • 05:10 AM

S100B and schizophrenia meta-analysed

by Paul Whiteley in Questioning Answers

I don't know if it's just me but this year (2014) I seem to be covering a lot more meta-analysis papers on this blog. I assume that's because of the increasing volume of peer-reviewed research being created year-on-year leading to greater volumes of research fodder for such grand reviews. Whatever the reason(s), there are some really interesting conclusions being reached in that literature as per the meta-analysis by Aleksovska and colleagues [1] (open-access) focusing on S100B blood levels and schizophrenia."My name is Gladiator"I've talked about S100B previously on this blog in relation to autism (see here) including some of the possible whys and wherefores. Very briefly, S100B - S100 calcium binding protein B - is a protein primarily secreted by glial cells which seems to be involved in various important functions including those in relation to synaptic plasticity and the innate immune response among others. S100B levels have also been examined in relation to brain injury, although some uncertainty seems to persist about their value here [2].With schizophrenia in mind, there is a growing research base suggestive of some role for S100B in the condition (see here). Not all the evidence has universally pointed to a connection between protein and condition, bearing in mind the similar issue of heterogeneity and 'spectrums' being discussed in schizophrenia circles as they have in autism circles (albeit with caveats).The Aleksovska paper reported that based on their analysis of the combined literature (using the PRISMA guidance) "S100B in peripheral blood was significantly increased in schizophrenia patients, with an almost double level in cases than controls". Results drawn from 20 studies which survived their filtering (all case-control reports) also indicated: "no evidence of difference in subgroups regarding detection of S100B in plasma or serum, medication status, stage of the disease, ethnicity, selection of cases and controls and source of controls". Interestingly too, the authors make reference to the "the traditional reductionist assessments based on single-pathways analyses and categorical diagnoses" used in schizophrenia as not being all that useful. They call their alternative 'Systems Medicine'. I would say however that they're describing something like RDoC (see here).What's more to say on this area of schizophrenia research? Well, further investigations on the reason(s) for elevated S100B might be a good starting point including that related to glial cell activation in relation to schizophrenia [3]. But... and it is an important point, investigations also need to consider the variety of other factors which might account for elevated levels of S100B and are comorbid to psychiatric symptoms such as weight and insulin resistance [4], potentially all the more pertinent in light of the findings from van Beveren and colleagues [5] discussed in a recent post (see here).Music to close. Cue the 70's detectives... Sabotage.----------[1] Aleksovska K. et al. Systematic Review and Meta-Analysis of Circulating S100B Blood Levels in Schizophrenia. PLoS One. 2014 Sep 9;9(9):e106342.[2] Hansen-Schwartz J. & Bouchelouche PN. Use of biomarker S100B for traumatic brain damage in the emergency department may change observation strategy. Dan Med J. 2014 Sep;61(9):A4894.[3] Rothermundt M. et al. Glial cell activation in a subgroup of patients with schizophrenia indicated by increased S100B serum concentrations and elevated myo-inositol. Prog Neuropsychopharmacol Biol Psychiatry. 2007 Mar 30;31(2):361-4.[4] Steiner J. et al. Elevated S100B levels in schizophrenia are associated with insulin resistance. Mol Psychiatry. 2010 Jan;15(1):3-4.[5] van Beveren NJ. et al. Evidence for disturbed insulin and growth hormone signaling as potential risk factors in the development of schizophrenia. Transl Psychiatry. 2014 Aug 26;4:e430.----------Aleksovska K, Leoncini E, Bonassi S, Cesario A, Boccia S, & Frustaci A (2014). Systematic Review and Meta-Analysis of Circulating S100B Blood Levels in Schizophrenia. PloS one, 9 (9) PMID: 25202915... Read more »

  • October 2, 2014
  • 05:04 PM

The Mysterious Origins of HIV Discovered

by Gabriel in Lunatic Laboratories

There have been a lot of theories on where HIV came from, anywhere from the mundane, it spread from other animals. To the down right crazy, the government created it to wipe out homosexuals. Well bad news for conspiracy theorists, a new study suggests that the HIV pandemic with us today is almost certain to have begun its global spread from Kinshasa, the capital of the Democratic Republic of the Congo (DRC).... Read more »

Nuno R. Faria1, Andrew Rambaut, Marc A. Suchard, Guy Baele, Trevor Bedford, Melissa J. Ward, Andrew J. Tatem, João D. Sousa, Nimalan Arinaminpathy, Jacques Pépin,.... (2014) The early spread and epidemic ignition of HIV-1 in human populations. Science. info:/10.1126/science.1256739

  • October 2, 2014
  • 02:01 PM

Survivin: You wouldn’t be alive without it

by Clay Clark in Biochem Blogs

  Enzymes perform numerous tasks in order to contribute to the global goal of organism survival. One such enzyme is Survivin. Survivin wears many “hats” within the cell and is a vital part of cellular homeostasis. Here I will introduce you to two of the main processes Survivin regulates. Survivin is a multifunctional protein involved […]... Read more »

  • October 2, 2014
  • 08:03 AM

Coeliac disease risk not affected by early feeding practices

by Paul Whiteley in Questioning Answers

I'd like to bring three papers to your attention, all united by their discussion of coeliac (celiac) disease, that most classic of autoimmune conditions in the most part managed by the use of a lifelong gluten-free diet.First up are the papers by Elena Lionetti and colleagues [1] and Sabine Vriezinga and colleagues [2] which unfortunately pour cold water on the notion that the risk of developing coeliac disease (CD) can be somehow mitigated via the use of either the early or delayed introduction of gluten nor seemingly affected by breastfeeding habits. Indeed, as science has known about for sometime, genes and specifically the HLA genotype linked to CD, seem to be the important predictors of disease outside of gluten consumption itself.Both the Lionetti and Vriezinga papers were published in the New England Journal of Medicine and were accompanied by an editorial by Jonas Ludviggson among others (he of the 'not CD but something else potentially linking gluten and some autism'). Both studies were based on randomised controlled trials.The Lionetti study involved either the introduction of gluten at 6 or 12 months to at-risk infants (those with a first-degree relative with CD) and then examining: "the prevalence of celiac disease autoimmunity and of overt celiac disease among the children at 5 years of age". The numbers of participants involved featured in the hundreds so this was by no means an under-powered trial. The authors concluded that: "Neither the delayed introduction of gluten nor breast-feeding modified the risk of celiac disease among at-risk infants, although the later introduction of gluten was associated with a delayed onset of disease".The Vriezinga study looked at whether introducing gluten early (between 4-6 months) might also offset the risk of CD. Again based on a pretty impressive participant number (N=944) comprising children with a first-degree relative with CD as well as being "positive for HLA-DQ2 or HLA-DQ8", participants were randomly assigned to either "100 mg of immunologically active gluten daily" or a placebo. Again, biopsy confirmed CD and some of the various serology associated with CD were the outcomes. The authors concluded: "As compared with placebo, the introduction of small quantities of gluten at 16 to 24 weeks of age did not reduce the risk of celiac disease by 3 years of age in this group of high-risk children".The final paper to discuss today is that published by Elfström and colleagues [3] (open-access here) and the findings of their systematic review and meta-analysis looking at "associations between coeliac disease and type 1 diabetes". Type 1 diabetes, distinct from type 2 diabetes, is an autoimmune condition whereby the insulin producing cells of the body have been destroyed. The Elfström paper coincidentally carrying Dr Ludviggson as a co-author, concluded that: "More than one in twenty patients with type 1 diabetes have biopsy-verified coeliac disease" and onwards that there may be some substance to the idea that birds of an autoimmune feather flock together (see here). Indeed, I've previously covered the possibility of a connection between Type 1 diabetes and CD (see here) and how, for example, some of the research on [General] zonulin might be potentially very informative to this area (see here).There's little more for me to say in this post aside from reiterating that when it comes to CD, genotype combined with gluten exposure seems to be the most important factors in disease onset and progression. That's not to say that a gluten-free diet might be the only tool in the management arsenal (see here) nor that other variables might not potentially impact on CD risk (see here) but for now, screening and where indicated, gluten avoidance, seem to be the primary measures to be undertaken.----------[1] Lionetti E. et al. Introduction of Gluten, HLA Status, and the Risk of Celiac Disease in Children. N Engl J Med. 2014 Oct 2;371(14):1295-1303.[2] Vriezinga SL. et al. Randomized Feeding Intervention in Infants at High Risk for Celiac Disease. N Engl J Med. 2014 Oct 2;371(14):1304-1315.[3] Elfström P. et al. Systematic review with meta-analysis: associations between coeliac disease and type 1 diabetes. Aliment Pharmacol Ther. 2014 Oct 1. doi: 10.1111/apt.12973.----------Lionetti E, Castellaneta S, Francavilla R, Pulvirenti A, Tonutti E, Amarri S, Barbato M, Barbera C, Barera G, Bellantoni A, Castellano E, Guariso G, Limongelli MG, Pellegrino S, Polloni C, Ughi C, Zuin G, Fasano A, Catassi C, & the SIGENP (Italian Society of Pediatric Gastroenterology, Hepatology, and Nutrition) Working Group on Weaning and CD Risk (2014). Introduction of Gluten, HLA Status, and the Risk of Celiac Disease in Children. The New England journal of medicine, 371 (14), 1295-1303 PMID: 25271602Vriezinga SL, Auricchio R, Bra... Read more »

Lionetti E, Castellaneta S, Francavilla R, Pulvirenti A, Tonutti E, Amarri S, Barbato M, Barbera C, Barera G, Bellantoni A.... (2014) Introduction of Gluten, HLA Status, and the Risk of Celiac Disease in Children. The New England journal of medicine, 371(14), 1295-1303. PMID: 25271602  

Vriezinga SL, Auricchio R, Bravi E, Castillejo G, Chmielewska A, Crespo Escobar P, Kolaček S, Koletzko S, Korponay-Szabo IR, Mummert E.... (2014) Randomized Feeding Intervention in Infants at High Risk for Celiac Disease. The New England journal of medicine, 371(14), 1304-1315. PMID: 25271603  

  • October 2, 2014
  • 06:37 AM

What do sperm have to do with brain tumors?

by pknoepfler in the Node

  This post was originally published in the Knoepfler Lab Stem Cell Blog.      Sometimes in science there are unexpected threads tying seemingly very different things together. Unraveling the knots in these threads can lead to new insights into important developmental processes and mechanisms of disease. My lab studies epigenomic and transcription factors including […]... Read more »

Yuen, B., Bush, K., Barrilleaux, B., Cotterman, R., & Knoepfler, P. (2014) Histone H3.3 regulates dynamic chromatin states during spermatogenesis. Development, 141(18), 3483-3494. DOI: 10.1242/dev.106450  

  • October 2, 2014
  • 06:00 AM

6 Tooth Found in Fossil Leg Bone Is ‘First Evidence’ of Clash Between Ancient Apex Predators

by Blake de Pastino in Western Digs

A tooth found embedded in a fossil leg bone is evidence of an unlikely battle between two top predators in the American Southwest some 220 million years ago — one of them hunted on land, the other lived in the water.... Read more »

  • October 2, 2014
  • 04:57 AM

Volatile organic compounds and autism

by Paul Whiteley in Questioning Answers

As harsh as the phrase volatile organic compounds (VOCs) might appear at first glance, all this refers to is a class of compounds containing carbon which have a tendency to evaporate at room temperature assuming normal air pressure. VOCs have been associated with pollutants as per their inclusion in various literature on the topic of things like indoor air pollution (see here) and the fact that just about everything around us in the modern home or office is likely to release VOCs. Whilst not trying to belittle the potential effects of some of those VOCs (see here) it is important to note however that living things also produce and release VOCs [1] as by-product of metabolism too.The reason for the chatter about VOCs in today's post relates to a paper by Rosaria Cozzolino and colleagues [2] and their preliminary advances into investigating whether VOCs might have some potential as biomarkers for the autism spectrum disorders (ASDs). In amongst the authorship list on the Cozzolino paper I also note a familiar name - Laura de Magistris - who some people might recognise as being the lead on some of that very interesting leaky gut work (see here).A few details from the paper first:Regular readers on this blog might already know that I like talking about analytical chemistry, particularly when applied to autism or other potentially related conditions. In the case of the Cozzolino paper it was all about preparing urine samples from 24 children with autism and 21 asymptomatic controls via something called solid-phase extraction, sorry, solid-phase microextraction (SPME) and then applying the solute to analysis via gas chromatography - mass spectrometry (GC-MS) "to obtain metabolomic information patterns". Metabolomics by the way, is basically the collected analysis of small molecules (metabolites) in one or more biofluids.Following some discriminant function analysis (DFA) of results from both groups prepared under both acid and alkaline conditions, authors presented quite a bit of data on what compounds, VOCs, might have some discriminatory function between the autism (A) group and the control (C) group. So: "Among these [compounds], 3-methyl-cyclopentanone, 3-methyl-butanal, 2-methyl-butanal, and hexane under acid conditions, and 2-methyl-pyrazine, 2,3-dimethyl-pyrazine, and isoxazolo under alkaline pH had statistically higher levels in urine samples from autistic children than from the control group".Authors suggested quite a bit more analysis might be needed to look at the "metabolic origins of these variables" and "verify the usefulness... for early-stage [autism] diagnosis".I know, I know. Mention of the word 'biomarker(s)' when it comes to such a heterogeneous and possibly plural condition like 'the autisms' is still something rather problematic as things currently stand. I'm not saying that there may not be specific types of autism (endophenotypes) which might be amenable to certain biomarkers such as VOCs, but I don't quite think we are there yet in determining the hows and whys. And then there are the very small participant numbers reported on by Cozzolino et al...But this is not the first times that VOCs have turned up in autism research. The paper by De Angelis and colleagues [3] (open-access) talked about levels of VOCs detected in poop samples being "markedly affected in PDD-NOS [Pervasive Developmental Disorder Not Otherwise Specified ] and, especially, AD [autism] children". Stool analysis and the gut microbiome, as regular readers of this blog might know, is of increasing interest to autism research.Keeping in mind discussions on VOCs in relation to [some?] autism, I'll also introduce the paper by Kalkbrenner and colleagues [4] which, following a review of the some of the literature on environmental chemical (yes, that word again) exposures and autism, suggested that there may be more to see when it comes to specific environmental factors. So: "some environmental exposures showed associations with autism, especially traffic-related air pollutants, some metals, and several pesticides, with suggestive trends for some volatile organic compounds (e.g., methylene chloride, trichloroethylene, and styrene) and phthalates". This on the back of previous research from this author on this topic [5].Accepting that VOCs cover a whole slew of different compounds and that not every VOC has been analysed with an autism link (or not) in mind, the various papers hint that we should be a little more wary of this class of compounds and perhaps a little more inquisitive when it comes to a condition like autism.----------[1] Shirasu M. & Touhara K. The scent of disease: volatile organic compounds of the human body related to disease and disorder. J Biochem. 2011 Sep;150(3):257-66.[2] Cozzolino R. et al. Use of solid-phase microextraction coupled to gas chromatography–mass spectrometry for determination of urinary volatile organic compounds in autistic children compared with healthy controls. Analytical & Bioanalytical Chemistry. 2014. 10.1007/s00216-014-7855-z[3] De Angelis M. et al. Fecal microbiota and metabolome of children with autism and pervasive developmental disorder not otherwise specified. PLoS One. 2013 Oct 9;8(10):e76993.[4] Kalkbrenner AE. et al. Environmental Chemical Exposures and Autism Spectrum Disorders: A Review of the Epidemiological Evidence. Curr Probl Pediatr Adolesc Health Care. 2014 Sep 4. pii: S1538-5442(14)00074-1.[5] Kalkbrenner AE. et al. Perinatal exposure to hazardous air pollutants and autism spectrum disorders at age 8. Epidemiology. 2010 Sep;21(5):631-41.----------Cozzolino R, De Magistris L, Saggese P, Stocchero M, Martignetti A, Di Stasio M, Malorni A, Marotta R, Boscaino F, & Malorni L (2014). Use of soli... Read more »

  • October 1, 2014
  • 02:23 PM

MERS-CoV: update 2.0

by thelonevirologist in Virology Tidbits

Five different fragments of MERS-CoV S1 receptor binding domain were tested for their receptor affinity and an ability to induce the formation of neutralizing antibodies. Results suggest that the induction of high antibody titers is dependent on the absence of extended N- and C-terminal ends. ... Read more »

Wang N, Shi X, Jiang L, Zhang S, Wang D, Tong P, Guo D, Fu L, Cui Y, Liu X.... (2013) Structure of MERS-CoV spike receptor-binding domain complexed with human receptor DPP4. Cell research, 23(8), 986-93. PMID: 23835475  

  • October 1, 2014
  • 01:41 PM

The Ever Plastic Brain and Intellectual Disabilities

by Gabriel in Lunatic Laboratories

The plasticity of the brain is always somewhat of a shock. It's near incredible what the brain can achieve, look at people who have strokes, or any other sort of brain injury and yet still somehow manage to get up and move, or perform tasks. So I guess it should be no surprise, but still amazing that studying mice with a genetic change similar to what is found in Kabuki syndrome (an inherited disease of humans) researchers report they have used an anticancer drug to improve mental function.... Read more »

Hans T. Bjornsson, Joel S. Benjamin, Li Zhang, Jacqueline Weissman, Elizabeth E. Gerber, Yi-Chun Chen, Rebecca G. Vaurio, Michelle C. Potter, Kasper D. Hansen, & Harry C. Dietz. (2014) Histone deacetylase inhibition rescues structural and functional brain deficits in a mouse model of Kabuki syndrome. Science Translational Medicine. info:/10.1126/scitranslmed.3009278

  • October 1, 2014
  • 09:46 AM

Video Tip of the Week: MEGA, Molecular Evolutionary Genetics Analysis

by Mary in OpenHelix

This week’s tip of the week highlights the MEGA tools–MEGA is a collection of tools that perform Molecular Evolutionary Genetics Analysis. MEGA tools are not new–they’ve been developed and supported over many years. In fact, on their landing page you can see the first reference to MEGA was in 1994. How much computing were you […]... Read more »

  • October 1, 2014
  • 09:00 AM

What Is Love, Anyway?

by Bill Sullivan in The 'Scope

Inspired by the recent discovery of a couple still holding hands after 700 years, this article ponders the question, "What Is Love, Anyway?"... Read more »

Love TM. (2014) Oxytocin, motivation and the role of dopamine. Pharmacology, biochemistry, and behavior, 49-60. PMID: 23850525  

Domingue, B., Fletcher, J., Conley, D., & Boardman, J. (2014) Genetic and educational assortative mating among US adults. Proceedings of the National Academy of Sciences, 111(22), 7996-8000. DOI: 10.1073/pnas.1321426111  

  • October 1, 2014
  • 08:00 AM

One Thing Is Just Like The Other – Sort Of

by Mark Lasbury in As Many Exceptions As Rules

Recent studies have illustrated how complicated evolution by descent with adaptation can be. Convergent evolution and parallel evolution explain the fingerprints of koalas and the marsupial and placental saber-toothed cats. Dollo’s Law of Irreversibility has been shown to be plastic, as frogs have re-evolved mandibular teeth and stick insects have lost and regained wings several times. ... Read more »

Lahti, D. C., N. A. Johnson, et al. (2009) Relaxed selection in the wild. . Trends in Ecology and Evolution, , 24(9), 487-496. info:/

Stone G, & French V. (2003) Evolution: have wings come, gone and come again?. Current biology : CB, 13(11). PMID: 12781152  

  • October 1, 2014
  • 05:11 AM

Maternal complement C1q and offspring psychosis

by Paul Whiteley in Questioning Answers

"In conclusion, exposure to maternal C1q activity during pregnancy may be a risk factor for the development of schizophrenia and psychosis in offspring". That was the primary observation made by Emily Severance and colleagues [1] at Johns Hopkins, extending their scientific interest in immune system involvement being potentially linked to psychiatry [2]."Serve the public trust, protect the innocent, uphold the law"I've already talked about Dr Severance's previous research forays into complement factor C1q and psychiatry on this blog (see here) and how C1q seropositivity was pretty significantly associated with both recent and non-recent onset schizophrenia in their cohort. Said complexing of C1q also turning up food components (gluten and casein) as potentially being involved [3] which has rumbles of Dohan's hypothesis [4] mixed in.The most recent Severance paper takes things another stage further by trying to "determine if maternal C1q was associated with offspring schizophrenia and psychosis". Archived serum samples provided during pregnancy were therefore analysed for 55 "matched case-control" pairs of mothers - mothers with offspring who went on to develop psychoses as adults and those with offspring who were asymptomatic from such psychiatric issues. "IgG markers of C1q, bovine milk casein, egg ovalbumin, and wheat gluten were measured". Authors reported that: "C1q was significantly elevated in case mothers" and in that case group, where offspring developed psychoses: "C1q was significantly correlated with antibodies to both food and infectious antigens: gluten..., herpes simplex virus type 2..., and adenovirus".Accepting that the total number of participants included in this latest trial was relatively small, also relying on archived samples collected as part of the US Collaborative Perinatal Project (CPP) [5], these are interesting results. That both food and infectious agent antigens seemed to correlate with C1q adds to other interesting work by Dr Severance and colleagues on, for example, the protozoan Toxoplasma gondii potentially joining forces with food antigens (see here) in some fashion. I don't know enough about the processes potentially involved in any relationship to provide any definitive answers as to the hows and whys but one hazards a guess that something like an effect on gastrointestinal barrier function might play some role [6]. This and other research from people such as the late Paul Patterson [7] continue to drive home the notion that maternal infection, or rather the immune processes and consequence of infection during pregnancy, seem to be able to influence later life outcomes for offspring. We still need to know more about the specific biological processes involved in any relationship including the rising scientific star that is epigenetics [8] (something covered in a recent blog post) and also how subsequent life events (whether biological, social or psychological) contribute to any psychiatric diagnosis. Whether for certain people or groups of people, there may be some merit at looking further at gastrointestinal (GI) functions (see here) or even dietary changes (see here) is perhaps something else worth investing a little more research time and effort into too...Ben Folds Five to close...----------[1] Severance EG. et al. Maternal complement C1q and increased odds for psychosis in adult offspring. Schizophrenia Res. 2014. 4 September.[2] Severance EG. et al. Autoimmune diseases, gastrointestinal disorders and the microbiome in schizophrenia: more than a gut feeling. Schizophr Res. 2014 Jul 14. pii: S0920-9964(14)00319-3.[3] Severance EG. et al. Complement C1q formation of immune complexes with milk caseins and wheat glutens in schizophrenia. Neurobiol Dis. 2012 Dec;48(3):447-53.[4] Dohan FC. Genetic hypothesis of idiopathic schizophrenia: its exorphin connection. Schizophr Bull. 1988;14(4):489-94.[5] Klebanoff MA. The Collaborative Perinatal Project: a 50-year retrospective. Paediatr Perinat Epidemiol. 2009 Jan;23(1):2-8.[6] Nouri M. et al. Intestinal barrier dysfunction develops at the onset of experimental autoimmune encephalomyelitis, and can be induced by adoptive transfer of auto-reactive T cells. PLoS One. 2014 Sep 3;9(9):e106335.[7] Brown AS. & Patterson PH. Maternal infection and schizophrenia: implications for prevention. Schizophr Bull. 2011 Mar;37(2):284-90.[8] Tang B. et al. Epigenetic changes at gene promoters in response to immune activation in utero. Brain Behav Immun. 2013 May;30:168-75.----------Emily G. Severance, Kristin L. Gressitt, Stephen L. Buka, Tyrone D. Cannon, & Robert H. Yolken (2014). Maternal complement C1q and increased odds for psychosis in adult offspring Schizophrenia Research : 10.1016/j.schres.2014.07.053... Read more »

Emily G. Severance, Kristin L. Gressitt, Stephen L. Buka, Tyrone D. Cannon, & Robert H. Yolken. (2014) Maternal complement C1q and increased odds for psychosis in adult offspring. Schizophrenia Research. info:/10.1016/j.schres.2014.07.053

  • September 30, 2014
  • 07:10 PM

A Warm Winter Legacy: Leaf Flushing and Senescence Long-Term

by Melissa Chernick in Science Storiented

Fall is in the air. Here in North Carolina that means drastic temperature swings that cause me to dress incorrectly on any given day. It also means the arrival of fall colors. Indeed, fall colors are incredibly beautiful, but biologically speaking, you are watching death happen. This autumn splendor got me to thinking about these colors a little closer, specifically the phenology of trees.Phenology is the study of the annual timing of recurring life cycle events. The timing of these events is typically influenced by seasonal environmental changes. In the case of trees, specifically hardwood forests, this is the leafing-out (flushing) and dropping-off (senescence) of leaves. But what actually triggers a plant to leaf-out? This can vary a bit by species or even individual, but there are a couple of general categories you can look to. The first is changes in air temperature, the chilling in the winter and warming in the spring. The other is photoperiod, or the day length, which often interacts with temperature, allowing plants to quickly respond to changing conditions.Considering that these events are triggered by environmental changes, it is logical to assume that global climate change can force changes in the phenology of many species and communities. This is another think-about-the-plants moment. How plants respond to climate change has huge consequences for world ecosystems – growing seasons, species ranges, carbon and water cycling, interactions with animals, etc. A paper published earlier this year in PNAS took a look at variations in leaf flushing and senescence dates in relation to warming. Many phonological studies focus on specific phenophases (like leaf-out in the spring), but this study is unique in that it looks at subsequent phenological events. The authors aimed to see if effects of warming lasted longer than the current growing season. To do this, in December 2009 they took seventy 3-4 year old cloned oak and beech trees and put them in growth chambers where they could very carefully control the winter environmental conditions. They manipulated the temperatures of the growth chambers to create treatment groups of winter-spring warming, winter-only warming, and spring-only warming. Then, in spring of 2010 when the flushing was complete, they moved the trees out of the chambers and into a field. The trees stayed outside and were measured until the following spring of 2011. Leaf-out rates were determined using a scale that went from undeveloped bud to unfolded leaf, and leaf senescence was recorded as the date at which half of the leaves were colored or dropped. These measurements allowed for a quantification of growing season length. Additional measurements of numbers of leaf per tree, specific leaf area, total leaf area per tree, number of buds, dry weights of various parts of the trees, carbohydrate content, and carbon and nitrogen content were taken. They also combined their data with that of the European phenology network to get both a larger sample size and a wider geographic area.The researchers found both leaf flushing and senescence in both species to be advanced 15-18 days by winter-spring warming. In the long-term, the timing of autumn leaf senescence was found to be positively correlated with spring leaf flushing dates, and advanced leaf flushing lead to earlier leaf flushing the following year. This suggests that the physiological impacts of a warmer winter last longer than just one growing season. Advanced leaf flushing in this winter-spring-warming treatment was also associated with some physiological and morphological changes, particularly in the oaks. These included higher leaf number, higher leaf area per tree, and higher starch accumulation.The trends of the experiment were also observed in the mature trees in the long-term field-based phenology observations of the European phenology network. The underlying cause in both cases is likely that the plants never really fulfill the winter chilling requirements necessary for them to enter dormancy. Currently, the most widely accepted mechanism for leaf senescence is the environmental control hypothesis, which proposes that leaf senescence is triggered with the unfavorable autumn season comes (changes in photoperiod, temperature, or both). This study shows that perhaps that isn’t all that’s going on.*sigh* nothing is ever simple is it?Fu, Y., Campioli, M., Vitasse, Y., De Boeck, H., Van den Berge, J., AbdElgawad, H., Asard, H., Piao, S., Deckmyn, G., & Janssens, I. (2014). Variation in leaf flushing date influences autumnal senescence and next year's flushing date in two temperate tree species Proceedings of the National Academy of Sciences, 111 (20), 7355-7360 DOI: 10.1073/pnas.1321727111For lots of really great info on the science of leaf-out, I recommend this review article:Polgar, C., & Primack, R. (2011). Leaf-out phenology of temperate woody plants: from trees to ecosystems New Phytologist, 191 (4), 926-941 DOI: 10.1111/j.1469-8137.2011.03803.x... Read more »

Fu, Y., Campioli, M., Vitasse, Y., De Boeck, H., Van den Berge, J., AbdElgawad, H., Asard, H., Piao, S., Deckmyn, G., & Janssens, I. (2014) Variation in leaf flushing date influences autumnal senescence and next year's flushing date in two temperate tree species. Proceedings of the National Academy of Sciences, 111(20), 7355-7360. DOI: 10.1073/pnas.1321727111  

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