In 348/7 BC, fearing anti-Macedonian sentiment or disappointed with the control of Plato’s Academy passing to Speusippus, Aristotle left Athens for Asian Minor across the Aegean sea. Based on his five years — before returning to Macedonia to tutor Alexander the Great — studying of the natural history of Lesbos, he wrote the pioneering work […]... Read more »
Recently, scientists discovered a new learning rule for a specific type of excitatory synaptic connection in the hippocampus. These synapses are located in the so-called CA3 region of the hippocampus, which plays a critical role for storage and recall of spatial information in the brain. One of its hallmark properties is that memory recall can even be triggered by incomplete cues. This enables the network to complete neuronal activity patterns, a phenomenon termed pattern completion.
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Mishra, R., Kim, S., Guzman, S., & Jonas, P. (2016) Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative networks. Nature Communications, 11552. DOI: 10.1038/ncomms11552
"Dance like nobody's watching" is fine advice, unless somebody is watching, and she needs to translate your dance steps into instructions to find food. That's the case for honeybees. But even though the rest of the colony must interpret their dance moves carefully, it turns out honeybees are pretty sloppy dancers.
When honeybees return to the hive after finding nectar or other food, they famously do a "waggle dance" to tell their sisters where the food was. The waggle is a shimmying run t... Read more »
Schürch R, Ratnieks FL, Samuelson EE, & Couvillon MJ. (2016) Dancing to her own beat: honey bee foragers communicate via individually calibrated waggle dances. The Journal of experimental biology. PMID: 26944504
by Casper van der Kooi in genome ecology evolution etc
Many male and female-specific traits share a common genetic basis. Selection on these traits may, however, differ between the sexes, leading to sexual conflict. Sex-dependent dominance, where the dominant allele in one sex is recessive in the other, is expected … Continue reading →... Read more »
Barson, N., Aykanat, T., Hindar, K., Baranski, M., Bolstad, G., Fiske, P., Jacq, C., Jensen, A., Johnston, S., Karlsson, S.... (2015) Sex-dependent dominance at a single locus maintains variation in age at maturity in salmon. Nature, 528(7582), 405-408. DOI: 10.1038/nature16062
Two papers provide some brief discussion today. The first by Janice Goldschmidt  titled: 'What Happened to Paul? Manifestation of Abnormal Pain Response for Individuals With Autism Spectrum Disorder' provides an account of a young man with autism who during a "pilot nutrition intervention designed to teach cooking skills to young adults with autism spectrum disorder (ASD)" fell quite seriously. We are told that: "After his accident, which resulted in broken and dislocated bones in his ankle, his demeanor was dramatically altered, program gains were lost, and staff noted the appearance of many new challenging behaviors."The second paper by Andrea Courtemanche and colleagues  continues a theme looking to "measure expressions of pain among young children being evaluated for autism and other neurodevelopmental disabilities." Authors concluded that their results among other things "support that individuals with self-injury may have enhanced expressions of pain."The commonality in these papers, aside from looking at pain, is the idea that autism might 'lead' to a "blunted pain response" is not necessarily one that fits uniformly across the autism spectrum. To quote: "The consequence is not a reduction in pain sensation, but a different expression of pain, determined by that individual's particular communicative, cognitive, or physiological challenges." Of course science already knows much of what is being said here as I've covered topics such as the fact that yes, people on the autism spectrum do get headaches (see here) and how pain may be quite a significant predictor of things like sleeping problems in relation to autism (see here). I might add that some of the source of that pain could also be linked to some of the over-represented comorbidity that can/does follow a diagnosis of autism (see here) (and hence should be perfectly treatable).The discussions about self-injury being potentially linked to the expression of pain also ties into related topics covered on this blog insofar as such 'challenging behaviours' normally having some reasoning behind them (see here). Self-injurious behaviour (SIB) can often be a harrowing thing to see (no parent or sibling wants to see a loved one hurting themselves) but with the right investigative approach can sometimes provide important information about a person and their wants and wishes (see here). I don't say that to somehow encourage SIB nor to lessen the impact that biology can have on its expression; merely that some other person perspective-taking should accompany analysis of any behaviours that challenge as and when they present (before reaching for the anti-challenging behaviour meds) as well as making moves towards breaking down things like communication barriers (see here) that potentially contribute to such behavioural manifestations.Pain is very much part of the human experience. Whilst efforts should indeed continue to ensure that everyone lives a life as pain-free as possible, the importance of short-term pain or rather the importance of short-term pain expression should not be under-estimated. Likewise, sweeping generalisations about altered pain sensitivity applying across the autism spectrum need not necessarily apply. I'm also happy to report that pain is a topic being discussed at IMFAR today...---------- Goldschmidt J. What Happened to Paul? Manifestation of Abnormal Pain Response for Individuals With Autism Spectrum Disorder. Qual Health Res. 2016 Apr 26. pii: 1049732316644415. Courtemanche AB. et al. The Relationship Between Pain, Self-Injury, and Other Problem Behaviors in Young Children With Autism and Other Developmental Disabilities. Am J Intellect Dev Disabil. 2016 May;121(3):194-203.----------Goldschmidt J (2016). What Happened to Paul? Manifestation of Abnormal Pain Response for Individuals With Autism Spectrum Disorder. Qualitative health research PMID: 27117957Courtemanche AB, Black WR, & Reese RM (2016). The Relationship Between Pain, Self-Injury, and Other Problem Behaviors in Young Children With Autism and Other Developmental Disabilities. American journal on intellectual and developmental disabilities, 121 (3), 194-203 PMID: 27119211... Read more »
Goldschmidt J. (2016) What Happened to Paul? Manifestation of Abnormal Pain Response for Individuals With Autism Spectrum Disorder. Qualitative health research. PMID: 27117957
Courtemanche AB, Black WR, & Reese RM. (2016) The Relationship Between Pain, Self-Injury, and Other Problem Behaviors in Young Children With Autism and Other Developmental Disabilities. American journal on intellectual and developmental disabilities, 121(3), 194-203. PMID: 27119211
The air in a cinema contains a chemical cocktail emitted by the audience - and the emotional tone of the movie influences the molecular composition of the cloud.
That's according to a striking set of results from researchers Johnathan Williams and colleagues who took air samples from two 230-seater screens of a cinema in Germany over a period of two weeks.
Here's an example of the chemical trace associated with shows of the movie "The Hunger Games 2: Catching Fire", featuring three... Read more »
Williams J, Stönner C, Wicker J, Krauter N, Derstroff B, Bourtsoukidis E, Klüpfel T, & Kramer S. (2016) Cinema audiences reproducibly vary the chemical composition of air during films, by broadcasting scene specific emissions on breath. Scientific reports, 25464. PMID: 27160439
Emerge into Brazil’s swamp, with Chiara and the Wildlife Conservation Society.... Read more »
Rodrigo Luiz Simas de Aguiar, & Keny Marques Lima. (2012) A arte rupestre em cavernas da região noroeste de Mato Grosso do Sul discussões preliminares. Espeleo-Tema, 23(2). info:/
Small animals in a big forest
Recognizing different species is crucial for all zoological studies. The study of many animal groups went through different periods with new data changing established beliefs about the number and distribution of known species. Recently, one more piece of story has been added to the history of tardigrade genus Milnesium, a new species living in the tree canopy.
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YOUNG, A., CHAPPELL, B., MILLER, W., & LOWMAN, M. (2016) Tardigrades of the Tree Canopy: Milnesium swansoni sp. nov. (Eutardigrada: Apochela: Milnesiidae) a new species from Kansas, U.S.A. Zootaxa, 4072(5), 559. DOI: 10.11646/zootaxa.4072.5.3
I note the paper by Kara Gross Margolis and colleagues  (open-access available here) has been garnering a few media headlines with the suggestion that: "Gastrointestinal [GI] problems in autistic children may be linked to the same genetic mutations that cause other characteristics of autism spectrum disorder."The study, focusing on the idea that SERT (the serotonin transporter) encoded by the SLC6A4 gene might show some connection to 'some' autism , looked to model gastrointestinal (GI) development in a mouse model where SERT function were affected - SERT variant (Ala56). They compared results on various parameters with "those obtained in mice either lacking SERT or treated from gestation to weaning with the selective 5-HT reuptake inhibitor fluoxetine" and wild-type (WT) mice. I should point out that these results were expected to be published around about now and Dr Margolis, a paediatric gastroenterologist, seems to have quite a bit of interest in this whole area.Results: bearing in mind this was a study of mice, and included only quite a small number of mice, some interesting results are presented: "The ENS [enteric nervous system] was strikingly hypoplastic in SERT Ala56 mice." This 'under-development' of the 'thinking part' of the gut manifested as less neurons being found in various regions of the gut (yes, your gut does house neurons) compared to the other models looked at. The authors suggest that their findings are "consistent with the ideas that defective 5-HT signaling due to the increased 5-HT clearance of SERT Ala56 mice interferes with enteric neurogenesis." 5-HT by the way, is another name for serotonin. Further: "The data are also consistent with the hypothesis that a defect common to the ENS and CNS [central nervous system] could be responsible in ASD [autism spectrum disorder] for comorbid GI disturbances."They also reported that gut motility - "GI transit time and colonic transit" - was also affected in the SERT Ala56 mice where "slow GI transit [and] diminished peristaltic reflex activity" were more readily present compared to other models. The press release accompanying the study quotes the authors on these points: "Basically, the gut goes slower and the mice were constipated, which is a common complaint in kids with autism." Indeed it is (see here).And then to quite an interesting piece of information: "The SERT Ala56 mutation decreases crypt epithelial cell proliferation, stunts growth of villi, and decreases mucosal permeability." Decreases mucosal permeability eh? If I'm reading is right (and I'm not expert in this area), all that talk about increased gut permeability (intestinal hyperpermeability) and [some] autism (see here) might have something of a counter-balance under certain circumstances and serotonin (5-HT) might play something of a role...Finally: "Administration of a 5-HT4 agonist [prucalopride] to Ala56 mice during development prevented Ala56-associated GI perturbations, suggesting that excessive SERT activity leads to inadequate 5-HT4-mediated neurogenesis." The authors caution that although the drug seemed to affect GI issues in the Ala56 mice, this does not necessarily mean that it will do the same in humans carrying the same genetic issue.Despite the methodological issues associated with this type of study, there are quite a few avenues of further research indicated. Not least is the requirement to identify those people carrying the gain-of-function SERT Ala56 mutation and compare and contrast with other non-carriers in terms of things like gastrointestinal (GI) functions as well as perhaps on other behavioural parameters. This set in the context of functional bowel issues already being suggested to impact on behaviour (see here). The associated idea that offspring of those mice who were treated with the antidepressant fluoxetine during pregnancy might show a distinct pattern of GI issues is also worthy of further study without any big headlines. Accepting that such medication use and risk of offspring autism is still a bit of a scientific hot potato (see here), it looks like a little more science in this area could be indicated.Music to close, and when following Sunderland Association Football Club, this piece seems particularly apt... (blood pressure starting to return to normal).---------- Margolis KG. et al. Serotonin transporter variant drives preventable gastrointestinal abnormalities in development and function. J Clin Invest. 2016 Apr 25. pii: 84877. Muller CL. et al. The serotonin system in autism spectrum disorder: From biomarker to animal models. Neuroscience. 2016 May 3;321:24-41.----------Margolis KG, Li Z, Stevanovic K, Saurman V, Israelyan N, Anderson GM, Snyder I, Veenstra-VanderWeele J, Blakely RD, & Gershon MD (2016). Serotonin transporter variant drives preventable gastrointestinal abnormalities in development and function. The Journal of clinical investigation PMID: 27111230... Read more »
Margolis KG, Li Z, Stevanovic K, Saurman V, Israelyan N, Anderson GM, Snyder I, Veenstra-VanderWeele J, Blakely RD, & Gershon MD. (2016) Serotonin transporter variant drives preventable gastrointestinal abnormalities in development and function. The Journal of clinical investigation. PMID: 27111230
During the current outbreak of ZIKV in Brazil, ZIKV RNA was detected in amniotic fluid samples of women infected with ZIKV during pregnancy and ZIKV RNA has also been isolated from tissue (brain and CNS) of neonates born with microcephaly, suggesting that ZIKV infection of the mother might be a contributive factor in the observed increase of microcephaly cases in neonates. In addition to microcephaly, miscarriages have also been reported in ZIKV positive pregnant women, especially during the first trimester of pregnancy. Foetal deaths have been observed in women who were infected with ZIKV during the second and third trimester in addition to neonate death within 20 hrs following birth.
Here the contribution of TLR-3 mediated signalling in the induction of ZIKV induced apoptosis as well as the potential role of changes in the expression of genes in brain organoids compared to neuronal stem cells is discussed.... Read more »
Slavov SN, Otaguiri KK, Kashima S, & Covas DT. (2016) Overview of Zika virus (ZIKV) infection in regards to the Brazilian epidemic. Brazilian journal of medical and biological research , 49(5). PMID: 27143174
Ribeiro GS, & Kitron U. (2016) Zika virus pandemic: a human and public health crisis. Revista da Sociedade Brasileira de Medicina Tropical, 49(1), 1-3. PMID: 27163559
Noronha L, Zanluca C, Azevedo ML, Luz KG, & Santos CN. (2016) Zika virus damages the human placental barrier and presents marked fetal neurotropism. Memorias do Instituto Oswaldo Cruz. PMID: 27143490
Carod-Artal FJ. (2016) Epidemiology and neurological complications of infection by the Zika virus: a new emerging neurotropic virus. Revista de neurologia, 62(7), 317-328. PMID: 26988170
De Carvalho NS, De Carvalho BF, Fugaça CA, Dóris B, & Biscaia ES. (2016) Zika virus infection during pregnancy and microcephaly occurrence: a review of literature and Brazilian data. The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases. PMID: 27102780
Bayer A, Lennemann NJ, Ouyang Y, Bramley JC, Morosky S, Marques ET Jr, Cherry S, Sadovsky Y, & Coyne CB. (2016) Type III Interferons Produced by Human Placental Trophoblasts Confer Protection against Zika Virus Infection. Cell host . PMID: 27066743
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Plotkin, S. (1967) 33 A Mitotic Inhibitor Produced by Rubella Virus Infection of Human Fibroblasts. Pediatric Research, 1(3), 208-209. DOI: 10.1203/00006450-196705000-00040
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Qian X, Nguyen HN, Song MM, Hadiono C, Ogden SC, Hammack C, Yao B, Hamersky GR, Jacob F, Zhong C.... (2016) Brain-Region-Specific Organoids Using Mini-bioreactors for Modeling ZIKV Exposure. Cell. PMID: 27118425
Dang J, Tiwari SK, Lichinchi G, Qin Y, Patil VS, Eroshkin AM, & Rana TM. (2016) Zika Virus Depletes Neural Progenitors in Human Cerebral Organoids through Activation of the Innate Immune Receptor TLR3. Cell stem cell. PMID: 27162029
Miner, J., Cao, B., Govero, J., Smith, A., Fernandez, E., Cabrera, O., Garber, C., Noll, M., Klein, R., Noguchi, K.... (2016) Zika Virus Infection during Pregnancy in Mice Causes Placental Damage and Fetal Demise. Cell. DOI: 10.1016/j.cell.2016.05.008
Tang H, Hammack C, Ogden SC, Wen Z, Qian X, Li Y, Yao B, Shin J, Zhang F, Lee EM.... (2016) Zika Virus Infects Human Cortical Neural Progenitors and Attenuates Their Growth. Cell stem cell, 18(5), 587-90. PMID: 26952870
Pelka K, Shibata T, Miyake K, & Latz E. (2016) Nucleic acid-sensing TLRs and autoimmunity: novel insights from structural and cell biology. Immunological reviews, 269(1), 60-75. PMID: 26683145
Tabeta K, Hoebe K, Janssen EM, Du X, Georgel P, Crozat K, Mudd S, Mann N, Sovath S, Goode J.... (2006) The Unc93b1 mutation 3d disrupts exogenous antigen presentation and signaling via Toll-like receptors 3, 7 and 9. Nature immunology, 7(2), 156-64. PMID: 16415873
Kim J, Huh J, Hwang M, Kwon EH, Jung DJ, Brinkmann MM, Jang MH, Ploegh HL, & Kim YM. (2013) Acidic amino acid residues in the juxtamembrane region of the nucleotide-sensing TLRs are important for UNC93B1 binding and signaling. Journal of immunology (Baltimore, Md. : 1950), 190(10), 5287-95. PMID: 23585677
Casrouge A, Zhang SY, Eidenschenk C, Jouanguy E, Puel A, Yang K, Alcais A, Picard C, Mahfoufi N, Nicolas N.... (2006) Herpes simplex virus encephalitis in human UNC-93B deficiency. Science (New York, N.Y.), 314(5797), 308-12. PMID: 16973841
Lafaille FG, Pessach IM, Zhang SY, Ciancanelli MJ, Herman M, Abhyankar A, Ying SW, Keros S, Goldstein PA, Mostoslavsky G.... (2012) Impaired intrinsic immunity to HSV-1 in human iPSC-derived TLR3-deficient CNS cells. Nature, 491(7426), 769-73. PMID: 23103873
Estornes Y, Toscano F, Virard F, Jacquemin G, Pierrot A, Vanbervliet B, Bonnin M, Lalaoui N, Mercier-Gouy P, Pachéco Y.... (2012) dsRNA induces apoptosis through an atypical death complex associating TLR3 to caspase-8. Cell death and differentiation, 19(9), 1482-94. PMID: 22421964
Chuang JH, Chuang HC, Huang CC, Wu CL, Du YY, Kung ML, Chen CH, Chen SC, & Tai MH. (2011) Differential toll-like receptor 3 (TLR3) expression and apoptotic response to TLR3 agonist in human neuroblastoma cells. Journal of biomedical science, 65. PMID: 21861882
Suzuki Y, Nakabayashi Y, Nakata K, Reed JC, & Takahashi R. (2001) X-linked inhibitor of apoptosis protein (XIAP) inhibits caspase-3 and -7 in distinct modes. The Journal of biological chemistry, 276(29), 27058-63. PMID: 11359776
Frumence E, Roche M, Krejbich-Trotot P, El-Kalamouni C, Nativel B, Rondeau P, Missé D, Gadea G, Viranaicken W, & Desprès P. (2016) The South Pacific epidemic strain of Zika virus replicates efficiently in human epithelial A549 cells leading to IFN-β production and apoptosis induction. Virology, 217-26. PMID: 27060565
Vontell R, Supramaniam V, Wyatt-Ashmead J, Gressens P, Rutherford M, Hagberg H, & Thornton C. (2015) Cellular mechanisms of toll-like receptor-3 activation in the thalamus are associated with white matter injury in the developing brain. Journal of neuropathology and experimental neurology, 74(3), 273-85. PMID: 25668563
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Penkala I, Wang J, Syrett CM, Goetzl L, López CB, & Anguera MC. (2016) LNCRHOXF1: a long noncoding RNA from the X-chromosome that suppresses viral response genes during development of the early human placenta. Molecular and cellular biology. PMID: 27066803
Each year, an estimated 1.7 million people in the United States sustain traumatic brain injuries (TBIs), according to the U.S. Centers for Disease Control and Prevention. These injuries occur most frequently from falling, but can also result from military combat, car accidents, contact sports or domestic abuse. Recently, physicians and researchers have become increasingly concerned that even mild cases of repetitive brain trauma could have long-term, unanticipated consequences.
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Barekat, A., Gonzalez, A., Mauntz, R., Kotzebue, R., Molina, B., El-Mecharrafie, N., Conner, C., Garza, S., Melkani, G., Joiner, W.... (2016) Using Drosophila as an integrated model to study mild repetitive traumatic brain injury. Scientific Reports, 25252. DOI: 10.1038/srep25252
For years now we’ve been doing training and outreach on the UCSC Genome Browser. And there’s been a lot of change over the years–so much more data, so many new tools, new species. All that ENCODE information and a portal for that. But the look of the main site was largely the same. Here’s a […]... Read more »
In our continuing story of how being sick can save you, how about three genetic diseases and a genetic condition that can save you from malaria. The genetic diseases might kill you, but usually after you procreate, and that is better for the species than being killed by malaria as a child. Evolution is an emotionless mistress.... Read more »
Chootong P, Panichakul T, Permmongkol C, Barnes SJ, Udomsangpetch R, et al. (2012) Characterization of Inhibitory Anti-Duffy Binding Protein II Immunity: Approach to Plasmodium vivax Vaccine Development in Thailand. PLoS ONE , 7(4). DOI: 10.1371/journal.pone.0035769
I don't want to keep you too long today aside from directing you to the literature review by Hajar Mazahery and colleagues  (open-access available here) discussing the collected peer-review literature on the topic of vitamin D and autism to date.Anyone that stops by this blog might already know about my interest in the science around this issue (see here and see here for example) and how quite a few more resources really should be directed into this 'sunshine' research area. The Mazahery review pulls in the major themes included in the research literature including what has been published so far on levels of vitamin D and autism (and insufficiency/deficiency percentages), a possible role for ethnicity and migration, and use of vitamin D as a possible intervention option. They do also make mention of some of the genetics of vitamin D metabolism (see here) (and there is even more recent research on this ) and the potentially important link to areas such as autoimmunity with autism in mind (see here).I'll leave you with their closing remarks: "Conclusions are not yet possible due to the inconsistent results, different methodological approaches employed, and very few trials in the current literature. However, there are some indications that early exposure to inadequate vitamin D may interact with other factors and contribute to the aetiology of autism, low vitamin D status might be highly prevalent in populations with ASD, and intervention with vitamin D might be beneficial in reducing autism symptoms among those who have ASD." That combined with what NICE here in England have already proposed more generally (see here) and you can perhaps see that vitamin D and the 'English Disease' (rickets)  might be but one connection for this important vitamin/hormone.Oh, and as part of a wider group of variables 'linked' to autism, vitamin D is also discussed in the recent mini-review paper by Takeo Fujiwara and colleagues . Thick and fast people, thick and fast...And completely unrelated to today's post, IMFAR 2016 starts today.---------- Mazahery H. et al. Vitamin D and Autism Spectrum Disorder: A Literature Review. Nutrients. 2016 Apr 21;8(4). pii: E236. Coşkun S. et al. Association of polymorphisms in the vitamin D receptor gene and serum 25-hydroxyvitamin D levels in children with autism spectrum disorder. Gene. 2016 May 4. pii: S0378-1119(16)30361-4. Belton NR. Rickets--not only the "English disease". Acta Paediatr Scand Suppl. 1986;323:68-75. Fujiwara T. et al. Chemicals, Nutrition, and Autism Spectrum Disorder: A Mini-Review. Front. Neurosci. 2016; April 20.----------Mazahery H, Camargo CA, Conlon C, Beck KL, Kruger MC, & von Hurst PR (2016). Vitamin D and Autism Spectrum Disorder: A Literature Review. Nutrients, 8 (4) PMID: 27110819... Read more »
Mazahery H, Camargo CA, Conlon C, Beck KL, Kruger MC, & von Hurst PR. (2016) Vitamin D and Autism Spectrum Disorder: A Literature Review. Nutrients, 8(4). PMID: 27110819
(Also appeared on United Academics) Sleep cycles When we leave the day behind us and nestle ourselves in our cosy beds, we sleep. Sleep, however, comes in stages that repeat themselves. It’s a five-stage cycle that last about 90 minutes in humans. Four stages of non-REM sleep are followed by a period of REM (Rapid […]... Read more »
Ólafsdóttir HF, Barry C, Saleem AB, Hassabis D, & Spiers HJ. (2015) Hippocampal place cells construct reward related sequences through unexplored space. eLife. PMID: 26112828
Shein-Idelson M, Ondracek JM, Liaw HP, Reiter S, & Laurent G. (2016) Slow waves, sharp waves, ripples, and REM in sleeping dragons. Science (New York, N.Y.), 352(6285), 590-5. PMID: 27126045
In answer to the question posed in the title of this post: "A GFD [gluten-free diet] changes the gut microbiome composition and alters the activity of microbial pathways."So said the findings reported by Marc Jan Bonder and colleagues  (open-access) who presented results based on the "changes in the gut microbiomes of 21 healthy volunteers who followed a GFD for four weeks." Said research volunteers (12 women and 9 men) initially followed a GFD for 4 weeks following some baseline assessments that was followed by "a “wash-out” period of five weeks." At various time points along the study, they supplied blood samples and er, 'fecal samples' that alongside some food diary information, were analysed and processed. Outside the use of "454 pyrosequencing" to see what was living in said poo(p) samples, researchers also looked at a panel of various 'biomarkers' in those blood samples including some old friends - the cytokines.Results: bearing in mind 3-day food diaries are not without their methodological issues, the authors reported some group differences between use of a GFD and a habitual diet (not GFD) but nothing that came up as statistically significant in terms of energy, protein, carbohydrates or fats. They concluded that: "dietary macronutrient composition was not significantly changed by following a GFD." I might add that other research from other areas has suggested that when it comes to things like vegetable and fruit intake and corresponding nutrient intake, the horror that is a GFD as part of a gluten-free, casein-free (GFCF) strategy might actually not be so horrible...Next: "Inter-individual variation in the gut microbiota remained stable during this short-term GFD intervention." Allowing for the fact that the GFD was only in place for 4 weeks, the authors reported that adoption of such a dietary change did not seem to significantly affect the bacterial diversity noted in poo(p) samples. But... they did note that certain types of bacteria seemed to be affected by the implementation of a GFD: "On a taxonomic level we identified eight bacteria that change significantly in abundance on GFD: Veillonellaceae, Ruminococcus bromii, and Roseburia faecis decreased on GFD, and Victivallaceae, Clostridiaceae, ML615J-28, Slackia, and Coriobacteriaceae increased on GFD. The strongest effect was seen in the decrease of Veillonellaceae during GFD, Gram-negative bacteria known for lactate fermentation."Here's where it also gets a little bit interesting. "This is the first time that the Veillonellaceae family has been associated to a dietary intervention, but it was recently shown to be decreased in autistic patients." The citation in question covering that previous research is that from Kang et al  that has also been discussed on this blog (see here). Kang and colleagues did include some participants (a quarter) who were on a GFCF diet at the time of sampling suggesting the "the importance of including dietary information in analyses of microbiota in relation to diseases." I might add that I don't readily accept that autism is a 'disease' but can see the point the authors are trying to make about diet affecting the gut microbiome and what that might mean for research into various labels.Further on: "Veillonellaceae is considered to be a pro-inflammatory family of bacteria; an increase in Veillonellaceae abundance was consistently reported in IBD, IBS, and cirrhosis patients. It is conceivable that a decrease in Veillonellaceae abundance might be one of the mediators of the GFD’s beneficial effect observed in patients with IBS and gluten-related disorders." This is an interesting observation. Allowing for the fact that there is some blurring when it comes to binary notions of pro-inflammatory and anti-inflammatory actions of various compounds and so one has to be a little careful, the idea that the GFD might significantly affect the the presence of something like Veillonellaceae is deserving of quite a bit more research attention. On my previous 'wish-list' entry about the use of a GFD with autism in mind (see here) I did suggest that the gut microbiome might be an important part of future studies in this area...There is quite a bit more data included in the Bonder paper (including the conclusion that: "a GFD and its downstream effects on the microbiome do not cause major inflammatory or metabolic changes in gut function in healthy participants") and I would encourage readers to take some time over the findings. Keep in mind the short time-scale for dietary intervention and relatively small participants numbers however but don't lose sight of the idea that what we eat (or don't eat) might have quite a few 'effects' on the trillions of wee beasties that call us home.---------- Bonder MJ. et al. The influence of a short-term gluten-free diet on the human gut microbiome. Genome Medicine. 2016;8:45. Kang DW. et al. Reduced incidence of Prevotella and other fermenters in intestinal microflora of autistic children. PLoS One. 2013 Jul 3;8(7):e68322.----------Bonder MJ, Tigchelaar EF, Cai X, Trynka G, Cenit MC, Hrdlickova B, Zhong H, Vatanen T, Gevers D, Wijmenga C, Wang Y, & Zhernakova A (2016). The influence of a short-term gluten-free diet on the human gut microbiome. Genome medicine, 8 (1) PMID: 27102333... Read more »
Bonder MJ, Tigchelaar EF, Cai X, Trynka G, Cenit MC, Hrdlickova B, Zhong H, Vatanen T, Gevers D, Wijmenga C.... (2016) The influence of a short-term gluten-free diet on the human gut microbiome. Genome medicine, 8(1), 45. PMID: 27102333
Our paper “A Pragmatic Approach to Getting Published: 35 Tips for Early Career Researchers” just came out in Frontiers in Plant Science. This is the story behind the paper.
For my second postdoc, I was the fortunate receipient of a PLANT FELLOWS scholarship. PLANT FELLOWS is an international program that provides research grants to postdocs in the field of plant science. The fellows are based at many different host institutions throughout Europe. I myself am working at Bayer Crop Science in Gent, Belgium, in collaboration with the Dessimoz lab in London and Lausanne. Part of the PLANT FELLOWS mission is to provide training, mentoring, and networking to the postdocs—skills essential for career advancement.
Last year, the annual PF meeting was held in Männedorf, Switzerland from September 28 to October 1 2015. Training workshops took place at the Boldern Hotel, surrounded by meadows and with a nice view of Lake Zürich.
Group picture from the 3rd annual PLANT FELLOWS meeting
The meeting consisted of several days of trainings and workshops. For one of the days, I chose to participate in the workshop “Advanced Strategies for Dealing with the Publication Process.” I was especially keen on learning more about this particular subject. As a postdoc still trying to navigate the publication waters, I was looking for all the advice I could get. We’ve all heard the saying before: publish or perish. Publishing papers in your postdoc years is so important for an academic career.
There were about 15 postdocs in this day-long workshop. The facilitator, Philipp Mayer, came with a bunch of photocopied book chapters, articles, and USB keys full of pdfs for each of us to use on our laptops. The objective of the workshop was to, as a group, write a small paper about advanced publication strategies using the literature we were provided with. Our plan of attack was to pool our collective postdoc experience and come up with a list of our most useful recommendations on how to get a scientific paper published.
After feverishly reading websites, book chapters and papers, at the end of the day we came up with a draft: an introduction, our recommendations broken into 3 main sections, and a conclusion. We had a respectable number of references. But what would be the fate of our paper? About a third of the class was apathetic, a third thought we should aim for a blog post, and another third thought we should try for a “real” scientific journal. I had really enjoyed the workshop so I lobbied for publishing it in a real journal. I liked the experience of learning about a topic, working collaboratively with my peers, and then passing on the information for others to benefit.
I volunteered to take charge of the paper, edit it, and submit it to journals in hopes of getting it published. At the end of the day I left with a draft of the paper, many references, the contact information of all the attendees, and the full support of the facilitator (Philipp) for any future help that I might need. I looked at it as an opportunity take a leadership role in publishing a paper, from start to finish. And more importantly, it was a chance to put our own advice into practice.
Upon returning to Belgium, I quickly found out that one of the sentences we had written in the paper rang true: It is a common misconception among early career researchers that the presentation of the work in a manuscript is the last stage of a project. There is a long and complicated process associated with submission, review, and revision that must be taken into account. During the next month, I reread paper, finished writing short sections, added references, edited, and got feedback from the coauthors. We agreed on the author order, and shared the document using Authorea. Philipp and I went back and forth with several rounds of editing.
We decided to submit our manuscript to eLife, which is a prestigious peer reviewed open access journal with favorable policy toward early career researchers. I wrote a cover letter to the editor describing our paper and asking if the topic was suitable to be considered for eLife.
Within a few days, the editor read the manuscript but informed me that he was unable to send it out for review because it wasn’t “fresh” enough, meaning most of what we said had already be discussed many times in the scientific community. Despite the sting of having a paper rejected directly from the editor, I decided to take the advice we had written in the paper: Remove your personal feelings from the peer review process. Time to find the next journal.
During the following month and a half, the manuscript was pushed to the bottom of my To Do list, as other projects and tasks got my attention. Christmas holidays came and went, and admittedly this paper was the last thing on my mind.
In January, I sent a presubmission inquiry to PLOS Biology. The PLOS Biology editor wrote back within a few days to inform me that although they appreciated the attention to an important problem, they could not encourage us to submit because it didn’t present “novel strategies for increasing access to research, improving the quality of research results, or fixing flawed measures of impact.” Since this was the second time I had heard this same exact criticism, I realized it was time to take more advice from the paper: It is critical to highlight the novelty and importance in the article and cover letter. We were going to have to add something to the paper to make it more novel.
Shortly after, I contacted the Frontiers in Plant Science (FiPS) Editorial Office with a new and improved cover letter. FiPS is an open access online journal publishing many different peer reviewed articles: research, reviews, commentaries, and perspectives, among others. The editor and I discussed morphing the paper into something that would be more plant related, given the plant science background of all the coauthors. Over the next month, it was back to editing the paper. I proposed edits that would make our tips more plant-specific. We added advice about industry-academia collaborations, and more information about plant science journals. Philipp, the coauthors, and I went back and forth several times with rounds of edits, adding more references and polishing more details. I submitted the final version of the paper to Frontiers in Plant Science on March 15.
The experience of the collaborative peer review by FiPS was a pleasant and efficient one. Their webiste says “Frontiers reviews are standardized, rigorous, fair, constructive, efficient and transparent.” I enthusiastically agree. Within two weeks, we had received comments from the reviewers. There were some major points that needed to be addressed before Frontiers could offer publication. However, the points were all very relevant and only helped to make the paper stronger. During the process of the interactive review, I took more guidance from the paper: Go point by point through the reviewer comments and either make the suggested change or politely explain and clarify the misunderstanding.
April 21st : Acceptance achieved! Approximately 5 weeks after submitting the article, it was accepted and the provisional version of the manuscript was published online. This is an extremely fast turnover time, in part due to the responsiveness of the editor, quick but in-depth peer review, and the interactive, transparent review discussion.
What I learned
This collaboration with the PLANT FELLOWS postdocs resulted in a paper I can say I’m proud of. I learned many things about the publication process—not only through a literature review, but by actually experiencing the process first hand. Here are some of the main things that stuck with me:
There is a certain creative power in bringing people together in a beautiful location to brainstorm and produce an outcome within a short period of time. However, it is necessary for someone to take the reins and commit to the follow-through in order to get to a finished product. I think things like hackathons or other collaborative group efforts could lead to fruitful outcomes.
I learned how to coordinate a small project. This was a great collaborative effort, which gave me an opportunity to practice the recommendations we wrote about in the paper.
I discovered firsthand the importance of the initial contact with the editor. As soon as we reworked the paper to approach the topic from a plant-specific standpoint, this added novelty to the paper. We were able to highlight this novelty in the cover letter.
Don’t give up. Many times I got distracted or discouraged and thought to publish the manuscript on our blog, but I’m glad in the end we found a home for it at FiPS. Perseverance is key.
... Read more »
Glover, N., Antoniadi, I., George, G., Götzenberger, L., Gutzat, R., Koorem, K., Liancourt, P., Rutowicz, K., Saharan, K., You, W.... (2016) A Pragmatic Approach to Getting Published: 35 Tips for Early Career Researchers. Frontiers in Plant Science. DOI: 10.3389/fpls.2016.00610
A new study on the epigenetics of lactose intolerance may provide an approach to understanding schizophrenia and other complex, serious illnesses. While that may seem odd, both lactose intolerance and schizophrenia are inherited. In addition, neither condition emerges in the first years of life, but rather both appear years or even decades later.
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Labrie, V., Buske, O., Oh, E., Jeremian, R., Ptak, C., Gasiūnas, G., Maleckas, A., Petereit, R., Žvirbliene, A., Adamonis, K.... (2016) Lactase nonpersistence is directed by DNA-variation-dependent epigenetic aging. Nature Structural . DOI: 10.1038/nsmb.3227
By Hayley TrzinskiImage by Hayley TrzinskiThe Princess and the Frog is a very fun and imaginative children’s story… but not when pesticides are involved. Have you ever wondered how dangerous pesticides can be? Well, pesticides can harm more than just pests and weeds, and in the case of frogs, many pesticides and herbicides are causing problems. Atrazine, a chemical commonly used as an herbicide, can cause reproduction in male African clawed frogs to be impossible. In some cases, atrazine is even turning some male frogs into females! Tyrone Hayes, a biology professor at the University of California, Berkeley, and his research team looked at the effects of atrazine on African clawed frogs. The hypothesis of the researchers was to determine if exposure to atrazine would feminize or stop reproductive ability of male frogs. Tyrone Hayes and his team raised some frogs in atrazine dissolved in a weak ethanol solution and some in only a weak ethanol solution for a control group. Even though the ethanol solutions did not contain enough ethanol to impact the frogs, it is important to put the control group frogs in ethanol as well so both the treatment and control groups are equal in that way. Fertility in the frogs was later determined by looking at the number of developed embryos produced from atrazine-treated males and females, and from normal males and females. Atrazine is an endocrine disruptor, meaning that it contains chemicals that can change the hormone systems in animals. Some endocrine disruptors block hormone receptors, causing the hormones needed for reproduction to stop working. Atrazine works as an endocrine disruptor by increasing the production and activity of aromatase, a chemical that turns testosterone into estrogen. This decreases the amount of testosterone and increases the amount of estrogen in the male frogs. Tyrone Hayes and his team saw that aromatase was found in normal females and in atrazine-treated males, but not in normal males. The aromatase production caused a decrease in testosterone and an increase in estrogen in the atrazine-treated males. Subsequently, the atrazine-treated males' calls became less masculine, their sperm died, and they started forming characteristics such as female sex organs. In the long run, atrazine could affect whole frog populations by skewing the sex ratio, meaning that there will be many more of one sex of frog than the other, making it hard to keep a healthy frog population. The main way that atrazine could skew the sex ratio of frogs is by changing their behavior. This starts by male frogs not being able to mate or by their fertility decreasing. Tyrone Hayes found that the behavior of male frogs treated with atrazine was different than the behavior of male frogs not treated with atrazine. Non-treated males out-competed atrazine-treated males for females and only two atrazine-treated males obtained correct mating posture. Also, non-treated males had much higher testosterone levels when around females than atrazine-treated males. This behavior change in male frogs affected by atrazine could cause fewer of those males to act like males, and more of them to act like females or to not reproduce at all.Atrazine can skew the sex ratios of frog populations in other ways, too. African clawed frogs have the opposite type of sex determining chromosomes as humans. While human males have one Y and one X sex chromosome and human females have two X sex chromosomes, normal male African clawed frogs have two Z chromosomes and female African clawed frogs have one Z chromosome and one W chromosome. The sex ratio becomes skewed, in part, because even though some of the newly transitioned female frogs can successfully breed, they still have male genetics. When these newly transitioned female frogs mate with natural male frogs, all of the offspring will be males. This is because two frogs that both have original sex cells that are both Z’s create offspring that must inherit two Z chromosomes, making all of the babies male. This is dangerous for populations of frogs, because only one sex of frogs being created could lead to extinction of these creatures. Although you may like the idea of crops being pest and weed free, there are many negative side effects to the dangerous pesticide chemicals, including changing the reproduction of frogs and even fish, reptiles, birds, and mammals, sometimes including humans. Even though the effects of these pesticides are pretty interesting, I don’t know about you, but I would rather read a story where frogs turn into princes instead of princesses.SourcesHayes, T., Khoury, V., Narayan, A., Nazir, M., Park, A., Brown, T., Adame, L., Chan, E., Buchholz, D., Stueve, T., & Gallipeau, S. (2010). Atrazine induces complete feminization and chemical castration in male African clawed frogs (Xenopus laevis) Proceedings of the National Academy of Sciences, 107 (10), 4612-4617 DOI: 10.1073/pnas.0909519107Mnif, W., Hassine, A., Bouaziz, A., Bartegi, A., Thomas, O., & Roig, B. (2011). Effect of Endocrine Disruptor Pesticides: A Review International Journal of Environmental Research and Public Health, 8 (12), 2265-2303 DOI: 10.3390/ijerph8062265... Read more »
Hayes, T., Khoury, V., Narayan, A., Nazir, M., Park, A., Brown, T., Adame, L., Chan, E., Buchholz, D., Stueve, T.... (2010) Atrazine induces complete feminization and chemical castration in male African clawed frogs (Xenopus laevis). Proceedings of the National Academy of Sciences, 107(10), 4612-4617. DOI: 10.1073/pnas.0909519107
Mnif, W., Hassine, A., Bouaziz, A., Bartegi, A., Thomas, O., & Roig, B. (2011) Effect of Endocrine Disruptor Pesticides: A Review. International Journal of Environmental Research and Public Health, 8(12), 2265-2303. DOI: 10.3390/ijerph8062265
The Eatles are feasting on an African Grey Parrot. Come read about the natural history and conservation of this animal, courtesy of Animalia, Inc and the Organ Laboratory at Indiana University School of Medicine.... Read more »
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