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Brian D. Adkins Theresa A. Libby Marlene M. Mayberry Thomas W. Brady Justin B. Halls Stephanie Mallow Corbett Joseph Schoeny Eric P. Shields Jahan Chowdhury Amanda N. Kinsinger-Stickel Gay Wehrli Nicholas R. Jaeger Matthew P. Robertson Kathy M. Butler Stuart M. Lowson James Forrest Calland James D. Gorham 《Transfusion》2021,61(11):3066-3074
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Constanze A. Jakwerth Adam M. Chaker Ferdinand Guerth Madlen Oelsner Lisa Pechtold Lynn S. zur Bonsen Julia T. Ullmann Susanne Krauss-Etschmann Anna Erb Josephine Kau Mirjam Plaschke Marlene Winkler Alexandra Kurz Antonia Kloss Julia Esser-von Bieren Carsten B. Schmidt-Weber Ulrich M. Zissler 《Clinical and experimental allergy》2021,51(12):1577-1591
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Laure Ségurel Frederic Austerlitz Bruno Toupance Mathieu Gautier Joanna L Kelley Patrick Pasquet Christine Lonjou Myriam Georges Sarah Voisin Corinne Cruaud Arnaud Couloux Tatyana Hegay Almaz Aldashev Renaud Vitalis Evelyne Heyer 《European journal of human genetics : EJHG》2013,21(10):1146-1151
The high prevalence of type 2 diabetes and its uneven distribution among human populations is both a major public health concern and a puzzle in evolutionary biology. Why is this deleterious disease so common, while the associated genetic variants should be removed by natural selection? The ‘thrifty genotype'' hypothesis proposed that the causal genetic variants were advantageous and selected for during the majority of human evolution. It remains, however, unclear whether genetic data support this scenario. In this study, we characterized patterns of selection at 10 variants associated with type 2 diabetes, contrasting one herder and one farmer population from Central Asia. We aimed at identifying which alleles (risk or protective) are under selection, dating the timing of selective events, and investigating the effect of lifestyle on selective patterns. We did not find any evidence of selection on risk variants, as predicted by the thrifty genotype hypothesis. Instead, we identified clear signatures of selection on protective variants, in both populations, dating from the beginning of the Neolithic, which suggests that this major transition was accompanied by a selective advantage for non-thrifty variants. Combining our results with worldwide data further suggests that East Asia was particularly prone to such recent selection of protective haplotypes. As much effort has been devoted so far to searching for thrifty variants, we argue that more attention should be paid to the evolution of non-thrifty variants. 相似文献
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Beck Stefanie Ragab Haissam Hoop Dennis Meßner-Schmitt Aurélie Rademacher Cornelius Kahl Ursula von Breunig Franziska Haese Alexander Graefen Markus Zöllner Christian Fischer Marlene 《Journal of clinical monitoring and computing》2021,35(4):891-901
Journal of Clinical Monitoring and Computing - Surgery in the prolonged extreme Trendelenburg position may lead to elevated intracranial pressure and compromise cerebral hemodynamic regulation. We... 相似文献
69.
Miguel Alves-Ferreira Marlene Quintas Jorge Sequeiros Alda Sousa Jos Pereira-Monteiro Isabel Alonso Joo Luís Neto Carolina Lemos 《The journal of headache and pain》2021,22(1)
BackgroundMigraine is a multifactorial disorder that is more frequent (two to four times) in women than in men. In recent years, our research group has focused on the role of neurotransmitter release and its regulation. Neurexin (NRXN2) is one of the components of the synaptic vesicle machinery, responsible for connecting intracellular fusion proteins and synaptic vesicles.Our aim was to continue exploring the role and interaction of proteins involved in the control and promotion of neurotransmission in migraine susceptibility.MethodsA case-control study was performed comprising 183 migraineurs (148 females and 35 males) and 265 migraine-free controls (202 females and 63 males). Tagging single nucleotide polymorphisms of NRXN2 were genotyped to assess the association between NRXN2 and migraine susceptibility. The χ2 test was used to compare allele frequencies in cases and controls and odds ratios were estimated with 95% confidence intervals. Haplotype frequencies were compared between groups. Gene-gene interactions were analysed using the Multifactor Dimensionality Reduction v2.0.ResultsWe found a statistically significant interaction model (p = 0.009) in the female group between the genotypes CG of rs477138 (NRXN2) and CT of rs1158605 (GABRE). This interaction was validated by logistic regression, showing a significant risk effect [OR = 4.78 (95%CI: 1.76–12.97)] after a Bonferroni correction. Our data also supports a statistically significant interaction model (p = 0.011) in the female group between the GG of rs477138 in NRXN2 and, the rs2244325''s GG genotype and rs2998250’s CC genotype of CASK. This interaction was also validated by logistic regression, with a protective effect [OR = 0.08 (95%CI: 0.01–0.75)]. A weak interaction model was found between NRXN2-SYT1. We have not found any statistically significant allelic or haplotypic associations between NRXN2 and migraine susceptibility.ConclusionsThis study unravels, for the first time, the gene-gene interactions between NRXN2, GABRE - a GABAA-receptor - and CASK, importantly it shows the synergetic effect between those genes and its relation with migraine susceptibility.These gene interactions, which may be a part of a larger network, can potentially help us in better understanding migraine aetiology and in development of new therapeutic approaches.Supplementary InformationThe online version contains supplementary material available at 10.1186/s10194-021-01266-y. 相似文献
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Claudia A. Grillo Gerardo G. Piroli Robert C. Lawrence Shayna A. Wrighten Adrienne J. Green Steven P. Wilson Randall R. Sakai Sandra J. Kelly Marlene A. Wilson David D. Mott Lawrence P. Reagan 《Diabetes》2015,64(11):3927-3936
Insulin receptors (IRs) are expressed in discrete neuronal populations in the central nervous system, including the hippocampus. To elucidate the functional role of hippocampal IRs independent of metabolic function, we generated a model of hippocampal-specific insulin resistance using a lentiviral vector expressing an IR antisense sequence (LV-IRAS). LV-IRAS effectively downregulates IR expression in the rat hippocampus without affecting body weight, adiposity, or peripheral glucose homeostasis. Nevertheless, hippocampal neuroplasticity was impaired in LV-IRAS–treated rats. High-frequency stimulation, which evoked robust long-term potentiation (LTP) in brain slices from LV control rats, failed to evoke LTP in LV-IRAS–treated rats. GluN2B subunit levels, as well as the basal level of phosphorylation of GluA1, were reduced in the hippocampus of LV-IRAS rats. Moreover, these deficits in synaptic transmission were associated with impairments in spatial learning. We suggest that alterations in the expression and phosphorylation of glutamate receptor subunits underlie the alterations in LTP and that these changes are responsible for the impairment in hippocampal-dependent learning. Importantly, these learning deficits are strikingly similar to the impairments in complex task performance observed in patients with diabetes, which strengthens the hypothesis that hippocampal insulin resistance is a key mediator of cognitive deficits independent of glycemic control. 相似文献