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A 4.5-fold higher risk of developing breast cancer in the highest vs. lowest quintile of AMPA excretion was observed (ORQ5 vs. Q1 4.49; 95% CI 1.46-13.77; ptrend = 0.029). To our knowledge, this is the first study to prospectively examine associations between urinary AMPA excretion and breast cancer risk. Our preliminary findings suggest that AMPA exposure may be associated with increased breast cancer risk; however, these results require confirmation in a larger population to increase study power and permit careful examinations of race/ethnicity differences.
Traumatic injuries can have long-term negative impacts on health, especially psychological health. A biopsychosocial approach is recommended to identify those likely to experience psychosocial stress, however large individual differences exist in stress reactivity and post-injury health that remain unexplored. Therefore, we investigated autonomic nervous system (ANS) stress responses and pre-existing psychosocial vulnerability as contributors to health in individuals who sustained a traffic-related injury.
120 adults with traffic-related injury and 112 non-injury controls underwent an integrative ANS (cardiac and skin conductance) assessment and a health-related assessment at 3-6 weeks post-injury. Propensity score matching based on six pre-injury psychosocial vulnerability factors (age, sex, education, prior mental/physical health, socioeconomic status) guided the definition of high vulnerability (HV) and low vulnerability (LV) injury subgroups, with the LV subgroup having similar propensity scores to no. Post-stress recovery patterns may represent a novel physiological signature for a "biological intrinsic" vulnerability early after the injury. These findings provide direction for improved early identification and management of injured individuals, including innovative preventive interventions that target ANS regulation.Individuals vary in their response to psychological and physiological stressors, and this reactivity can be captured using measures of cortisol. Previous research suggests cortisol reactivity is under some degree of genetic control; however, the measures used have varied widely. selleck products This study (N = 524) examined potential differences in heritability across varying cortisol metrics of stress reactivity following the Trier Social Stress Test (TSST) and whether these measures are genetically or environmentally interrelated. Participants included twins aged 15-20 years (56% female). Cortisol reactivity to the TSST was assessed via serial salivary cortisol samples collected pre- and post-TSST. Modest to moderate heritability estimates (12% [95CI 1-36%] - 45% [95CI 16-69%]) were observed across measures purported to capture stress reactivity (peak, area under the curve [AUC], baseline-to-peak change). Findings also demonstrate both shared and unique genetic and environmental influences between baseline cortisol and cortisol reactivity. Minimal to no additional genetic innovations above and beyond the contributions of peak cortisol were found for other measures of cortisol reactivity such as AUC. This study is one of the largest twin-based samples to examine the heritability of cortisol reactivity, and results suggest that simpler measures of cortisol reactivity demonstrate higher heritability compared to more complex measurements.The development of enumeration skills over childhood is thought to reflect improvements in both subitizing (for small sets) and serial counting (for larger sets). However, investigations into the contribution of subitizing to advancing mathematics ability are limited by challenges in measuring subitizing capacity across developmental populations. Subitizing capacity in adults is traditionally assessed by calculating the bilinear inflection point for reaction times or accuracy across set sizes, but in children greater variability and dramatic improvements in counting ability introduce problems with this approach. This study demonstrates this limitation in a sample of elementary school children and proposes a novel probabilistic approach to measuring subitizing capacity. This metric captures well-established trends in the development of children's subitizing. Furthermore, the proposed metric predicts unique variance in symbolic arithmetic ability, corroborating previous research that suggests a foundational role for subitizing in the development of numerical cognition. Findings demonstrate the advantages of a probabilistic approach to determining subitizing capacity in young children and suggest that it may be practically and theoretically well-suited for investigating subitizing and its role in mathematics development.Gu-Ben-Fang-Xiao decoction (GBFXD), derived from the traditional Chinese medicine Yu-Ping-Feng-San, is widely used in clinical settings and has obvious curative effects in respiratory diseases. GBFXD regulates cholesterol transport and lipid metabolism in chronic persistent asthma. There is evidence for its beneficial effects in the remission stage of asthma; however, its metabolic regulatory effects and underlying mechanisms during asthma remission are unclear. In the present study, we used liquid chromatography-mass spectrometry (LC-MS) to analyse the metabolic profile of mouse serum during asthma remission. The acquired LC-MS data were subjected to a multivariate analysis for identification of significantly altered metabolites. In total, 42 metabolites were significantly differentially expressed among the control, model, and GBFXD groups. In particular, levels of fatty acids, acylcarnitines, phosphatidylcholines, phosphatidylethanolamines, phosphatidylinositols, triglycerides, and diacylglycerols were altered during asthma remission. GBFXD may maintain lipid homeostasis on the lung surface by modulating lipid metabolism and may thereby alleviate asthma. We further quantified hypogeic acid (FA 161) based on targeted metabolomics and found that GBFXD may regulate fatty acid metabolism by activating the AMP-activated protein kinase (AMPK) pathway. These results support the use of GBFXD in patients with asthma remission.Metformin is an oral antihyperglycemic drug widely used to treat type 2 diabetes mellitus (T2DM), acting via indirect activation of 5' Adenosine monophosphate-activated Protein Kinase (AMPK). Beyond the anti-diabetic effect, accumulative pieces of evidence have revealed that metformin also everts a beneficial effect in diverse kidney diseases. In various acute kidney diseases (AKI) animal models, metformin protects renal tubular cells from inflammation, apoptosis, reactive oxygen stress (ROS), endoplasmic reticulum (ER) stress, epithelial-mesenchymal transition (EMT) via AMPK activation. In diabetic kidney disease (DKD), metformin also alleviates podocyte loss, mesangial cells apoptosis, and tubular cells senescence through AMPK-mediated signaling pathways. Besides, metformin inhibits cystic fibrosis transmembrane conductance regulator (CFTR)-mediated fluids secretion and the mammalian target of rapamycin (mTOR)-involved cyst formation negatively regulated by AMPK in autosomal dominant polycystic kidney disease (APDKD).
Homepage: https://www.selleckchem.com/products/bay80-6946.html
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