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t difference exists between the values of HbA1c as a result of application of any type of DMS. The changes in HbA1c values, number and frequency of hypoglycemic episodes, and time in glucose range are the most valuable for assessing the appropriateness and effectiveness of DMS. Future more comprehensive studies assessing the effectiveness, cost-effectiveness, and comparative effectiveness of DMS are needed to stratify them for the most suitable diabetes patients' subgroups.
To explore the correlations between waist circumference, body mass index, calf circumference (CC), and waist-calf circumference ratio (WCR) and activities of daily living (ADLs) and instrumental activities of daily living (IADLs) in Hainan centenarians.
A total of 1,002 Hainan centenarians were selected by full sample household survey. ADLs and IADLs were used to investigate the ability of activity and instrumental activity in daily living. HDAC inhibitor The possible non-linear associations were further analyzed using restricted cubic spline.
After adjusting for demographic characteristics (gender, age, ethnicity, marital status, educational level, and type of residence) and lifestyle (smoking, drinking, and exercise), the odds ratio (OR) of CC (continuous variable) on ADL disability in centenarians was 0.90 (95% CI 0.85-0.96), while high WCR (continuous variable) was related with high risk of ADL disability (OR=1.73; 95% confidence interval[CI], 1.07-2.80). The ORs of CC and WCR for IADL severe disability were 0.86 (95% CI, 0.82-0.91) and 2.23 (95% CI, 1.52-3.28), respectively.
Central (WCR) and peripheral (CC) adiposity had different effects on disability (ADL and IADL) in centenarians. Even in centenarians, maintaining muscle mass (with higher calf circumference) and avoiding central obesity are of positive significance for the prevention of ADL/IADL disability.
Central (WCR) and peripheral (CC) adiposity had different effects on disability (ADL and IADL) in centenarians. Even in centenarians, maintaining muscle mass (with higher calf circumference) and avoiding central obesity are of positive significance for the prevention of ADL/IADL disability.Neonatal hypoglycemia is a common condition. A transient reduction in blood glucose values is part of a transitional metabolic adaptation following birth, which resolves within the first 48 to 72 h of life. In addition, several factors may interfere with glucose homeostasis, especially in case of limited metabolic stores or increased energy expenditure. Although the effect of mild transient asymptomatic hypoglycemia on brain development remains unclear, a correlation between severe and prolonged hypoglycemia and cerebral damage has been proven. A selective vulnerability of some brain regions to hypoglycemia including the second and the third superficial layers of the cerebral cortex, the dentate gyrus, the subiculum, the CA1 regions in the hippocampus, and the caudate-putamen nuclei has been observed. Several mechanisms contribute to neuronal damage during hypoglycemia. Neuronal depolarization induced by hypoglycemia leads to an elevated release of glutamate and aspartate, thus promoting excitotoxicity, and to an increased release of zinc to the extracellular space, causing the extensive activation of poly ADP-ribose polymerase-1 which promotes neuronal death. In this review we discuss the cerebral glucose homeostasis, the mechanisms of brain injury following neonatal hypoglycemia and the possible treatment strategies to reduce its occurrence.The hypothalamic neuroendocrine system is strongly implicated in body energy homeostasis. In particular, the degree of production and release of arginine vasopressin (AVP) in the hypothalamus is affected by plasma osmolality, and that hypothalamic AVP is responsible for thirst and osmolality-dependent water and metabolic balance. However, the osmolality-responsive intracellular mechanism within AVP cells that regulates AVP synthesis is not clearly understood. Here, we report a role for tonicity-responsive enhancer binding protein (TonEBP), a transcription factor sensitive to cellular tonicity, in regulating osmosensitive hypothalamic AVP gene transcription. Our immunohistochemical work shows that hypothalamic AVP cellular activity, as recognized by c-fos, was enhanced in parallel with an elevation in TonEBP expression within AVP cells following water deprivation. Interestingly, our in vitro investigations found a synchronized pattern of TonEBP and AVP gene expression in response to osmotic stress. Those results indicate a positive correlation between hypothalamic TonEBP and AVP production during dehydration. Promoter and chromatin immunoprecipitation assays confirmed that TonEBP can bind directly to conserved binding motifs in the 5'-flanking promoter regions of the AVP gene. Furthermore, dehydration- and TonEBP-mediated hypothalamic AVP gene activation was reduced in TonEBP haploinsufficiency mice, compared with wild TonEBP homozygote animals. Therefore, our result support the idea that TonEBP is directly necessary, at least in part, for the elevation of AVP transcription in dehydration conditions. Additionally, dehydration-induced reductions in body weight were rescued in TonEBP haploinsufficiency mice. Altogether, our results demonstrate an intracellular machinery within hypothalamic AVP cells that is responsible for dehydration-induced AVP synthesis.Described almost 50 years ago, the glycerophosphocholine lipid mediator Platelet-activating factor (PAF) has been implicated in many pathologic processes. Indeed, elevated levels of PAF can be measured in response to almost every type of pathology involving inflammation and cell damage/death. In this review, we provide evidence for PAF involvement in pathologic processes, with focus on cancer, the nervous system, and in photobiology. Importantly, recent insights into how PAF can generate and travel via bioactive extracellular vesicles such as microvesicle particles (MVP) are presented. What appears to be emerging from diverse pathologies in different organ systems is a common theme where pro-oxidative stressors generate oxidized glycerophosphocholines with PAF agonistic effects, which then trigger more enzymatic PAF synthesis via the PAF receptor. A downstream consequence of PAF receptor activation is the generation and release of MVP which provide a mechanism to transmit PAF as well as other bioactive agents.
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