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Noise pollution has become a common public health problem. The harm of noise exposure to human health cannot be ignored. Exposure to noise not only damages the auditory system but also affects the non-auditory system. At present, accumulating domestic and international epidemiological studies have suggested that noise exposure may be related to glycolipid metabolism disturbance. This article summarized recent epidemiological evidence of the association between noise exposure and glucose and lipid metabolism disorders, such as type 2 diabetes, obesity, metabolic syndrome, and hyperlipidaemia. The potential biological mechanisms connecting noise exposure to glucolipid metabolism were also introduced, e.g. noise as a stressor, sleep disorders, and intestinal flora regulation. This study discussed the impacts of noise exposure on glycolipid metabolism related diseases, providing a basis for further identifying noise related risk factors, conducting future related research, and formulating scientific and effective prevention and control measures.
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With the rapid development of aging around the world， the incidence and prevalence of age-related dementia have increased significantly， leading to a huge burden on patients， families and society. So far， there are no drugs that can completely reverse degeneration of the nervous system. The core pathological mechanisms of dementia are not clear， and the occurrence and progression of degenerative diseases in the nervous system appears to be only rely on the prevention through lifestyle interventions. Among lifestyle interventions， a large amount of laboratory evidence and a small amount of epidemiological evidence suggest that time restricted feeding have excellent effects on preventing the occurrence and progression of degenerative diseases in the nervous system. However， due to the lack of evidence in human population， the application of time restricted feeding lacks scientific basis. By synthesizing the existing evidence， this review discussed the pathway network of time restricted feeding that antagonizes the nervous system degradation， suggesting that future studies should focus on population evidence and the combined effects of multiple effect pathways.
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Background Global warming may increase the frequency of compound hot extreme (CHE).However, there is still a lack of studies assessing the associations between CHE and preterm birth (PTB), and the underlying biological mechanisms remain unclear. Objective To estimate the association of exposure to CHE during pregnancy with PTB, and to explore the roles of inflammatory, endothelial dysfunction, and oxidative stress in the association between CHE and PTB. Methods All participants were selected from the Prenatal Environments and Offspring Health (PEOH), a prospective birth cohort conducted in Guangzhou. In this study, a total of 2449 participants who gave birth from May to October in 2014 to 2017 were enrolled, and among them blood samples were collected from 311 preterm (n=43) and full-term (n=268) pregnant women at the time of delivery. A hot day/night was identified as a day when the daily maximum temperature/minimum temperature was higher than its 90th percentile in the study period, and a CHE was defined as having both a hot night and a following hot day. The meteorological data were obtained from the China Meteorological Data Sharing Service System. Anusplin was used to assess the daily maximum temperature, daily minimum temperature, and relative humidity of the participant residence. Enzyme-linked immunosorbent assay (ELISA) was used to measure C reactive protein (CRP), endothelin-1 (ET-1), and malondialdehyde (MDA) levels in maternal serum, and their results were transformed by natural logarithm. A distributed lag nonlinear model was used to investigate the associations of exposures to hot day, hot night, and CHE during pregnancy with PTB at different lag days, and a logistic regression model was used to investigate the associations of CRP, ET-1, and MDA with PTB. Results The incidence rate of PTB was 6.2% in all selected participants. Compared with the non-hot day, the RRs (95%CIs) of CHE in lag 3, 7, and 14 days on PTB were 1.43 (1.12-1.84), 1.24 (1.08-1.43), and 1.17 (1.05-1.30), respectively, and the cumulative effects (% difference) (95%CI) of CHE in lag 14 days on maternal serum CRP, ET-1, and MDA were 0.33% (−0.45%-1.12%), 0.59% (0.11%-1.07%), and 0.57% (0.09%-1.05%), respectively. Compared with the Q1 (lowest quartile) for CRP, ET-1 and MDA, the RRs (95%CIs) of Q4 (highest quartile) for PTB were 1.27 (0.50-3.22), 1.51 (0.61-3.72), and 2.07(0.81-5.27), respectively. Conclusion Maternal exposure to CHE during pregnancy might be associated with an increased risk of PTB. Prenatal exposure to CHE is positively associated with maternal serum CRP, ET-1, and MDA, and the three biochemical indicators are also positively associated with PTB. However, the above conclusions still need further confirmation.
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Abstract@#Exposure to atmospheric PM2.5 is closely related to the morbidity and mortality of kidney diseases such as chronic kidney disease, membranous nephropathy and kidney cancer. Acute and chronic PM2.5 exposure lead to the damage of glomerular filtration and kidney tissue of mice. PM2.5 induces cellular oxidative stress, inflammatory response, endoplasmic reticulum stress, renin angiotensin system and bradykinin system activation, so that causes renal blood vessel and tissue damage, decreases glomerular filtration rate and clearance capacity, and mediates the occurrence of kidney damage and diseases. This article reviews the studies into the impact of PM2.5 on kidney and its mechanism form 2016 to 2020, so as to provide the basis for the prevention and treatment of kidney injury induced by PM2.5.
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Objective: To explore the biological mechanisms of tibial transverse transport (TTT) for promoting microcirculation and tissue repair. Methods: The clinical application and animal model study of TTT were reviewed. Results: The possible biological mechanisms of TTT for promoting microvascular network formation and tissue repair: ① Tibial corticotomy reduces intramedullary pressure and improves microcirculation; ② Tension stress stimulation promotes microvascular regeneration and accelerates the formation of new "transcortical vessels" network; ③ Systemic mobilization of stem cells, mediating local inflammation, etc. Conclusion: TTT has been clinically proven to be effective for the management of lower limb ischemia and diabetic foot ulcers. The surgical procedure is relatively easy with little adverse effects on bone structures. The TTT has good application prospects despite the biological mechanisms of which still need further exploration.
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The symptoms of depressive disorder can be summarized into three dimensions:emotional symptoms,cognitive symptoms and somatic symptoms.Most patients with depressive disorders have various somatic symptoms.The existence of somatic symptoms is often related to the severity of the disease,poor efficacy,and prolonged disease duration.Depressive disorder with somatic symptoms may be a special subtype of depressive disorder.Therefore exploration for its biological mechanisms has an important significance in such patients.This article reviews the clinical characteristics,definitions,and biological mechanisms of somatic symptoms in depressive disorder,and hopes to contribute to an improved understanding of the pathology of depressive disorders.
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Depression and diabetes are difficult to cure chronic diseases.Both of them are in the clinical presence of the situation.There is a certain biological basis.Based on the analysis of relevant literatures both at home and abroad,this paper briefly reviewed the relationship on the aspect of biological mechanism between depression and diabetes,as well as its clinical treatment status.It provided new ideas for the treatment of two diseases,comorbidity and drug development.
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The purpose of this review is to discuss the debate concerning the interpretation of epidemiologic studies on particles and health effects. Study of the 1952 air pollution disaster in London established that very high levels of particulate-based smog can cause dramatic increases in daily mortality. However, recent epidemiologic studies have reported statistically significant health effects and mortality due to low levels of air pollution. The statistical significance does not prove causation in observational studies; therefore it is necessary to evaluate these associations. There are arguments for and against each of the numerous studies using Hill's criteria, however the body of accepted evidence supports the causal association. In particular, a high level of consistency in the estimated effect of PM10 has been observed across studies worldwide. The mechanism of the relationship between air pollution and health effects is not obvious. The mechanism of particle-induced injury may involve the production of an inflammatory response by the particulate. The harvesting and the threshold effect are also major concerns regarding the health effects of air pollution. However, current epidemiologic findings indicate that linear models lacking a threshold are appropriate for assessing the effect of particulate air pollution on daily mortality even at current levels.