RESUMEN
BACKGROUND: Little is known about the association between sarcopenia and cardiovascular disease (CVD) among middle-aged and older adults. Using the nationally representative data from the China Health and Retirement Longitudinal Study (CHARLS), we conducted cross-sectional and longitudinal analyses to investigate the association between sarcopenia status and CVD in middle-aged and older Chinese population. METHODS: The sample comprised 15,137 participants aged at least 45 years from the CHARLS 2015. Sarcopenia status was defined according to the Asian Working Group for Sarcopenia 2019 (AWGS 2019) criteria. CVD was defined as the presence of physician-diagnosed heart disease and/or stroke. A total of 11,863 participants without CVD were recruited from the CHARLS 2015 and were followed up in 2018. Cox proportional hazards regression models were conducted to examine the effect of sarcopenia on CVD. FINDINGS: The pre valence of CVD in total populations, no-sarcopenia, possible sarcopenia and sarcopenia individuals were 12.6% (1905/15,137), 10.0% (1026/10,280), 18.1% (668/3685), 18.0% (211/1172), respectively. Both possible sarcopenia [OR (95% CI): 1.29 (1.13-1.48)] and sarcopenia [1.72 (1.40-2.10)] were associated with CVD in total populations. During the 3.6 years of follow-up, 1,273 cases (10.7%) with incident CVD were identified. In the longitudinal analysis, individuals with the diagnosis of possible sarcopenia (HR:1.22, 95% CI: 1.05-1.43) and sarcopenia participants (HR:1.33, 95% CI: 1.04-1.71) were more likely to have new onset CVD than no-sarcopenia peers. INTERPRETATION: Both possible sarcopenia and sarcopenia, assessed using the AWGS 2019 criteria, were associated with higher CVD risk among middle-aged and older Chinese adults. FUNDING: None.
RESUMEN
AIM: To observe the effects of acute hypoxia and adenosine on splenic T lymphocyte proliferation. METHODS: Wistar rats were divided into control and hypoxic group, and the latter were exposed to hypoxia (5000 m simulated high altitude, 23 h/d). Three days later, spleen cells were collected and stimulated by 5.0 microg/ml and 2.5 microg/ml concanavalin A (ConA) to determine the splenocyte proliferation. The proliferation was also observed after addition of different amount of adenosine to culture medium. RESULTS: Acute hypoxia and adenosine had marked inhibitory effect on mitogenic response to Con A in splenic T cells, and the inhibitory effect induced by adenosine displayed concentration-dependent. CONCLUSION: Acute hypoxia may impair the T cell function and adenosine could be involved in this process.
Asunto(s)
Adenosina/farmacología , Proliferación Celular/efectos de los fármacos , Hipoxia , Linfocitos T/citología , Linfocitos T/efectos de los fármacos , Animales , Concanavalina A/farmacología , Medios de Cultivo/química , Masculino , Ratas , Ratas Wistar , Bazo/citologíaRESUMEN
To explore the effects of ATP concentration in the medium and hypoxia exposure on mitochondrial DNA expression at transcriptional and translational level, rats were exposed to hypoxia in a hypobaric chamber simulating 4000 m above sea level for 3 d (acute hypoxia) or 40 d (chronic hypoxia). Cerebral cortex mitochondria were isolated from control and hypoxia-exposed rats by centrifugation program. The activities of intramitochondrial RNA and protein synthesis were measured respectively by the methods of incorporation of (3)H-UTP or (3)H-Leucine in a cell-free system in vitro in isolated organelle. The effect of different ATP concentrations in medium on incorporation activity of mitochondria from control rat brains was observed. The results showed that there was a 40% reduction in RNA synthesis and a 60% inhibition in protein synthesis in isolated mitochondria in vitro in acute hypoxia exposure compared to control. But in chronic hypoxic exposure, the inhibition of both RNA synthesis and protein synthesis was alleviated, being 72% and 76% of the normoxic control, respectively. Furthermore, the effect of ATP concentration in medium on mitochondrial RNA and protein synthesis in vitro showed two phases. The mitochondrial RNA and protein synthesis were inhibited when ATP concentration was either above or below 1 mmol/L in the incubation medium. These results indicate that hypoxia exposure affects the expression of mtDNA at both transcription and translation levels. It also suggests that the improvement of mitochondrial semi-automation during chronic hypoxic exposure may be at least one of the cellular mechanisms of body adaptation to hypoxia. The regulation of ATP in mitochondrial RNA and protein synthesis is therefore an economic and effective mode of regulation.
Asunto(s)
Hipoxia/metabolismo , Mitocondrias/metabolismo , ARN/biosíntesis , Adenosina Trifosfato/metabolismo , Animales , Encéfalo/metabolismo , Masculino , Biosíntesis de Proteínas , ARN Mitocondrial , Ratas , Ratas WistarRESUMEN
This study was intended to evaluate the effects of hypoxic exposure on gene expression and coordination of cytochrome oxidase (COX) subunits I (COX I) and IV (COX IV) encoded by mtDNA and nDNA respectively in rat cerebral cortex. Male Wistar rats were exposed to hypoxia in a hypobaric chamber simulating high altitude at 5000 m for 2, 5, 15 and 30 d. Control rats were fed outside the hypobaric chamber (the height was 300 m above sea level). Rats were sacrificed and mitochondria from cerebral cortex were isolated by differential centrifugation at each time point. COX I and COX IV proteins in isolated rat cerebral cortex mitochondria were detected by Western blot analysis and mRNA in the cerebral cortex by RT-PCR. The ratios of protein and mRNA were used to estimate the coordinative expression of two subunits. The results showed that COX I mRNA increased significantly at 2 and 5 d, and decreased to the control level at 15 and 30 d; COX IV mRNA remarkably increased at 2, 5 and 15 d, and dropped below the control level at 30 d. The mRNA ratio of COX IV to COX I reached a peak at 15 d, but showed no differences between other time points. The Western blot analysis of COX I and COX IV in isolated rat cerebral cortex mitochondria showed no obvious changes during hypoxic exposure. Our findings demonstrate that hypoxia can affect mRNA expression of COX I and COX IV and their coordination, while protein expression of both subunits are stable and coordinative. This study suggests that the expression of COX I and COX IV proteins during hypoxic exposure is coordinately regulated by post-transcriptional mechanisms.