ABSTRACT
Objectives: We tended to explore the association of indoor air pollution (IAP) and non-neoplastic digestive system diseases (NNDSD) among the Chinese middle-aged and older population. Methods: From 2011 to 2018, we included 7884 NNDSD-free adults from the China Health and Retirement Longitudinal Study (CHARLS). Physician-diagnosed NNDSD was obtained by self-reported information at baseline and updated across follow-up surveys. We investigated the associations between baseline exposure of solid fuel use for cooking and/or heating and NNDSD diagnosed during follow-up through Cox proportional hazard models. Furthermore, we examined the relationship between cooking fuel switching and NNDSD diagnosed during follow-up. Results: Solid fuel use for cooking and/or heating was positively associated with NNDSD after adjusting for potential confounders. The risk of NNDSD among subjects who always use solid fuel for cooking (adjusted hazard ratio [aHR]: 1.42; 95% confidence interval [CI]: 1.09, 1.84) was higher than those with always clean fuels. Moreover, we found a lower NNDSD risk among participants who switched from solid to clean cooking fuel (aHR: 0.65; 95% CI: 0.49, 0.87) than those with always solid fuels. Conclusion: Our present study shows that indoor solid fuel use is a dependent risk factor for NNDSD. Moreover, switching to clean fuel may contribute to the prevention of digestive system illnesses.
Subject(s)
Digestive System Diseases , East Asian People , Adult , Middle Aged , Humans , Aged , Cohort Studies , Longitudinal Studies , Risk Factors , China/epidemiologyABSTRACT
OBJECTIVE: To investigate the clinical efficacy of coenzyme Q10 (CoQ10) plus trimetazidine (TMZ) in treating acute viral myocarditis (AVMC) and the combination's influence on the oxidative stress markers and the patients' quality of life (QoL). METHODS: This retrospective analysis enrolled 156 patients with AVMC admitted to the Department of Cardiology of the Affiliated Hospital of Chengdu University of Traditional Chinese Medicine between February 2018 and February 2019. Based on the treatment method each patient was administered, the patients were classified into a control group (n=72, CoQ10 therapy) and a combination group (n=84, CoQ10+TMZ therapy). The clinical effectiveness was observed in the two groups two weeks after the treatment, and the changes in the patients' serum inflammatory factor levels, oxidative stress indexes, myocardial enzyme levels, and cardiac function were compared. RESULTS: The combination group had a far superior total effective rate than the control group (90.5% vs. 77.8%, P<0.05). After the treatment, the serum inflammatory factor levels, including tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), and C-reactive protein (CRP), decreased in both groups, and the index levels in the combination group were significantly better than they were in the control group (P<0.05). The oxidative stress indicators, such as superoxide dismutase (SOD), malondialdehyde (MDA) and nitric oxide (NO), improved more significantly in the combination group compared to the control group (P<0.05). The myocardial zymogram creatine kinase (CK), cardiac troponin (cTnI), creatine kinase isoenzyme MB (CK-MB), and lactate dehydrogenase (LDH) levels were reduced in the two groups, with lower levels in the combination group. The left ventricular systolic function and the patients' QoL were better in the combination group compared with the control group (P<0.05). CONCLUSIONS: CoQ10 plus TMZ yields a favorable clinical effectiveness in the treatment of AVMC, and it can effectively promote cardiac function recovery, alleviate oxidative stress and inflammatory reactions, and bolster patients' QoL.
ABSTRACT
BACKGROUND: Liver X receptor alpha (Lxrα) is a sterol-regulated transcription factor that limits atherogenesis by regulating cholesterol homeostasis and inflammation in macrophages. Transcriptional profiling identified the reverse cholesterol transport protein Arf-like 7 (Arl7, Arl4c) as a Lxrα target gene. We hypothesized that the LXR response element (LXRE) sequence on the murine macrophage Arl7 promoter may play a critical role in Lxrα's atherosuppressive effects. METHODS: Employing low density lipoprotein receptor-deficient mice with macrophage-specific Lxrα overexpression (Ldlr-/- MΦ-Lxrα), we constructed a novel in vivo Ldlr-/- MΦ-Lxrα Arl7MutLXRE model possessing macrophage-specific mutations within the Arl7 promoter LXRE sequences (Arl7MutLXRE) using the CRISPR/spCas9 genome editing technique. In vitro and in vivo transplantation studies were conducted using bone marrow-derived macrophages (BMDMs) and peritoneal macrophages (PMs). RESULTS: Ldlr-/-, Ldlr-/- MΦ-Lxrα, and Ldlr-/- MΦ-Lxrα Arl7MutLXRE mice on a 60% high-fat diet displayed no significant differences in body weight, fat mass, glucose homeostasis, or lipid metabolism. Macrophage Lxrα promoted Arl7 expression, enhanced cholesterol efflux, and reduced foam cell formation in an Arl7 LXRE-dependent manner. In contrast, Lxrα reduced macrophage activation, inflammatory cytokine expression, and efferocytosis independent of Arl7 LXRE. Western diet-fed Ldlr-/- mice reconstituted with transgenic BMDMs revealed that macrophage Lxrα reduced atherosclerotic plaque formation independent of Arl7 LXRE. CONCLUSION: Lxrα's anti-atherosclerotic effects in Ldlr-/- mice are not primarily attributable to Lxrα's influence on Arl7 expression. This evidence suggests that Lxrα's effects on plaque inflammation may be more critical to in vivo atherogenesis than its effects on macrophage cholesterol efflux and foam cell development.
