Health-related quality of life and associated factors among people living with HIV/AIDS in Sichuan, China: A cross-sectional study.

Purpose: This study aimed to explore health-related quality of life (HRQoL) and its associated factors among people living with HIV/AIDS (PLWH) in Sichuan, China. Methods: A total of 401 PLWH were recruited from the city of Panzhihua between August 2018 and January 2019. Demographic characteristics and disease-related data were collected by self-administered questionnaires and medical system records. Health-related quality of life (HRQoL) was measured by the medical outcome study HIV health survey (MOS-HIV), which measured ten subdimensions and two summarized dimensions, the physical health summary score (PHS) and the mental health summary score (MHS). Logistic regression models were used to explore the variables independently associated with quality of life. Results: The PHS and MHS measured by MOS-HIV were 53.66 ± 6.80 and 51.31 ± 7.66, respectively. Younger age, higher educational level, no methadone use, higher CD4 lymphocyte counts, less symptom counts and heathy BMI significantly were associated with higher HRQOL in the univariate χ2-test analysis. Education level was found to have a significant influence on patients' quality of life, both in physical health (P = 0.022) and mental health (P = 0.002) dimensions. Younger age (P = 0.032), higher CD4 lymphocyte counts (P = 0.007), less symptom counts (P < 0.001) and health BMI level (P < 0.001) were positively related to the PHS of quality of life in the multivariable logistic regression model. Conclusion: The HRQoL of PLWH in Sinchuan Province was relatively low. Age, educational level, methadone use, CD4 lymphocyte counts, symptom counts and BMI were positively related to quality of life. This study indicates that health caregivers should pay more attention to comorbidity issues and mental health in PLWH, especially for those with lower education levels, unhealthy body mass index, more symptomatic presentation and older age.

microRNA-135a-5p regulates NOD-like receptor family pyrin domain containing 3 inflammasome-mediated hypertensive cardiac inflammation and fibrosis via thioredoxin-interacting protein.

Hypertension is a severe public health problem that induces cardiac injury with alterations of gene expressions. The current study sought to evaluate the mechanism of microRNA(miR)-135a-5p in NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome-mediation of cardiac inflammation and hypertensive cardiac fibrosis. Firstly, hypertensive mouse models were established using angiotensin II (Ang II), followed by miR-135a-5p agomir treatment. Subsequently, mouse blood pressure and basic cardiac function indexes, histopathological changes, and cardiac fibrosis were all determined, in addition to detection of factors related to inflammation and fibrosis. Additionally, mice cardiac fibroblasts (CFs) were isolated and treated with Ang II. The binding relationship of miR-135a-5p and thioredoxin-interacting protein (TXNIP) was predicted and testified, while the interaction of TXNIP and NLRP3 was detected by means of a co-immunoprecipitation assay. It was found that miR-135a-5p was poorly-expressed in Ang II-treated mice and further exerted cardioprotective effects against hypertensive heart diseases. Moreover, over-expression of miR-135a-5p resulted in inhibition of inflammatory infiltration and almost eliminated cardiac fibrosis, as evidenced by decreased Collagen (COL)-I, COL-III, a-smooth muscle actin, NLRP3, tumor necrosis factor-α, and interleukin-6. Mechanically, miR-135a-5p inhibited TXNIP expression to block the binding of TXNIP and NLRP3. On the other hand, TXNIP up-regulation reversed the protective role of miR-135a-5p over-expression in CFs. Collectively, our findings indicated that miR-135a-5p over-expression inhibited TXNIP expression to block the binding of TXNIP and NLRP3, thereby alleviating hypertensive cardiac inflammation and fibrosis.

miR-449a induces EndMT, promotes the development of atherosclerosis by targeting the interaction between AdipoR2 and E-cadherin in Lipid Rafts.

EndMT plays an important role in the relationship between endothelial dysfunction and atherosclerosis. This work will elucidate the biofunction induced by miR-449a and lipid rafts in EndMT and development of atherosclerosis. The differential miRNA expression between atherosclerotic plaques and normal arteries were analyzed. The luciferase activities of AdipoR2 3' UTR treated with miR-449a were determined. ECs were dealt with miR-449a mimics or inhibitors, then cell proliferation and migration were assessed. Moreover, the expression of AdipoR2 and mesenchymal cell markers were analyzed. The influences of lipid rafts related to reciprocity between E-cadherin and AdipoR2 on TNF-α-induced damage in ECs were investigated. ApoE KO diabetic mice were used to explore the potential roles of miR-449a on atherosclerosis. Our results indicated that compared with normal arteries, 17 miRNAs were upregulated and 3 miRNAs were down-regulated in atherosclerotic plaques. The relative expression of miR-449a in plaques was significantly higher than that in normal arteries. MiR-449a suppressed AdipoR2 expression, additionally its interaction protein E-cadherin in ECs. MiR-449a enhanced expression of mesenchymal cell markers, induced cell proliferation and migration of ECs, regulated the interaction between E-cadherin and AdipoR2 interceded by lipid rafts. The miR-449a antagomir could protect against the development process of atherosclerosis in ApoE KO diabetic mice. In conclusion, miR-449a targeted to AdipoR2, and was a crucial mediator of EndMT and atherosclerosis in ECs through regulating E-cadherin bindability with AdipoR2 in lipid rafts. These results suggested that aim to lipid rafts and miR-449a in chronic EC inflammation response, was a feasible therapy strategy for atherosclerosis.

Effects of vibration in forced posture on biochemical bone metabolism indices, and morphometric and mechanical properties of the lumbar vertebra.

Epidemiological studies have shown a relatively strong association between occupational lower back pain (LBP) and long-term exposure to vibration. However, there is limited knowledge of the impact of vibration and sedentariness on bone metabolism of the lumbar vertebra and the mechanism of bone-derived LBP. The aim of this study was to investigate the effects of vibration in forced posture (a seated posture) on biochemical bone metabolism indices, and morphometric and mechanical properties of the lumbar vertebra, and provide a scientific theoretical basis for the mechanism of bone-derived LBP, serum levels of Ca(2+), (HPO4)(2-), tartrate-resistant acid phosphatase (TRAP), bone-specific alkaline phosphatase (BALP), and bone gla protein (BGP),the pathological changes and biomechanics of lumbar vertebra of New Zealand white rabbits were studied. The results demonstrate that both forced posture and vibration can cause pathological changes to the lumbar vertebra, which can result in bone-derived LBP, and vibration combined with a seated posture could cause further damage to bone metabolism. Serological changes can be used as early markers for clinical diagnosis of bone-derived LBP.

Immunosuppression induced by apoptosis of mixed lymphocyte culture is associated with p53.

A lymphocyte inhibition model was created using a co-culture of donor and host lymphocytes, resulting in apoptosis of the latter, and subsequently, inducing immune tolerance. This method may be used to resolve the immune rejection problem prior to organ transplantation. Using mixed lymphocyte culture (MLC) and/or addition of anti-anti-IL-2 neutralizing monoclonal antibody, we successfully developed a lymphocyte inhibition model in vitro. In this model, the apoptosis of recipient lymphocytes co-cultured with donor lymphocytes was observed by Wright-Giemsa stain, electron microscopy imaging and flow cytometry. The growth and proliferation of mixed lymphocytes were detected by XTT and BrdU assays. Cell viability was determined using CCK-8 cell viability assay. The activity of the recipient lymphocytes was very high when stimulated by antigens alone [PMLC+D2 (Bm) group] but markedly lowered by anti-anti-IL-2 neutralizing monoclonal antibody [PMLC+D2 (Bm)+anti­IL-2 group]. The suppression of recipient lymphocyte activity was due to apoptosis mediated by p53 and caspase-3, and the optimal ratio of donor and recipient lymphocytes for apoptosis was explored. With the exception of the control group, the ratio of apoptotic cells was highest in the PMLC+D2 (Bm)+anti-IL-2 group and lowest in the PMLC+D2 (Bm) group. Blockade of IL-2 with anti-IL-2 neutralizing antibody resulted in an increased number of apoptotic lymphocytes in our experiment, which suggested that IL-2 inhibits the apoptosis of lymphocytes. These data suggest that IL-2 is involved in MLC-induced apoptosis of recipient lymphocytes, and that apoptosis may be associated with p53 and caspase-3 pathways.