The expression of MEG8 was upregulated, while miR-15a-5p and miR-15b-5p were downregulated in NSCLC cell lines. The depletion of MEG8 inhibited NSCLC cell proliferation, migration, and invasion in vitro. MEG8 contributed to NSCLC progression by targeting miR-15a-5p/miR-15b-5p in vitro. LncRNA MEG8 contributes to tumor growth of NSCLC via the miR-15a/b-5p/PSAT1 axis in vivo. Thus, we concluded that lncRNA MEG8 promotes NSCLC progression by modulating the miR-15a/b-5p/PSAT1 axis. Our findings demonstrated that lncRNA MEG8 plays a critical role in NSCLC development. LncRNA MEG8, miR-15a-5p, miR-15b-5p, and PSAT1 may serve as potential targets for NSCLC therapy. Our findings demonstrated that lncRNA MEG8 plays a critical role in NSCLC development. LncRNA MEG8, miR-15a-5p, miR-15b-5p, and PSAT1 may serve as potential targets for NSCLC therapy. Acute myocardial infarction (MI) remains a frequent health event and a major contributor to long-term impairments globally. So far, research on social inequalities in MI incidence and mortality with respect to MI severity is limited. Furthermore, evidence is lacking on disparities in the length of life affected by MI. This study investigates social inequalities in MI incidence and mortality as well as in life years free of MI and affected by the consequences of mild or severe MI. The study is based on data of a large German statutory health insurance provider covering the years 2008 to 2017 (N = 1,253,083). Income inequalities in MI incidence and mortality risks and in life years with mild or severe MI and without MI were analysed using multistate analyses. The assessment of MI severity is based on diagnosed heart failure causing physical limitations. During the study period a total of 39,832 mild MI, 22,844 severe MI, 276,582 deaths without MI, 15,120 deaths after mild MI and 16,495 deaths after severe MI occurred. Clear inequalities were found in MI incidence and mortality, which were strongest among men and in severe MI incidence. Moreover, substantial inequalities were found in life years free of MI in both genders to the disadvantage of those with low incomes and increased life years after mild MI in men with higher incomes. Life years after severe MI were similar across income groups. Social inequalities in MI incidence and mortality risks led to clear disparities in the length of life free of MI with men with low incomes being most disadvantaged. Our findings stress the importance of primary and secondary prevention focusing especially on socially disadvantaged groups. Social inequalities in MI incidence and mortality risks led to clear disparities in the length of life free of MI with men with low incomes being most disadvantaged. Our findings stress the importance of primary and secondary prevention focusing especially on socially disadvantaged groups. Atherosclerosis (AS) is a chronic inflammatory disorder. The aim of our study was to explore the role of circular RNA (circRNA) transmembrane 7 superfamily member 3 (circTM7SF3) in AS progression. Experiments were conducted using oxidized low-density lipoprotein (ox-LDL)-induced THP-1-derived macrophages and differentiated human monocyte-derived macrophages (hMDMs). https://www.selleckchem.com/products/rmc-9805.html Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of circTM7SF3, its linear form TM7SF3, microRNA-206 (miR-206) and aspartyl (asparaginyl) β-hydroxylase (ASPH) messenger RNA (mRNA). Cell viability and apoptosis were examined by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry. Cell inflammation was analyzed by measuring the production of tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) using enzyme-linked immunosorbent assay (ELISA) kits. Cell oxidative stress was assessed through analyzing the levels of oxidative stress markers using their correspond through up-regulating the expression of ASPH via targeting miR-206. CircTM7SF3 contributed to ox-LDL-induced injury in AS cell model through up-regulating the expression of ASPH via targeting miR-206. Health workers are crucial to the successful implementation of infection prevention and control strategies to limit the transmission of SARS-CoV-2 at healthcare facilities. The aim of our study was to determine SARS-CoV-2 infection prevention and control knowledge and attitudes of frontline health workers in four provinces of South Africa as well as explore some elements of health worker and health facility infection prevention and control practices. A cross-sectional study design was utilised. The study population comprised both clinical and non-clinical staff working in casualty departments, outpatient departments, and entrance points of health facilities. A structured self-administered questionnaire was developed using the World Health Organization guidance as the basis for the knowledge questions. COVID-19 protocols were observed during data collection. A total of 286 health workers from 47 health facilities at different levels of care participated in the survey. The mean score on the 10 knowledge ing adequate infection prevention and control training for all staff and universal access to appropriate PPE were identified as key areas that needed to be addressed. Interim and final reports which identified key shortcomings that needed to be addressed were provided to the relevantprovincial departments of health. The attitudes of participants reflected a willingness to engage in appropriate SARS-CoV-2 infection prevention and control practices as well as a commitment to be involved in COVID-19 patient care. Ensuring adequate infection prevention and control training for all staff and universal access to appropriate PPE were identified as key areas that needed to be addressed. Interim and final reports which identified key shortcomings that needed to be addressed were provided to the relevant provincial departments of health. Age-related hearing loss (ARHL), also known as presbycusis, is the most common sensory impairment seen in elderly people. However, the cochlear aging process does not affect people uniformly, suggesting that both genetic and environmental (e.g., noise, ototoxic drugs) factors and their interaction may influence the onset and severity of ARHL. Considering the potential links between thyroid hormone, mitochondrial activity, and hearing, here, we probed the role of p43, a N-terminally truncated and ligand-binding form of the nuclear receptor TRα1, in hearing function and in the maintenance of hearing during aging in p43 mice through complementary approaches, including in vivo electrophysiological recording, ultrastructural assessments, biochemistry, and molecular biology. We found that the p43 mice exhibit no obvious hearing loss in juvenile stages, but that these mice developed a premature, and more severe, ARHL resulting from the loss of cochlear sensory outer and inner hair cells and degeneration of spiral ganglion neurons.