In this review, we explore recent advances and accumulating evidence uniting immune dysregulation, inflammaging and recurring mutations in the pathogenesis of MDS.Occupational lung diseases (OLDs) are caused, aggravated or exacerbated by exposures at the workplace. OLDs encompass a wide range of respiratory diseases similar to that found outside the work environment. Occupational asthma is the most commonly diagnosed OLD. Other OLDs may include acute and chronic conditions, ranging from hypersensitivity pneumonitis to chronic obstructive pulmonary disease (COPD) to pulmonary fibrosis. Historically, research into OLDs has centered on diseases resulting from exposures relevant to high-income countries and more obvious hazardous occupations, such as silicosis in coal miners. Peer-reviewed publications in 2019 have broadened the focus to include low- and middle-income countries and once-overlooked occupations such as dry cleaning and animal husbandry. Technological advances and greater understanding of disease etiology have allowed researchers and clinicians to implement improved risk analysis, screening and mitigation strategies to not only treat disease once it occurs, but to identify at-risk populations and institute protections to prevent or limit the negative impacts of workplace hazards. As recognition of OLDs as a worldwide threat in a variety of occupations increases, research is allowing for the development of better treatments and preventive measures that advance workers' rights and ensure their continued good health.Depression is currently one of the most common psychiatric disorders and the number of patients receiving antidepressant treatment is increasing every year. Therefore, it is essential to understand the underlying mechanisms that are associated with higher prevalence of depression. The main component leading to the change in functioning, in the form of apathy, anhedonia, lack of motivation and sleep disturbances, is stress. This is the factor that in recent decades-due to the civilization speed, dynamic technological development as well as competitiveness and competition in relationships-significantly affects the psychophysical condition, which results in an increase in the prevalence of civilization diseases, including depression. To understand the mechanism of susceptibility to this disease, one should consider the significant role of the interaction between immune and nervous systems. Their joint development from the moment of conception is a matrix of later predispositions, both associated with the mobilization of the proinflammatory pathways (TNFα, IL-1β, IL-6) and associated with psychological coping with stress. Such an early development period is associated with epigenetic processes that are strongly marked in prenatal development up to 1 year of age and determinate the characteristic phenotype for various forms of pathology, including depression. Regarding the inflammatory hypothesis of depression, interleukin 17 (IL-17), among other proinflammatory cytokines, might play an important role in the development of depressive disorders. It is secreted by Th17 cells, crossed the placental barrier and acts on the brain structures of the fetus by increasing IL-17 receptor levels and affecting the intensity of its signaling in the brain. Retigabine belongs to the novel generation of antiepileptic drugs but its complex mechanism of action causes that the drug might be effective in other diseases, for instance, alcohol dependence. It is known that ethanol abuse impaired the function of brain structures associated with memory and learning such as the hippocampus. In our previous study, retigabine reduced hippocampal changes induced by ethanol in the EEG rhythms in rabbits. This study is focused on the impact of retigabine on memory processes in male rats receiving alcohol. Memory was evaluated in various experimental models Morris water maze, Contextual, and Cued Fear Conditioning tests. Retigabine was administered for 3weeks directly to the stomach via oral gavage at a dose of 10mg/kg. Rats received also 20% ethanol (5g/kg/day in two doses) via oral gavage for 3weeks and had free access to 5% ethanol in the afternoon and at night. Morris water maze was performed after 1 and 3weeks of ethanol administration and after 1week from the discontinuation of ethanol administration. Contextual and Cued Fear Conditioning tests were carried out after 24h and 72h of alcohol discontinuation. The drug significantly decreased ethanol-induced memory disturbances during alcohol administration as well as slightly improved learning processes after the discontinuation of ethanol administration. This beneficial effect of retigabine-ethanol interaction on memory may be a relevant element of the drug's impact on the development of addiction.This beneficial effect of retigabine-ethanol interaction on memory may be a relevant element of the drug's impact on the development of addiction.Mitochondrial (MT) dysfunction is a hallmark of aging and has been associated with most aging-related diseases as well as immunological processes. However, little is known about aging, lifestyle and genetic factors influencing mitochondrial DNA (mtDNA) abundance. Selleckchem Seladelpar In this study, mtDNA abundance was estimated from the weighted intensities of probes mapping to the MT genome in 295,150 participants from the UK Biobank. We found that the abundance of mtDNA was significantly elevated in women compared to men, was negatively correlated with advanced age, higher smoking exposure, greater body-mass index, higher frailty index as well as elevated red and white blood cell count and lower mortality. In addition, several biochemistry markers in blood-related to cholesterol metabolism, ion homeostasis and kidney function were found to be significantly associated with mtDNA abundance. By performing a genome-wide association study, we identified 50 independent regions genome-wide significantly associated with mtDNA abundance which harbour multiple genes involved in the immune system, cancer as well as mitochondrial function. Using mixed effects models, we estimated the SNP-heritability of mtDNA abundance to be around 8%. To investigate the consequence of altered mtDNA abundance, we performed a phenome-wide association study and found that mtDNA abundance is involved in risk for leukaemia, hematologic diseases as well as hypertension. Thus, estimating mtDNA abundance from genotyping arrays has the potential to provide novel insights into age- and disease-relevant processes, particularly those related to immunity and established mitochondrial functions.