Pathophysiology regarding Obesity

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Tebuconazole (TEB) is a broad-spectrum conazole fungicide that has been used in agriculture in the control of foliar and soil-borne diseases of many crops. The present study has investigated the adverse effects of subchronic exposure to TEB on the kidney of male rats. Animals were divided into four equal groups and treated with TEB at increasing doses 0.9, 9 and 27 mg/kg body weight for 28 consecutive days. The results showed that TEB induced oxidative stress in the kidney demonstrated by an increase in malondialdehyde (MDA), protein carbonyl (PC), advanced oxidation protein product (AOPP) levels and DNA damage, as compared to the controls. Furthermore, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities were increased in the renal tissue of treated rats. Moreover, significant decrease in reduced glutathione (GSH) content in TEB-treated rats was observed, while oxidized glutathione (GSSG) levels were increased, thus a marked fall in GSH/GSSG ratio was registered in the kidney. Glutathione reductase (GR) activity showed a significant increase after TEB exposure. Moreover, TEB down-regulated the expression of Bcl2 and up-regulated the expression of Bax and caspase 3, which triggered apoptosis via the Bax/Bcl2 and caspase pathway. Also, TEB administration resulted in altered biochemical indicators of renal function and varying lesions in the overall histo-architecture of renal tissues. Taken together, our findings brought into light the renal toxicity induced by TEB, which was found to be significant at low doses.In terms of public health, the 21st century has been characterized by coronavirus pandemics in 2002-03 the virus SARS-CoV caused SARS; in 2012 MERS-CoV emerged and in 2019 a new human betacoronavirus strain, called SARS-CoV-2, caused the unprecedented COVID-19 outbreak. During the course of the current epidemic, medical challenges to save lives and scientific research aimed to reveal the genetic evolution and the biochemistry of the vital cycle of the new pathogen could lead to new preventive and therapeutic strategies against SARS-CoV-2. Up to now, there is no cure for COVID-19 and waiting for an efficacious vaccine, the development of "savage" protocols, based on "old" anti-inflammatory and anti-viral drugs represents a valid and alternative therapeutic approach. As an alternative or additional therapeutic/preventive option, different in silico and in vitro studies demonstrated that small natural molecules, belonging to polyphenol family, can interfere with various stages of coronavirus entry and replication cycle. Here, we reviewed the capacity of well-known (e.g. quercetin, baicalin, luteolin, hesperetin, gallocatechin gallate, epigallocatechin gallate) and uncommon (e.g. scutellarein, amentoflavone, papyriflavonol A) flavonoids, secondary metabolites widely present in plant tissues with antioxidant and anti-microbial functions, to inhibit key proteins involved in coronavirus infective cycle, such as PLpro, 3CLpro, NTPase/helicase. Due to their pleiotropic activities and lack of systemic toxicity, flavonoids and their derivative may represent target compounds to be tested in future clinical trials to enrich the drug arsenal against coronavirus infections.In age-related macular degeneration, inflammatory events are presumed to contribute to disease development. A primary suspect of this contribution is the microglia, the innate immune cell of the retina. In addition, retinal pigment epithelium (RPE) cells can be inflammatorily activated. In this study, we investigate the effect of activated RPE cells on retinal microglia and on neuronal cells. RPE cells and microglia were harvested from porcine eyes. In addition, a neuronal cell line (SHSY-5Y) of human origin was used. For inflammatory activation, agonists of toll-like receptors in different concentrations were used Pam2CSK4 (Pam; TLR-2), Polyinosinicpolycytidylic acid (Poly IC; TLR-3) and lipopolysaccharid (LPS; TLR-4). Cell viability was investigated with an MTT assay. The secretion of cytokines was assessed in an ELISA and their expression in real-time PCR. There was no effect of the agonists on cell viability in RPE cells. All agonists induced the secretion of IL-6 and IL-8 in RPE cells with the strongest mmatory activated RPE cells have a regulatory effect on the pro-inflammatory activation of microglia, stressing the importance of the interaction between these two retinal cell types. Microglia treated with RPE supernatant reduced viability of a neuronal cell line, indicating a neurotoxic effect.To avoid negative environmental impacts of escapees and potential inter-breeding with wild populations, the Atlantic salmon farming industry has and continues to extensively test triploid fish that are sterile. However, they often show differences in performance, physiology, behavior and morphology compared to diploid fish, with increased prevalence of vertebral deformities and ocular cataracts as two of the most severe disorders. Here, we investigated the mechanisms behind the higher prevalence of cataracts in triploid salmon, by comparing the transcriptional patterns in lenses of diploid and triploid Atlantic salmon, with and without cataracts. We assembled and characterized the Atlantic salmon lens transcriptome and used RNA-seq to search for the molecular basis for cataract development in triploid fish. Transcriptional screening showed only modest differences in lens mRNA levels in diploid and triploid fish, with few uniquely expressed genes. In total, there were 165 differentially expressed genes (DEGs) between the cataractous diploid and triploid lens. Of these, most were expressed at lower levels in triploid fish. ODM-201 mw Differential expression was observed for genes encoding proteins with known function in the retina (phototransduction) and proteins associated with repair and compensation mechanisms. The results suggest a higher susceptibility to oxidative stress in triploid lenses, and that mechanisms connected to the ability to handle damaged proteins are differentially affected in cataractous lenses from diploid and triploid salmon.Exposure to high ambient temperatures (HAT) is associated with increased mortality, weight loss, immunosuppression, and metabolic malfunction in birds, all of which are likely downstream effects of reduced food intake. While the mechanisms mediating the physiological responses to HAT are documented, the neural mechanisms mediating behavioral responses are poorly understood. The aim of the present study was thus to investigate the hypothalamic mechanisms mediating heat-induced anorexia in four-day old broiler chicks. In Experiment 1, chicks exposed to HAT reduced food intake for the duration of exposure compared to controls in a thermoneutral environment (TN). In Experiment 2, HAT chicks that were administered an intracerebroventricular (ICV) injection of neuropeptide Y (NPY) increased food intake for 60 min post-injection, while TN chicks that received NPY increased food intake for 180 min post-injection. In Experiment 3, chicks in both the TN and HAT groups that received ICV injections of corticotropin-releasing factor (CRF) reduced food intake for up to 180 min post-injection.