Hansonmelgaard7934

Angiotensin converting enzyme 2 (ACE2) is the door for SARS-CoV-2, expressed in critical metabolic tissues. So, it is rational that the new virus causes pleiotropic alterations in glucose metabolism, resulting in the complication of pre-existing diabetes's pathophysiology or creating new disease mechanisms. However, it seems that less attention has been paid to this issue. This review aimed to highlight the importance of long-term consequences and pleiotropic alterations in glucose metabolism following COVID-19 and emphasize the need for basic and clinical research in metabolism and endocrinology.

SARS-CoV-2 shifts cellular metabolism from oxidative phosphorylation to glycolysis, which leads to a decrease in ATP generation. Together with metabolic imbalance, the impaired immune system elevates the susceptibility of patients with diabetes to this deadly virus. SARS-CoV-2-induced metabolic alterations in immune cells can result in hyper inflammation and a cytokine storm. Metabolic dysfunction may affect theolic and clinical features, supporting a potential role of COVID-19 in the development of diabetes.Pathological cardiac hypertrophy is associated with many diseases including hypertension. Recent studies have identified important roles for microRNAs (miRNAs) in many cardiac pathophysiological processes, including the regulation of cardiomyocyte hypertrophy. However, the role of miR-145-5p in the cardiac setting is still unclear. In this study, H9C2 cells were overexpressed with microRNA-145-5p, and then treated with Ang-II for 24 h, to study the effect of miR-145-5p on Ang-II-induced myocardial hypertrophy in vitro. Results showed that Ang-II treatment down-regulated miR-145-5p expression were revered after miR-145-5p overexpression. Based on results of bioinformatics algorithms, paxillin was predicted as a candidate target gene of miR-145-5p, luciferase activity assay revealed that the luciferase activity of cells was substantial downregulated the following co-transfection with wild paxillin 3'UTR and miR-145-5p compared to that in scramble control, while the inhibitory effect of miR-145-5p was abolished after transfection of mutant paxillin 3'UTR. Additionally, overexpression of miR-145-5p markedly inhibited activation of Rac-1/ JNK /c-jun/ NFATc3 and ANP expression and induced SIRT1 expression in Ang-II treated H9c2 cells. Jointly, our study suggested that miR-145-5p inhibited cardiac hypertrophy by targeting paxillin and through modulating Rac-1/ JNK /c-jun/ NFATc3/ ANP / Sirt1 signaling, therefore proving novel downstream molecular pathway of miR-145-5p in cardiac hypertrophy.Colorectal cancer (CRC) is between the top three occurring cancers worldwide. The anticancer effects of Cannabinoid receptor 2 (CB2) agonist (GW833972A) in the presence and absence of its inverse agonist (SR144528) on Human colorectal adenocarcinoma cells (HT-29) was investigated. Following cell viability assays on HT-29 and HFF cells, the molecular mechanism(s) of cytotoxicity and apoptotic pathways of cell death were analyzed. The anticancer effects of CB2 agonist were measured with tumor cell migration and colony-forming assays. Real-time PCR and Western blotting techniques were used to examine any alterations in the expression of apoptotic genes. A concentration and time-dependent cytotoxicity of CB2 agonist with IC50 value of 24.92 ± 6.99 μM was obtained. The rate of lipid peroxidation was elevated, while the TNF-α concentration was declined, significantly (p  less then  0.05). CB2 agonist (50 μM) reduced the colony-forming capability by 83% and tumor cell migration by 50%. Apoptotic effects of CB2 agonist were revealed with the increase of apoptotic cells in Acridine orange/Ethidium bromide staining, clear DNA fragmentation, pro-apoptotic genes and proteins upregulation (Caspase-3 and p53), and significant downregulation of anti-apoptotic Bcl-2. All assessments demonstrated that CB2 agonist-induced effects were reversed by CB2 inverse agonist. These data suggest that CB2 agonists at micro-molar concentrations might be considered in the CRC treatment, and their effectiveness attributes to the apoptosis induction via upregulation of caspase-3 and p53 and downregulation of Bcl-2.Multiple sclerosis (MS) is an autoimmune chronic inflammatory disease of the central nervous system with a wide range of symptoms, like executive function defect, cognitive dysfunction, blurred vision, decreased sensation, spasticity, fatigue, and other symptoms. This neurological disease is characterized by the destruction of the blood-brain barrier, loss of myelin, and damage to neurons. It is the result of immune cells crossing the blood-brain barrier into the central nervous system and attacking self-antigens. Heretofore, many treatments proved that they can retard the progression of the disease even though there is no cure. Therefore, treatments aimed at improving patients' quality of life and reducing adverse drug reactions and costs are essential. In this review, the treatment approaches to alleviate the progress of MS include the following pharmacotherapy, antibody therapy, cell therapy, gene therapy, and surgery. GSK2830371 manufacturer The current treatment methods of MS are described in terms of the prevention of myelin shedding, the promotion of myelin regeneration, and the protection of neurons.Cancer therapies have undergone a tremendous progress over the past decade. Precision medicine provides a more tailored approach, making the combination of existing therapies more precise. Different types of cancers are characterized by unique biomarkers that are targeted using various genomic approaches by clinicians and companies worldwide to achieve efficient treatment with minimal side effects. Precision medicine has two broad approaches namely stratified and personalized medicine. The driver mutations could vary within a subtype while the same driver mutations could be found across different subtypes. Precision medicine has recently gained a lot of importance for breast cancer therapy. Various kinds of mutations like hotspot mutations, gene alterations, gene amplification mutations are targeted to design a more specific therapy. Apart from these known gene mutations there are various unknown mutations. Thus, tumor heterogeneity can pose a challenge to precision medicine. For breast cancer, one of the most successful models developed in case of precision medicine is the anti-HER2 therapies as HER2 was considered to have the worst prognosis being highly malignant.