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BACKGROUND: The most common symptoms of coronavirus infections are fever, cough, shortness of breath, headache, ache of joints, a loss of smell and loss of taste, and etc. Early studies suggested that smell and taste receptors were associated with pathogenic detection and immunity. Thus, we aimed to evaluate the expression profile of gene receptors that are related to taste, smell, and appetite control in COVID-19 patients and their putative correlation with SARS-CoV-19 variants. METHOD: Gene expression levels of TAS1R2, TAS1R3, TAS2R38, OR51E1, LEPR, GHRL were analyzed in 100 COVID-19 patients and 100 SARS-CoV-2 RT-qPCR negative group. RESULTS: The expression levels of TAS1R2 and TAS1R3 genes were significantly decreased in COVID-19 patients who were infected with Delta variant. However, the TAS2R38 gene expression level was significantly lower when compared to the control group. The TAS1R2 gene expression was positively correlated with TAS1R3, and TAS2R38 genes (p = 0.001, p = 0.025, respectively). CONCLUSION: TAS1R2, TAS1R3, and TAS2R38 gene expression levels were decreased in the Delta variant compared to the Omicron BA.1 variant in the studied groups. These results provided a significant clue for the temporary taste loss, especially in patients infected with the Delta variant, which is the most disruptive and symptomatic variant causing hospitalizations, and deaths compared to other variants may be because ACE2 is expressed in the taste buds and high replication of SARS-CoV-2 in the infected gustatory cells in the taste bud generates inflammation and then could eventually destroy the cells. This gustatory cell damage may cause malfunction of the gustatory system.

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Avermectins are a group of macrocyclic lactones that are commonly used as pesticides to treat pests and parasitic worms. Some members of the avermectin family, such as ivermectin, have been found to exhibit anti-proliferative activity toward cancer cells. This study aimed to investigate the potential anti-cancer activities of avermectin B1a using the HCT-116 colon cancer cell line. The MTT assay was used to calculate the IC50 by incubating cells with increasing doses of avermectin B1a for 24, 48, and 72 h. Flow cytometry was used to evaluate apoptosis following the 24 h incubation of cells. The migration capacity of the HCT-116 cells in the absence or presence of avermectin B1a was also investigated. Finally, tubulin polymerization in the presence of avermectin B1a was evaluated. Avermectin B1a presented anti-proliferative activity with an IC50 value of 30 µM. Avermectin B1a was found to promote tubulin polymerization at 30 µM. In addition, avermectin B1a induced apoptosis in HCT-116 cells and substantially diminished their ability to migrate. Avermectin B1a exhibits significant anti-cancer activity and enhances tubulin polymerization, suggesting that it can be used as a promising microtubule-targeting agent for the development of future anticancer drugs.

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Cancer is the leading cause of death among women all over the world. Female tissue-specific cancers are the most commonly diagnosed among women and account for most cancer-related deaths. The main risk factors for women's cancer are hereditary factors, specific exposure to dangerous chemicals, disorders such as hormone imbalance, and lifestyle. High body mass index, low physical activity, low intake of fruit and vegetables, smoking, excessive alcohol consumption, lack of cancer screening and treatment are the most common risk factors. Nutrigenetics and nutrigenomics are both part of nutritional genomics. Nutrigenetics is how a person's body reacts to nutrients based on his/her genotype. It can be used to create a personalized diet, maintain a person's health, avoid disease, and if necessary to sustain therapy. Nutrigenomics studies the impact of nutrition on gene expression and the epigenomic, proteomic, transcriptomic and metabolomic effects of dietary intake. There is evidence that diet matters for different women's cancers, and is related to cancer progression, survival and treatment. The optimum combination for cancer prevention is a diet rich in vitamins and fibre, with low meat consumption, low milk intake and moderate use of alcohol. The Mediterranean diet looks to be an optimal diet with a good nutrition pattern, qualifying it as a therapy to prescribe.

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Abamectin, a blend of the natural avermectins B1a and B1b, is a widely-used insecticide/miticide with relatively low toxicity to mammals. Exposure to high doses of it, however, leads to cholinergic-like neurotoxic effects. Butyrylcholinesterase, which is best known for its abundant presence in plasma, is a serine hydrolase loosely coupled with the cholinergic system. It protects and supports the neurotransmitter function of its sister enzyme acetylcholinesterase. Here, using experimental and computational studies, we provide evidence demonstrating that abamectin is a potent (IC50 = 10.6 µM; Ki = 2.26 ± 0.35 µM) inhibitor of horse serum butyrylcholinesterase and that it interacts with the enzyme in a reversible, competitive manner predictively to block the mouth of the active-site gorge of the enzyme and to bind to several critical residues that normally bind/hydrolyze choline esters.

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AIMS: Medical treatment of arterial thrombosis is mainly directed against platelets and coagulation factors, and can lead to bleeding complications. Novel antithrombotic therapies targeting immune cells and neutrophil extracellular traps (NETs) are currently being investigated in animals. We addressed whether immune cell composition of arterial thrombi induced in mouse models of thrombosis resemble those of human patients with acute myocardial infarction (AMI). METHODS AND RESULTS: In a prospective cohort study of patients suffering from AMI, 81 human arterial thrombi were harvested during percutaneous coronary intervention and subjected to detailed histological analysis. In mice, arterial thrombi were induced using two distinct experimental models, ferric chloride (FeCl3) and wire injury of the carotid artery. We found that murine arterial thrombi induced by FeCl3 were highly concordant with human coronary thrombi regarding their immune cell composition, with neutrophils being the most abundant cell type, as well as the presence of NETs and coagulation factors. Pharmacological treatment of mice with the protein arginine deiminase (PAD)-inhibitor Cl-amidine abrogated NET formation, reduced arterial thrombosis and limited injury in a model of myocardial infarction. CONCLUSIONS: Neutrophils are a hallmark of arterial thrombi in patients suffering from acute myocardial infarction and in mouse models of arterial thrombosis. Inhibition of PAD could represent an interesting strategy for the treatment of arterial thrombosis to reduce neutrophil-associated tissue damage and improve functional outcome.

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