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Viper bites pose a significant public health issue in Armenia, even within urban areas, often resulting in clotting disorders, hypofibrinogenemia, and tissue necrosis in humans. This study investigates histopathological changes in various tissues during mice envenomation by West-Asian blunt-nosed viper (Macrovipera lebetina obtusa) venom, as well as the recovery process aided by experimental antivenom derived from sheep. The high venom dose caused substantial damage to the heart, lungs, liver, and kidneys in mice, indicating systemic harm. While antivenom administration can prevent mortality in mice envenomation, it may not fully mitigate histological damage in affected organs. Additionally, the study highlights the importance of timing antivenom administration, as the severity of tissue alterations can vary depending on the duration of envenomation. These findings shed light on antivenom's effects on viper envenomation and stress the need for further research to optimize its timing and dosage for minimizing histological damage and enhancing clinical outcomes.

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High-altitude environments present extreme conditions characterized by low barometric pressure and oxygen deficiency, which can disrupt brain functioning and cause edema formation. The objective of the present study is to investigate several biomolecule expressions and their role in the development of High Altitude Cerebral Edema in a rat model. Specifically, the study focuses on analyzing the changes in total arginase, nitric oxide, and lipid peroxidation (MDA) levels in the brain following acute hypobaric hypoxic exposure (7620 m, SO2=8.1 %, for 24 h) along with the histopathological assessment. The histological examination revealed increased TNF-α activity, and an elevated number of mast cells in the brain, mainly in the hippocampus and cerebral cortex. The research findings demonstrated that acute hypobaric hypoxic causes increased levels of apoptotic cells, shrinkage, and swelling of neurons, accompanied by the formation of protein aggregation in the brain parenchyma. Additionally, the level of nitric oxide and MDA was found to have increased (p<0.0001), however, the level of arginase decreased indicating active lipid peroxidation and redox imbalance in the brain. This study provides insights into the pathogenesis of HACE by evaluating some biomolecules that play a pivotal role in the inflammatory response and the redox landscape in the brain. The findings could have significant implications for understanding the neuronal dysfunction and the pathological mechanisms underlying HACE development.

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Purpose: The hematological changes in COVID-19 patients continue to receive great attention, especially in the field of public health. To our knowledge, coronavirus disease may be identified based on the severity of illness, and the study of peripheral blood smears may offer important information to facilitate the identification. Thus, we evaluated the morphological abnormalities (atypical and immature lymphocytes, lymphocytes with micronuclei, various nuclear abnormalities among erythrocytes) and quantitative changes in peripheral blood cells among 48 individuals with COVID-19 disease. Methods: The present study is a retrospective analysis of 48 individuals, including 24 hospitalized patients diagnosed with COVID-19 disease. The blood smears of all patients were subjected to a hematological examination to identify various morphological abnormalities in white and red blood cells. In addition, a micronucleus test was conducted to assess the incidence of chromosomal damage in lymphocytes. Furthermore, the complete blood count (CBC) was performed to evaluate changes in peripheral blood cells, particularly the differential total leukocyte count, which could indicate the immune response against viral infection in COVID-19 patients. Results: The findings of the hematological study conducted on patients diagnosed with COVID-19 disease revealed neutrophilia, eosinophilia, mild monocytosis, decreased hematocrit level, elevated erythrocyte sedimentation rate (ESR), and immature leukocytes. It was observed that patients who were infected with coronavirus demonstrated mild thrombocytopenia. Furthermore, the micronucleus test indicated the presence of immature cells with micronuclei among lymphocytes and numerous nuclear abnormalities in red blood cells. These results help to shed light on the hematological changes that occur in COVID-19 patients, and could potentially contribute to the development of more effective treatments for the disease. Conclusions: The examination of complete blood counts (CBCs) in conjunction with peripheral blood smears offers a potential means of identifying the impact of SARS-CoV-2 infection on the hematopoietic and immune systems, thereby providing early indications of inflammation. Based on a study, it has been suggested that SARS-CoV-2 may affect red and white blood cells causing morphological alterations thereby establishing a corresponding relationship with disease severity.

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High altitude sickness is a life-threatening disease that occurs among acclimatized individuals working or living at a high altitude accompanied by hypobaric hypoxia exposure. The prolonged influence of hypobaric hypoxia on the brain may trigger neuronal damage and cell death due to an oxygen deficiency. The purpose of the current study was to investigate the histomorphological changes in the hippocampus, cerebral cortex, cerebellar cortex, and striatum of the rat's brain following chronic hypobaric hypoxia. Fourteen albino rats were used for this investigation. The animals were exposed to chronic hypobaric hypoxia in the special decompression chamber at an altitude of 7000 m for 7 days. The histological analysis was conducted via toluidine staining and silver impregnation. DNA damage and cell apoptosis were assessed via Feulgen staining. The histochemical assessment revealed increased dark neurons in the hippocampus with cell swelling. Silver impregnation showed increased argyrophilic neurons in the cerebellar cortex, striatum, CA1 subfield of the hippocampus, and cerebral cortex. The cytochemical analysis determined the increased apoptotic cells with hyperchromatic condensation and pyknosis in the hippocampus subfields and cerebral cortex. In addition, it has been observed that hypoxia has resulted in small hemorrhages and perivascular edema within the cerebellar and cerebral cortex. The results indicate brain injury observed in the various parts of the brain towards hypobaric hypoxia, however, the hippocampus showed greater vulnerability against hypoxic exposure in comparison to the striatum, cerebellum, and cerebral cortex. These changes support our insights regarding brain intolerance under conditions of hypoxia-induced oxygen deficiency and its histomorphological manifestations.

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