Journal of investigative medicine : the official publication of the American Federation for Clinical Research
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The COVID-19 pandemic has infected millions of people worldwide and many countries have been suffering from a large number of deaths. Acknowledging the ability of SARS-CoV-2 to mutate into distinct strains as an RNA virus and investigating its potential to cause reinfection is important for future health policy guidelines. It was thought that individuals who recovered from COVID-19 generate a robust immune response and develop protective immunity; however, since the first case of documented reinfection of COVID-19 in August 2020, there have been a number of cases with reinfection. ⋯ Overall, 68.8% (11/16) had similar severity; 18.8% (3/16) had worse symptoms; and 12.5% (2/16) had milder symptoms with the second episode. Our case series shows that reinfection with different strains is possible, and some cases may experience more severe infections with the second episode. The findings also suggest that COVID-19 may continue to circulate even after achieving herd immunity through natural infection or vaccination, suggesting the need for longer-term transmission mitigation efforts.
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Undoubtedly, identification of the chemical composition of organic extracts or secondary metabolites of plant materials and evaluation of their potential bioactivity are among the main objectives of natural products-based investigations. In the present study, we report the chemical composition and antidiabetic activity of Sophora pachycarpa (Family Fabaceae) seeds extract (SPE) for the first time. First, the plant seeds were macerated in ethanol. ⋯ The statistical analyses revealed there are no significant differences between the ability of SPE and metformin in the regulation of fasting blood sugar level and liver enzymes (ALP, SGPT, and SGOT). A quinolizidine alkaloid, namely sophoridine, along with fatty acids, viz oleic, linoleic, and n-hexadecanoic acid, were characterized as the major compounds in S. tachycardia seeds extract. The plant extract was also found as a potent agent to reduce blood glucose and liver enzymes.
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Previous animal models of gastroesophageal reflux disease (GERD) were not physiological and required a variety of surgical procedures. Therefore, the animal model developed by conditions that are similar to the pathogenesis of GERD is necessary. The aim is to establish a non-surgical animal model with GERD caused by overeating induced in mice. ⋯ The higher frequency of fasting and overeating could cause GERD effectively. The dietary control can make mice overeat, which elicits the change of lower esophageal mucosa similar to GERD. Thus, the overeating-induced mouse may be used as a GERD mouse model.
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This study investigated the influences of EphA10 and Gli3 on breast cancer (BC) cell proliferation, invasion and migration. Immunohistochemistry was used to reveal the expressions of EphA10 and Gli3 in 18 intraductal carcinomas, 124 invasive carcinomas, 50 paracancerous tissues (2 cm away from the tumor, when possible or available), 50 lobular hyperplastic tissues and 30 normal breast tissues. qRT-PCR and Western blotting were applied to detect the expressions of EphA10 and Gli3 in invasive BC cells (MDA-MB-231, BT20 and Hs578T) and normal human mammary epithelial cells (MCF10A). MDA-MB-231 and BT20 cells were transfected with sh-EphA10, sh-Gli3 or sh-EphA10+sh-Gli3. ⋯ Knockdown of EphA10 or Gli3 suppressed activities of BC cells. Knockdown of both EphA10 and Gli3 was more effective than knockdown of Gli3 alone. Taken together, coexpression of EphA10 and Gli3 promotes BC cell proliferation, invasion and migration.
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To investigate the effort of mitochondrial calcium transport and calcium-induced membrane permeability transition in alleviating atherosclerosis. The experimental mice were divided into three groups: the control group (C57BL/6 mice with normal diet), the atherosclerosis group (apolipoprotein E-deficient (ApoE-/-) mice with high-fat diet) and the mitochondrial targeting agent group (ApoE-/- mouse with high-fat diet). The mean fluorescence intensity of Ca2+ in the atherosclerosis group is significantly higher than control group and mitochondrial targeting agent group. ⋯ The macrophage recruitment (F4/80 positive area) and the expression of tumor necrosis factor alpha, interleukin-6, pyrin domain containing protein 3, intercellular cell adhesion molecule-1, p38 mitogen-activated protein kinase and Jun kinase 1/2 phosphorylation in the atherosclerosis group are higher that other groups. Treatment with mitochondrial targeting agents reduced the levels of elevated cyt C and cleaved caspase-3 in atherosclerotic mice (p<0.05). Mitochondrial targeting agents interfere with mitochondrial calcium transport and calcium-induced membrane permeability transition, inhibit MAPK/JNK pathway activation, inhibit foam cell formation and alleviate the process of atherosclerosis.