The aim of the study is to examine the relationship between secondhand smoke (SHS) and angina using the National Health and Nutrition Examination Survey database over a 12-year period. Self-reported smoking status and cotinine levels were used to identify exposure groups (smokers, nonsmokers, and secondhand smokers), and medical history of angina was also collected via a self-report survey. The association between exposure to SHS and angina was analyzed using odd ratios with 95% confidence intervals calculated using two logistic regression models.
View Article and Find Full Text PDFBackground: The Arab region is highly affected by the COVID-19 pandemic. Local governments have already started to act against the disease. However, only a few countries provided COVID-19 vaccination.
View Article and Find Full Text PDFMutations in the human NBEAL2 gene cause gray platelet syndrome (GPS), a bleeding diathesis characterized by a lack of α granules in platelets. The functions of the NBEAL2 protein have not been explored outside platelet biology, but there are reports of increased frequency of infection and abnormal neutrophil morphology in patients with GPS. We therefore investigated the role of NBEAL2 in immunity by analyzing the phenotype of Nbeal2-deficient mice.
View Article and Find Full Text PDFAim: To evaluate the feasibility of reducing the dose of iodinated contrast agent in computed tomography pulmonary angiography (CTPA).
Methods: One hundred and twenty-seven patients clinically suspected of having pulmonary embolism underwent spiral CTPA, out of whom fifty-seven received 75 mL and the remaining seventy a lower dose of 60 mL of contrast agent. Both doses were administered in a multiphasic injection.
The antiviral restriction factor IFN-induced transmembrane protein 3 (IFITM3) inhibits cell entry of a number of viruses, and genetic diversity within IFITM3 determines susceptibility to viral disease in humans. Here, we used the murine CMV (MCMV) model of infection to determine that IFITM3 limits herpesvirus-associated pathogenesis without directly preventing virus replication. Instead, IFITM3 promoted antiviral cellular immunity through the restriction of virus-induced lymphopenia, apoptosis-independent NK cell death, and loss of T cells.
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