Risk Factors Associated with Pulmonary Disease Among Hospitalized Patients in The United States

Background: The etiology of pulmonary disease is complex and influenced by various factors, resulting in a significant public health issue, with 16 million Americans living with chronic obstructive pulmonary disease (COPD) and 24 million with asthma, and cases are on the rise. The purpose of this study was to explore demographic, health status, and lifestyle behaviors with pulmonary disease so patterns of risk can be understood and inform interventions. Methods: This cross-sectional study utilized the National Inpatient Sample Data from 2019 (NIS 2019). The predictor variables consisted of: demographics (age (18+), sex, race), health status (obesity, depression, diabetes), lifestyle behaviors (smoking, alcohol use, and aspirin use), and the outcome variable was pulmonary disease. To ensure accuracy, the data was weighted by the variable discharge weight (DISCWT), and chi-square analyses and ANOVA tests were conducted to determine the independence of categorical and numerical predictor variables. Descriptive statistics were conducted for all variables, simple and multiple logistic regression analyses were performed to identify factors that contribute to the likelihood of having pulmonary disease. Results: The sample of the NIS 2019 data included 6,043,654 cases of which, 22.65% of inpatients had pulmonary disease. The collective sample demographic characteristics were: mean age of 58.4 years, and more than half of inpatients were females (57.05% compared to 42.95% males). In terms of health, 17.75% of the sample were obese, 28.8% had diabetes, and 14.25% were depressed. Within the collective sample, 16.8% of inpatients reported smoking, 9.09% drank alcohol, and 14.51% consumed aspirin (long-term (current) use of aspirin). Results of the multivariate statistical analyses reveal that individuals who were obese were 68.3% more likely to have pulmonary disease compared to non-obese patients (aOR = 1.683, CI 1.679-1.686, pConclusion: Results of our study provide important insights between pulmonary disease and associated risk patterns. As pulmonary symptoms have risen in the wake of the COVID-19 pandemic, there is an urgent public health need to explore disruption of risk pathways to avoid overwhelming fragile global healthcare systems

Temporal changes in immune blood cell parameters in COVID-19 infection and recovery from severe infection

10.1111/bjh.16847BRITISH JOURNAL OF HAEMATOLOGY190133-3

A Small-Molecule Inhibitor of PIM Kinases as a Potential Treatment for Urothelial Carcinomas

The proto-oncogene proviral integration site for moloney murine leukemia virus (PIM) kinases (PIM-1, PIM-2, and PIM-3) are serine/threonine kinases that are involved in a number of signaling pathways important to cancer cells. PIM kinases act in downstream effector functions as inhibitors of apoptosis and as positive regulators of G1-S phase progression through the cell cycle. PIM kinases are upregulated in multiple cancer indications, including lymphoma, leukemia, multiple myeloma, and prostate, gastric, and head and neck cancers. Overexpression of one or more PIM family members in patient tumors frequently correlates with poor prognosis. The aim of this investigation was to evaluate PIM expression in low- and high-grade urothelial carcinoma and to assess the role PIM function in disease progression and their potential to serve as molecular targets for therapy. One hundred thirty-seven cases of urothelial carcinoma were included in this study of surgical biopsy and resection specimens. High levels of expression of all three PIM family members were observed in both noninvasive and invasive urothelial carcinomas. The second-generation PIM inhibitor, TP-3654, displays submicromolar activity in pharmacodynamic biomarker modulation, cell proliferation studies, and colony formation assays using the UM-UC-3 bladder cancer cell line. TP-3654 displays favorable human ether-à-go-go-related gene and cytochrome P450 inhibition profiles compared with the first-generation PIM inhibitor, SGI-1776, and exhibits oral bioavailability. In vivo xenograft studies using a bladder cancer cell line show that PIM kinase inhibition can reduce tumor growth, suggesting that PIM kinase inhibitors may be active in human urothelial carcinomas