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Introduction: To evaluate factors associated with severe coronavirus disease 2019 (COVID-19) among patients with rheumatoid arthritis (RA) in the US. Methods: Adults with RA who had a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, based on molecular or antigen test or clinical diagnosis, were identified from the Optum® COVID-19 Electronic Health Record dataset (March 1, 2020–April 28, 2021). The primary outcome was the occurrence of severe COVID-19 (hospitalization or death) within 30 days from SARS-CoV-2 infection. Adjusted odds ratios (aOR) and 95% confidence intervals (CI) were estimated using multivariable logistic regression models to assess the association between severe COVID-19 and patient characteristics, including demographics, baseline comorbidities, and recent RA treatments. Results: During the study period, 6769 SARS-CoV-2 infections were identified in patients with RA, among whom 1460 (22%) developed severe COVID-19. Multivariable logistic regression analysis showed that being older, male, and non-White and having diabetes and cardiovascular conditions are associated with greater odds of severe COVID-19. In addition, compared with no use, the adjusted odds of severe COVID-19 were lower with recent use of tumor necrosis factor inhibitors (aOR 0.60, 95% CI 0.41–0.86) and higher with recent use of corticosteroids (aOR 1.38, 95% CI 1.13–1.69) or rituximab (aOR 2.87, 95% CI 1.60–5.14), respectively. Conclusion: Nearly one in five patients with RA developed severe COVID-19 disease within 30 days after SARS-CoV-2 infection. In patients with RA, recent use of corticosteroids and rituximab were two factors associated with a greater risk of severe COVID-19 in addition to the risk factors among demographics and comorbidities previously identified in the general population. [ABSTRACT FROM AUTHOR]

The purpose of this study was to determine whether cis-dichlorodiammineplatinum (cisplatin) causes mitochondrial DNA (mtDNA) damage. A specific and sensitive method for quantitation of damage to mtDNA was used, by which the physical forms of mtDNA (supercoiled, open circular and linear forms) were separated by gel electrophoresis. The DNA specificity was then obtained by hybridizing with a mtDNA probe. In vitro incubation of mtDNA with cisplatin showed that the drug did not induce any changes in the proportion of physical forms; similar results were obtained in vivo. Since cisplatin did not cause any strand scission in mtDNA but induces strand breaks in nuclear DNA, which is an indirect effect, a lack of repair for cisplatin-induced adducts in mtDNA is suggested. [ABSTRACT FROM AUTHOR]

Under a suitable ellipticity condition, we show that classical SG-pseudodifferential operators of nonnegative order possess complex powers. We show that the powers are again classical and derive an explicit formula for all homogeneous components. Keywords: Complex power, Weighted symbols, Noncompact manifolds [ABSTRACT FROM AUTHOR]

We prove in details the higher codimensional version of Theorem 1.1 [11]. This provides a complete proof of Fefferman’s SAK Principle for a class of PDO’s with symplectic characteristic manifold. Keywords: A priori estimates, General theory of PDO’s [ABSTRACT FROM AUTHOR]

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We obtain a Weyl formula for a class of positive md-elliptic operators on manifolds with finitely many cylindrical exits. Weyl formula is deduced by a classical Tauberian theorem through the asymptotic expansion at t=0 of the trace of the heat parametrix. The constant of the leading term is expressed invariantly by means of the usual principal symbol and exit symbols. [ABSTRACT FROM AUTHOR]

The objective of this study was to determine if the nephrotoxic effects induced by cisplatin were correlated to mitochondrial DNA damage. Comparisons were made with the liver since hepatotoxicity is rarely observed. Cisplatin doses of 10, 20 and 40 mg/kg were administered intraperitoneally to C57BL/6J mice. Mitochrondrial DNA was isolated from both the hepatic and renal tissues and quantitated by hybridization with a specific mitochondrial probe. Cisplatin caused differential effects on mouse hepatic and renal mitochondrial DNA. The 10 and 20 mg/kg dose caused an elevation in mitochondrial DNA levels in the hepatic, but no increase in the renal tissue was observed. This is the first study demonstrating an organ specific effect of cisplatin at the DNA level. [ABSTRACT FROM AUTHOR]