There is an established literature on the symptoms and complications of COVID-19 but the after-effects of COVID-19 are not well understood with few studies reporting persistent symptoms and quality of life. We aim to evaluate the pooled prevalence of poor quality of life in post-acute COVID-19 syndrome (PCS) and conducted meta-regression to evaluate the effects of persistent symptoms and intensive care unit (ICU) admission on the poor quality of life. We extracted data from observational studies describing persistent symptoms and quality of life in post-COVID-19 patients from March 10, 2020, to March 10, 2021, following PRISMA guidelines with a consensus of two independent reviewers. We calculated the pooled prevalence with 95% confidence interval (CI) and created forest plots using random-effects models. A total of 12 studies with 4828 PCS patients were included.We found that amongst PCS patients, the pooled prevalence of poor quality of life

Background COVID‐19 pandemic is a global health crisis. Very few studies have reported association between obesity and severity of COVID‐19. In this meta‐analysis, we assessed the association of obesity and outcomes in COVID‐19 hospitalized patients. Methods Data from observational studies describing the obesity or body mass index (BMI) and outcomes of COVID‐19 hospitalized patients from December 1, 2019, to August 15, 2020, was extracted following PRISMA guidelines with a consensus of two independent reviewers. Adverse outcomes defined as intensive care units (ICU), oxygen saturation <90%, invasive mechanical ventilation (IMV), severe disease and in‐hospital mortality. The odds ratio (OR) and 95% confidence interval (95%CI) were obtained and forest plots were created using random‐effects models. Results A total of 10 studies with 10,233 confirmed COVID‐19 patients were included. The overall prevalence of obesity in our study was 33.9% (3473/10,233). In meta‐analysis, COVID‐19 patient with obesity had higher odds of poor outcomes compared to better outcomes with a pooled OR of 1.88 (95%CI:1.25–2.80; p=0.002), with 86% heterogeneity between studies (p<0.00001). Conclusion Our study suggests a significant association between obesity and COVID‐19 severity and poor outcomes. Our results findings may have important suggestions for the clinical management and future research of obesity and COVID‐19. This article is protected by copyright. All rights reserved.

Tempol corrects hypertension without a compensatory sympathoadrenal activation or salt retention. The response is independent of nitric oxide, endothelin, or catecholamines and occurs despite increased PRA. It is accompanied by a reduction in oxidative stress and is maintained during increased salt intake.

Tempol is an amphipathic radical nitroxide (N) that acutely reduces blood pressure (BP) and heart rate (HR) in the spontaneously hypertensive rat (SHR). We investigated the hypothesis that the response to nitroxides is determined by SOD mimetic activity or lipophilicity. Groups (n ϭ 6 -10) of anesthetized SHRs received graded intravenous doses of Ns: tempol (T), 4-amino-tempo (AT), 4-oxotempo (OT), 4-trimethylammonium-2,2,6,6-tetramethylpiperidine-1-oxyl iodide (CAT-1), 3-carbamoyl-proxyl (3-CP), or 3-carboxyproxyl (3-CTPY). Others received native or liposomal (L) Cu/Zn SOD. T and OT are uncharged, AT is positively charged and cell-permeable, and CAT-1 is positively charged and cell-impermeable. 3-CP and 3-CTPY have five-member pyrrolidine rings, whereas T, AT, OT, and CAT-1 have six-member piperidine rings. T and AT reduced mean arterial pressure (MAP) similarly (Ϫ48 Ϯ 2 mmHg and Ϫ55 Ϯ 8 mmHg) but more (P Ͻ 0.05) than OT and CAT-1. 3-CP and 3-CTPY were ineffective. The group mean change in MAP with piperidine Ns correlated with SOD activity (r ϭ Ϫ0.94), whereas their ED50 correlated with lipophilicity (r ϭ 0.89). SOD and L-SOD did not lower BP acutely but reduced it after 90 min (Ϫ32 Ϯ 5 and Ϫ31 Ϯ 6 mmHg; P Ͻ 0.05 vs. vehicle). Pyrrolidine nitroxides are ineffective antihypertensive agents. The antihypertensive response to piperidine Ns is predicted by SOD mimetic action, and the sensitivity of response is by hydrophilicity. SOD exerts a delayed hypotensive action that is not enhanced by liposome encapsulation, suggesting it must diffuse to an extravascular site. (39), by enhancing the peripheral sympathetic nervous system (37, 38), or by enhancing renal tubular NaCl reabsorption (17,22,23).Oxidative stress accompanies hypertension in many models of hypertension, including the spontaneously hypertensive rat (SHR) (25). Mitchell, Krishna, and colleagues (15,18,24) have shown that tempol (T) is a permeant amphipathic radical nitroxide (N) that detoxifies oxygen metabolites by redox cycling through one-electron transfer reactions. The nitroxide/ oxoammonium cation pair form an efficient redox coupling that mimics the enzymic action of SOD and confers catalaselike action to heme proteins (14, 15). Although T lowers blood pressure (BP) in many animal models of hypertension accompanied by oxidative stress, including the SHR (9, 21, 26, 27, 29, 36 -38), the mechanisms of its in vivo action are not clearly established.Fink and colleagues (38) have shown that T given to deoxycorticosterone acetate-salt rats reduces BP before it has dissipated O 2 Ϫ ⅐ in the aorta. This acute antihypertensive response is accompanied by reduced renal sympathetic nervous system activity. It is unclear whether these neural actions of T depend on SOD mimetic action. Nevertheless, intravenous injection of liposomal (L), polyethylene-glycol, or heparin-bonded SOD lowers BP in SHR (20) or ANG-II-infused hypertensive rats (19) or restores ACh-induced relaxation in blood vessels from atherosclerotic rabbits (34).We investigated the hypothesis t...

Acute intravenous Tempol reduces mean arterial pressure (MAP) and heart rate (HR) in spontaneously hypertensive rats. We investigated the hypothesis that the antihypertensive action depends on generation of hydrogen peroxide, activation of heme oxygenase, glutathione peroxidase or potassium conductances, nitric oxide synthase, and/or the peripheral or central sympathetic nervous systems (SNSs). Tempol caused dose-dependent reductions in MAP and HR (at 174 micromol/kg; DeltaMAP, -57+/- 3 mmHg; and DeltaHR, -50 +/- 4 beats/min). The antihypertensive response was unaffected by the infusion of a pegylated catalase or by the inhibition of catalase with 3-aminotriazole, inhibition of glutathione peroxidase with buthionine sulfoximine, inhibition of heme oxygenase with tin mesoporphyrin, or inhibition of large-conductance Ca(2+)-activated potassium channels with iberiotoxin. However, the antihypertensive response was significantly (P < 0.01) blunted by 48% by the activation of adenosine 5'-triphosphate-sensitive potassium (K(ATP)) channels with cromakalim during maintenance of blood pressure with norepinephrine and by 31% by the blockade of these channels with glibenclamide, by 40% by the blockade of nitric oxide synthase with N(omega)-nitro-L-arginine methyl ester (L-NAME), and by 40% by the blockade of ganglionic autonomic neurotransmission with hexamethonium. L-NAME and hexamethonium were additive, but glibenclamide and hexamethonium were less than additive. The central administration of Tempol was ineffective. The acute antihypertensive action of Tempol depends on the independent effects of potentiation of nitric oxide and inhibition of the peripheral SNS that involves the activation of K(ATP) channels.

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Biopharmaceuticals (biologics) represent one of the fastest growing sectors of cancer treatment. They are recommended for treating underlying cancer and as supportive care for management of treatment side effects. Given the high costs of cancer care and the need to balance health care provision and associated budgets, patient access and value are the subject of discussion and debate in the USA and globally. As the costs of biologics are high, biosimilars offer the potential of greater choice and value, increased patient access to treatment, and the potential for improved outcomes. Value-based care aims to improve the quality of care, while containing costs. The Centers for Medicare & Medicaid Services (CMS) has developed value-based care programs as alternatives to fee-for-service reimbursement, including in oncology, that reward health care providers with incentive payments for improving the quality of care they provide. It is anticipated that CMS payments in oncology care will be increasingly tied to measured performance. This review provides an overview of value-based care models in oncology with a focus on CMS programs and discusses the contribution of biosimilars to CMS value-based care objectives. Biosimilars may provide an important tool for providers participating in value-based care initiatives, resulting in cost savings and efficiencies in the delivery of high-value care through expanded use of biologic treatment and supportive care agents during episodes of cancer care.