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Fractional excretion of sodium was decreased from baseline when dogs received 0.5, 1, or 4 mg of prednisone/kg, compared with results for the control condition. Several expected changes in clinicopathologic values were observed after prednisone administration at any dose. Changes in serum NT-proBNP concentration, plasma renin activity, and SAP did not differ from changes for the control condition at any prednisone dose. PROTAC tubulin-Degrader-1 in vitro CONCLUSIONS AND CLINICAL RELEVANCE Oral prednisone administration did not affect SAP, NT-proBNP concentration, or measures of renin-angiotensin-aldosterone system activation in healthy laboratory-housed dogs but was associated with relative increases in GFR and serum glucose concentration.The novel SARS coronavirus SARS-CoV-2 pandemic may be particularly deleterious to patients with underlying cardiovascular disease (CVD). The mechanism for SARS-CoV-2 infection is the requisite binding of the virus to the membrane-bound form of angiotensin-converting enzyme 2 (ACE2) and internalization of the complex by the host cell. Recognition that ACE2 is the coreceptor for the coronavirus has prompted new therapeutic approaches to block the enzyme or reduce its expression to prevent the cellular entry and SARS-CoV-2 infection in tissues that express ACE2 including lung, heart, kidney, brain, and gut. ACE2, however, is a key enzymatic component of the renin-angiotensin-aldosterone system (RAAS); ACE2 degrades ANG II, a peptide with multiple actions that promote CVD, and generates Ang-(1-7), which antagonizes the effects of ANG II. Moreover, experimental evidence suggests that RAAS blockade by ACE inhibitors, ANG II type 1 receptor antagonists, and mineralocorticoid antagonists, as well as statins, enhance ACE2 which, in part, contributes to the benefit of these regimens. In lieu of the fact that many older patients with hypertension or other CVDs are routinely treated with RAAS blockers and statins, new clinical concerns have developed regarding whether these patients are at greater risk for SARS-CoV-2 infection, whether RAAS and statin therapy should be discontinued, and the potential consequences of RAAS blockade to COVID-19-related pathologies such as acute and chronic respiratory disease. The current perspective critically examines the evidence for ACE2 regulation by RAAS blockade and statins, the cardiovascular benefits of ACE2, and whether ACE2 blockade is a viable approach to attenuate COVID-19.Introduction Bladder cancer is the second most common genitourinary tract cancer and is often recurrent and/or chemoresistant after tumor resection. Cigarette smoking, exposure to aromatic amines, and chronic infection/inflammation are bladder cancer risk factors. NF-κB is a transcription factor that plays a critical role in normal physiology and bladder cancer. Bladder cancer patients have constitutively active NF-κB triggered by pro-inflammatory cytokines, chemokines, and hypoxia, augmenting carcinogenesis and progression.Areas covered NF-κB orchestrates protein interactions (PTEN, survivin, VEGF), regulation (CYLD, USP13) and gene expression (Trp 53) resulting in bladder cancer progression, recurrence and resistance to therapy. This review focuses on NF-κB in bladder inflammation, cancer and resistance to therapy.Expert opinion NF-κB and bladder cancer necessitate further research to develop better diagnostic and treatment regimens that address progression, recurrence and resistance to therapy. NF-κB is a master regulator that can act with or on minimally one cancer hallmark gene or protein, leading to bladder cancer progression (Tp53, PTEN, VEGF, HMGB1, CYLD, USP13), recurrence (PCNA, BcL-2, JUN) and resistance to therapy (P-gp, twist, SETD6). Thus, an understanding of bladder cancer in relation to NF-κB will offer improved strategies and efficacious targeted therapies resulting in minimal progression, recurrence and resistance to therapy.Introduction Treatment options for patients suffering from neuromyelitis optica spectrum disorders (NMOSD) so far have relied on off-label and empiric drugs. The first drug for the therapy of anti-aquaporin-4 (AQP4) antibody-seropositive NMOSD patients has been approved in 2019 the C5 complement inhibitor eculizumab. The interleukin-6 receptor inhibitor satralizumab and anti-CD19 antibody inebilizumab have published positive phase III trial results and await approval in the near future.Areas covered We sum up current treatment options and portray in detail the new developments in NMOSD drugs focusing on phase III clinical trials, followed by an overview of emerging drugs in less advanced clinical trial stages.Expert opinion Eculizumab's approval by the competent authorities marks a milestone in NMOSD treatment. Satralizumab and inebilizumab will most likely follow in approval given their presented results in efficacy and safety. All three drugs have shown efficacy in reducing relapse rates in NMOSD patients with anti-AQP4 antibodies. Although we will have even more evidence-based therapy options in the future, empirically used medications will keep their importance for now. The potential effect of new medications in AQP4 antibody-seronegative NMOSD and patients with an NMOSD phenotype and antibodies to myelin oligodendrocyte glycoprotein remains to be determined.Background The rs368234815 polymorphism of interferon-λ4 (IFN-λ4) gene (IFNL4) is involved in HBV surface antigen (HBsAg) clearance in non-uremic subjects. The rs368234815 ΔG/ΔG genotype can express IFN-λ4 while the TT/TT genotype cannot. We investigated whether rs368234815 is associated with the development of HBsAg antibodies (anti-HBs) in response to vaccination or infection, and HBsAg loss after infection in uremic patients on extracorporeal dialysis.Research design and methods Dialyzed patients (n = 467) were genotyped for rs368234815 by the polymerase chain reaction-restriction fragment length polymorphism method. Non-responders to HBV vaccination we compared with responders. HBsAg positive patients not able to develop anti-HBs we compared with individuals who eliminated HBsAg and generated anti-HBs. HBsAg positive patients we compared with subjects who eliminated HBsAg.Results The ∆G allele was associated with the 1.6-fold higher risk not to develop anti-HBs titers ≥10 IU/L in response to HBV vaccination and infection (P = 0.