Background: The European Confederation of Medical Mycology (ECMM) Quality of Clinical Candidaemia Management (EQUAL) score is a tool designed by the ECMM to measure guideline adherence. The current study investigated the association between EQUAL scores and clinical outcomes. Methods: This retrospective study was conducted in three hospitals in Taiwan. Patients with candidaemia between January 2014 and July 2018 were enrolled. Guideline adherence was evaluated using EQUAL score indicators. Clinical outcomes and predictors of 30-day mortality were investigated. Results: A total of 384 patients were enrolled. The overall mean EQUAL score was 8.91 ± 3.42 (9.42 ± 3.60 in survivors vs. 8.10 ± 2.94 in non-survivors, p < 0.001). Higher scores were positively correlated with survival (p < 0.001). Scores of 16e22 indicated the highest survival rates (p for trend <0.001). The Kaplan eMeier plot revealed that patients with EQUAL scores 10 exhibited significantly higher survival rates (p < 0.001) than those with scores <10. Multivariable analysis revealed that EQUAL scores 10 (odds ratio (OR) 0.37, 95% confidence interval (CI) 0.19e0.74), advanced age (OR 1.02, 95% CI 1.00e1.04), septic shock (OR 4.42, 95% CI 2.09e9.36), high sequential organ failure assessment scores (OR 4.28, 95% CI 2.15 e8.52), intravascular catheter-related source (OR 0.42, 95% CI 0.19e0.94) and central venous catheter retention (OR 5.41, 95% CI 2.06e14.24) were independent predictors of 30-day mortality. Discussion: Greater guideline adherence with a higher EQUAL score was significantly associated with survival. An EQUAL score cutoff point <10 predicted 30-day mortality.

Resveratrol, an anti-inflammatory agent, can inhibit pro-inflammatory mediators by activating Sirt1, which is a class III histone deacetylase. However, whether resveratrol can regulate inhibitory or anti-inflammatory molecules has been less studied. FcγRIIB, a receptor for IgG, is an essential inhibitory receptor of B cells for blocking B-cell receptor-mediated activation and for directly inducing apoptosis of B cells. Because mice deficient in either Sirt1 or FcγRIIB develop lupus-like diseases, we investigated whether resveratrol can alleviate lupus through FcγRIIB. We found that resveratrol enhanced the expression of FcγRIIB in B cells, resulting in a marked depletion of plasma cells in the spleen and notably in the bone marrow, thereby decreasing serum autoantibody titers in MRL/lpr mice. The upregulation of FcγRIIB by resveratrol involved an increase of Sirt1 protein and deacetylation of p65 NF-κB (K310). Moreover, increased binding of phosphor-p65 NF-κB (S536) but decreased association of acetylated p65 NF-κB (K310) and phosphor-p65 NF-κB (S468) to the −480 promoter region of Fcgr2b gene was responsible for the resveratrol-mediated enhancement of FcγRIIB gene transcription. Consequently, B cells, especially plasma cells, were considerably reduced in MRL/lpr mice, leading to improvement of nephritis and prolonged survival. Taken together, we provide evidence that pharmacological upregulation of FcγRIIB expression in B cells via resveratrol can selectively reduce B cells, decrease serum autoantibodies and ameliorate lupus nephritis. Our findings lead us to propose FcγRIIB as a new target for therapeutic exploitation, particularly for lupus patients whose FcγRIIB expression levels in B cells are downregulated.

Vitamin D is a hormone involved in many physiological processes. Its active form, 1,25(OH)2D3, modulates serum calcium–phosphate homeostasis and skeletal homeostasis. A growing body of evidence has demonstrated the renoprotective effects of vitamin D. Vitamin D modulates endothelial function, is associated with podocyte preservation, regulates the renin–angiotensin–aldosterone system, and has anti-inflammatory effects. Diabetic kidney disease (DKD) is a leading cause of end-stage kidney disease worldwide. There are numerous studies supporting vitamin D as a renoprotector, potentially delaying the onset of DKD. This review summarizes the findings of current research on vitamin D and its role in DKD.