Fibromyalgia syndrome is a chronic pain disorder and defies definitively efficacious therapy. In this review, we summarize the results from the early treatment research as well as recent research evaluating the pharmacological, interventional and nonpharmacological therapies. We further discuss future directions of fibromyalgia syndrome management; we specifically focus on the issues that are associated with currently available treatments, such as the need for personalized approach, new technologically oriented and interventional treatments, the importance of understanding and harnessing placebo effects and enhancement of patient engagement in therapy.

Compared with CsA continuation, conversion to reduced TAC target trough concentrations resulted in significantly improved renal function without increasing the risk of rejection. Conversion to TAC, regardless of target concentration, resulted in improved serum lipid profiles in kidney transplant recipients at 12 months.

Since the discovery of Cu/Zn superoxide dismutase (SOD1) gene mutation, in 1993, as the first genetic abnormality in amyotrophic lateral sclerosis (ALS), over 50 genes have been identified as either cause or modifier in ALS and ALS/frontotemporal dementia (FTD) spectrum disease. Mutations in C9orf72, SOD1, TAR DNA binding protein 43 (TARDBP), and fused in sarcoma (FUS) genes are the four most common ones. During the last three decades, tremendous effort has been made worldwide to reveal biological pathways underlying the pathogenesis of these gene mutations in ALS/FTD. Accordingly, targeting etiologic genes (i.e., gene therapies) to suppress their toxic effects have been investigated widely. It includes four major strategies: (i) removal or inhibition of abnormal transcribed RNA using microRNA or antisense oligonucleotides (ASOs), (ii) degradation of abnormal mRNA using RNA interference (RNAi), (iii) decrease or inhibition of mutant proteins (e.g., using antibodies against misfolded proteins), and (iv) DNA genome editing with methods such as clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein (CRISPR/Cas). The promising results of these studies have led to the application of some of these strategies into ALS clinical trials, especially for C9orf72 and SOD1. In this paper, we will overview advances in gene therapy in ALS/FTD, focusing on C9orf72, SOD1, TARDBP, and FUS genes.

Objective To examine factors associated with hospital safety net burden and its impact on survival for patients with sinonasal squamous cell carcinoma (SNSCC). Study Design Retrospective database study. Setting National Cancer Database from 2004 to 2016. Methods SNSCC cases were identified in the National Cancer Database. Hospital safety net burden was defined by percentage of uninsured/Medicaid patients treated, namely ≤25% for low-burden hospitals, 26% to 75% for medium-burden hospitals, and >75% for high-burden hospitals (HBHs). Univariate and multivariate analyses were used to investigate patient demographics, clinical characteristics, and overall survival. Results An overall 6556 SNSCC cases were identified, with 1807 (27.6%) patients treated at low-burden hospitals, 3314 (50.5%) at medium-burden hospitals, and 1435 (21.9%) at HBHs. On multivariate analysis, Black race (odds ratio [OR], 1.39; 95% CI, 1.028-1.868), maxillary sinus primary site (OR, 1.31; 95% CI, 1.036-1.643), treatment at an academic/research program (OR, 20.63; 95% CI, 8.868-47.980), and treatment at a higher-volume facility ( P < .001) resulted in increased odds of being treated at HBHs. Patients with grade III/IV tumor (OR, 0.70; 95% CI, 0.513-0.949), higher income ( P < .05), or treatment modalities other than surgery alone ( P < .05) had lower odds. Survival analysis showed that hospital safety net burden status was not significantly associated with overall survival (log-rank P = .727). Conclusion In patients with SNSCC, certain clinicopathologic factors, including Black race, lower income, treatment at an academic/research program, and treatment at facilities in the West region, were associated with treatment at HBHs. Hospital safety net burden status was not associated with differences in overall survival. Level of evidence 4.

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