Citations

ABSTRACT Objective To derive precise estimates of anxiety and depressive disorder prevalence in patients with common vestibular disorders. Data Sources CINAHL, Cochrane Library, PubMed, PsycINFO, and SCOPUS. Review Methods This systematic review and meta‐analysis was reported per PRISMA guidelines. Outcomes included continuous measures (mean), proportions (%), and relative risks (RR) with 95% confidence intervals. Results Eighty‐five studies ( n = 764,403) examining anxiety, depression, and vestibular disorders in adults were included. Mean ages were 50.3 (vestibular) and 46.7 (control); females comprised 63.8% and 64.3%, respectively. Patients with vestibular disorders had significantly higher rates and risks of anxiety (31.4% vs. 8.3%, p < 0.0001; RR = 1.50, 95% CI: 1.1–2.0) and depression (28.3% vs. 4.7%, p < 0.0001; RR = 2.9, 95% CI: 1.8–4.4) than controls. Elevated rates were observed in benign paroxysmal positional vertigo (30.6%, 23.6%), Meniere's disease (47.0%, 43.1%), vestibular migraine (46.5%, 35.7%), and vestibular neuritis (19.4%, 20.7%) (all p < 0.0001). Episodic disorders showed higher prevalence than vestibular neuritis. Patients with unspecified peripheral vestibular disorders also had significantly higher anxiety (12.1%) and depression (13.2%) rates than controls. Meta‐regression revealed significant associations between Dizziness Handicap Inventory (DHI) scores and Hospital Anxiety and Depression Scale (HADS) anxiety and depression subscales. Conclusions This meta‐analysis offers the most precise prevalence and relative risk estimates of anxiety and depressive disorders in vestibular illness. The greater risk in episodic versus single‐event vestibular disorders may inform the understanding of vestibular–psychiatric comorbidity mechanisms.

BACKGROUND: Patients with functioning pituitary adenomas (FPA) require a multidisciplinary team-based approach to select best medical, surgical, and radiation treatments, including stereotactic radiosurgery (SRS). OBJECTIVE: The aim of this study was to provide evidence-based recommendations on the use of SRS for adult patients with FPA. METHODS: PubMed and Embase were searched from data base inception to June 8, 2021. Full-text articles were then screened using published exclusion/inclusion criteria. Evidence tables were developing based on data extraction from the full-text reviews, and evidence-based recommendations were finalized. RESULTS: Of the total 1842 abstracts pertinent to this topic, 343 full articles met eligibility. Of these, 21 met entry criteria and were included in the evidence tables. The provided Class III evidence supported 2 Level III recommendations: 1. SRS, hypofractionated SRS, fractionated (>5 fractions) radiotherapy, and conventional radiation therapy provide excellent radiographic control with variable hormonal reduction and endocrine remission rates. For SRS and fractionated radiotherapy hormonal reduction may continue for up to 10 years after treatment. 2. Clinicians may continue to administer endocrine suppressive medical treatment before SRS as this may not affect radiographic control. CONCLUSION: This systematic review provides evidence-based recommendations to guide providers caring for adult patients with FPA when making decisions pertinent to radiosurgery. The CNS Guidelines Committee will continue to pursue timely updates to further improve the care of patients with this diagnosis.

ABSTRACT Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disease that is caused by mutations in PKD genes. Glucagon‐like peptide‐1 (GLP‐1) receptor agonists (GLP‐1RAs) are a class of medications that mimic the actions of the hormone GLP‐1, conferring beneficial effects on weight management and other metabolic conditions. However, whether GLP‐1RA plays a kidney‐protective action in ADPKD remains unknown. In this study, we define the role and mechanisms of one of the most popular GLP‐1RA agonists, Semaglutide, in ADPKD. We show that the expression of GLP‐1R is decreased in Pkd1 mutant renal epithelial cells and kidneys. Treatment with Semaglutide delays cyst growth in aggressive and long‐lasting Pkd1 mutant mouse models. Treatment with Semaglutide (1) decreases glucose uptake, ATP generation, and glycolysis, (2) deactivates PKD‐associated signaling pathways, including Rb, S6, and Stat3, resulting in a decrease in cell proliferation, (3) deactivates NF‐kB signaling pathways, resulting in a decrease in the expression of cytokines and the recruitment of macrophages, (4) normalizes mitochondrial morphology and function, (5) induces Pkd1 mutant renal epithelial cell death, (6) induces ketosis characterized by an increase in serum level of beta‐hydroxybutyrate (BHB) and the activation of AMPK, and (7) alleviates renal fibrosis through deactivation of TGF‐b signaling in Pkd1 mutant mouse kidneys. This study highlights the potential of GLP‐1R agonists as a novel therapeutic strategy for ADPKD treatment.

Background: Fat grafting is a common procedure in plastic and reconstructive surgery. It is associated with several disadvantages and complications, especially in patients undergoing recurrent procedures. Researchers are exploring the implications of cryopreserving adipose tissue and stem cells in plastic surgery. This article aimed to evaluate whether autologous fatty tissue and adipose-derived stem cells obtained through liposuction can be safely stored via cryopreservation for future surgical use. Methods: A comprehensive literature search was conducted across 3 databases, including PubMed, ScienceDirect, and Ovid MEDLINE, using specific keywords, yielding 75 articles. Studies that were not written in English or conducted in vitro were excluded. Only studies published in English within the last 5 years, and focusing on the use of cryopreservation of adipose tissue, were included. After review, a total of 22 articles met the inclusion criteria and were analyzed. Results: Cryopreserving adipose tissue and adipose-derived stem cells shows great potential in plastic surgery. Patient factors such as harvesting site, age, and obesity significantly impact the yield. The highest yield was obtained by harvesting from the abdomen and thigh. Additionally, cryopreservation requires cryoprotective agents, among which a combination of dimethyl sulfoxide and human serum albumin was most effective. Despite the advancement in cryoprotective agents, thawing adipose tissue results in cell death and impaired extracellular matrix integrity. However, cryopreserved stromal vascular fraction gel demonstrated fewer complications and better retention. Conclusions: The cryopreservation of adipose tissue and stromal vascular fraction gel demonstrates promising advancements for future applications in plastic surgery and regenerative medicine.

Abstract Background and Aims Type 1 short QT syndrome (SQT1) is a genetic channelopathy caused by gain-of-function variants in KCNH2, resulting in shortened cardiac repolarization and QT intervals, which predispose patients to ventricular arrhythmias and sudden cardiac death. This study aimed to investigate the therapeutic efficacy of KCNH2-specific suppression-and-replacement (KCNH2-SupRep) gene therapy in a transgenic rabbit model of SQT1. Methods KCNH2-SupRep was developed by combining a KCNH2-shRNA with its corresponding shRNA-immune KCNH2-cDNA into an AAV9 vector, delivered directly into the aortic root (1 × 1010 vg/kg). Therapeutic efficacy was evaluated in vivo by electrocardiogram, ex vivo by optical mapping, and at cellular levels by patch-clamp, calcium imaging, and qPCR in ventricular cardiomyocytes (VCMs). Results In vivo, KCNH2-SupRep normalized the heart rate-corrected QT interval (QTc) in SQT1 rabbits, without affecting repolarization heterogeneity. Ex vivo, KCNH2-SupRep corrected the action potential duration (APD90) and resolved the increased apicobasal APD90 heterogeneity observed in untreated (UT)-SQT1 hearts, supporting an antiarrhythmic effect, which was further validated by reduced re-entry formation in silico. At cellular levels, KCNH2-SupRep prolonged APD90 in VCMs from SupRep-SQT1 rabbits closer to wildtype levels compared with UT- and sham-SQT1. Additionally, KCNH2-SupRep restored the cellular surrogate of the electro-mechanical window and normalized IKr in nearly 50% of VCMs, in line with a 50%–60% suppression of the mutant KCNH2 transcript. Conclusions This proof-of-concept study is the first to demonstrate the efficacy of gene therapy for SQT1 in a medium-sized animal model. KCNH2-SupRep gene therapy successfully corrected the pathologic phenotype in vivo, ex vivo, and at cellular levels in transgenic SQT1 rabbits.