Predictors of behavioral health unit readmission within 30 days of discharge: A retrospective study.

Several studies have aimed to describe associated demographic and psychiatric risk factors that would lead to readmission to a behavioral health unit within 30 days of discharge. Here we considered 1,095 patients that were discharged from Millcreek Community Hospital (MCH) in Erie, Pennsylvania between June 2018 and June 2019. We extracted electronic medical data and analyzed various risk factors using a SPSS software and performed Chi square analysis to determine significance. We determined that patients between the age 30-39 that were diagnosed with major depressive disorder or bipolar disorder, and patients that had 12 or more previous behavioral health admissions were significantly more likely to be readmitted within 30 days of discharge. By analyzing risk factors that lead to a higher percentage of readmission rates, physicians can be more readily equipped and prepared while treating inpatient psychiatric patients. These physicians can take more precautionary measures when discharging patients with specific characteristic profiles to prevent the risk of being readmitted within 30 days of discharge.

Comparative proteomics reveals elevated CCN2 in NGLY1-deficient cells.

N-glycanase 1(NGLY1) catalyzes the removal of N-linked glycans from newly synthesized or misfolded protein. NGLY1 deficiency is a recently diagnosed rare genetic disorder. The affected individuals present a broad spectrum of clinical features. Recent studies explored several possible molecular mechanisms of NGLY1 deficiency including defects in proteostasis, mitochondrial homeostasis, innate immunity, and water/ion transport. We demonstrate abnormal accumulation of endoplasmic reticulum-associated degradation (ERAD) substrates in NGLY1-deficient cells. Global quantitative proteomics discovered elevated levels of endogenous proteins in NGLY1-defective human and mouse cells. Further biological validation assays confirmed the altered abundance of several key candidates that were subjected to isobarically labeled proteomic analysis. CCN2 was selected for further analysis due to its significant increase in different cell models of NGLY1 deficiency. Functional assays show elevated CCN2 and over-stimulated TGF-ß signaling in NGLY1-deficient cells. Given the important role of CCN2 and TGF-ß pathway in mediating systemic fibrosis, we propose a potential link of increased CCN2 and TGF-ß signaling to microscopic liver fibrosis in NGLY1 patients.