Effects of functional performance and national health insurance cost on length of hospitalization for postacute care in stroke: a retrospective observational study.

Background: The postacute care for cerebrovascular disease (PAC-CVD) program was launched in Taiwan nearly a decade ago. However, no clear regulations regarding length of stay (LOS) in the program and extension standards exist. Thus, the allocation of limited medical resources such as hospital beds is a major issue.

Efficacy and Cost over 12 Hospitalization Weeks of Postacute Care for Stroke.

Few studies have investigated changes in functional outcomes and economic burden in patients in the postacute care cerebrovascular disease (PAC-CVD) program. We, for the first time, retrospectively investigated changes in functional performance and the national health insurance (NHI) cost over 12 PAC-CVD hospitalization weeks and evaluated the therapeutic effects of the PAC-CVD program on the NHI cost. Specifically, the functional outcomes and NHI cost of 263 stroke patients in the PAC-CVD program were analyzed.

Increased Anxiety and Depression Symptoms in Post-Acute Care Patients with Stroke during the COVID-19 Pandemic.

This study aimed to explore the quality and stability of post-acute care for patients with stroke, including their functional outcomes, mental health and medical care in Taiwan during the COVID-19 pandemic. In this retrospective case-control study-based on propensity score matching-we assessed 11 patients admitted during the pandemic period (in 2021) and 11 patients admitted during the non-pandemic period (in 2020). Functional outcomes, including the scores of the modified Rankin Scale, Barthel Index, EuroQoL-5 Dimension, Lawton-Brody instrumental activities of daily living, Berg Balance Scale, 5-metre walking speed and 6-min walking distance, were determined.

Curcumin Attenuates Adipogenesis by Inducing Preadipocyte Apoptosis and Inhibiting Adipocyte Differentiation.

Patients with metabolic syndrome are at an increased risk of developing type 2 diabetes and cardiovascular diseases. The principal risk factor for development of metabolic syndrome is obesity, defined as a state of pathological hyperplasia or/and hypertrophy of adipose tissue. The number of mature adipocytes is determined by adipocyte differentiation from preadipocytes.

Methylosome protein 50 promotes androgen- and estrogen-independent tumorigenesis.

Methylosome protein 50 (MEP50) is a component of methylosome where MEP50 binds protein substrates and activates the oncogenic protein arginine methyl transferase 5 (PRMT5). MEP50 is also a coactivator for androgen receptor (AR) and estrogen receptor (ER), and transforms cells in the presence of androgen or estrogen. To extend the understanding of how MEP50 transforms cells, we investigated whether MEP50 could transform cells independent of AR and ER, and clarified whether PRMT5 could contribute to the MEP50-caused tumor formation.

Protein arginine methyltransferase 5 is a potential oncoprotein that upregulates G1 cyclins/cyclin-dependent kinases and the phosphoinositide 3-kinase/AKT signaling cascade.

Increasing evidence suggests that PRMT5, a protein arginine methyltransferase, is involved in tumorigenesis. However, no systematic research has demonstrated the cell-transforming activity of PRMT5. We investigated the involvement of PRMT5 in tumor formation.

Coenzyme Q10 suppresses oxLDL-induced endothelial oxidative injuries by the modulation of LOX-1-mediated ROS generation via the AMPK/PKC/NADPH oxidase signaling pathway.

Scope: The lectin-like oxidized low-density lipoprotein receptor (LOX-1) is one pivot receptor for oxidized low-density lipoprotein (oxLDL) in human endothelial cells. Co-enzyme Q10 (Co Q10) has been widely used in clinical intervention. However, the molecular mechanisms underlying its protective effects against oxidative stress in endothelial cells are still largely unknown.

A novel mechanism of coenzyme Q10 protects against human endothelial cells from oxidative stress-induced injury by modulating NO-related pathways.

Background: Atherosclerosis is a chronic inflammatory disease of the vessel wall associated with oxidized low-density lipoprotein (oxLDL)-induced apoptosis of endothelial cells. Coenzyme Q10 (CoQ10), a potent antioxidant and a critical intermediate of the electron transport chain, has been reported to inhibit LDL oxidation and thus the progression of atherosclerosis. However, its molecular mechanisms on endothelial cells remain still unclarified.

Enhanced radiosensitivity and radiation-induced apoptosis in glioma CD133-positive cells by knockdown of SirT1 expression.

CD133-expressing glioma cells play a critical role in tumor recovery after treatment and are resistant to radiotherapy. Herein, we demonstrated that glioblastoma-derived CD133-positive cells (GBM-CD133(+)) are capable of self-renewal and express high levels of embryonic stem cell genes and SirT1 compared to GBM-CD133(-) cells. To evaluate the role of SirT1 in GBM-CD133(+), we used a lentiviral vector expressing shRNA to knock-down SirT1 expression (sh-SirT1) in GBM-CD133(+).