Validity of the Clinical Frailty Scale in Korean older patients at a geriatric clinic.

BACKGROUND/AIMS: We aimed to assess the validity of the Korean translated version of the Clinical Frailty Scale (CFS) in determining the frailty status in geriatric outpatients. METHODS: The records of 123 ambulatory outpatients who had undergone CFS and comprehensive geriatric assessments (CGAs) including measurements for the Cardiovascular Health Study (CHS) frailty scale and the frailty index (CGA-FI) were analyzed. Correlations between CFS, CHS frailty scale, and CGA-FI were assessed. The ability of CFS to classify frailty status was calculated using the CHS frailty scale and CGA-FI as references. RESULTS: The mean CFS score was 3.2 in the study population, with a mean age of 77.49 years (45.5% men). Individuals with higher CFS scores were older, had a greater burden of chronic diseases, and worse daily functions and cognitive performance. CFS scores positively correlated with CGA-FI (B = 0.78, p < 0.001) and CHS frailty scale (B = 0.67, p < 0.001) scores. For CFS, C-statistics to classify frailty by CGA-FI and CHS scale were 0.905 and 0.826, respectively. The cut-off value of CFS ≥ 4 maximized Youden's J to classify frailty by both the CHS scale and CGAFI. CONCLUSION: The CFS is a valid screening tool to assess the frailty status in outpatients of a geriatric clinic in Korea. As a simple and quick measure, the CFS may facilitate frailty assessments in real-world clinical practice.

Gastrokine 1 regulates NF-κB signaling pathway and cytokine expression in gastric cancers.

Gastrokine 1 (GKN1) plays an important role in the gastric mucosal defense mechanism and also acts as a functional gastric tumor suppressor. In this study, we examined the effect of GKN1 on the expression of inflammatory mediators, including NF-κB, COX-2, and cytokines in GKN1-transfected AGS cells and shGKN1-transfected HFE-145 cells. Lymphocyte migration and cell viability were also analyzed after treatment with GKN1 and inflammatory cytokines in AGS cells by transwell chemotaxis and an MTT assay, respectively. In GKN1-transfected AGS cells, we observed inactivation and reduced expression of NF-κB and COX-2, whereas shGKN1-transfected HFE-145 cells showed activation and increased expression of NF-κB and COX-2. GKN1 expression induced production of inflammatory cytokines including IL-8 and -17A, but decreased expression of IL-6 and -10. We also found IL-17A expression in 9 (13.6%) out of 166 gastric cancer tissues and its expression was closely associated with GKN1 expression. GKN1 also acted as a chemoattractant for the migration of Jurkat T cells and peripheral B lymphocytes in the transwell assay. In addition, GKN1 significantly reduced cell viability in both AGS and HFE-145 cells. These data suggest that the GKN1 gene may inhibit progression of gastric epithelial cells to cancer cells by regulating NF-κB signaling pathway and cytokine expression.