Paynemalling3188

s of the facilities or summary quality scores. Development of risk reduction approaches requires assessment of processes and quality beyond the current quality measures.

We investigated whether the FRAIL scale questionnaire is consistent with the Fried criteria, predicts all-cause mortality, and reflects physical dysfunction in patients with heart failure (HF).

Secondary analysis of FRAGILE-HF, a cohort study that enrolled participants from 2016 to 2018 and followed-up for 1-year of discharge.

A prospective multicenter cohort study in which 15 hospitals in Japan (8 university hospitals and 7 nonuniversity teaching hospitals) participated. We prospectively enrolled 1332 consecutive hospitalized patients ≥65years old with HF and analyzed 1028 patients after excluding 304 patients with missing data on the FRAIL scale.

The FRAIL scale, the Fried model, and physical function were measured before discharge. The endpoint was all-cause mortality.

According to the FRAIL scale, 459 (44.6%) and 491 (47.8%) were classified as frail and prefrail, respectively. The Kappa coefficient between the FRAIL scale and the Fried criteria were 0.39 [95% confidence interval (CI) 0.34-0.44; P<.001]. The area under the receiver-operating characteristic curves for frailty diagnosed by the Fried criteria of the FRAIL scale was 0.74 (95% CI 0.71-0.76; P<.001). A total of 118 deaths occurred during 1year of follow-up. After adjusting for the MAGGIC risk score and log-BNP, The FRAIL scale predicted all-cause mortality (hazard ratio 1.17; 95% CI 1.01-1.36; P=.035). The FRAIL scale was also associated with various physical dysfunctions that correlated with poor prognosis.

The FRAIL scale had moderate consistency with the Fried criteria, predicted all-cause mortality, and reflected clinically important physical dysfunctions.

The FRAIL scale had moderate consistency with the Fried criteria, predicted all-cause mortality, and reflected clinically important physical dysfunctions.

Slow walking speed (WS) is predictive of mortality but may be difficult to measure, which compromises the assessment of frailty, based on Fried etal's phenotype. The timed Moberg picking-up test (MPUT), developed to evaluate hand's function, was found moderately but significantly correlated with WS. We compared the relationship between slowness, assessed by MPUT and WS tests, and mortality.

Observational (prospective cohort study).

4731 community-dwelling adults included in 2004, 2009, or 2014 in the ongoing Lausanne cohort 65+ (Lc65+) were assessed at the age of 66-71years.

Mortality was compared for individuals above and below percentile 80 of MPUT, and respectively WS performance time, according to the Fried criterion. Multivariable analyses using Cox's regression models were adjusted for age, sex, height and grip strength. The predictive capability of MPUT and WS was assessed in adjusted models using Harrell C.

Slowness in MPUT and in WS test was associated with mortality at 4, 9, and 14years (Pernative to WS in the assessment of slowness has similar predictive capability for mortality and avoids biased estimates because of nonrandom exclusion of individuals unable to complete WS.

Previous studies reported that mild inflammation promotes retinal ganglion cell (RGC) survival and axonal regeneration after optic nerve (ON) injury with involvement of infiltrating macrophages and neutrophils. Here we aimed to evaluate the involvement and regulation of the main inflammatory chemokine pathway CXCL5/CXCR2 in the inflammation-mediated RGC survival and axonal regeneration in mice after ON injury.

The expressions and cellular locations of CXCL5 and CXCR2 were confirmed in mouse retina. Treatment effects of recombinant CXCL5 and CXCR2 antagonist SB225002 were studied in the explant culture and the ON injury model with or without lens injury. The number of RGCs, regenerating axons, and inflammatory cells were determined, and the activation of Akt andSTAT3 signaling pathways were evaluated.

Cxcr2 and Cxcl5 expressions were increased after ON and lens injury. Guanosine 5'-monophosphate compound library chemical Addition of recombinant CXCL5 promoted RGC survival and neurite outgrowth in retinal explant culture with increase in the number of activtarget for RGC survival promotion after ON injury.Uveal melanoma (UM), as the most common primary intraocular carcinoma, is a relatively rare but lethal tumor. Upregulated eukaryotic translation initiation factor 4E family member 2 (EIF4E2) promotes the progression of multiple human carcinomas. However, its role remains unclear in UM. To identify the prognostic value of EIF4E2 in UM, we downloaded RNA-sequencing data along with clinical information from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets. EIF4E2 mRNA was significantly increased in three different subgroups in the TCGA-UM dataset. High mRNA expression was correlated with shorter overall survival (OS) and shorter recurrence-free survival (RFS). Moreover, we constructed a prognostic signature using Cox regression analyses in our training cohort TCGA-UM dataset as follows risk score = 0.04335 × Age +0.49639 × expression of EIF4E2. Based on the risk score, each patient was classified as high-risk or low-risk. Additional survival analyses suggested that patients in the high-risk score group had an unfavorable OS compared with patients in the low-risk score group, which was validated in two external GEO datasets, including GSE84976 and GSE22138. Functional enrichment analysis demonstrated that UM was correlated with hypoxia-related functions. Gene set enrichment analysis (GSEA) indicated significant enrichments of the p53 and Notch pathways. In addition, EIF4E2 was genetically altered in 12.5% (10/80) of UM patients. Epigenetically, higher expression of cg03852847 was correlated with longer OS and longer RFS. In conclusion, our findings demonstrated that high EIF4E2 expression is an independent prognostic risk factor for UM patients. EIF4E2 might play an important role in hypoxia-related signaling pathways during UM progression. Both genetic and epigenetic alterations may contribute to UM pathogenesis. These findings could offer individualized clinical prognostication and potential novel treatment targets for UM patients.