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INTRODUCTION@#We developed a Clinical Frailty Scale algorithm (CFS-A) to minimise inter-rater variability and to facilitate wider application across clinical settings. We compared the agreement, diagnostic performance and predictive utility of CFS-A against standard CFS.@*MATERIALS AND METHODS@#We retrospectively analysed data of 210 hospitalised older adults (mean age, 89.4 years). Two independent raters assessed frailty using CFS-A. Agreement between CFS-A raters and with previously completed CFS was determined using Cohen's Kappa. Area under receiver operator characteristic curves (AUC) for both measures were compared against the Frailty Index (FI). Independent associations between these measures and adverse outcomes were examined using logistic regression.@*RESULTS@#Frailty prevalence were 81% in CFS and 96% in CFS-A. Inter-rater agreement between CFS-A raters was excellent (kappa 0.90, <0.001) and there was moderate agreement between CFS-A and standard CFS (kappa 0.42, <0.001). We found no difference in AUC against FI between CFS (0.91; 95% CI, 0.86-0.95) and CFS-A (0.89; 95% CI, 0.84-0.95; <0.001). Both CFS (OR, 3.59; 95% CI, 2.28-5.67; <0.001) and CFS-A (OR, 4.31; 95% CI, 2.41-7.69; <0.001) were good predictors of mortality at 12 months. Similarly, CFS (OR, 2.59; 95% CI, 1.81-3.69; <0.001) and CFS-A (OR, 3.58; 95% CI, 2.13-6.02; <0.001) were also good predictors of institutionalisation and/or mortality after adjusting for age, sex and illness severity.@*CONCLUSION@#Our study corroborated the results on inter-rater reliability, diagnostic performance and predictive validity of CFS-A which has the potential for consistent and efficient administration of CFS in acute care settings.
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<p><b>OBJECTIVE</b>To review the functions of these intracellular signals in their regulation of retinal ganglion cell (RGC) axon regeneration.</p><p><b>DATA SOURCES</b>Relevant articles published in English or Chinese from 1970 to present were selected from PubMed. Searches were made using the terms "intrinsic determinants, axon regeneration, RGC, optic nerve regeneration, and central nervous system axon regeneration."</p><p><b>STUDY SELECTION</b>Articles studying the mechanisms controlling RGC and central nervous system (CNS) axon regeneration were reviewed. Articles focusing on the intrinsic determinants of axon regeneration were selected.</p><p><b>RESULTS</b>Like other CNS neurons of mammals, RGCs undergo a developmental loss in their ability to grow axons as they mature, which is a critical contributing factor to the failure of nerve regeneration and repair after injury. This growth failure can be attributed, at least in part, by the induction of molecular programs preventing cellular overgrowth and termination of axonal growth upon maturation. Key intracellular signals and transcription factors, including B cell lymphoma/leukemia 2, cyclic adenine monophosphate, mammalian target of rapamycin, and Krüppel-like transcription factors, have been identified to play central roles in this process.</p><p><b>CONCLUSIONS</b>Intense effort and substantial progress have been made to identify the various intrinsic growth pathways that regulate RGC axon regeneration. More work is needed to elucidate the mechanisms of and the interrelationship between the actions of these factors and to successfully achieve regeneration and repair of the severed RGC axons.</p>
