[Development of Nursing Clinical Judgment Scale].

PURPOSE: This study aimed to develop a nursing clinical judgment scale (NCJS) and verify its validity and reliability in assessing the clinical judgment of nurses. METHODS: A preliminary instrument of the NCJS comprising 38 items was first developed from attributes and indicators derived from a literature review and an in-depth/focus interview with 12 clinical nurses. The preliminary tool was finalized after 7 experts conducted a content validity test based on a data from a preliminary survey of 30 hospital nurses in Korea. Data were collected from 443 ward, intensive care unit, emergency room nurses who voluntarily participated in the survey through offline and online for the verification of the construct validity and reliability of the scale. RESULTS: The final scale comprised 23 items scored on a 5-point Likert scale. Six factors- integrated data analysis, evaluation and reflection on interventions, evidence on interventions, collaboration among health professionals, patient-centered nursing, and collaboration among nurse colleagues - accounted for 64.9% of the total variance. Confirmatory factor analysis supported the fit of the measurement model, comprising six factors (root mean square error of approximation = .07, standardized root mean square residual = .04, comparative fit index = .90). Cronbach's α for all the items was .92. CONCLUSION: The NCJS is a valid and reliable tool that fully reflects the characteristics of clinical practice, and it can be used effectively to evaluate the clinical judgment of Korean nurses. Future research should reflect the variables influencing clinical judgment and develop an action plan to improve it.

Sequencing and characterization of Varicella-zoster virus vaccine strain SuduVax.

BACKGROUND: Varicella-zoster virus (VZV) causes chickenpox in children and shingles in older people. Currently, live attenuated vaccines based on the Oka strain are available worldwide. In Korea, an attenuated VZV vaccine has been developed from a Korean isolate and has been commercially available since 1994. Despite this long history of use, the mechanism for the attenuation of the vaccine strain is still elusive. We attempted to understand the molecular basis of attenuation mechanism by full genome sequencing and comparative genomic analyses of the Korean vaccine strain SuduVax. RESULTS: SuduVax was found to contain a genome that was 124,759 bp and possessed 74 open reading frames (ORFs). SuduVax was genetically most close to Oka strains and these Korean-Japanese strains formed a strong clade in phylogenetic trees. SuduVax, similar to the Oka vaccine strains, underwent T- > C substitution at the stop codon of ORF0, resulting in a read-through mutation to code for an extended form of ORF0 protein. SuduVax also shared certain deletion and insertion mutations in ORFs 17, 29, 56 and 60 with Oka vaccine strains and some clinical strains. CONCLUSIONS: The Korean VZV vaccine strain SuduVax is genetically similar to the Oka vaccine strains. Further comparative genomic and bioinformatics analyses will help to elucidate the molecular basis of the attenuation of the VZV vaccine strains.

PKR protein kinase is activated by hepatitis C virus and inhibits viral replication through translational control.

Hepatitis C virus (HCV) infection is currently treated with IFNalpha-based therapy but little is known how IFNalpha inhibits HCV replication. We show here that HCV JFH1 infection of human hepatoma Huh-7 cells leads to the activation of IFN-inducible protein kinase PKR and phosphorylation of the translation initiation factor eIF2alpha. Compared to a control cell HCV replication was significantly elevated in a PKR-knockdown cell, giving rise to a 10-fold higher viral titer, and was less sensitive to IFNalpha treatment. Conversely, transient expression of PKR inhibited HCV replication in a kinase-dependent manner with concomitant increase of eIF2alpha phosphorylation. Further, expression of a phospho-mimetic eIF2alpha mutant moderately inhibited HCV replication. Together, these results demonstrate that PKR is activated by HCV infection and plays a critical antiviral role through inhibition of viral protein translation.

Hepatitis C virus NS2 protein activates cellular cyclic AMP-dependent pathways.

Chronic infection of the hepatitis C virus (HCV) leads to liver cirrhosis and cancer. The mechanism leading to viral persistence and hepatocellular carcinoma, however, has not been fully understood. In this study, we show that the HCV infection activates cellular cAMP-dependent pathways. Expression of a luciferase reporter gene controlled by a basic promoter with the cAMP response element (CRE) was significantly elevated in human hepatoma Huh-7 cells infected with the HCV JFH1. Analysis with viral subgenomic replicons indicated that the HCV NS2 protein is responsible for the effect. Furthermore, the level of cellular transcripts whose stability is known to be regulated by cAMP was specifically reduced in cells harboring NS2-expressing replicons. These results allude to the HCV NS2 protein having a novel function of regulating cellular gene expression and proliferation through the cAMP-dependent pathway.