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1.
Journal of Korean Society of Medical Informatics ; : 123-132, 2007.
Article in English | WPRIM | ID: wpr-49846

ABSTRACT

OBJECTIVE: The main complaints of users in existing electronic medical record systems are the complexity of recording system and long recording time. The records of patient moving and the diagnostic test performed outside emergency room are important. But emergency nurses can't record such information exactly and completely because of the highest priorities of emergency treatment and its record in overcrowded emergency room. METHODS: Emergency electronic medical record team of Asan Medical Center developed the automatic recording system of patient moving and diagnostic test information in 2006. The effectiveness of this system was evaluated by comparing the number of records in manual and automatic documentations before and after the system application. RESULTS: The numbers of total records per patient-order were not changed statistically, but the number of manual patient moving and diagnostic test records significantly reduced from 0.50+/-0.69 to 0.31+/-0.47 (p < 0.01). The number of automatic patient moving and diagnostic test records per patient-order was 1.98+/-0.99. CONCLUSION: This automatic recording system can reduce indirect nursing time and give more exact and complete information to emergency medical personnel. The effort to simplify documentation in electronic medical record systems is important, but 'automatic recording' strategy is also needed.


Subject(s)
Humans , Automation , Diagnostic Tests, Routine , Documentation , Electronic Health Records , Emergencies , Emergency Service, Hospital , Emergency Treatment , Moving and Lifting Patients , Nursing
2.
Experimental & Molecular Medicine ; : 267-277, 2007.
Article in English | WPRIM | ID: wpr-201428

ABSTRACT

In vascular smooth muscle cells (VSMCs), induction of the heme oxygenase-1 (HO-1) confers vascular protection against cellular proliferation mainly via its up-regulation of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) that is involved in negative regulation of cellular proliferation. In the present study, we investigated whether the phytochemical curcumin and its metabolite tetrahydrocurcumin could induce HO-1 expression and growth inhibition in rat VSMCs and, if so, whether their antiproliferative effect could be mediated via HO-1 expression. At non-toxic concentrations, curcumin possessing two Michael-reaction acceptors induced HO-1 expression by activating antioxidant response element (ARE) through translocation of the nuclear transcription factor E2-related factor-2 (Nrf2) into the nucleus and also inhibited VSMC growth triggered by 5% FBS in a dose-dependent manner. In contrast, tetrahydrocurcumin lacking Michael-reaction acceptor showed no effect on HO-1 expression, ARE activation and VSMC growth inhibition. The antiproliferative effect of curcumin in VSMCs was accompanied by the increased expression of p21(WAF1/CIP1). Inhibition of VSMC growth and expression of p21(WAF1/CIP1) by curcumin were partially, but not completely, abolished when the cells were co- incubated with the HO inhibitor tin protoporphyrin. In human aortic smooth muscle cells (HASMCs), curcumin also inhibited growth triggered by TNF-alpha and increased p21(WAF1/CIP1) expression via HO-1-dependent manner. Our findings suggest that curcumin has an ability to induce HO-1 expression, presumably through Nrf2-dependent ARE activation, in rat VSMCs and HASMCs, and provide evidence that the antiproliferative effect of curcumin is considerably linked to its ability to induce HO-1 expression.


Subject(s)
Animals , Humans , Rats , Active Transport, Cell Nucleus , Aorta/cytology , Cell Nucleus/metabolism , Cell Proliferation/drug effects , Cells, Cultured , Curcumin/analogs & derivatives , Cyclin-Dependent Kinase Inhibitor p21/biosynthesis , Gene Expression Regulation , Heme Oxygenase (Decyclizing)/biosynthesis , Heme Oxygenase-1/biosynthesis , Metalloporphyrins/pharmacology , Muscle, Smooth, Vascular/drug effects , Myocytes, Smooth Muscle/drug effects , NF-E2-Related Factor 2/metabolism , Protoporphyrins/pharmacology , Regulatory Sequences, Nucleic Acid , Response Elements , Tumor Necrosis Factor-alpha/pharmacology
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