Effects of Supplemented Remifentanil/Meperidine to Sevoflurane Anesthesia on the Recovery in the Pediatrics Undergoing Tonsillectomy

BACKGROUND: Recovery from anesthesia, postoperative pain, nausea and vomiting are very important after pediatric tonsillectomy surgery. We compared the effects of supplemented opioids (remifentanil, meperidine) combined with sevoflurane on the recovery and side effects. METHODS: Patients were randomized to receive meperidine (group M, n = 41) or remifentanil (group R, n = 43). Group R received a bolus dose of normal saline, and group M 1 mg/kg of meperidine. A continuous infusion of normal saline was followed in the group M, and remifentanil 0.25micro/kg/min in the group R. In all patients, signs of inadequate anesthesia were treated with an increase of sevoflurane concentration. Intraoperative hemodynamics, recovery profiles, and side effects were assessed. RESULTS: Supplemented remifentanil resulted in significantly lower systolic blood pressure and heart rate during operation (P < 0.05). The emergence from anesthesia was not different between groups. Although the patients in the group R had early recovery characteristics at recovery room, time to discharge at recovery room was longer in the group R than in the group M (P < 0.05). The incidence of retching and vomiting was not different between groups. Supplemented meperidine resulted in less analgesic requirements than the other group (P < 0.05). CONCLUSIONS: Supplemented remifentanil was associated with hemodynamic stability, however it provided later discharge time at recovery room. Postoperative analgesic requirements were reduced by the supplemented meperidine without increasing postoperative nausea, vomiting.

Molecular Genetics of Primary Intracerebral Hemorrhage / 대한뇌혈관외과학회지

Intracerebral hemorrhage (ICH) is more deadly than ischemic stroke but is also rarer and more difficult to study. Genetic and environmental risk factors likely play a role in the occurrence of ICH. The genetics of cerebral amyloid angiopathy like mutation at beta-amyloid peptide positions 22 and 23, cystatin C, presenilin 1 and 2 or apolipoprotein E have been studied for both familial and sporadic forms. In addition, genetic variation in the hemostasis pathway likewise might affect the likelihood of sporadic ICH. Furthermore, polymorphisms of candidate genes such as endoglin, cytochrome P450 enzyme, lipoproteins, or proteolytic enzyme are all known to be risk factors of ICH. Recent advances in molecular biology provide evidence that genetic variants of different candidate genes are associated with the occurrence of ICH. The aim of this review is to expose the current status of these various hypotheses and their contribution to the pathogenesis of ICH in order to provide a basis for future investigations in this field.

Expression of the DNA Repair Gene, N-Methylpurine-DNA Glycosylase in Astrocytic Tumors

OBJECTIVE: This study is designed to investigate the association of tumorigenesis with DNA repair gene, N-methylpurine-DNA-glycosylase(MPG) in astrocytic tumors. METHODS: MPG mRNA expression and localization in the 30 astrocytic tumors and 7 tumor-adjacent brain tissues was examined by reverse transcriptase-polymerase chain reaction(RT-PCR) and RNA in situ hybridization. Expression and intracellular localization of MPG protein was determined by immunohistochemistry. Statistical analysis was performed by ANOVA with a p value<0.05 considered statistically significant. RESULTS: MPG mRNA expression in RT-PCR was significantly higher in grade IV tumor tissues than in brain tissues adjacent to tumor or in grade II-III astrocytic tumor tissues(p<0.05). MPG mRNA in in situ hybridization was detected both in brain tissues adjacent to tumor and in astrocytic tumor tissues, regardless of the tumor grades. However, MPG protein localization in immunohistochemical study was detected only in the nucleus of all tumor tissues. In brain tissues adjacent to tumor, immunohistochemical study for MPG was not stained both in the nucleus and in cytoplasm. CONCLUSION: These results suggest MPG's role in human astrocytic tumors and raise the possibility that the increased mRNA level and intracellular localization could be associated with astrocytic tumorigenesis. Further studies about control of MPG gene expression in astrocytic tumors are warranted.