RESUMO
Aim: To investigate if any mutations in hepatitis C virus (HCV) internal ribosome entry site (IRES) can inhibit the translation of viral polyprotein. Materials and Methods: A 26-year-old male patient infected with HCV 10 years ago was followed up. After 9 years of chronic infection. The patient had managed to resolve the infection for a period of 9 months, after which the patient experienced a viral recurrence characterized by high viral load and diverse HCV quasispecies. The IRES structures of the viral strains that disappeared were comparable with those that are currently active using structural mutational analysis. Results: A novo mutational position 254 combined with a rarely observed mutation at position 253 in the stem of the IIId subdomain were observed and the new conformation had an octa-apical loop (AGUGUUGG) and a shift in the 3 ` GU from the loop to the stem. Conclusions: These mutations were found to be highly deleterious, and they affected the direct binding of the IIId loop to the 40S ribosomal subunit with a subsequent inhibition of translation of viral polyprotein and clearance of the virus.
RESUMO
To evaluate the foetal condition by assessment of foetal umbilical artery acid base balance and blood gases in high risk pregnancies compared to normal pregnancy. Forty female patients were included in this study, twenty served as normal controls, ten preeclamptic patients and ten diabetic patients. Post delivery umbilical artery blood sampling was withdrawn to measure pH, PaO[2], PaCO[2]. There was a significant difference in umbilical artery blood acid base parameters [pH, PaO[2], PaCO[2]] between normal pregnancies and high risk pregnancies [Diabetes mellitus and hypertension]. In addition the acid-base showed a good condition with mode of delivery. It appears that umbilical artery acid-base is an accurate assessment of foetal metabolic status and much more accurate than APGAR scoring system in diagnosis of asphyxia