Radiomodulation by Hoechst 33258 against radiation- induced damage in murine splenocytes.

In this study modulatory effect of Hoechst 33258 on radiation induced membrane related signaling events which ultimately leads to apoptosis has been investigated. Splenocytes from swiss albino mice were irradiated in air at room temperature in a gamma chamber (240 TBq 60Co Model 4000 A) at the dose-rate of 0.052 Gys-1. Membrane lipid peroxidation, fluidity, specific activities of antioxidant enzymes, levels of nitric oxide, glutathione and apoptosis in presence and absence of different concentrations of Hoechst 33258 has been assayed. DNA binding activity of nuclear factor kappa B and activator protein–1 was also assayed by electrophoretic mobility shift assay. Modulatory effect of Hoechst 33258 was examined at 3 and 5 Gy using different concentrations (10, 20 and 30 µM). Hoechst 33258 was found to inhibit radiation induced peroxidative damage and fluidity and lowered the level of nitric oxide and apoptosis - as evident by DNA ladder assay and FACS, indicating free radicals scavenging potential. Dot plot diagramme clearly showed that 30 µM Hoechst 33258 caused 14% and 19% decrease in apoptotic cells at 3 Gy and 5 Gy of radiation respectively (compared to irradiated control group). Further DNA binding activity of nuclear factor kappa B and activator protein–1 was also inhibited but the antioxidant potential of the cells was enhanced. These findings support that Hoechst 33258 protects the cell from undergoing apoptosis. Hoechst 33258 may have interacted and has an ability to protect splenocytes against radiation induced apoptosis through modulation of membrane-related signaling events and antioxidant status.

Longitudinal growth patterns of Pakistani infants in a clinic based growth promotion program.

OBJECTIVE: To describe the operation of growth monitoring and promotion (GMP) clinic and longitudinal growth patterns of children. DESIGN: Prospective observation and intervention. SETTING: Outpatient department of a teaching hospital. METHODS: Less than 6 months old infants were registered at GMP clinic and followed for up to two years of age. Mothers were provided information, education and counselling about healthy growth of their infants. The outcome measure was change in weight after follow-up. RESULTS: We enrolled a cohort of 553 children in the first 6 months of life, of which 318 were males. Mean follow up period was 15.7 (SD+/-6.4) months. At enrollment 207 were underweight [weight-for-age Z score (WAZ<-2], of which 153 were from low-income families. The children from poorer families also gained weight regularly, although it was less than the higher income families. Of 346 infants with normal weight at registration, 305 maintained their weight gain by last follow-up visit. Of 207 underweight infants at enrollment 128 improved their weight gain by the last follow-up visit. Overall 433 infants followed-up at our GMP clinic either maintained or improved their weight gain. CONCLUSIONS: Children at risk of undernutrition should be identified at an early age and through effective interaction between health workers and the family, their growth can be improved. Children of poor families can also benefit from this activity, provided a comprehensive approach is made available.