[Spermicides for contraception and STD prevention: current status].
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Biomedical subjects
Publications and source records attributed to S Townsend.
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This study establishes the association between early onset severe hyperbilirubinaemia (serum bilirubin (SBR) level greater than or equal to 272 mumol/L) with no assigned cause and breast feeding. The rates of breast feeding at hospital discharge increased from 46.4 to 75.4% in non-insured (public) women and 58.6 to 89.2% in insured (private) women between 1975 and 1987, and were accompanied by an increase in severe hyperbilirubinaemia from 1.6 to 3.1% in public and 0.9 to 3.6% in private babies. The case control study involved 125 term breast feeding infants born between 1 July 1985 and 1 July 1986 with severe hyperbilirubinaemia (SBR level 272 mumol/L) with no assigned cause who were compared with 125 matched controls who had peak SBR levels less than or equal to 272 mumol/L. Severe hyperbilirubinaemia was associated with primiparous and non-Caucasian mothers, non-smoking and oxytocin usage. Univariate analysis of feeding practice variables revealed that less frequent breast feeds, greater weight loss and less frequent stools over the first 3 days related to severe hyperbilirubinaemia (P less than 0.05). Multivariate analysis of the eight significant univariate factors revealed that maternal non-smoking, less frequent breast feeding, less frequent stooling and excessive infant weight loss were the best predictors of severe hyperbilirubinaemia. With the wide promotion of breast feeding, the contribution of individual feeding practices to severe hyperbilirubinaemia demands ongoing analysis and review.
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The effect of combined ultrasound and heat treatments on Chinese hamster multicellular spheroids of varying size was investigated using growth rate, single cell survival and ultrastructural damage as endpoints. Ultrasonic irradiation at 37 degrees C had no effect on the growth rate of 200-730 microns spheroids. Similarly there was no effect on the growth rate of 350 microns spheroids when irradiated during a 60 min exposure to 41.5 degrees C. However, spheroids of 200-700 mm diameter showed growth delay when held at 43 degrees C for 1 h. The effect was enhanced with concomitant ultrasound irradiation but was not dependent on spheroid size. When 200 and 400 microns spheroids held at 43 degrees C for 60 min were irradiated with different ultrasonic intensities a dose-dependent decrease in surviving fraction and a dose-dependent increase in growth delay was obtained. When surviving fraction was plotted as a function of growth delay a good correlation was obtained, suggesting that the combination of heat and ultrasound irradiation does not produce cytostasis in the surviving cells of either 200 or 400 microns spheroids. At the ultrastructural level increased cytoplasmic vacuolation was the only result of ultrasonic irradiation at 37 degrees C. Exposure to 43 degrees C for 60 min was required to elicit thermal damage. This took the form of membrane evagination at the spheroid surface, vacuolation of the cytoplasm, grouping of organelles around the periphery of the nucleus, and fragmentation of the nucleolus. These effects were enhanced with concomitant ultrasonic irradiation but other features were also noted, viz. disaggregation of polyribosomes, dilation of the rough endoplasmic reticulum and blebbing of the nuclear membrane. Damage was independent of spheroid size. These results are in agreement with previous data obtained from single-cell studies. Indicating that there is a non-thermal, non-cavitational component to the cell killing in multicellular spheroids resulting from combined heat and ultrasound treatment.
The direct-acting mutagen 4-nitro-o-phenylenediamine (NOP) was activated in vitro by pea or tobacco S-9 into a more potent mutagen in Salmonella typhimurium strain TA98. NOP mutagenicity was not altered by Aroclor 1254-induced rat liver S-9. The plant S-9 activation of NOP was heat-sensitive but was not NADPH-dependent, did not involve superoxide radicals, and was not inhibited by CO. A direct relationship between plant peroxidase and NOP activation was established. Several purified peroxidases including horseradish peroxidase, chloroperoxidase, and lactoperoxidase also activated NOP. The perodoxidative process was not H2O2-dependent but was partially inhibited by a peroxidase inhibitor.
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