Routine template bleeding time determinations before cardiac procedures.
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Biomedical subjects
Publications and source records attributed to W Berry.
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"This paper systematically relates local survey data to national census data in an investigation of one peripheral form of counter-urbanization now regarded as widely present in developed countries. The recent growth and spatial distribution of long-distance English migration to the Highlands and Islands of Scotland is described, and then 'explained' through multivariate analysis of cross-sectional data and through the stated motivations and characteristics of surveyed migrants to some of the remoter, rural parts of the region. The study reveals the importance of environmental and quality of life considerations." (summary in FRE, GER)
We have confirmed the observations of Tsunoo et al. (Toxicol. Lett. 4:253, 1979) that (a) DBA/2 mice are resistant to cadmium mortality than C3H mice and (b) DBA/2 mice accumulate more 109Cd into hepatic metallothionein than do C3H mice in response to an injection of 30 mumol CdCl2/kg, a dose of CdCl2 which is lethal to C3H mice. We now report, using a nonlethal dose of 8 mumol CdCl2/kg, that the rates of both the synthesis and the degradation of cadmium-induced hepatic metallothionein are increased in C3H mice. The rate of metallothionein synthesis, measured 6 hr after cadmium administration and expressed as the percentage of injected [35S]cysteine incorporated into metallothionein/g liver, was 0.33 +/- 0.04% (SD) in C3H mice, compared to 0.19 +/- 0.06% in DBA/2 mice (significantly different rates by Students' t test. P less than 0.01). Also, at this dose, hepatic 35S-labeled metallothionein was degraded with a half-life of 22.5 +/- 0.7 hr in C3H mice, compared to 30.1 +/- 2.5 hr in DBA/2 mice (significantly different half-lives by F test, within 95% confidence limits). The increased accumulation of metallothionein in resistant DBA/2 mice compared to sensitive C3H mice after cadmium exposure appears to be due primarily to a difference in metallothionein degradation, rather than metallothionein synthesis.
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