The Chilliwack Respiratory Survey, 1963: Part I. Methodology

In order to ascertain the prevalence of chronic respiratory disease in residents of a rural town and to determine the relative importance of tobacco smoking and air pollution, a survey was conducted of 726 persons living at Chilliwack, British Columbia, in May and June, 1963. Over 95% of a random sample of adults was interviewed and performed simple tests of respiratory function. The sample was selected from a commercial census. An analysis of the demographic characteristics of the sample indicated that the group, aged 25 to 74 years, was reasonably representative for detailed study of chronic respiratory disease.     

Synergistic inhibition of metabolic cooperation by oleic acid or 12-0-tetradecanoylphorbol-13-acetate and dichlorodiphenyltrichlorethane (DDT) in Chinese hamster V79 cells: Implication of a role for protein kinase C in the regulation of gap junctional intercellular communication

The effects of TPA and/or DDT and oleic acid and/or DDT on gap junction-mediated intercellular communication (i.e. metabolic cooperation) between Chinese hamster V79 cells was examined. Addition of TPA, DDT or oleic acid alone to cocultures of 6t-hioguanine-resistant (6-TG ^R ) and 6-thioguanine-sensitive (6-TG ^S ) V79 cells significantly increased the recovery of 6-TG ^R cells indicating inhibition of metabolic cooperation. In the presence of TPA and DDT or oleic acid and DDT the observed recovery of 6-TG ^R cells was significantly greater than the expected (calculated) additive 6-TG ^R cell recovery. No synergistic increases in 6-TG ^R cell recovery were observed when co-cultures of V79 cells were exposed to dieldrin and DDT. These results indicate that TPA and DDT or oleic acid and DDT can act synergistically to inhibit metabolic cooperation. These data suggest a role for protein kinase C in the regulation of gap junction-mediated intercellular communication.Abbreviations DDT dichlorodiphenyltrichlorethane - MC metabolic cooperation defective - 6-TG 6thioguanine - TPA 12-0-tetradecanoylphorbol-13-acetate     

The primary effect of the Ity locus is on the rate of growth of Salmonella typhimurium that are relatively protected from killing

The Ity locus affects the net increase in numbers of Salmonella typhimurium in the liver and spleen of infected mice. There has been controversy, however, about whether the effects of this locus are due to differential killing of S. typhimurium or differential growth rates of S. typhimurium in mice. Our studies using S. typhimurium aroA mutants, which do not grow in vivo, demonstrate that growth of the infecting salmonella is necessary for the observation of the Ity phenotype. To examine the effects of the Ity locus on the growth and killing of fully virulent salmonella, we infected Ity-congenic mice i.v. with stationary phase S. typhimurium containing a single copy of the plasmid pHSG422. This plasmid exhibits defective replication at body temperature and is diluted out during salmonella growth in vivo. Thus, the frequency of plasmid-containing salmonella recovered from mice provides a measure of salmonella cell divisions in vivo. Inasmuch as the numbers of plasmid-containing salmonella are only slightly affected by bacterial division, any decline in the numbers of plasmid-containing salmonella is an unbiased measure of killing. By infecting mice with these plasmid-containing salmonella we observed that: 1) during the first four h post infection (during blood clearance of injected salmonella) there is about 3-fold more killing of salmonella in Ityr mice than in Itys mice; 2) from 4 to 44 h postinfection (after blood clearance is completed) there is little if any additional killing in either Itys or Ityr mice; and 3) during the first 48 h postinfection there is about 18-fold more growth of salmonella in Itys mice than in Ityr mice. Thus, the major effect of the Ity locus on resistance to salmonella, is the regulation of growth within a "safe" (relatively nonbactericidal) site in the liver and spleen.