Hyperplasia of jejunal smooth muscle in the myenterically denervated rat

Summary Application of a cationic surfactant, benzalkonium chloride, to the serosa of rat jejunum results in an increase in thickness of both longitudinal and circular smooth muscle layers. The increase in thickness is due primarily to an increase in the number of smooth muscle cells (hyperplasia). Little cellular hypertrophy was observed. The time sequence of surfactant-induced effects on the muscle layers was determined. Within 24 h, total destruction of the longitudinal muscle and partial destruction of the circular muscle was evident. The myenteric plexus was also necrotic; however, the submucosal plexus remained intact. By 48 h after surfactant treatment, the smooth muscle cells remaining in the circular muscle layer had begun to divide, as indicated by the presence of mitotic figures and incorporation of ³H-thymidine. A repopulation of the longitudinal muscle layer began at this time, apparently the result of migration of cells arising in the circular muscle layer. By 5 days post-treatment, both muscle layers had regenerated to their original states. The myenteric plexus was totally absent. The denervated smooth muscle cells proceeded to divide until approximately day 15, resulting in hyperplasia of both muscle layers. Between 15 and 105 days, the number of muscle cells in the circular layer progressively declined, eventually returned to the value seen in control tissue. In contrast, the number of smooth muscle cells in the longitudinal layer remained elevated through the period of study (165 days). We hypothesize that the smooth muscle hyperplasia observed after serosal benzalkonium chloride application results from loss of the myenteric nerves.     

Congenital cataract linked to the Y chromosome]

A possible Y linked form of congenital cataract is reported, but an autosomal dominant mode of inheritance cannot be ruled out.     

A Pooled Response Strategy for Combining Multiple Lines of Evidence to Quantitatively Estimate Impact

The impacts of sediment contaminants can be evaluated by different lines of evidence, including toxicity tests and ecological community studies. Responses from 10 different toxicity assays/tests were combined to arrive at a “site score.” We employed a relatively simple summary measure, pooled P-values where we quantify a potential decrement in response in a contaminated site relative to nominally clean reference sites. The response-specific P-values were defined relative to a “null” distribution of responses in reference sites, and were then pooled using standard meta-analytic methods. Ecological community data were also evaluated using an analogous strategy. A distribution of distances of the reference sites from thecentroid of the reference sites was obtained. The distance from each of the test sites from the centroid of the reference sites was then calculated, and the proportion of reference distances that exceed the test site difference was used to define an empirical P-value for that test site. A plot of the toxicity P-value versus the community P-value was used to identify sites based on both alteration in community structure and toxicity, that is, by weight-of-evidence. This approach provides a useful strategy for examining multiple lines of evidence that should be accessible to the broader scientific community. The use of a large collection of reference sites to empirically define P-values is appealing in that parametric distribution assumptions are avoided, although this does come at the cost of assuming the reference sites provide an appropriate comparison group for test sites.     

A study of the localization of polynucleotide phosphorylase within rat liver cells and of its distribution among rat tissues and diverse animal species

1. Rat liver polynucleotide phosphorylase was localized in the mitochondrion, but may also occur in the nucleus. 2. The mitochondrial enzyme was found in rat heart, kidney, liver, muscle and spleen. 3. Mitochondrial polynucleotide phosphorylase is also present in calf, chicken, guinea-pig and rabbit liver and in goldfish muscle. 4. A possible physiological role for the enzyme in the control of the intramitochondrial ADP concentration is suggested.