A reappraisal of non-specific genital infection with reference to the work of the late Dr E. Weston Hurst.

It is easy to overlook work that is before its time, especially if it has been done in the recent past. In his animal experimental work with Chlamydia spp, the late Dr E. Weston Hurst found that although he was able to effect a clinical cure in his intraperitoneally infected mice, he was unable to eradicate their infections. As his work appears to have relevance to today's growing problems concerning genital infections associated with chlamydiae, it should not fall into obscurity.     

Rectal potential difference in the diagnosis of aldosterone excess.

Rectal potential difference (pd) is directly related to the plasma aldosterone concentration, and rises when aldosterone is stimulated by sodium deprivation. However, when the measurement of rectal pd was tested at a screening test for hyperaldosteronism in 19 hypertensive subjects, four of the eight with primary hyperaldosteronism had a normal pd and four of the eight without aldosterone excess had an abnormally raised potential difference. The technique cannot therefore be recommended as a routine screening test for hyperaldosteronism. No relationship was found between rectal pd and hypertension associated with excess of deoxycorticosterone. Rectal pd rises in response to the mineralocorticoid-like agent carbenoxolone.     

Caries and periodontitis associated with an unerupted third molar

Radiographic, gross, and histologic evidence is provided to demonstrate the development of caries and periodontal disease over a 5-year period in an unerupted tooth. The authors speculate on the pathogenesis of these disease processes.     

Toxicology of vindesine (desacetyl vinblastine amide) in mice, rats, and dogs.

Comparative acute intravenous toxicity studies of vinblastine sulfate (VLB), vincristine sulfate (VCR), and vindesine in mice and rats indicated that vindesine was more toxic than VLB and less toxic than VCR. Rats were able to tolerate larger repeated doses of vindesine than dogs. Rats given intravenous doses totaling 0.15 mg/kg-wk vindesine for 3 months developed no remarkable signs of toxicity. Doses of 0.3 mg/kg-wk or greater produced anorexia, depressed blood cell counts, atrophic intestinal mucosa, inhibition of spermatogenesis, extramedullary hematopoiesis, and infections. Dogs were given total weekly intravenous doses of 0.04, 0.08, 0.1, or 0.16 mg/kg vindesine for 3 months. The only observed effect in the two lower dose groups was inhibition of spermatogenesis. Groups receiving 0.1 or 0.16 mg/kg developed leukopenia, slight erythropenia, inhibition of spermatogenesis, focal skeletal muscle degeneration, elevated lactic dehydrogenase, and an increase in bone marrow myeloid: erythroid ratio. No evidence of functional or structural changes in neural tissues was found. The above effects are common to animals given VCR at lower doses and for a shorter test period. It is therefore concluded that vindesine is less toxic in animals than VCR.     

Clinical involvement of mesenteric and antimesenteric borders of small bowel loops

Anatomic features of the mesentery, as it contributes to the characteristic course and coiled nature of small bowel loops, are analyzed in detail. An understanding of the anatomic definition and relationships of the loops of small intestine permits roentgen identification of their mesenteric and antimesenteric borders. It is established that (a) the concave margin of a small bowel loop, facing toward the axis of the root of the mesentery, is the mesenteric border; and (b) the convex margin of a small bowel loop, facing away from the axis of the root of the mesentery, constitutes the antimesenteric border. The ability to distinguish between the mesenteric and antimesenteric borders of small bowel loops further refines the capabilities of radiologic diagnosis in a variety of intraabdominal disease processes.