An in vitro hemolytic characteristic of Vibrio parahaemolyticus is closely correlated with human pathogenicity. A pathogenic halophile, Vibrio parahaemolyticus, has been well known as the causative agent of the most prevalent food poisoning in Japan. The organism has come to the attention of taxonomists outside Japan and was the subject of discussion at a recent international symposium (2, 4). In Japan, nationwide cooperative studies were initiated after the discovery of the causative agent during outbreaks of mackerel-borne food poisoning along the coast of the Pacific Ocean in 1959 (7). The 1959 outbreak was the second major occurrence since 1955 (5). Since then, extensive studies, including epidemiology and bacteriology, have been in progress, mainly by the Japanese workers. Evidence of the widespread distribution of V. parahaemolyticus in the sea of Southeast Asia and the Central Pacific has been reported by Yasunaga and Aoki et al. (personal communication), in the coastal areas of the United States by Baross and Liston (1), Colwell (personal communication), and Ward (9), and in Europe (i.e., in the Baltic Sea) by Nakanishi et al. (8).

SUMMARY : In recent years, it was demonstrated that cultures of Vibrio parahaemolyticus isolated from human diarrheal stools were different from those from sea fish and sea water in a hemolytic activity on a special blood agar, which was named the Kanagawa phenomenon.In the present studies, the finding has been confirmed by using 3370 cultures of the vibrios. Ninety-six % of the vibrios isolated from human patients gave positive (hemolytic) reaction in the test of the phenomenon, while only one % of the vibrios from sea fish and sea water gave positive results in the test.No relationship was observed between the phenomenon and serological and biochemical characteristics.Enteropathogenicity of the cultures of the vibrios positive in the Kanagawa phenomenon was evident by the results of feeding tests according to Takikawa and Aiiso and Fujiwara and by a case of laboratory infection of the culture to a male who took gastroenteritis by administration of approximately 106 viable cells of the hemolytic vibrios in the test of the phenomenon.On the other hand, feeding tests were carried out with 15 human volunteers to clarify enteropathogenicity of the negative (non-hemolytic) vibrios. None of them took illness, although over 109 cells of the vibrios were administered.Thus, the authors considered, as a rule, that the vibrios giving negative Kanagawa phenomenon may be nonpathogenic to human beings.

We have developed a method of measuring anterior displacement of the calcaneus on the talus in instability of the subtalar joint and have used the technique to demonstrate anterior instability in 50 patients (72 feet) showing a positive drawer sign. The angle of the posterior facet of the talus was also measured to assess the bony configuration. Our patients with subtalar joint instability could be divided into three categories. The first group had a history of trauma leading to ankle instability (26 cases), the second showed generalised joint laxity (10 cases) and the third were young females with a history of chronic stress on the foot and a poor bony block (14 cases). Satisfactory results were obtained by treating the instability with a brace or by reconstruction of the interosseous talocalcaneal ligament.

To examine a relation between the production of acetylcholine-induced endothelium-derived contracting factor and an increase in blood pressure, endothelium-dependent contraction and relaxation were evaluated by measuring the isometric tension of aortic rings from spontaneously hypertensive rats and Wlstar-Kyoto rats at 5,10, 20, and 30 weeks of age. In norepinephrine-precontracted rings, acetylcholine (10"' to 10"' M)-induced relaxations diminished at the doses of 10"' to 10" 5 M in both strains except at 5 weeks of age. Treatment with a thromboxane A 2 /prostaglandin H 2 antagonist (ONO-3708) prevented this reduction in acetylcholine-induced relaxations in both strains and induced dose-dependent relaxations, which were completely inhibited by treatment with a nitric oxide inhibitor, A rG -nitro-L-arginine methyl ester. In aorta treated with /V G -nitro-L-arginine methyl ester without precontraction, acetylcholine induced dose-dependent contractions, which were greater in spontaneously hypertensive rats than in Wistar-Kyoto rats. These acetylcholine-induced contractions, which were observed only in rings with endothelium, were completely inhibited by treatment with ONO-3708 but not with a thromboxane A 2 synthetase inhibitor (OKY-046). There was a statistically significant correlation between the acetylcholine-induced contractions and blood pressure. Release of 6-ketoprostaglandln F, o by acetylcholine from the aorta was greater in spontaneously hypertensive rats. In vivo administration of another thromboxane A 2 /prostaglandin H 2 antagonist (ONO-8809) (10 or 30 /ig per body per day) for 3 weeks (5-8 weeks of age) did not affect blood pressure in either rat strain. These results suggest that the production of acetylcholine-induced endothelium-derived contracting factor, which is most likely prostaglandin H 2 , is closely associated with the increase in blood pressure that occurs in young to adult rats. (Hypertension 1992;19-J26-332) KEY WORDS • endothelium • endothelium-derived contracting factor • endothelium-derived relaxing factor • prostaglandin H 2 • spontaneously hypertensive rats T he endothelium produces various vasoactive substances and controls vascular smooth muscle tone. Since Furchgott and Zawadzki 1 first reported the presence of endothelium-derived relaxing factor (EDRF) in 1980, many vessels were found to produce EDRF in response to a variety of stimuli. -3The primary component of EDRF was thereafter shown to be nitric oxide. 4 ' 5 It was also clarified that endothelium-derived contracting factor (EDCF) is also produced by stimulated vessels, 6 and increased production of EDCF has been reported in anoxia, 7 hypertension, 8 and aging. 9 The nature of EDCF varies with the species and the anatomical site of its production, but thromboxane A 2 (TXA 2 ), 10 superoxide anion, 1112 endothelin, 13 and prostaglandin H 2 (PGH 2 ) 14 have been suggested as EDCF. The EDCF released from the rat thoracic aorta by acetylcholine stimulation is likely to be PGH 2 , as we have previously suggested.14 From the ...

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