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Biomedical subjects

J Sakurai

Publications and source records attributed to J Sakurai.

At least 109 records · Page 6Linked to original sources
PubMed1988

[Operative results of acquired valvular disease with blood cardioplegia followed by terminal cardioplegia].

Cold blood cardioplegia followed by terminal cardioplegia was employed as a method of myocardial protection for acquired valvular disease. Postoperative clinical results of both cardiac iso-enzyme and cardiac function were discussed from the effect of the myocardial protection. In operative procedures of 62 cases, 30 cases underwent mitral valve replacement and other mitral repair, 17 cases aortic valve replacement, 10 cases double valve replacement and 5 cases modified Bentall operation. Iso-enzymes of Creatine-Kinase (CK) and Lactate-Dehydrogenase (LDH) were measured by the constant time-interval. Cardiac function was estimated in acute postoperative phase and late phase. Hospital mortality was 1.5%. The cause of death was thought to be postoperative Graft Versus Host Disease with skin rash and pancytopenia. Cardiac function during acute phase well recovered in 62 cases of which two cases were controlled with intra-aortic balloon pumping. The values of CK-MB were measured during aortic cross-clamp, 30 min, 3 hours, 6 hours and 24 hours after cross-clamp release. Peak CK-MB value was detected 3 hours or 6 hours in almost cases. In contrast, peak LDH-1 value was detected 24 hours after cross-clamp release. Perioperative myocardial infarction was occurred in one case with modified Bentall operation whose CK-MB value was elevated over 150 IU/L at 3rd hour and 24th hour. However, the cardiac radio-isotope data of this case revealed good cardiac function with left ventricular ejection fraction (LVEF) 76% by cardiac pool imaging in spite of small postero-lateral perfusion defect by Thallium 201 scintigram.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Enteritis necroticans among Khmer children at an evacuation site in Thailand.

A severe illness characterised by bloody diarrhoea and intestinal dysfunction was recognised at an evacuation site on the Thai-Kampuchean border. From June, 1985, to July, 1986, the illness occurred in 62 Khmer children aged 10 months to 10 years (mean 4 years); it was characterised by bloody diarrhoea (94%), fever (90%), and abdominal pain (78%). The overall mortality rate was 58%. Among 16 children who died and underwent necropsy, small-intestinal necrosis of varying severity was found; in 5 of these children small-intestinal lesions with areas of full-thickness necrosis were seen that histologically resembled those in cases of enteritis necroticans (pigbel) in Papua New Guinea. Beta-toxin-producing Clostridium perfringens type C was isolated from 2 of 23 children from whom specimens for anaerobic cultures were collected, and antibodies to beta toxin were detected in 5 of 9 survivors but not in 10 healthy, age-matched control children. These cases show that enteritis necroticans can cause substantial morbidity and mortality outside Papua New Guinea.

Adult↗
PubMed1987

Purification and characterization of Clostridium perfringens beta toxin.

A new procedure for the purification of beta toxin from culture supernatant fluid of Clostridium perfringens was established. The procedure consists of ammonium sulfate fractionation, affinity chromatography on zinc-chelate Sepharose and gel filtration on Toyopearl HW 60. Beta toxin was purified about 460-fold from the ammonium sulfate fraction with a yield of about 60% in terms of lethality of the toxin. The molecular weight of the toxin, determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and sucrose gradient centrifugation, was approximately 40,000. The isoelectric point was 5.6. The minimal necrotic dose for guinea pigs was approximately 2 ng. The 50% lethal doses for adult mice were 310 ng/kg and 4.5 micrograms/kg, when injected i.v. and i.p., respectively.

Acid Phosphatase↗
PubMed1987

The inactivation of Clostridium perfringens epsilon toxin by treatment with tetranitromethane and N-acetylimidazole.

When one residue of tyrosine per molecule of epsilon toxin was nitrated by tetranitromethane, the modified toxin lost more than 90% of its original activity. The toxin also was inactivated by treatment with N-acetylimidazole. The lethality was restored when the inactive N-acetylimidazole-treated toxin was treated with hydroxylamine. The inactive N-acetylimidazole-treated toxin was not nitrated by tetranitromethane under conditions where one residue of Tyr per molecule of the untreated toxin is nitrated. These data suggest that only one Tyr residue in the toxin is important for the lethal activity.

Acetylation↗
PubMed1987

Carboxyl groups in Clostridium perfringens epsilon toxin.

The maximal number of norleucine methyl ester (NME) incorporated into carboxyl groups in epsilon toxin of Clostridium perfringens by the carbodiimide-nucleophile procedure was 7 and 17 in the absence and presence of 8 M urea, respectively. The introduction of 3-4 nucleophilic modifying agents such as NME, glycine methyl ester or taurine into carboxyl groups of the toxin reduced the lethality to approximately 10% of the original activity. The incorporation of 6-7 of these agents resulted in complete loss of the activity. On the other hand, circular dichroism spectra and the reaction between the toxin or the NME-incorporated toxin and antiepsilon toxin reaction showed no difference between the intact toxin and the NME-incorporated toxin. The data suggested that at least 4 out of 7 carboxyl groups on the surface of the toxin are important in maintaining the lethal activity of toxin.

Animals↗
PubMed1987

A unique amino acid sequence of the B subunit of a heat-labile enterotoxin isolated from a human enterotoxigenic Escherichia coli.

The purified B subunit of heat-labile enterotoxin produced from a human strain, 240-3, of enterotoxigenic Escherichia coli (LTh(240-3] was carboxymethylated, succinylated, digested with chymotrypsin and subjected to high performance liquid chromatography (HPLC), and the amino acid compositions of the peptide peaks from the column were analyzed and compared with the data reported by Yamamoto and Yokota (J. Bacteriol. 155, 728.1983), who deduced the amino acid sequence of LTh(H10407) from the DNA sequence of a human strain H10407. Only one fraction differed in amino acid composition from that reported by them. This fraction was found to consist of peptides with the sequences Arg-Asn-Thr-Gln-Ile-Tyr and Arg-Ile-Ala-Tyr. Yamamoto and Yokota reported the sequence of the latter peptide as Arg-Ile-Thr*-Tyr, which corresponds to the peptide from 73rd to 76th from amino (N-) terminus. Thus amino acid residue 75 from the N-terminus of LTh-B(240-3) is alanine, not threonine. The B subunit of cholera toxin also has alanine at position 75. LTh(240-3) appeared similar to LTh(H10407) in an Ouchterlony test, vascular permeability test and GMI ganglioside ELISA. These data show that substitution of threonine for alanine at position 75 from the N-terminus does not affect the immunological and biological characteristics of LTh.

Amino Acid Sequence↗
PubMed1987

[A case of acute occlusion of the left common iliac artery due to blunt abdominal trauma].

A 56-year-old man was involved in an automobile accident and had abdominal blunt injury with the steering wheel. He developed slight abdominal distension and pulseless, cold sensation and peripheral cyanosis of the left lower extremity which suggested acute arterial occlusion. DSA revealed complete obstruction of the common iliac artery near its origin and the leakage of contrast medium at peripheral branch of the SMA. Four and a half hours after injury, surgical exploration was carried out. Laparotomy showed the laceration of the mesentery with accumulation of massive fresh and clotted blood in the abdominal cavity. Obstructed portion of the left common iliac artery was resected and arterial reconstruction was performed with prosthetic graft (8mm Gore-Tex for end to end left common-left external iliac bypass, 6mm Gore-Tex for side to end right common-left hypogastric bypass). A resected specimen demonstrated completely disrupted intima, resulting in the obstruction of the lumen associated with distal fresh thrombosis. The postoperative course was uneventful with successful patency of both grafts.

Accidents, Traffic↗
PubMed1986

Amino groups in Clostridium perfringens epsilon prototoxin and epsilon toxin.

Modification with succinic anhydride (SA) of Clostridium perfringens epsilon prototoxin or toxin resulted in a loss of activation by trypsin or lethal activity, respectively. The prototoxin was more sensitive to succinylation than the toxin. On the other hand, the succinylated prototoxin was activated and cleaved by chymotrypsin, but not by trypsin. The lethal activity of the toxin was also lost after treatment with 2,3-dimethylmaleic anhydride (DMA) or 2,4,6-trinitrobenzenesulfonic acid (TNBS). When the DMA-treated toxin treated with SA or TNBS was incubated under acidic condition, it regained lethal activity. Thus modification of amino groups (lysine residues) prevented activation of the prototoxin by trypsin, and abolished lethal activity of the toxin.

Bacterial Toxins↗
PubMed1986

Excitatory effect of Clostridium perfringens alpha toxin on the rat isolated aorta.

Clostridium perfringens alpha toxin caused contraction of the isolated aorta of the rat in a dose-dependent manner. The contractile action caused by the toxin was inhibited or abolished by calcium antagonists such as nifedipine, verapamil and cinnarizine, or a Ca-free medium, but was not affected by phentolamine, chlorpheniramine, atropine, tetrodotoxin or a low Na medium. The toxin stimulated Ca uptake into the aorta in a dose-dependent manner. 8-N,N'-diethylaminooctyl-3,4,5-trimethoxybenzoate (TMB-8) blocked significantly both the toxin- and noradrenaline (NA)-induced contractions. Trifluoperazine (TFP) and N-(6-aminohexyl)-5-chloro-1-naphtharene sulphonamide (W-7) did not affect the contractile activity of the toxin but blocked the NA-induced contraction. The toxin also stimulated the 32P phosphate labelling of phosphatidylinositol (PI) and phosphatidic acid (PA) in the preparation. These results indicate that the toxin-induced contraction, which is different from that induced by NA, is the result of a direct action of the toxin on the aorta and is due to an increased Ca2+ permeability across the smooth muscle membrane. It is suggested that the contractile response to the toxin is associated with activation of phospholipid metabolism and enhanced entry of Ca into the aorta.

Amino Acids↗
PubMed1986

Identity of hemolysins produced by Vibrio cholerae non-O1 and V. cholerae O1, biotype El Tor.

Hemolysins purified from non-O1 Vibrio cholerae (non-O1 hemolysin) and a Vibrio cholerae O1, biotype El Tor (El Tor hemolysin) were investigated for their homology. The hemolysins were isolated from the culture supernatant fluids by ammonium sulfate precipitation and gel filtration on Sephadex G-100 columns. The purified hemolysins gave single bands with an identical mobility on conventional polyacrylamide gel disc electrophoresis. The molecular weights of the non-O1 and El Tor hemolysins were estimated to be about 60,000 by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and the amino acid compositions of the hemolysins were very similar. The specific activities of the hemolysins were identical, and both hemolysins were neutralized to the same extent with antisera against the homologous and heterologous hemolysins. Ouchterlony double immunodiffusion tests with both hemolysins and antihemolysin serum gave a common (fused) precipitin line. These data indicate that the non-O1 hemolysin is biologically, physicochemically, and immunologically indistinguishable from the El Tor hemolysin.

Amino Acids↗
PubMed1986

In vivo studies on age dependency of DNA repair with age in mouse skin.

Since the capacity for DNA repair relative to other cellular processes is an important parameter relevant to mutagenesis, carcinogenesis, and also aging, its assessment should preferably be carried out in intact animals. For this reason we developed an autoradiographic technique for measuring DNA repair directly in vivo. By this method unscheduled DNA synthesis (UDS) can be detected quantitatively as silver grains over epithelial cells of mouse skin after treatment with chemical carcinogens or ultraviolet (UV) irradiation. Possible age-related change in UDS response was examined by this skin technique using 2- and 18-mo-old mice. Similar dose-dependent induction of UDS was observed in mice of both ages after treatment with 4-hydroxyaminoquinoline 1-oxide. The dose-response curves for young and aged animals after UV irradiation also showed similar increases to a plateau level at low doses, but their responses to high doses were very different. In aged mice the UDS level decreased markedly with increase in dose, whereas in young mice it remained at the same plateau level. This suggests that, in aged animals, high doses of UV irradiation cause deterioration of DNA repair systems, and that aged animals cannot repair extensive UV-induced DNA damage efficiently.

4-Hydroxyaminoquinoline-1-oxide↗