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Biomedical subjects

H Hashimoto

Publications and source records attributed to H Hashimoto.

At least 91 records · Page 5Linked to original sources

Characterization of baculovirus-expressed hemagglutinin and fusion glycoproteins of the attenuated measles virus strain AIK-C.

With measles virus cDNA of the avirulent vaccine strain AIK-C, two cDNAs of H or F genes were amplified by the polymerase chain reaction. The amplified cDNAs were inserted respectively to the baculovirus transfer vector pAcYM1 derived from the nuclear polyhedrosis virus of Autographa californica (AcNPV). After co-transfection of the transfer vectors with AcNPV DNA to Spodoptera frugiperda cells, recombinant baculoviruses were screened by plaque assay, and the viruses containing H-cDNA or F-cDNA were named H-AIK or F-AIK, respectively. By Western blot analyses, the band around 80 kDa and some smaller bands were appeared in the H-AIK infected S. frugiperda cells, and the band around 40 kDa was detected in the F-AIK infected cells. Immunofluorescence studies on unfixed S. frugiperda cells infected with H- or F-AIK recombinants showed that both antigens were transported to the cell surface. When green monkey red blood cells were added to the recombinant infected cells, H-AIK infected cells showed haemadsorption, and cells infected with F-AIK lysed the red blood cells. The recombinant proteins elicited the neutralizing antibodies against measles virus.

Animals

Studies on antimutagenic effect of milk cultured with lactic acid bacteria on the Trp-P2-induced mutagenicity to TA98 strain of Salmonella typhimurium.

The inhibitory effects of cultured milk using 76 strains of lactic acid bacteria isolated from milk products were investigated on the mutagenicity of 3-amino-1-methyl-5H-pyrido[4,3-b]indole (Trp-P2), a tryptophan pyrolysate for Salmonella typhimurium TA98. Each cultured milk sample displayed its characteristic antimutagenic effect against the mutagenicity of Trp-P2. The milk cultured with Lactobacillus acidophilus LA106 (LA2) showed the highest inhibition of 82.1% among the strains used. Milk samples cultured with Lactococcus lactis subsp. lactis, Lll103 (10-3) and Lll102 (KM) also exhibited higher inhibition percentages.

Animals

Spindle cell hemangioendothelioma exhibits the ultrastructural features of reactive vascular proliferation rather than of angiosarcoma.

A patient with spindle cell hemangioendotheliomas was followed from 1964 to the present time, allowing the authors the opportunity to examine the lesions in the early, mature, and old phases. Organizing thrombi of different stages associated with slit-like vascular proliferation were always observed, whereas cavernous vascular spaces predominated as the lesions became older. Each spindle cell hemangioendothelioma initially developed relatively rapidly and was sometimes painful but then persisted as a silent nodule for decades. Transmission and scanning electron microscopic studies revealed that endothelial cells tended to digitate into the slit-like proliferating channels, became attached to other cells by means of tight junctions, and thus obstructed the channels at sites where thrombi developed repeatedly. The vascular spaces, ranging in nature from slit-like to cavernous, were outlined further by a relatively sparse mantle of ramified or dendritic interstitial cells that corresponded to spindle cells. Most of the cells appeared simply to be fibroblasts, but they developed the features of pericytes when they were close to the endothelial lining of well-developed vascular lumens. Large vascular spaces and phleboliths were surrounded by smooth muscle cells. Approximately 20% of the interstitial cells were dendritic macrophages characterized by phagocytic activity, presence of many lysosomes, and Factor XIIIa expression. The long and characteristic clinical course, the histologic evidence that thrombosis and its organization was continually occurring within the lesions, and the ultrastructural finding that spindle cell hemangioendotheliomas were composed of different microvascular segments from capillaries to veins, suggest that spindle cell hemangioendotheliomas may develop from a cycle of recanalization after thrombosis that occurs repeatedly because of the unique endothelial growth that was noted. This is in contrast with the previous conception that they were low-grade angiosarcomas.

Adult

Enhancement of GST-P-positive liver cell foci development by nivalenol, a trichothecene mycotoxin.

In order to elucidate whether T-2 toxin (T-2) and nivalenol (NIV), the naturally occurring trichothecene mycotoxins in food and feed, are carcinogenic or possess an ability to modulate aflatoxin B1 (AFB1)-induced hepatocarcinogenicity, a medium-term liver bioassay was carried out. F344 male rats were given a single i.p. injection of diethylnitrosamine (DEN, 200 mg/kg), and then fed the test trichothecenes in diet (2 and 5 p.p.m. T-2 or 6 p.p.m. NIV) for 6 weeks beginning 2 weeks after the injection. Some control groups received DEN alone. For synergism between AFB1 and the trichothecenes, DEN-initiated rats as above were given a single i.p. injection of AFB1 (0.5 mg/kg) 2 weeks later and were fed a NIV-containing diet (6 p.p.m.) for 6 weeks. The other control group received the vehicle alone. Control rats not initiated with DEN were also treated with AFB1, NIV or T-2 alone as above. All rats were subjected to a two-thirds partial hepatectomy (PH) at week 3 and killed at week 8, and liver sections were analyzed by glutathione S-transferase placental form (GST-P) expression. In rats that did not receive DEN, AFB1 alone enhanced both the numbers and areas of GST-P-positive foci as reported earlier, while NIV or T-2 alone induced no marked changes. In rats initiated with DEN, AFB1 caused a marked expression of GST-P, and thus the hepatocarcinogenicity of AFB1 was reconfirmed. The expression of GST-P foci in rats fed T-2 or NIV was found to be at background level, indicating that the hepatocarcinogenicity was not predicted for the trichothecene mycotoxins such as T-2 and NIV by this medium-term bioassay system. In the group initiated by DEN followed by AFB1, on the other hand, an elevation of both the numbers and areas of GST-P-positive foci was observed by the subsequent feeding of rats with NIV, and this elevation was statistically significant from the sum totals of individual data of AFB1 or NIV alone. From this evidence, it is predicted that NIV causes an enhancing effect on AFB1-induced hepatocarcinogenesis.

Animals

Changes in ventricular 1,2-diacylglycerol content in rats following monocrotaline treatment.

OBJECTIVE: 1,2-Diacylglycerol may initiate cardiac hypertrophy, probably by activating protein kinase C. To test this hypothesis we determined the 1,2-diacylglycerol content of hypertrophied tissue. METHODS: Rats were treated with monocrotaline and developed severe right ventricular hypertrophy followed by congestive heart failure. 1,2-Diacylglycerol content and fatty acid composition, DNA concentrations, and RNA concentrations in the right ventricle from monocrotaline treated rats were compared with values obtained from the left side or from control rats. RESULTS: During the first week, the right ventricle showed no significant change in 1,2-diacylglycerol content and a small increase in RNA concentration. However, the 1,2-diacylglycerol content was significantly increased by 55% at two weeks after monocrotaline injection, when DNA and RNA synthesis was also enhanced to its highest level when compared with control rats (37% and 18%, respectively). At four weeks after monocrotaline injection, conversely, the 1,2-diacylglycerol content was decreased by 25% in the right ventricle from monocrotaline treated rats, most of which had pleural and peritoneal effusions indicating congestive heart failure, although RNA synthesis was sustained at a high level. The fatty acid composition of 1,2-diacylglycerol did not differ significantly between the right and left ventricles or control rat ventricles. CONCLUSIONS: These results suggest that 1,2-diacylglycerol accumulation is associated with development of hypertrophy in monocrotaline treated rats. In contrast, at a stage of congestive heart failure 1,2-diacylglycerol production decreased, suggesting that intracellular transduction mechanisms may be attenuated.

Animals

Effects of SUN-1165, N-(2,6-dimethylphenyl)-8-pyrrolizidine acetamide hydrochloride hemihydrate, a new class I antiarrhythmic drug, on ventricular arrhythmias, intraventricular conduction, and the refractory period in canine myocardial infarction.

Effects of SUN-1165, a class I antiarrhythmic drug, on ventricular arrhythmias, intraventricular conduction, and the effective refractory period (ERP) were examined in a canine model of myocardial infarction and compared with those of lidocaine. The antiarrhythmic effects were examined on the arrhythmias developed 24 h after left anterior descending coronary artery (LAD) ligation and ventricular premature stimulation-induced arrhythmias 5-7 days after LAD ligation. Effects on intraventricular conduction and ERP were also examined in animals 5-7 days after LAD ligation. The intraventricular conduction time (CT) was determined by excitation induced by a ventricular stimulation at various coupling intervals from 200 to 1,000 ms. SUN-1165 (1 and 3 mg/kg) showed a marked reduction in the frequency of ventricular ectopic beats 24 h after LAD ligation and was more potent than lidocaine. SUN-1165 (1 and 3 mg/kg) prolonged CT in the infarcted zones over a wide range of the coupling intervals and produced block of severely delayed conduction. In contrast, lidocaine prolonged CT only at short coupling intervals. Ventricular premature stimulation produced ventricular arrhythmias, which were prevented by pretreatment with SUN-1165 (3 mg/kg). ERP was prolonged by SUN-1165 (3 mg/kg). In conclusion, SUN-1165 showed antiarrhythmic effects in a canine model of myocardial infarction. A selective depression of delayed conduction in the infarcted zone and a prolongation of ERP probably contribute to this antiarrhythmic effect.

Animals

Phage pattern and antibiotic resistance pattern of coagulase-negative staphylococci obtained from immunocompromised patients.

A total of 152 coagulase-negative staphylococcal strains were isolated from clinical samples of 14 patients hospitalized after bone-marrow transplantation in a specialized hospital ward in Hungary, during an 18-month period between 1987 and 1989. Two species, Staphylococcus epidermidis and Staphylococcus haemolyticus, predominated (each, 45%). Using Pulverer and co-workers' phage set for typing, 68% of the isolates were typable; 16 phage patterns were observed. A characteristic long pattern with phages Ph10/Ph13/Ph15/U4/U15/U16/U20/U33 /U46 appeared only in S. epidermidis, among 5 of 11 colonized patients (8.5% of all strains). Single lysis with phage Ph13 was observed in 7 of the 14 patients (49% of all strains), in species S. capitis, S. epidermidis, S. haemolyticus, S. hominis, and S. warneri. In S. haemolyticus, non-typable strains predominated (66%); this character occurred only in 2% among other species. The strains colonizing the immunocompromised patients differed from each other in phage pattern, antibiotic resistance pattern, and/or slime production. No hospital infection was suggested. On the other hand, high incidence of two well-definable phage patterns raises some relationship between phage receptors or some regulatory systems in phage multiplication and factors responsible for special colonization as common surface properties.

Bacterial Typing Techniques

Occurrence of the nfxB type mutation in clinical isolates of Pseudomonas aeruginosa.

Seven spontaneous norfloxacin (NFLX)-resistant mutants obtained in vitro from 20 NFLX-susceptible clinical isolates and 3 NFLX-resistant clinical isolates of Pseudomonas aeruginosa were transformed with the pNF111 plasmid, whose BamHI fragment is responsible for conferring susceptibility to NFLX, by complementing the nfxB mutation. The resulting patterns of MICs of NFLX, beta-lactams, aminoglycosides, and chloramphenicol and the observed increased accumulation of NFLX were consistent with the occurrence of the nfxB type mutation in these clinical isolates.

Carbenicillin

Vibrio cholerae non-O1 isolated from ayu fish (Plecoglossus altivelis) in Japan.

A fish pathogen, Vibrio cholerae non-O1, was isolated from diseased ayu fish (Plecoglossus altivelis) collected from rivers in eight prefectural districts of Japan. This organism was found to have biochemical characteristics similar to those of V. cholerae non-O1, except that our isolates were negative for ornithine decarboxylase. Antiserum against an ayu isolate did not agglutinate with the majority of environmental V. cholerae non-O1 isolates, but a major O antigen was common among the ayu isolates. All strains were hemolytic to sheep erythrocytes, and oral administration of culture supernatants induced fluid accumulation in suckling mice. However, the crude toxin was not lethal to adult mice, and no cholera toxin-like enterotoxins were detected.

Agglutination Tests

Immunoadsorbent plasmapheresis for a patient with antiphospholipid syndrome during pregnancy.

The case of a 34 year old woman with systemic lupus erythematosus with a history of three previous recurrent abortions and lupus anticoagulant and anticardiolipin antibodies is reported. Immunoadsorbent plasmapheresis with a dextran sulphate column was used to remove lupus anticoagulant, anticardiolipin antibodies, and antibodies to DNA during her fourth pregnancy in combination with low doses of aspirin and prednisolone. Although during the course of treatment prednisolone was transiently increased to 30 mg/day owing to an asymptomatic increase of lupus anticoagulant and anticardiolipin antibodies, the levels of lupus anticoagulant, anticardiolipin antibodies, and antibodies to DNA were decreased by immunoadsorbent plasmapheresis and a baby girl was delivered successfully by caesarean section. Therefore, immunoadsorbent plasmapheresis with dextran sulphate seems to reduce the risk of recurrent abortion in patients with the antiphospholipid syndrome.

Adult

Autoantibodies to T and B cell lines detected in serum samples from patients with systemic lupus erythematosus with lymphopenia and hypocomplementaemia.

Antibodies to lymphocytes in serum samples from 88 patients with systemic lupus erythematosus (SLE) and 15 normal control subjects were examined by a cell enzyme linked immunosorbent assay (ELISA) with four human T and B cell lines as antigens. The antibodies reacted with the Wa B cell line and the T cell lines P12 (CD4-, CD8+), Jurkat (CD4-, CD8-), and Hut78 (CD4+, CD8-). Antibody titres in serum samples from patients with SLE were higher than in those from normal control subjects. Titres of antibodies to P12 were correlated with titres of antibodies to Wa, Jurkat, and Hut78 in serum samples from patients with SLE. IgG antibodies to P12 were associated with lymphopenia and reduced haemolytic complement. By thin layer chromatography immunostaining, the antibodies in serum samples from two of 10 patients with SLE with high titres of IgG antibodies to P12 and lymphopenia were shown to react with three monosialoglycosphingolipids and two neutral glycosphingolipids from P12 cells. Antibodies to lymphocytes in serum samples from patients with SLE react with T and B cell lines, recognise a series of cell membrane glycosphingolipids and are associated with the lymphopenia and hypocomplementaemia typical of active disease.

Adult

Soluble interleukin 2 receptors in patients with polymyositis/dermatomyositis.

The concentration of soluble interleukin 2 receptor was determined in serum samples from 19 patients with polymyositis/dermatomyositis by an enzyme linked immunosorbent assay (ELISA). The concentration of soluble interleukin 2 receptor in serum samples from patients with polymyositis/dermatomyositis was higher than that in samples from normal subjects.

Adult

Hypoxia-elicited contraction of aorta and coronary artery via removal of endothelium-derived nitric oxide.

To characterize endothelium-derived contracting factor 1 (EDCF1) released under hypoxia, vascular rings isolated from spontaneously hypertensive rat (SHR) aorta and canine coronary artery were suspended for isometric tension recording in an organ chamber filled with a Krebs-Henseleit buffer. In SHR aorta precontracted with norepinephrine (10(-7) M), severe hypoxia induced an initial increase in tension by 36.7 +/- 7.5% followed by a 56.9 +/- 5.7% relaxation; moderate hypoxia induced only a sustained increase in tension by 20.6 +/- 2.5%. Inhibition of nitric oxide (NO) production with N omega-nitro-L-arginine methyl ester (L-NAME) (10(-3) M) augmented norepinephrine-induced precontraction by 76.1 +/- 12.3% and totally eliminated the hypoxic contraction. In canine coronary arteries precontracted with KCl (30 mM) in the presence of indomethacin (10(-5) M), severe hypoxia caused a sustained increase in tension by 68.9 +/- 7.3%, which was also abolished with L-NAME. When L-NAME (10(-3) M) was given after the precontraction, both of these vessels developed sustained contractions under normoxia and moderate hypoxia. These results suggest that the vasocontraction currently considered to be induced by EDCF1 is not caused by a contracting factor but rather is a contracting phenomenon derived from continuous inhibition of basal NO synthesis during hypoxia.

2,4-Dinitrophenol

Correlation with blood pressure of the acetylcholine-induced endothelium-derived contracting factor in the rat aorta.

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 Wistar-Kyoto rats at 5, 10, 20, and 30 weeks of age. In norepinephrine-precontracted rings, acetylcholine (10(-8) to 10(-5) M)-induced relaxations diminished at the doses of 10(-6) to 10(-5) M in both strains except at 5 weeks of age. Treatment with a thromboxane A2/prostaglandin H2 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, NG-nitro-L-arginine methyl ester. In aorta treated with NG-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 A2 synthetase inhibitor (OKY-046). There was a statistically significant correlation between the acetylcholine-induced contractions and blood pressure. Release of 6-ketoprostaglandin F1 alpha by acetylcholine from the aorta was greater in spontaneously hypertensive rats. In vivo administration of another thromboxane A2/prostaglandin H2 antagonist (ONO-8809) (10 or 30 micrograms per body per day) for 3 weeks (5-8 weeks of age) did not affect blood pressure in either rat strain.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha

Effects of flecainide on ventricular arrhythmias, abnormal automaticity and activation in a canine model of myocardial infarction.

Effects of flecainide, a class I antiarrhythmic drug, on ventricular arrhythmias, ventricular abnormal automaticity and ventricular activation were examined in a canine model of myocardial infarction, and compared with those of lidocaine. The effects of the drugs were examined on (1) the arrhythmias developed 24 h after the left anterior descending coronary artery (LAD) ligation, (2) ventricular premature stimulation-induced arrhythmias 5 to 7 d after LAD ligation, (3) ventricular abnormal automaticity about 24 h after LAD ligation and (4) ventricular activation induced by a ventricular stimulation at various coupling intervals in animals 5 to 7 d after LAD ligation. Flecainide (1 and 3 mg/kg) showed a marked reduction in the frequency of ventricular ectopic beats 24 h after LAD ligation, and was more potent than lidocaine. The ventricular abnormal automaticity was inhibited by flecainide (1 and 3 mg/kg) and lidocaine (10 mg/kg). Flecainide (1 and 3 mg/kg) prolonged the activation time in the infarcted zones over a wide range of the coupling intervals, and produced block of seriously delayed activation. In contrast, lidocaine produced similar effects only at short coupling intervals. Ventricular premature stimulation produced ventricular arrhythmias, which were prevented by pretreatment with flecainide (3 mg/kg). In conclusion, flecainide showed antiarrhythmic effects in a canine model of myocardial infarction. A marked inhibition of ventricular abnormal automaticity and selective depression of delayed activation in the infarcted zone probably contribute to its antiarrhythmic effect.

Animals

Inducible resistance to a 16-membered macrolide, mycinamicin, in Staphylococcus aureus resistant to 14-membered macrolides and streptogramin B antibiotics.

Staphylococcus aureus 8325(pEP2104), a transductant derived from S. aureus PM2104 isolated clinically in Hungary (L. Janosi, and E. Ban, Acta Microbiol. Acad. Sci. Hung., 29: 187-200, 1982), exhibited an inducible resistance to the 14-membered macrolides [erythromycin (EM) and oleandomycin (OL)] and streptogramin B (MKM-B) antibiotics, but not to the 16-membered macrolides and lincosamides. This resistance was referred to as PMS-resistance phenotype (L. Jánosi, Y. Nakajima, and H. Hashimoto, Microbiol. Immunol., 34: 723-735, 1990). In addition to EM, OL, and MKM-B, however, the strain was recently and first observed to have inducible resistance to mycinamicin, a 16-membered ring macrolide. Thereby, we propose that the reference stated just above as PMS-resistance has to be extended to such 16-membered macrolides as mycinamicin. An optimum concentration of erythromycin or oleandomycin for induction of PMS-resistance was 1.35 mu g/ml in the strain 8325(pEP2104). The concentration was about 30 times as great as that (0.05 mu g/ml) required for induction of well-known co-resistance to macrolide-lincosamide-streptogramin B antibiotics in S. aureus ISP447.

Anti-Bacterial Agents

Comparison of the effects of halothane and propranolol on the effective refractory period and the ventricular activation in a canine myocardial infarction model.

The effects of halothane on the effective refractory period (ERP) and the ventricular activation were examined in a canine myocardial infarction model, and compared with those of propranolol. Halothane reduced the heart rate and prolonged the ERP in both normal and infarcted zones. A prolongation of ERP with halothane was also observed during atrial pacing at the same rate as in control, but the effect was less than during sinus rhythm. Halothane (1 MAC) further delayed or blocked the delayed activation in the infarcted zones with only slight effects on the activation of the normal zones. Propranolol (0.2 mg/kg) prolonged ERP during sinus rhythm, but it did not affect either the ERP or ventricular activation during atrial pacing. In conclusion, halothane produced a selective depression of the delayed activation and the prolongation of ERP, which may be caused by both direct effects on the myocardium and secondary effects such as a reduction of the heart rate. These effects of halothane may contribute to its antiarrhythmic effects in the myocardial infarction model which have been previously reported.

Animals