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Biomedical subjects

S Arai

Publications and source records attributed to S Arai.

At least 397 records · Page 22Linked to original sources
PubMed1985

Emetic effect of triazolopyrimidine, a pyrimidine compound, in dogs.

The intention of this study was to determine the minimum required dosage of triazolpyridine (TAP) to consistently induce emesis in canines. We administered single oral doses of TAP to 42 adult beagle dogs. The effect of TAP dosage on emesis was highly significant. The effective emetic dosages were 4.0 mg/10 ml water/animal (p less than 0.05) and 8.0 mg/10 ml water/animal (p less than 0.01). In all the dogs tested, 8.0 mg of TAP successfully induced emesis. The mean latency of emesis in the beagle group studied was 15 min, 54 sec (95% confidence limits = 8 min, 11 sec to 23 min, 38 sec). Intravenous apomorphine HCL was used to demonstrate the effectiveness of anti-emetic pretreatment with subcutaneous chlorpromazine (CPZ). Pretreatment with CPZ appeared to inhibit apomorphine-induced emesis, but did not modify the emetic response elicited by TAP. Emesis following the administration of TAP was considered a result of direct action of TAP upon the gastrointestinal mucosa. Eighty adult mongrel dogs were also given TAP doses of 8.0 mg/10 ml water/animal, with 100% effectiveness in inducing emesis.

Animals↗
PubMed1985

Damage in DNA irradiated with 1.2 MHz ultrasound and its effect on template activity of DNA for RNA synthesis.

When aqueous DNA solution was irradiated with 1.2 MHz continuous ultrasound in the presence of cysteamine, the number of ultrasound-induced double-strand breaks of DNA was not influenced, but the number of ultrasound-induced single-strand breaks of DNA was reduced to about one-fifth that of the irradiated control. When the effect of cysteamine on the template activity of the ultrasound-irradiated DNA was investigated, the cysteamine was found to exert a leveling effect on the linear decrease of the template activity against ultrasonic intensity. Since cysteamine was known as an effective radical scavenger, the results of the experiment were regarded to suggest that (1) the double-strand breaks were exclusively induced by the mechanical effect of ultrasound, (2) the majority of single-strand breaks were produced by water radicals arising from cavitation, (3) the initial part in the decrease of the template activity was due to the double-strand breaks arising from mechanical effect, and (4) the further decrease of the template activity depended mainly on the single-strand breaks arising from water radicals.

Cysteamine↗
PubMed1984

Carbohydrates as antigenic determinants of tumor-associated antigens recognized by monoclonal anti-tumor antibodies produced in a syngeneic system.

Two monoclonal antibodies (KH-1 and KH-2) against a transplanted fibrosarcoma (KMT-17) in WKA rats were produced by fusing a mouse myeloma (P3-X63-Ag8.653) with spleen cells from syngeneic rats hyperimmunized with KMT-17. Both antibodies showed complement-dependent cytotoxicity against KMT-17. By absorption of cytotoxicity, KH-1 reacted with homologous tumor, other syngeneic fibrosarcomas (KMT-80 and KMT-75), and lung and kidney from normal rats. However, KH-2 reacted with many kinds of tumors and various normal tissues. Antigen specificity was tested by complement fixation and/or solid-phase radioimmunoassay using glycolipids isolated from KMT-17 cells and authentic glycolipids. KH-1 reacted with globotriglycosyl ceramide which was not detected on KMT-17 cells and in cross-reacted weakly with IV3-alpha-galactosyl-lactoneotetraglycosyl ceramide, one of the major glycolipids of KMT-17. The immune reaction was inhibited by alpha-methyl-galactose. KH-2 reacted with lactosyl ceramide and lactoneotetraglycosyl ceramide. The reaction was more potently inhibited by lactose than by beta-methyl-galactose. Antibodies with similar specificity to either KH-1 or KH-2 were elevated in syngeneic rat sera after serial immunization with viable KMT-17 cells.

Animals↗
PubMed1984

Left ventricular function of concentric hypertrophied heart after chronic pressure overload as studied in the isolated canine heart preparation.

The function of the pressure-overload left ventricle was studied in relation to the chamber geometry of the isolated canine heart. The occurrence of concentric hypertrophy was confirmed in dogs with aortic constriction 40 weeks after operation. The effect of the concentric hypertrophy on left ventricular function was then studied in five pressure-overload dogs. The end-diastolic pressure of the preparation was preset at 20 mmHg. In the pressure-overload ventricle, the end-diastolic volume was smaller by 47% (p less than 0.01) and the peak systolic pressure was higher by 24% (p less than 0.01) than the control at isovolumic beats. Ejection pressure was controlled by our afterload controlling system at various levels and kept constant during the ejection phase. When ejection pressure was the same, the difference in stroke volume between the experimental and control groups was not significant. In the pressure-overload ventricle, the slope (the reciprocal is Emax) of the regression line of the end-systolic volume on ejection pressure decreased (p less than 0.01) to 0.095 ml/mmHg by 47% from 0.186 ml/mmHg in the control. The volume-axis intercept (Vd) of the line was reduced to 55% of the control. A decrease in the regression line slope was in linear proportion to the degree of concentric hypertrophy, namely, to the change in chamber geometry. These results indicated that: Despite reduction of the end-diastolic volume, the concentric hypertrophied ventricle showed no reduction in stroke volume at the same level of ejection pressure, because of its improved capability to generate pressure. Emax was dependent on ventricular geometry.

Animals↗
PubMed1984

In vitro antibacterial activity and beta-lactamase stability of cefodizime, a new cephalosporin antibiotic.

The in vitro activity and beta-lactamase stability of cefodizime (HR 221), a new cephalosporin, were compared with those of other cephem antibiotics. HR 221 was highly active against Gram-negative bacteria. The compound inhibited growth of all tested Haemophilus influenzae strains at 0.10 microgram/ml and showed strong activity even against penicillin-resistant Neisseria gonorrhoeae strains, but it was less effective against Pseudomonas aeruginosa than the other antibiotics tested. Against Gram-positive bacteria, HR 221 showed 100% inhibition of growth of Streptococcus pneumoniae at 0.39 microgram/ml, and it was slightly less active against Staphylococcus aureus (MIC90:12.5 micrograms/ml) than other antibiotics such as cefotaxime (CTX). The bactericidal activity of HR 221 against E. coli was dose-related and comparable to that of CTX, cefoperazone and latamoxef. The bactericidal activity of the compound at medium concentrations simulating human serum levels was higher than that of CTX and cefmetazole, and no cell regrowth was noted after beta-lactamase-induced inactivation of the compound. HR 221 was stable to most drug-inactivating enzyme preparations from various bacterial species.

Cefoperazone↗
PubMed1984

In vivo antibacterial activity of cefodizime, a new cephalosporin antibiotic.

The in vivo activity of cefodizime (HR 221) was compared with that of cefotaxime (CTX), cefmenoxime, latamoxef, cefazolin and cefmetazole (CMZ). The protective effects of HR 221 on experimental infections in mice caused by Staphylococcus aureus Smith, Escherichia coli C-11, Proteus vulgaris GN-76 and Serratia marcescens No. 2 were directly related to its in vitro activity against these strains. In contrast, the compound showed the smallest ED50 values, among the 5 antibiotics tested (not including CMZ), for Klebsiella pneumoniae 3K-25 and Pseudomonas aeruginosa PI 67 against which it had relatively low in vitro activity, and its ED50 for Citrobacter freundii GN-346 was as small as 1.821 mg/mouse in spite of its MIC of greater than 100 micrograms/ml. HR 221 exerted potent bactericidal activity against Streptococcus pneumoniae Sp-1 inoculated into the mouse lung; the duration of action was prolonged. When tested against the E. coli Ec-89 infection induced in the rat uterus, the activity of HR 221 given to rats once daily was equal to that of CTX or CMZ given at the same dose twice daily.

Animals↗
PubMed1984

Activation of cytotoxic polymorphonuclear leukocytes by in vivo administration of a streptococcal preparation, OK-432.

Injection ip of a streptococcal preparation, OK-432, into WKA and DONRYU rats induced in vitro cytotoxicity of polymorphonuclear leukocytes (PMN) against tumor cells in terms of their cytostasis and cytolysis. PMN were obtained from peritoneal exudates of WKA and DONRYU rats. Cytotoxicity of activated PMN was immunologically nonspecific, although a certain target selectivity was observed in PMN cytotoxicity. The titer of cytotoxicity of PMN was dependent on the dose of injected OK-432 and on the number of PMN in the cytotoxicity assay. Activated PMN appeared very early (6 hr) after OK-432 injection, and the cytotoxic titer of PMN decreased from 24 hours and disappeared at 96 hours after injection of the reagent. In vitro culture of PMN with OK-432 also evoked cytotoxicity of PMN.

Animals↗
PubMed1983

Progressive pulmonary vascular disease after surgery in a case of patent ductus arteriosus with pulmonary hypertension.

In a 15-month-old girl with patent ductus arteriosus (PDA) with pulmonary hypertension, division of the PDA was undertaken, but she died of heart failure 7 months post-operatively. Morphometric study of biopsy and autopsy lungs showed that medial hypertrophy and pulmonary intimal lesions developed markedly after surgery. Severe pulmonary hypertension and hypoxemia were present preoperatively. The pulmonary hypertension remaining postoperatively and aggravated pulmonary hypoxemia are thought to have caused postoperative constriction of the pulmonary vessels and to bring about unusual medial hypertrophy. Since it is known that marked hypertrophy of the media can easily cause vasospasms, it is thought that, in the present case, the smooth muscle cells of the media became necrotic, which brought about damage to endothelial cells. Such damage, in turn, led to the development of occlusive pulmonary vascular disease.

Ductus Arteriosus, Patent↗
PubMed1983

Suppressive effect of human natural killer cells on pokeweed mitogen-induced B cell differentiation.

The suppressive effect of human natural killer (NK) cells on B cell differentiation induced by pokeweed mitogen (PWM) was investigated. By using Percoll discontinuous density gradient centrifugation, peripheral blood nonphagocytic and nonadherent mononuclear cells were divided into low and high density fractions for which NK cells (Large granular lymphocytes, LGL) and T cells were enriched, respectively. These fractionated mononuclear cells were co-cultured with purified autologous B cells in the presence of PWM, and were examined for their helper and suppressor activities on differentiation of B cells to immunoglobulin-(IgM and IgG) producing cells by a highly sensitive reversed hemolytic plaque assay. The T cell-enriched high density fractions provided help for B cell differentiation to levels higher than that of unfractionated mononuclear cells. On the other hand, the NK-enriched low density fractions did not show helper activity, and when added to the culture of B cells plus helper T cells, they markedly suppressed B cell differentiation. This suppressive activity, as well as the NK cytotoxicity of the NK-enriched fractions, was abrogated by treatment of the cells with monoclonal antibody against human NK cells (HNK-1), but not against T cells (OKT3) in the presence of complement. NK cells also suppressed PWM-driven B cell differentiation in the presence of T4+ (helper/inducer T) but not T8+ (cytotoxic/suppressor T) cells; however, they showed no inhibition of soluble factor-induced B cell differentiation assayed in the absence of helper T cells. It is thus concluded that human peripheral blood NK cells exhibit an ability to suppress PWM-driven B cell differentiation, possibly by acting through the effect on helper T cells but not directly on B cells.

Antibody Formation↗