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Biomedical subjects

H Iwai

Publications and source records attributed to H Iwai.

At least 163 records · Page 9Linked to original sources
PubMed1985

Spontaneous arthritis in nude rats of Rowett hooded strain.

Spontaneous arthritis was found in 19 of 55 Rowett hooded strain rats with rnu gene. Most cases were in the male rnu/rnu (15/19) but a few occurred in the male rnu/+ (3/10) and female rnu/rnu (1/8). The lesions were first noted as reddened swelling due to exudative inflammation of periarticular soft tissues including synovial membranes in the tarsal and/or carpal joints. Most of the affected animals cured leaving slight induration but in a few male rnu/rnu ankylosis with pannus formation and exostosis developed. No sign of mycoplasmal or bacterial infection was noticed in the colony.

Age Factors↗
PubMed1985

[Problems in the standardization of radiotherapy in cervical cancer].

In Japan there exists a interinstitutional difference in the response rate of cervical cancer, which is ascribed to the lack of intracavitary radiotherapy instruments. Provided the standardized treatment schedules are followed in all institutes, the over all responses will be definitely improved. Currently there are two major problems to be solved. Firstly, we have discussed IOR and hyperthermia to individualize locally advanced cervical cancers which are excluded from current standardized treatment method. Next we discussed indications for high dose rate intracavitary brachytherapy and the dose fractionation of it in relation to external beams.

Brachytherapy↗
PubMed1984

Immunoglobulin classes of anti-Sendai virus antibody detected by ELISA in infected nude mouse serum.

Sendai virus-infected nude mouse sera obtained on the seventh day after infection or later, in which anti-Sendai virus antibodies were undetectable by hemagglutination-inhibition and neutralization tests, were found to be reactive with the virus antigen by ELISA using horseradish peroxidase-conjugated anti-mouse IgG rabbit IgG. The reactivity was blocked by rabbit anti-Sendai virus antiserum and was not observed against influenza virus which served as a control antigen. Anti-Sendai virus antibody activity of fractions from Sephadex G-200 gel filtration was detected in the IgM fraction when anti-mouse mu chain-specific antiserum was used and in both IgG and IgM fractions when heavy and light chain-specific anti-mouse IgG serum was employed in ELISA. ELISA of the fractions from protein A-Sepharose affinity chromatography of Sendai virus-infected nude mouse sera showed that the eluates at pH 6.0 and pH 3.5 contained IgG1 and IgG2b anti-Sendai virus anti-bodies, respectively, and that the eluate at pH 4.5 contained both IgG2a and IgG3 antibodies.

Animals↗
PubMed1984

[Effect of diuretic, azosemide (SK-110), in combination with antibiotic, cephaloridine, on kidney].

This study was performed to compare the acute-renal toxicity of azosemide (SK-110) or furosemide (FM) treatment in combination with cephaloridine (CER). 1) Initially, the acute-renal toxicity of CER was studied after a subcutaneous administration at dose levels of 500, 1000, 1500 and 2000 mg/kg. The values of BUN, creatinine and relative kidney weights were increased in rats given CER at dose levels above 1500 mg/kg. consequently, it was considered that the threshold of CER with regard to acute-renal toxicity was 1000 mg/kg. 2) Secondarily, the acute-renal toxicity of SK-110 or FM were studied after oral administration of 40, 80, 160 or 320 mg/kg doses alone or in combination with CER. Acute-renal toxicity was evident in the 320 mg/kg-treated rats after both SK-110 and FM alone, as revealed by analysis of a number of parameters, i.e., BUN, serum creatinine, urine sediment and composition and pathological data composing both kidney weights and studies at the microscope level. However, the increase of BUN and relative kidney weights values, elevated numbers of epithelial cells in the urine and necrosis observed in the uriniferous-tubular epithelium on histopathological examination of kidneys were noted in rats given at dose levels of only 80 mg/kg with SK-110 + CER, whereas they were seen in animals treated with FM even at the lowest applied dose of 40 mg/kg in combination with CER. In conclusion, this study showed that the minimum dose of SK-110 or FM in combination with CER which causes acute-renal toxicity were, respectively, 80 mg/kg or less than 40 mg/kg.

Administration, Oral↗
PubMed1984

[Effect of triphenyltin chloride on superoxide (O2-.) production in human neutrophils].

Brief treatment (3 min at 37 degrees C) of human neutrophils with triphenyltin chloride (TPTC1) resulted in a dose-dependent inhibition of superoxide (O2-.) production stimulated by concanavalin A+ cytochalasin D. It was considered from the following findings that the inhibition may be caused by some functional disorders of neutrophils: 1) O2-. generated by xanthine oxidase-acetaldehyde system was not inhibited by TPTC1. 2) There was no change in cell viability after treatment with TPTC1. When the other phenyltin compounds were examined, the relative potencies of inhibitory effect were shown to be in the order of TPTC1 greater than diphenyltin dichloride greater than phenyltin trichloride greater than tetraphenyltin on a molar basis. Lysosomal enzyme release caused by neutrophils stimulated by N-formyl-methionyl-leucyl-phenylalanine (FMLP) was also inhibited by TPTC1. These results suggest that TPTC1 inhibits the common pathway(s) of the two stimulus responses.

Glucuronidase↗
PubMed1983

Hypoglycemic activity of 1-alpha-(3,4-dimethoxyphenethylaminomethyl) -2-hydroxybenzylalcohol 1/2 fumarate (TA-078) in the mouse, rat and dog.

1-alpha-(3,4-Dimethoxyphenethylaminomethyl)-2-hydroxybenzylalcohol 1/2 fumarate (TA-078) is a new hypoglycemic agent structurally different from any existing hypoglycemic drug. It depresses the rise of blood glucose when it is orally administered to glucose-loaded mice, rats and beagle dogs at minimal doses of 1, 10 and 2.5 mg/kg, respectively. In contrast with tolbutamide, TA-078 hardly affected fasting blood glucose levels in rats and dogs and only weakly reduced fasting blood glucose levels in mice. Oral administration of TA-078 to KK mice also improved glucose tolerance, while no improvement was observed in streptozotocin-diabetic rats. TA-078 elevated plasma immunoreactive insulin (IRI) levels in mice and rats soon after its oral administration. In fasted rats, TA-078 caused only a transient increase in plasma IRI but did not affect plasma immunoreactive glucagon (IRG) levels in the early phase after its administration. On the other hand, tolbutamide induced a sustained increase in plasma IRI and a transient but marked decrease in plasma IRG. In perfused rat pancreas, TA-078 stimulated insulin secretion. The stimulation by 10 micrograms/ml TA-078 in the perfusion liquid required the presence of a normal concn (5.6 mM) of glucose, whereas the same concn of tolbutamide stimulated insulin release even at a low glucose concn (2.8 mM).

Animals↗
PubMed1983

[The effect of triphenyltin fluoride on aggregation, ATP secretion and malondialdehyde formation of rabbit platelets in vitro].

Recent studies have demonstrated that triphenyltin fluoride (TPTF), widely used as an agricultural chemical and a marine antifoulant, inhibits collagen-induced platelet aggregation and ATP secretion in rabbits ex vivo. The aim of the present investigation was to elucidate the mechanism of the inhibitory action of TPTF by investigating platelet malondialdehyde (MDA) formation, aggregation and ATP secretion following the stimulation by various stimuli of rabbit platelets treated in vitro with TPTF, other triphenyl metals and aspirin. Although no inhibitory effect of TPTF was found on sodium arachidonate-induced platelet aggregation and ATP secretion, TPTF inhibited dose-dependently both platelet aggregation and ATP secretion induced by collagen. The antiaggregating (IC50) concentration of TPTF was 6.0 X 10(-6) M against collagen. In addition, TPTF prevented the collagen-, and thrombin-induced formation of MDA, but had little inhibitory effect on the conversion of exogenous arachidonic acid to MDA in platelets. In contrast, aspirin (10(-3) M) inhibited platelet aggregation, ATP secretion and MDA formation induced by all the stimuli tested. Other triphenyl metals did not any inhibitory effect on collagen-, and sodium arachidonate-induced platelet aggregation and ATP secretion even at a final concentration at 10(-3) M. These results suggest that TPTF has a specific inhibitory effect on platelet aggregation and ATP secretion by acting at some step(s) of platelet membrane between the binding site of collagen and thrombin and the release of arachidonic acid.

Adenosine Triphosphate↗
PubMed1983

[Experimental induction of atherosclerosis in guinea pigs fed a cholesterol and vitamin D2-rich diet].

Atherosclerotic lesions of aorta and arteries were induced in guinea pigs fed a diet supplemented with 1% cholesterol and vitamin D2 (0.75 million IU/kg of diet) for 6 weeks. Histopathological observation revealed intimal proliferation and calcification of the intima and media, but no atheroma was present at the sites of arterial injury. However, the biochemical findings revealed accumulation of cholesterol, mainly esterified, and calcium in the aorta. Significant correlation between the calcium and phosphorus contents in the aorta indicates the presence of a probable calcium-phosphate complex. Synergism for the induction of atherosclerotic lesions was shown between high cholesterol and excess vitamin D2. Sodium 4-(hexadecylamino)benzoate (cetaben) (90 mg/kg/day, p.o.) and trisodium ethane-1-hydroxy-1,1-diphosphonate (EHDP) (5 mg/kg/day, s.c.) inhibited the development of atherosclerotic lesions induced in this manner. These effects were associated with a significant reduction of serum and aortic cholesterol levels and a significant elevation of HDL-cholesterol levels caused by cetaben, and a significant reduction in aortic calcium caused by EHDP. These two drugs and clofibrate, however, had no significant effect on the regression of pre-established atherosclerotic lesions.

4-Aminobenzoic Acid↗
PubMed1982

Intestinal uptake site, enterohepatic circulation, and excretion of tetra- and trialkyltin compounds in mammals.

The intestinal uptake site, enterohepatic circulation, and excretion into bile, feces, and urine of alkyltins (tetra and trialkyltin) were investigated after oral, sc, or intestinal administration of the compounds to rats and rabbits. Assays of tetra- and trialkyltins in biological materials were carried out by gas chromatography. The main uptake sites in the small intestine were the jejunum and duodenum for tetraalkyltins and the ileum and jejunum for trialkyltins. Tetra- and trialkyltins were detected in the small intestine and contents of the intestinal lumen after sc injection of these compounds in rats. These facts suggest that tetra- and trialkyltins are transported in the body through enterohepatic circulation. The route, rate, and amount of excretion of tetra and trialkyltins seem to depend on the velocity of dealkylation, doses, physical and chemical properties, and route of administration of the compounds.

Administration, Oral↗
PubMed1982

[Elimination of mouse hepatitis virus infection in human malignant tumors transplanted into athymic (nude) mice (author's transl)].

Mouse hepatitis virus (MHV) infection occurred in athymic (nude) mice transplanted with human malignant tumors and 28 out of 38 tumor lines were contaminated with MHV. These 28 tumor lines were passaged in pathogen-free nude mice and 15 of these tumor lines (53.6%) became MHV-free. The MHV infection was eliminated in more than half of the tumor lines by passaging.

Animals↗
PubMed1982

Body weight changes of mice with different immunity to Sendai virus after challenge infection.

Four groups of mice immunized with Sendai virus in different ways, namely convalescent (CT), intrapertoneally (IP) or intranasally (IN) immunized with the inactivated virus and non-immunized (NOI), were challenged and examined degree of immunity and body weight changes. Degree of immunity assessed based on the antibodies, the lung lesions and the lung viral titers was higher in order of CT, IP, IN and NOI. Body weight changes, expressed by both the decrease in mean body weights and the correlation coefficients between pre- and post-challenge, were less in the mice with higher immunity against Sendai virus.

Animals↗
PubMed1982

[Resistance of mice with active and maternally passive immunity against Sendai virus].

Resistance of mice with active and maternally passive immunity to Sendai virus infection was investigated. Mice with active immunization were convalescent ones from intranasal infection with 10(3) TCID50 of the virus [CT], ones immunized with 4 weekly intranasal injections of about 4 X 10(3) hemagglutinating units (HAU) of formalin-inactivated virus (FV) [IN], or ones immunized with 4 weekly intraperitoneal injections of about 2 X 10(3) HAU of FV [IP]. The serum neutralizing (NT) antibody titers ranged 1 : 10 to 1 : 20 in CT and IN, and 1 : 20 to 1 : 40 in IP at 4 weeks after initial immunization. NT antibody in the lung lavage was detected only in IP in 3/5. After intranasal challenge infection with 10(6) TCID50 of the virus, little or no gross lung lesion, no virus recovery and no body weight loss were observed throughout experiment, in these 3 immunized groups, whereas, control mice showed lung lesions in 4/5 (7 days), virus recovery in 4/5 at 3 days and in 1/5 at 7 days post-challenge, and body weight loss. In additional histological study, bronchiolar epithelial methaplasia and alveolar septal thickening, which were characteristic findings in non-immunized infected mice, were not observed in mice immunized with 2 biweekly injection of about 250 HA of FV and then challenged. Maternal immunity was investigated in offsprings from convalescent dams infected with 10(3) TCID50 at mating [mCT] and from dams immunized intraperitoneally with 4 X 10(3) HAU of FV at 0, 1 and 2 weeks after mating and, 1 and 2 weeks after parturition [mIP]. Serum NT antibody was not detected in mCT, but the titers ranging 1 : 20 to 1 : 40 were detected in mIP. After intranasal challenge of mCT, mIP and offsprings from non-immune mice with 10(3) TCID50 of the virus, virus recovery on day 3 was 2/4, 1/4 and 3/3, and incidence of total lung lesions on day 7 and 12 was 11/21, 2/13 and 16/16, respectively. Body weight gain was suppressed slightly in the immune groups but markedly in the non-immune control.

Animals↗