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H Sugawara

Publications and source records attributed to H Sugawara.

At least 19 recordsLinked to original sources
PubMed1995

A handy database for culture collections worldwide: CCINFO-PC.

Culture collections are reservoirs of cultivable microbes, cell lines and gene libraries. Their role and duty are to supply biological resources to biomedical communities; nevertheless, their visibility from the public is low because most culture collections still have poor accesses via the Internet. Therefore the WFCC World Data Center on Micro-organisms (WDCM) developed a database that runs on IBM PCs and compatibles, which are the most popular computer and will be as powerful as workstations. The database includes various information: activities of 484 culture collections from 58 countries; an integrated list of their holdings of bacteria, fungi and yeast; and data entry system for culture collections.

Bacteria↗
PubMed1994

Helper T cell-independent proliferation of CD8+ cytotoxic T lymphocytes transduced with an IL-1 receptor retrovirus.

Although the proliferation of CD8+ CTL typically requires cytokine support provided by helper T cells, a subset of naturally occurring CD8+ CTL are capable of proliferating independently of T cell help. Such helper-independent CTL have previously been shown to possess IL-1 receptors (IL-1R) and to proliferate in response to IL-1 through endogenous production of IL-2. In this study, we have transduced conventional helper-dependent CTL clones with a retroviral vector encoding the murine type I IL-1R. Transduced CTL selected in G418 expressed vector-derived transcripts encoding IL-1R and displayed approximately 1000 cell surface receptors with an IL-1 affinity typical for the type I IL-1R. In contrast to parental cells, transduced CTL proliferated in response to IL-1 in the presence of Ag, without a requirement for helper T cells, IL-2, or other cytokine support. Stimulation with both IL-1 and Ag was necessary for the proliferative response. No endogenous synthesis of IL-2 could be detected in the IL-1R transduced cells in response to IL-1 stimulation, in the presence or absence of Ag. The IL-1R-induced phenotype was demonstrated in two independent T cell clones, both of which retained Ag-specific cytolytic activity. No such conversion to a helper-independent phenotype was induced by a retroviral vector encoding only the neo gene. The behavior of the IL-1R-transduced CTL in proliferation assays thus resembled that of the naturally occurring helper-independent CTL.

Animals↗
PubMed1994

Absence of antioxidant effects of nifedipine and diltiazem on myocardial membrane lipid peroxidation in contrast with those of nisoldipine and propranolol.

Both the production of active oxygen species and cellular damage due to concurrent lipid peroxidation are believed to be important factors in the pathogenesis of cardiovascular diseases and the ageing process. Since cardiovascular drugs are often administered over a long term, it might be advantageous if they reduced lipid peroxidation. There have been conflicting reports concerning the antiperoxidant effect of nifedipine. Therefore, we investigated whether nifedipine could inhibit lipid peroxidation in a nonenzymatic active oxygen-generating system, utilizing rat crude myocardial membranes, and compared its effect with those of propranolol, nisoldipine, and diltiazem. Nifedipine and diltiazem had no inhibitory effects on the lipid peroxidation of myocardial membranes. In contrast, nisoldipine and propranolol had a concentration-dependent antiperoxidant effect, with IC50 values of 28.2 and 50.1 microM, respectively. In addition, nisoldipine appeared to possess dual antiperoxidant mechanisms, involving both preventive and chain-breaking properties.

Animals↗
PubMed1994

Effects of the acetylene compound from Atractylodes rhizome on experimental gastric ulcers induced by active oxygen species.

This study was conducted to determine the beneficial effects of treating digestive disorders of (6E,12E)-tetradecadiene-8,10-diyne-1,3-diol diacetate (TDEYA) detected in the plasma in hydrolyzed form: (6E,12E)-tetradecadiene-8,10-diyne-1,3-diol (TDEY), following the oral administration of a decoction of Atractylodes rhizome to rats. Assessment was also made of the efficacy of TDEYA in experimental gastric disorder models. Oral administration of TDEYA at doses of 300 to 500 mg/kg suppressed the formation of gastric lesions induced by indometacin in a dose-dependent manner. TDEYA at a dose of 200 mg/kg suppressed gastric lesions induced by an ischemia-reperfusion injury model. TDEYA at doses of 100 to 300 mg/kg did not show suppressive effects on water immersion stress-induced gastric lesions. TDEYA showed no active oxygen species scavenging action, nor did it have any effect on superoxide dismutase activity in the stomach tissue. TDEYA at doses of 200 to 500 mg/kg significantly suppressed xanthine oxidase (XO) activity in the stomach tissue following its oral administration. The suppressive effects of TDEYA on lesion formation induced by indometacin and ischemia-reperfusion injury models would thus appear to be due in part to the inhibition of XO activity in the stomach tissue.

Acetylene↗
PubMed1994

[Therapeutic effectiveness of prednisolone in Mycoplasma pulmonis-infected pneumonia in mice].

The present investigation was designed to analyze the therapeutic efficacy of prednisolone in the development of pulmonary lesions in Mycoplasma pulmonis-infected mice. Mice were treated every day from day 3 to day 9 after M. pulmonis inoculation with minocycline (group M), prednisolone (group P), or with minocycline and prednisolone (group MP) and a control group was left untreated. Mice from each group were sacrificed at days 7, 14, and 21. The macroscopic lung lesion scores of group MP at days 7, 14, 21, and of group M at day 7 were significantly lower (p < 0.05) compared with the control group. Pathological findings in group M and MP showed reduction of the polymorphonuclear leukocyte response in the alveoli compared with the controls. However, infiltration of lymphocytes around the bronchioles and blood vessels of group M was not less than that in group MP. The titer of CF antibody in group MP was the lowest of the four groups. Among the four groups, M. pulmonis was cultured in the joints of group P. These results suggest that combination therapy with minocycline and prednisolone was effective because the mice of group MP had a more marked reduction of infiltration of lymphocytes around the bronchioles and blood vessels as compared with group M. Simultaneously, with prednisolone alone therapy, a risk of dissemination of the mycoplasma organism and diminution of antibody production were suggested.

Animals↗
PubMed1992

Circulating intercellular adhesion molecule-1 (ICAM-1) antigen in sera of patients with idiopathic pulmonary fibrosis.

Intercellular adhesion molecule-1 (ICAM-1), a member of immunoglobulin supergene family with a five-domain structure, is known to play an important role in inflammatory diseases. An ELISA was developed using two MoAbs against human ICAM-1 in order to detect the soluble shedding ICAM-1 antigen in sera. We measured levels of circulating ICAM-1 antigen in sera of patients with idiopathic pulmonary fibrosis (IPF), pulmonary sarcoidosis, hypersensitive pneumonitis, bacterial and mycoplasmal pneumonia, and inflammatory diseases of other organs. The results clearly demonstrated that IPF had significantly high levels of circulating ICAM-1 in sera as compared with other disorders or normal controls. Moreover, immunohistochemical analysis with MoAb against human ICAM-1 disclosed that in IPF, the expression of ICAM-1 was intensively enhanced on alveolar epithelial cells. These results suggest that ICAM-1 may contribute to the pathogenesis of IPF.

Adult↗
PubMed1992

Effects of nitric oxide synthase inhibitors on gastric alkaline secretion in rats.

The effects of NG-nitro-L-arginine methyl ester (L-NAME), the nitric oxide (NO) synthase inhibitor, on gastric HCO3- secretion were examined in anesthetized rats. Intravenous administration of L-NAME (1, 2.5, 5 mg/kg) increased HCO3- secretion in a dose-related manner. This effect of L-NAME was mimicked by NG-mono-methyl-L-arginine (50 mg/kg, i.v.) and was antagonized significantly by concurrent administration of L-arginine but not D-arginine (200 mg/kg, i.v.). These results indicate that gastric HCO3- secretion is stimulated by inhibition of NO biosynthesis.

Amino Acid Oxidoreductases↗
PubMed1992

The difference in immunological properties between lymph node metastatic and non-metastatic cell lines of MCA-induced fibrosarcoma of C4W mice.

To pursue the process of lymph node metastasis, i.e, the preferential tumor growth in lymph node, we have established the non-metastatic M2B cell line which was derived from 3-methylcholanthrene-induced fibrosarcoma of C4W mouse and a metastatic cell line, M2BLN-M+ which was obtained from metastatic lymph nodes of irradiated C4W mouse which was subcutaneously implanted with cultured tumor cells, because implanted tumor cells were derived from the spontaneous metastatic lymph node of the parental M2B tumor, but regressed in naive C4W mouse. We examined the characteristics of both tumor cell lines in terms of the immunological cellular interactions. M2BLN-M+ showed unexpectedly to be more susceptible to cytotoxicity of immune effectors (NK cell, macrophage and cytotoxic T lymphocyte) than M2B did. When cultured both tumor cells with these effector cells, the growth inhibition of M2BLN-M+ was greater than that of M2B. The regional lymph node of tumor-bearer, however, showed no effective cytotoxic activity as reported by others. On the contrary, when cultured both tumor cells with non-immune lymph node cells, to be surprised, the proliferation of M2B was markedly suppressed, while that of M2BLN-M+ was slightly inhibited. The lymph node cells of M2B-bearing mice showed stronger cytostatic activity to M2B. The results suggest that the cytostatic activity of lymph node cells will be a pivotal factor, concerning the establishment of lymph node metastasis.

Animals↗
PubMed1992

[Hybridoma Data Bank (HDB)].

A Hybridoma Data Bank (HDB) has been developed with the collaboration of ATCC (USA), Cerdic (Europe) and RIKEN (Japan). The database holds more than 23000 records of the monoclonal antibodies. HDB is designed to meet diverse research requirements. HDB describes the development, isotype, specificity, applications, availability and literature citations for an individual monoclonal antibody. The World Data Center (WDC) at RIKEN in Japan is currently giving users' access to HDB on INTERNET, packet switching system and telephone line. The procedures for access to WDC and the interactive information retrieval system in WDC are introduced. The extraction of HDB data to create the visual table, showing reactivity patterns of monoclonal antibodies, are also shown, as an example of intelligent usage of HDB.

Antibodies, Monoclonal↗
PubMed1992

Nicardipine infusion improved hepatic function but failed to reduce hepatic venous pressure gradient in patients with cirrhosis.

We investigated the effects of nicardipine on systemic and splanchnic hemodynamics and on liver function in 16 patients with cirrhosis and portal hypertension. Patients received a continuous infusion of 0.3 mg/min of nicardipine (n = 10) and a control infusion (n = 6). No significant changes were observed after a control infusion. In contrast, systemic vasodilatation, evidenced by a significant fall in mean arterial pressure (-14%, p less than 0.01) and systemic vascular resistance (-30%, p less than 0.01), increased heart rate (+8%, p less than 0.01) and cardiac output (+21%, p less than 0.01), and increased hepatic blood flow (+43%, p less than 0.01) were observed at 60 min after a continuous infusion of nicardipine. Although nicardipine improved hepatic function (intrinsic clearance from 0.29 +/- 0.13 to 0.33 +/- 0.15 L/min, p less than 0.05), portal pressure evaluated by hepatic venous pressure gradient was not reduced significantly (from 16.3 +/- 4.9 to 15.1 +/- 5.7 mm Hg; NS). We conclude that a continuous infusion of nicardipine improves liver function but has no beneficial effect on portal pressure in patients with cirrhosis.

Adult↗
PubMed1991

CD4+ T cell clones specific for the human p97 melanoma-associated antigen can eradicate pulmonary metastases from a murine tumor expressing the p97 antigen.

p97 is a human tumor-associated Ag present on most melanoma cells that represents a possible target for immunologic attack. To evaluate the capacity of T cells reactive with this protein to promote elimination of melanoma cells expressing p97, a murine model was developed by transfecting a C3H/HeN melanoma with the p97 cDNA, generating p97-specific CD4+ T cells by in vivo immunization of C3H/HeN mice with a vaccinia/p97 recombinant virus followed by in vitro cloning with soluble p97 protein, and determining whether these CD4+ T cells could mediate rejection of pulmonary metastases. Characterization of the T cell clones demonstrated the presence of both I-Ak and I-Ek-restricted clones, although the majority of clones recognized p97 in the context of I-Ek. Analysis of clonal specificity using truncated p97 proteins revealed that at least three epitopes were immunogenic, and further studies with overlapping 15-amino acid peptides from a region of the p97 molecule defined by these truncated proteins identified an immunodominant epitope responsible for the majority of the I-Ek response. The T cell clones were not capable of directly recognizing the p97-expressing melanoma cells but responded to the tumor if syngeneic APC were present to process the tumor-derived p97 Ag. The therapeutic efficacy of these CD4+ T cell clones was evaluated in an adoptive therapy model in which mice bearing metastatic pulmonary lesions were treated by i.v. administration of the p97-specific cells. Despite the inability of the CD4+ clones to directly respond to or lyse the tumor cells, the clones were effective in promoting tumor eradication. In vitro studies demonstrated that this may have reflected secretion of lymphokines that activated macrophages to lyse the tumor. The results suggest that noncytolytic p97-specific CD4+ T cell clones can be effective in therapy of pulmonary melanoma metastases. Moreover, if human T cells reactive with the p97 protein could be generated, the expression of this tumor-associated Ag in melanoma cells might be adequate for such T cells to mediate a therapeutic antitumor response.

Animals↗
PubMed1991

Possible involvement of 3-hydroxymethylglutaryl-CoA reductase in determining the side-chain length of ubiquinone in rat heart.

The biosynthetic mechanism for determining the side-chain length of ubiquinone in rat heart mitochondria was investigated. The biosynthesis of nonaprenyl ubiquinone (UQ-9) and decaprenyl ubiquinone (UQ-10) in the mitochondria from rat hearts previously perfused with mevalonolactone was accelerated depending on the concentration of mevalonolactone. Furthermore the synthesis ratio between UQ-10 and UQ-9 (UQ-10/UQ-9) increased in accordance with the increasing concentration of mevalonolactone used. In addition, an enhancement of the synthesis ratio (UQ-10/UQ-9) was observed when the rats were treated with isoproterenol to increase the activity of 3-hydroxymethylglutaryl-CoA (HMG-CoA) reductase, a rate-limiting enzyme which forms mevalonate. Moreover, the addition of isopentenyl pyrophosphate, which is a metabolite of mevalonate, elevated the synthetic ratios UQ-10/UQ-9 in intact mitochondria and decaprenyl pyrophosphate/solanesyl pyrophosphate in the partially purified polyprenyl pyrophosphate synthetase from rat heart. These results suggest that the HMG-CoA reductase could be involved as a determining factor of the side-chain length of ubiquinone in rat heart.

Animals↗
PubMed1991

The effects of trapidil on left ventricular function and platelet aggregation in patients with coronary artery disease subjected to pacing.

The effects of the intravenous administration of 100 mg of trapidil on systolic and diastolic left ventricular functions and coronary sinus blood flow, as well as on myocardial lactate metabolism and platelet aggregation, were investigated before and after pacing in 12 patients with coronary artery disease. Pacing without administration of trapidil provoked angina in 6 of these patients. During rest, trapidil decreased the mean blood pressure by an average of 5 mmHg (from 112 +/- 15 to 107 +/- 8 mmHg, p less than 0.05) and the left ventricular end-diastolic pressure by an average of 4 mmHg (from 10 +/- 3 to 6 +/- 2 mmHg, p less than 0.05). Trapidil also caused both the max dp/dt and the coronary sinus blood flow to increase slightly, although it had no significant effect on diastolic function, myocardial lactate metabolism, or platelet aggregation. During the pacing that followed trapidil administration, chest pain was not provoked in the same 6 patients who had previously experienced chest pain on pacing. The extent of ST-segment depression also improved from -1.6 +/- 0.3 to -0.9 +/- 0.7 mm (p less than 0.05) and there was a significant suppression of the production of myocardial lactate. When pacing was terminated, trapidil caused a decrease in left ventricular systolic pressure from 173 to 156 mmHg (p less than 0.05), and also caused a decrease of the left ventricular end-diastolic pressure, from 16 +/- 4 to 8 +/- 2 mmHg (p less than 0.05). Trapidil had no significant effect on platelet aggregation activity with either a 1 microM or a 2 microM dose of ADP (adenosine diphosphate). However, the beta-TG level was suppressed, decreasing from 119 +/- 14 to 99 +/- 19 ng/ml in the arterial blood (p less than 0.1) and from 114 +/- 9 to 103 +/- 17 ng/ml (p less than 0.1) in the coronary sinus blood. Reductions in the preload and afterload by trapidil were of far greater magnitude than either its coronary dilatory or positive chronotropic effects in patients with coronary artery disease. Thus trapidil, a new antianginal agent appears to inhibit the production of platelet derived growth factors and may, therefore, protect the arteries from atherosclerosis as it promotes beneficial systemic hemodynamics in patients with depressed ventricular function.

Aged↗
PubMed1990

Possible existence of an intermediate pool of ubiquinone in rat heart mitochondria.

1. The existence of an intermediate pool of ubiquinone in intact mitochondria of rat heart was investigated. 2. The incorporation of [3H-methyl]S-adenosylmethionine into ubiquinone-9 was not influenced by the co-synthesis of the intermediate, 3-nonaprenyl-4-hydroxybenzoate. 3. In the intermediate-depleted mitochondria, the synthetic rate of the intermediate, 3-nonaprenyl-4-hydroxybenzoate was similar to that of ubiquinone. 4. The possible existence of 3-nonaprenyl-4-hydroxybenzoate as a metabolic pool under physiological condition is discussed.

Animals↗
PubMed1990

Inhibition of ubiquinone synthesis in isolated rat heart under an ischemic condition.

1. The biosynthesis of ubiquinone (UQ) in isolated rat heart under ischemic and hypoxic conditions was investigated. 2. Under ischemic perfusion, a greater amount of biosynthetic intermediates, 3-nonaprenyl and 3-decaprenyl-4-hydroxybenzoate (PPHBs) was accumulated and a smaller amount of UQ-9 and -10 was synthesized when compared with normal conditions. 3. The accumulation of PPHBs was observed without forming UQs during anaerobic perfusion. 4. Hydroxylation which is the following reaction of PPHBs for the biosynthesis of UQ in rat heart, was proceeded by the monooxygenase(s) depending upon the oxygen concentrations.

Animals↗
PubMed1990

Effects of a low, oral dose of nisoldipine on the systemic and coronary hemodynamics and the prostaglandin metabolism of ischemic heart disease patients.

This study investigated the effects of a low dose of nisoldipine (5 mg, p.o.) in 10 patients with ischemic heart disease. The patients were subjected to a 90-min exercise regimen before and after a 5 mg dose of nisoldipine, using a supine bicycle ergometer adjusted to each patient's limitations. The mean blood plasma level of nisoldipine was 3.8 +/- 3.1 (SD) ng/ml. The drug significantly decreased the systolic arterial pressure in patients throughout the experimental session, whereas a change in the diastolic arterial pressure appeared only at the submaximal stage of the exercise. Additionally, at maximal exercise, nisoldipine caused a decrease in the mean coronary sinus pressure from 11.4 +/- 7 mmHg to 6.5 +/- 5 mmHg (p less than 0.01). By contrast, while at rest, nisoldipine decreased the coronary vascular resistance from 1.5 +/- 0.7 mmHg/ml/min to 1.0 +/- 0.7 mmHg/ml/min (p less than 0.05). After exercise, the drug decreased thromboxane B2 levels from 1133 +/- 907 pg/ml to 720 +/- 379 pg/ml (p less than 0.05) in the coronary sinus blood, and increased the 6 keto-prostaglandin F1 alpha levels from 465 +/- 135 pg/ml to 559 +/- 167 pg/ml (p less than 0.05) in brachial artery blood. This suggests that a low, oral dose of nisoldipine can moderately improve the systemic and coronary hemodynamics and afterloads, and may assist in improving the prostaglandin metabolism in ischemic heart disease patients.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Identification of regulatory sites in the biosynthesis of ubiquinone in the perfused rat heart.

The biosynthesis of ubiquinone was studied in an isolated perfused beating heart preparation from adult male rats to determine rate-limiting steps in the biosynthetic pathway. The isolated heart could incorporate p-hydroxy[U-14C]benzoate into ubiquinones (ubiquinone-9 and -10) and two other lipids which were identified as 3-nonaprenyl 4-hydroxybenzoate and 3-decaprenyl 4-hydroxybenzoate. No other lipids could be detected. Addition of unlabeled mevalonolactone to the perfusate stimulated the rate of incorporation of p-hydroxy[U-14C]benzoate into 3-nonaprenyl 4-hydroxybenzoate and 3-decaprenyl 4-hydroxybenzoate. The level of radioactivity in these intermediates was much greater than that in ubiquinone-9 and -10. These results show that in the intact heart there is a large excess capacity to form postmevalonate isoprenoid precursors of ubiquinone and suggest a possible regulatory step at the premevalonate level. Moreover, the accumulation of prenylated derivatives of 4-hydroxybenzoic acid indicates further rate limitation at one or more of the subsequent steps in conversion of these intermediates to ubiquinone.

Animals↗