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Biomedical subjects

T Fujisawa

Publications and source records attributed to T Fujisawa.

At least 271 records · Page 15Linked to original sources
PubMed1995

Detection of MspI RFLP in human THY1 gene by the polymerase chain reaction.

THY1 gene encodes a cell surface glycoprotein predominantly expressed in brain and peripheral nerves. Human THY1 gene region on chromosome 11q23 has been implicated in susceptibility to type 1 diabetes (Wong et al., 1991). Two primers derived from the sequences flanking the polymorphic MspI site in intron 2 of the human THY1 gene (Gatti et al., 1988) were selected for RCP to amplify a 566 bp fragment that spans the MspI polymorphism. Polymorphism was detected by MspI digestion of the PCR product.

Base Sequence↗
PubMed1995

Response to interferon therapy in children with chronic hepatitis C.

We evaluated the effect of interferon therapy and investigated factors that may influence the outcome in 18 children with chronic hepatitis C. A complete response was obtained in 10 children (56%). The titer for pretreatment serum virus ribonucleic acid (< or = 10(7) copies/ml) was correlated significantly with a complete response to therapy.

Alanine Transaminase↗
PubMed1995

Absorption of fructose by isolated small intestine of rats is via a specific saturable carrier in the absence of glucose and by the disaccharidase-related transport system in the presence of glucose.

Previous studies have shown that the absorption of fructose is aided by simultaneous ingestion of glucose. The aim of the present study was to reproduce this finding in vitro to better understand the mechanism of the effect of glucose on absorption of fructose. The phenomena could not be reproduced with everted sleeves of rat intestine or brush border vesicles. In a perfused segment of isolated intestine, it was possible to demonstrate that the transport of fructose was accelerated when glucose was present in the perfusion medium. The enhanced transport was inhibited by sucrose and also by acarbazone, an inhibitor of intestinal alpha-disaccharidases. Phlorizin had no effect on the transport of fructose. The results of these studies indicate that there is a specific carrier for fructose saturated with a low concentration of the sugar, and that in the presence of glucose there is joint absorption of the two sugars by the disaccharidase-related transport system.

Animals↗
PubMed1995

New selective media for isolation of clostridia from faecal specimens.

Two selective media, novobiocin-colistin agar (NCA) and colistin-crystal violet agar (CCA), were developed for isolating clostridia from human and animal faeces. The basal medium was modified Eggerth-Gagnon agar. The NCA medium contains novobiocin (8 micrograms ml-1) and colistin (8 micrograms ml-1) and the CCA medium contains colistin (10 micrograms ml-1) and crystal violet (10 micrograms ml-1). Nine faecal specimens were cultured. Clostridia isolated on these media were similar to those on non-selective media, and higher than those isolated after heat treatment. However, more clostridial species were isolated on the new selective media compared with the non-selective medium. These selective agars were particularly useful for enumerating and isolating clostridia from human faeces.

Animals↗
PubMed1995

Neonatal cholestasis in two siblings: a variant of Dubin-Johnson syndrome?

OBJECTIVE: Two Japanese brothers with neonatal cholestasis associated with pigment granules in the hepatocytes and hepatosteatosis were evaluated for the possible role of hepatosteatosis in the Dubin-Johnson syndrome. METHODOLOGY AND RESULTS: The morphology of pigment accumulation and the laboratory data in these cases were examined. The elevation of urinary coproporphrin isomer I to more than 90% and the presence cholestasis resembled that in the Dubin-Johnson syndrome, but the hypertriglyceridaemia ( > 1.13 mmol/L as triolein) and the hepatosteatosis differed. Both infants were thought to have familial hypertriglyceridaemia. However, this diagnosis was difficult to confirm in the absence of data on the normal values of apolipoprotein and lipoprotein isomer for infants. CONCLUSIONS: A neonatal variant of the Dubin-Johnson syndrome may account for the unusual findings in these infants.

Cholestasis↗
PubMed1995

Comprehensive treatment of advanced neuroblastoma involving autologous bone marrow transplant.

Encouraging results are reported with high-dose chemotherapy and total body irradiation followed by autologous bone marrow transplantation in the treatment of advanced neuroblastoma. However, relapse remains a significant problem. We used high-dose chemotherapy, surgery, intraoperative radiation and an autologous bone marrow transplant treated in vitro to remove tumor cells followed by 13-cis-retinoic acid to treat 36 children with advanced neuroblastoma. This comprehensive treatment appears to improve the survival rate of patients with advanced neuroblastoma, including those with N-myc amplification and bony involvement. The disease-free survival rate was 66% (95% confidence interval, 49-84%) at 3 years. All patients who received 13-cis-retinoic acid developed cheilitis, but no bone marrow depression occurred in these patients. Five patients developed hemolytic uremic syndrome (HUS) post-transplant. This may have been related to the procedure used for total body irradiation. Patients who had their kidneys shielded during this procedure did not develop this syndrome. Patients who received local irradiation at the primary site showed no evidence of relapse in this region, indicating that such therapy may help to prevent a relapse. These data suggest a high rate of 3 year disease-free survival with this treatment strategy. The nonrandomized nature of the study and use of multiple modalities precludes analysis of the specific contribution of each.

Adrenal Gland Neoplasms↗
PubMed1995

Inhibitory effect of transforming growth factor beta 1 on cytokine-enhanced eosinophil survival and degranulation.

The effects of transforming growth factor (TGF) beta 1 on cytokine-enhanced eosinophil survival and degranulation were investigated in vitro to determine whether it is an inhibitory regulator of allergic inflammation. Peripheral blood eosinophils purified by Percoll density gradient centrifugation and the CD16 negative selection technique were incubated in the presence of eosinophil-activating cytokines (interleukin-5 (IL-5), IL-3, granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon (IFN)-gamma) with and without TFG-beta 1 for 1-3 days. On day 1, eosinophil protein X release was measured by radioimmunoassay. Eosinophil viability on day 3 was determined by staining the cells with fluorescein diacetate and propidium iodide, and on the same day DNA was extracted and subjected to gel electrophoresis to test for fragmentation. TGF-beta 1 significantly inhibited eosinophil survival enhanced by IL-5, IL-3, GM-CSF and IFN-gamma in a dose-dependent manner. The inhibitory effects of TGF-beta 1 on IL-5-enhanced survival was partially reversed by high concentrations of IL-5 and was completely neutralized with anti-TGF-beta antibody. IL-5 inhibited DNA fragmentation of eosinophils in vitro. TGF-beta reversed the effect of IL-5, indicating that TGF-beta 1 activates the pathway of apoptosis. TGF-beta 1 significantly suppressed eosinophil protein X release induced by IL-5. These results suggest that TGF-beta 1 may play a role in the modulation of allergic inflammation.

Apoptosis↗
PubMed1995

Insulin receptor gene polymorphism and hyperinsulinemia in hypertensive patients.

Although insulin resistance often occurs in association with hypertension, considerable variation is observed in the degree of insulin resistance among hypertensive patients. Since there is evidence of a genetic basis in the development of insulin resistance in hypertension, we analyzed the contribution of genetic factors to insulin resistance in hypertensive patients. Sixty-six Japanese hypertensive patients were studied. These patients were divided into two groups (hyperinsulinemia group and normoinsulinemia group) according to plasma insulin response during a 75-g oral glucose tolerance test (75g-OGTT). Insulin receptor gene (INSR) was studied for association with insulin resistance in hypertensive patients. A microsatellite polymorphism in intron-2 of the insulin receptor gene was analyzed by the polymerase chain reaction method. Five alleles were detected in the INSR microsatellite. The frequency of C/C genotype in the hyperinsulinemia group was significantly higher than that in the normoinsulinemia group (73% vs. 43%, p = 0.02). There was no difference in genotype frequency of INSR between hypertensive patients and control subjects. When the hypertensive patients were divided into two groups, the frequency of C/C genotype in the hyperinsulinemia group was significantly higher than that in the control group (73% vs. 45%, p = 0.014). There was no significant difference between the normoinsulinemia group and control group. These data suggest that the insulin receptor gene may contribute to insulin resistance in hypertensive patients with hyperinsulinemia.

Alleles↗
PubMed1995

Angiotensin I-converting enzyme gene polymorphism is associated with myocardial infarction, but not with retinopathy or nephropathy, in NIDDM.

OBJECTIVE: To clarify the relationship between the angiotensin I-converting enzyme (ACE) gene polymorphism and diabetic micro- and macroangiopathy in patients with non-insulin-dependent diabetes mellitus (NIDDM). RESEARCH DESIGN AND METHODS: We examined 267 NIDDM patients with various stages of diabetic retinopathy, 61 patients with myocardial infarction (MI), and 136 patients without MI. An insertion/deletion polymorphism of the ACE gene was typed by polymerase chain reaction. RESULTS: Although no association was found between ACE gene polymorphism and diabetic retinopathy or nephropathy, this polymorphism was associated with MI in the patients with NIDDM. Homozygotes for the deletion polymorphism (DD genotype) were found more frequently in diabetic patients with MI (31.1%) than in diabetic patients without ischemic heart disease (16.9%), with a relative risk of 2.22 (95% confidence interval 1.11-4.46, P = 0.024). CONCLUSION: These data indicate that ACE gene polymorphism is associated with MI, but not with retinopathy or nephropathy, in patients with NIDDM and suggest that the ACE gene confers susceptibility to diabetic macroangiopathy but not to microangiopathy.

Alleles↗
PubMed1995

[Correlation between acute rejection and the role of donor specific cytotoxic T lymphocyte in canine lung allotransplantation].

We investigated the correlation between the donor specific CTL activities and pathological findings of the grafted lungs by using mononuclear cells obtained from BAL fluids (BAL), peripheral blood (PBL), spleen (SpL) and grafted lungs (GIL) in canine lung allotransplantation. Twenty eight mongrel dogs underwent left lung allotransplantation. Fifteen dogs were not given immunosuppressive drugs. Thirteen dogs were given cyclosporine a 20 mg/kg/day per os for ten days postoperatively. Dogs were monitored by chest roentgenograms and cytotoxic activity tests of which targets were donor's fibroblasts. Pathological findings were classified by Prop's classification. The results were as follows. In latent and vascular phases no elevations of cytotoxic activities were demonstrated in PBL, BAL and GIL. But in early alveolar phase the cytotoxic activity was elevated to 19.83 +/- 14.54% in BAL. In late alveolar phase the highest cytotoxicities of 30.83 +/- 15.28% in PBL, 72.63 +/- 7.36% in BAL and 70.07 +/- 6.34% in GIL at E:T = 100:1 were demonstrated. In pneumonia cytotoxicity did not elevate at all in any effectors. As a result of them, it clearly shows that BAL is a good tool for the diagnosis of lung rejection.

Animals↗
PubMed1995

[Influence of warm ischemia and reperfusion on no-derived cyclic GMP release in the perfused rabbit lung].

To elucidate the vascular endothelial function at pulmonary ischemia and reperfusion, cyclic GMP (cGMP) release in lung perfusate at reperfusion after ischemia was examined as a marker of nitric oxide (NO) release from the endothelium in an in situ perfused rabbit lung. The lung was perfused from the pulmonary artery with Krebs-Henselite buffer and cGMP in the lung effluent from the left ventricle was assayed in a time-dependent manner. The inhibition of cGMP release by NG-nitro-L-arginine methyl ester and the reversal of the effect by L-arginine indicated that cGMP released into the perfusate was elicited by NO from the endothelium. There was a significant decrease in cGMP release during reperfusion after warm ischemia (30 min and 60 min) compared with the immediately perfusion without intervening ischemia. These data suggest that NO release is impaired by the endothelial dysfunction at reperfusion after warm ischemia in the perfused rabbit lung and the biochemical studies of the perfusate is useful in assessing the vascular endothelial function.

Animals↗