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Biomedical subjects

T Uchida

Publications and source records attributed to T Uchida.

At least 721 records · Page 40Linked to original sources
PubMed1992

[Clinical evaluation of bone marrow fibrosis in non-Hodgkin's lymphomas].

A study was performed in 62 patients with non-Hodgkin's lymphoma (ATL included) who were hospitalized between 1985 and 1991 and who underwent bone marrow aspiration and biopsy before or after treatment or at the time of recurrence. The relationships between the extent of bone marrow fibrosis and other prognostic factors as well as the effects of chemotherapy and bone marrow fibrositic prognosis were examined. The results were as follows: 1) The periods of survival in patients with high degree of fibrosis in bone marrow were significantly shortened. 2) The extent of bone marrow fibrosis significantly correlated with the presence or general symptoms, bone marrow invasion, and blood levels of LDH and Ca on blood biochemical examinations. 3) Effective therapy reduced collagen fibers as well as reticulin fibers in bone marrow. 4) Sixty-four percent of relapsing cases showed increase of bone marrow fibrosis. These results suggest that understanding the state of bone marrow fibrosis over the clinical course may give a good guide of indication the prognosis of malignant lymphoma.

Bone Marrow↗
PubMed1992

[Analysis of pancreatic stone protein gene of hereditary pancreatitis].

To investigate the pathogenesis of hereditary pancreatitis we determined whether pancreatic stone protein (PSP) gene was structurally altered in two independent families diagnosed as hereditary pancreatitis. Because, it has been shown that a decrease in the activity of PSP which inhibits CaCO3 crystal formation in pancreatic juice is closely related to the development of chronic calcifying pancreatitis. Southern blot analysis revealed neither a rearrangement nor a gross deletion of PSP gene in genomic DNA of affected members of both families. Furthermore, six exons of PSP gene amplified by polymerase chain reaction from genomic DNA was directly sequenced, while no apparent base mutation was observed. The immunohistochemical study utilizing monoclonal antibody to PSP showed the presence of immunoreactive PSP in the section of pancreatic tissue obtained from a patient affected with hereditary pancreatitis. However, the level of immunoreactive PSP in the remaining acinar cells of the patient pancreas was not reduced when compared with that of normal pancreas. Results, therefore, indicate that genetic alteration of PSP gene may not be responsible for the pathogenesis of hereditary pancreatitis.

Adolescent↗
PubMed1992

[Mitoxantrone and conventional-dose cytosine arabinoside for relapsed and refractory acute leukemia].

Fourteen patients with relapsed or refractory acute leukemia received combination chemotherapy of mitoxantrone 6 mg/m2/day intravenously for three to six days and cytosine arabinoside 60 mg/m2/day intravenously over 24 hours continuously for five to ten days. Complete remission was attained in six patients (42.9%) and partial response in two patients (14.3%). Six patients (42.9%) had resistant disease, and four patients (28.6%) died during the myelosuppressive phase. Of the patients achieving complete remission, four relapsed and other two continued complete remission up to 27.3 months. Median remission duration was approximately 10.6 months. No significant difference was found with regard to the efficacy of our regimen between AML and ALL. Hematological toxicity was no more severe than the prior cumulative chemotherapy. Major non-hematologic side effects were nausea and vomiting (71.4%), stomatitis (64.3%) and liver dysfunction (57.1%), which were moderate and manageable, while no cardiotoxicity was observed in any patient. In conclusion, the combination chemotherapy of mitoxantrone and conventional dose cytosine arabinoside is an effective salvage therapy in relapsed or refractory acute leukemia, and our regimen has possible utility as first-line chemotherapy in de novo acute leukemia also.

Acute Disease↗
PubMed1992

[A case of granulomatous interstitial nephritis presented reversible renal failure treated with the steroid therapy: repeated renal biopsy case].

This report describes clinical and histopathological findings of a case of a 43-year-old male with granulomatous interstitial nephritis. The patient developed renal failure following renal insufficiency of 4 months duration. The patient presented with lethargy and nocturia. The first renal biopsy revealed granulomatous interstitial nephritis. There was no apparent evidence of a systemic granulomatous disease or drug hypersensitivity. Therapy with reducing regime of prednisolone produced a marked improvement in symptoms and renal function. Relapse occurred 3 months later in association with early discontinuation of the corticosteroid therapy. Ga-scintigraphy demonstrated an abnormal accumulation of gallium in both kidneys. The second renal biopsy did not show the obvious improvement. With the re-administration of the corticosteroid therapy, renal function rapidly improved again. Twelve months after the re-administration of the steroid therapy, Ga-scintigraphy showed no renal uptake. Corticosteroid therapy yielded a favorable outcome for renal function. The third renal biopsy showed disappearance of the granulomas lesion. Re-administration of the corticosteroid therapy continued for 22 months and the patient has not yet relapsed 9 months after the withdrawal of the steroid therapy.

Acute Kidney Injury↗
PubMed1992

[Valve repair for mitral regurgitation due to ruptured chordae tendineae--repaired valve function and late results].

Among 21 consecutive patients with significant mitral regurgitation due to ruptured chordae tendineae operated by an author (K.M.) between March, 1980 and August, 1990, the 18 patients who underwent mitral valve repair were studied to assess the repaired valve function and late results of the repair. The chordal rupture was due to idiopathic degenerative disease in 14 patients, infective endocarditis in three and trauma in one. Patients' ages ranged from 35 to 70 years (mean age 52). Nine patients were in New York Heart Association class II and the remaining nine in class III. In three patients with ruptured chordae of the anterior mitral leaflet, reconstruction of the chordae with xenograft pericardium was performed in two patients and partial closure of a commissure in one. In 15 patients with ruptured chordae of the posterior leaflet, Kay's repair was performed in 13 patients and leaflet resection technique in two. In addition to the chordal and leaflet repairs, Kay's mitral annuloplasty was performed in all. There was no hospital death and all patients showed significant hemodynamic improvement (systolic pulmonary arterial pressure from 43 +/- 20 mmHg preoperatively to 24 +/- 4 mmHg postoperatively, and pulmonary arterial wedge pressure from 17 +/- 10 mmHg to 6 +/- 3 mmHg, p less than 0.001 respectively). The repaired valves showed mild pressure gradient of 3.1 +/- 1.2 mmHg which was significantly lower than the gradient of 6.6 +/- 3.5 mmHg of SJM prostheses. Residual murmur was documented in six patients, in three of whom, however, the murmur disappeared within one year following the operation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Cytokine regulation of gut ornithine decarboxylase gene expression and enzyme activity.

BACKGROUND: The enzyme ornithine decarboxylase (ODC) catalyzes the rate-limiting step in polyamine biosynthesis and is important for gut mucosal repair after systemic injury (e.g., burns); however, the mechanisms responsible for the injury-mediated induction of ODC are not known. The purpose of this study was to determine whether interleukin-1 (IL-1) or tumor necrosis factor (TNF), which are released immediately after injury, regulates gut mucosal ODC enzyme activity and gene expression. METHODS: In vivo: In experiment 1, 64 male BALB/c mice received either recombinant IL-1 beta (2 x 10(4) units/kg administered intraperitoneally) or saline solution. In experiment 2, 64 mice received either recombinant TNF-alpha (100 micrograms/kg administered intraperitoneally) or saline solution. We determined ODC enzyme activity and ODC mRNA levels in small intestine and kidneys at 2, 4, 12, and 24 hours after injection. In vitro: We also determined the ODC enzyme activity in intestinal epithelial crypt cells after either IL-1 beta or TNF-alpha treatment. RESULTS: IL-1, but not TNF, increased small intestinal ODC enzyme activity. In addition, IL-1 increased ODC enzyme activity in intestinal epithelial crypt cells at 5 and 6 hours after treatment. Both IL-1 and TNF increased small intestinal ODC mRNA levels. Neither agent affected ODC enzyme activity or ODC mRNA levels in the kidney. CONCLUSIONS: These results suggest that the cytokine-mediated induction of ODC in the small intestine is tissue specific, that the induction occurs at multiple cellular levels, and that ODC may play a vital role in the restoration of gut mucosa that occurs after injury.

Animals↗
PubMed1991

Anti-aldosteronergic effect of torasemide.

The diuretic actions of torasemide and furosemide were studied in normotensive rats and in deoxycorticosterone acetate (DOCA)-saline-loaded hypertensive rats. Torasemide (0.3-3 mg/kg) and furosemide (3-30 mg/kg) had a dose-dependent and significant diuretic action in normotensive rats. Potassium retention was only observed in the case of torasemide. Torasemide also had a dose-dependent and significant diuretic action in DOCA-saline-loaded hypertensive rats, whereas furosemide did not. Higher doses of torasemide (10 mg/kg) and furosemide (100 mg/kg) increased both plasma renin activity and aldosterone concentration in normotensive rats in a similar manner. In vivo aldosterone receptor binding was determined to test the possible anti-aldosteronergic effect of torasemide. Torasemide inhibited the binding of aldosterone to its receptor in the cytoplasmic fraction of rat kidney in a dose-dependent manner, while furosemide produced no effect. These results suggest strongly that an anti-aldosteronergic action of torasemide contributes to producing less kaliuresis.

Administration, Oral↗
PubMed1991

Purification of diphtheria toxin receptor from Vero cells.

Diphtheria toxin receptor has been solubilized from Vero cell membranes with octyl beta-D-glucoside. CRM197, the product of a mutated diphtheria toxin gene, was used for the identification of the receptor. The binding activity of the solubilized receptor was assayed by precipitating the receptor with acetone in the presence of phospholipids and carrier proteins. The solubilized receptor was purified by the combination of several chromatographic steps in the presence of the detergent, resulting in about a 10(6)-fold purification of the receptor. The purified receptor showed essentially a single band of 14.5 kDa by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. When partially purified receptor fractions were subjected to ligand blotting analysis using 125I-CRM197 as the probe, the 14.5-kDa protein and a few minor protein bands were identified as diphtheria toxin-binding molecules. These results show clearly that the 14.5-kDa protein is the diphtheria toxin receptor, or at least the major diphtheria toxin-binding molecule. When partially purified receptor was applied to a Sephacryl S-300 column in the presence of detergent, the receptor was eluted in the fractions corresponding to the 60-90-kDa size range. This suggests that the protein forms a complex with itself or with another protein.

Animals↗
PubMed1991

An antibody that inhibits the binding of diphtheria toxin to cells revealed the association of a 27-kDa membrane protein with the diphtheria toxin receptor.

A monoclonal antibody that blocks the binding of diphtheria toxin to Vero cells was isolated by immunizing mice with Vero cell membrane. The antibody inhibits the binding of diphtheria toxin and also CRM197, a mutant form of diphtheria toxin, to Vero cells, and consequently inhibits the cytotoxicity of diphtheria toxin. This antibody does not directly react with the receptor molecule of diphtheria toxin (DTR14.5). Immunoprecipitation and immunoblotting studies revealed that this antibody binds to a novel membrane protein of 27 kDa (DRAP27). When diphtheria toxin receptor was passed through an affinity column made with this antibody, the receptor was trapped only in the presence of DRAP27. These results indicate that DRAP27 and DTR14.5 closely associate in Vero cell membrane and that the inhibition of the binding of diphtheria toxin to the receptor is due to the binding of the antibody to the DRAP27 molecule. Binding studies using 125I-labeled antibody showed that there are many more molecules of DRAP27 on the cell surface than diphtheria toxin-binding sites. However, there is a correlation between the sensitivity of a cell line to diphtheria toxin and the number of DRAP27 molecules on the cell surface, suggesting that DRAP27 is involved in the entry of diphtheria toxin into the target cell.

Animals↗
PubMed1991

A novel brain-specific 25 kDa protein (p25) is phosphorylated by a Ser/Thr-Pro kinase (TPK II) from tau protein kinase fractions.

A novel brain-specific 25 kDa protein (p25) was purified from a bovine brain extract. The protein was phosphorylated by Ser/Thr-Pro kinase (TPK II) in tau protein kinase fractions at the Ser residues of Ser-Pro sequences. Using immunoblot analysis, the protein was found only in brain extracts, and was most abundant in the brain regions such as cerebrum and hippocampus, but less abundant in cerebellum, medulla oblongata and olfactory bulb. The protein was detected in rat, bovine and human brain extracts, indicating that this protein specifically exists in mammalian brain tissues.

Amino Acid Sequence↗
PubMed1991

A serine/threonine proline kinase activity is included in the tau protein kinase fraction forming a paired helical filament epitope.

Previously we partially purified a novel protein kinase which phosphorylated tau and formed a paired helical filament (PHF) epitope. In this paper we show that the kinase fraction contains a protein kinase activity recognizing serine/threonine proline sequence. The kinase phosphorylated tau at the tau-1 site previously reported as one of the phosphorylation sites on PHF by other groups. The kinase also phosphorylated extraordinarily insoluble portion located on C-terminal region of tau in PHF. It is worth considering that tau phosphorylated by this kinase activity is incorporated into PHF.

Amino Acid Sequence↗
PubMed1991

Phosphoramidon inhibits the conversion of intracisternally administered big endothelin-1 to endothelin-1.

It is suggested that endothelin-1 (ET-1), a potent vasoconstrictor peptide, is involved in the pathogenesis of cerebral vasospasm following subarachnoid hemorrhage (SAH). We examined the effects of intracisternal administration of big ET-1 on the cerebral arteries in the absence or presence of pretreatment with phosphoramidon, an inhibitor of ET converting enzyme, in anesthetized dogs. After intracisternal administration of big ET-1 (10 micrograms/dog), the caliber of the basilar artery on the angiogram was decreased to about 59% of the control. This was accompanied by a marked increase in immunoreactive ET in the cerebrospinal fluid. Systemic arterial pressure was markedly elevated following big ET-1 injection. All changes induced by big ET-1 were effectively prevented with phosphoramidon. These data suggest that intracisternally administered big ET-1 is converted to ET-1 and that the generated ET-1 produces cerebral vasospasm and hypertension. A phosphoramidon-sensitive metalloproteinase appears to contribute to this conversion.

Animals↗
PubMed1991

Oncogene expression in the liver tissue of patients with nonneoplastic liver disease.

The expression of cellular oncogenes in nonneoplastic human liver tissue was examined to determine if there was a correlation between oncogene expression and physiologic regeneration in liver disease. Human liver tissue specimens from 70 patients with various histologic findings from almost normal to cirrhosis were examined (using northern blot analysis) for the expression of nine cellular oncogenes. With c-K-ras, four RNA bands (5.6-kilobase [kb], 2.1-kb, 1.5-kb, and 1.2-kb RNA species) were detected in all liver tissue examined. Expression of c-fos was also detected in a few samples examined when 50-micrograms samples of total RNA were applied. Other oncogenes such as H-ras, myc, erbB, raf, fms, fes, and myb were not detected. These results indicate that particular oncogene(s) may not be highly expressed during liver regeneration in human liver disease, or that populations of regenerating hepatocytes may be too small to show significant elevations of oncogene expression. The new finding of a constant expression of c-K-ras in human liver tissue suggests that it is linked to essential hepatocellular function rather than carcinogenesis.

Adult↗
PubMed1991

Expression of hepatitis B virus surface antigen in adult rat liver. Co-introduction of DNA and nuclear protein by a simplified liposome method.

We established a simple and efficient method for gene transfer in vitro (to cultured cells) and in vivo (to an adult organ) using liposomes. Plasmid DNA and proteins were efficiently co-encapsulated in liposomes by agitation and sonication, and were co-introduced into cells by hemagglutinating virus of Japan (HVJ)-mediated membrane fusion. Introduction of the Escherichia coli beta-galactosidase gene with non-histone chromosomal protein high mobility group 1 (HMG1) into LLCMK2 cells resulted in about 3 times higher beta-galactosidase activity than that on introduction of the gene alone. Two days after injection of HVJ-liposomes containing the beta-galactosidase gene and HMG1 under the perisplanchnic membrane of adult rat liver, hepatic cells near the injection site were found by 5-bromo-4-chloro-3-indolyl beta-D-galactoside staining to have beta-galactosidase activity. After similar injection of HVJ-liposomes containing the hepatitis B virus surface antigen (HBsAg) gene and HMG1, HBsAg was detected in the serum for 9 days with a maximum of 25-45 ng/ml on day 2 after the injection.

Animals↗
PubMed1991

Immunochemical and immunohistochemical studies, using antisera against porcine 25 kDa amelogenin, 89 kDa enamelin and the 13-17 kDa nonamelogenins, on immature enamel of the pig and rat.

Enamel proteins were extracted from the newly formed layer of immature porcine enamel, and the 25 kDa amelogenin, 89 kDa enamelin and 13-17 kDa nonamelogenins were purified. Specific antisera were raised against these proteins. Antibodies specific to the C-terminal region (residues 149-173) of the 25 kDa amelogenin were generated by absorption of the anti-25 kDa amelogenin serum with 20 kDa amelogenin, which contains residues 1-148 of the antigen. Immunoelectro-transfer blotting of the extracted porcine enamel proteins showed that the anti-25 kDa amelogenin serum recognized the 25 kDa and other low and high molecular weight amelogenins. The C-terminal specific anti-25 kDa amelogenin serum reacted only with amelogenins having molecular weights over 23 kDa. The anti-89 kDa enamelin serum recognized the 89 kDa enamelin and lower molecular weight proteins, but neither the amelogenins nor the 13-17 kDa nonamelogenins. The antiserum against the 13-17 kDa nonamelogenins showed no cross reactivity to the 89 kDa enamelin, but recognized higher molecular weight nonamelogenins. In immunohistochemical preparations of the porcine tooth germs, the 25 kDa amelogenin-like immunoreactivity over immature enamel decreased in a gradient from the enamel surface to the middle layer. In the inner layer immunoreactivity was concentrated over the prism sheaths. The C-terminal specific 25 kDa amelogenin-like immunoreactivity was intense at the outer layer of immature enamel and decreased sharply toward the middle layer. Prism sheaths were intensely stained by the antiserum to the 13-17 kDa nonamelogenins.(ABSTRACT TRUNCATED AT 250 WORDS)

Amelogenin↗
PubMed1991

Monoclonal antibodies specific for human chromosome 5 obtained with a monochromosomal hybrid can be used to sort out cells containing the chromosome with a FACS.

Using a human-mouse monochromosomal hybrid, BG15-6, that contains an intact human chromosome 5, we isolated four monoclonal antibodies, 2A10, 3H9, 5G9, and 6G12, as chromosome marker antibodies recognizing cell surface antigens specific for human chromosome 5. The binding patterns of these antibodies to BG15 subclones containing fragments of human chromosome 5 indicated that 2A10, 3H9, and 6G12 recognized the antigens produced by genes located on 5pter-q22, and that 5G9 recognized the antigen produced by a gene located on 5q23. Cells containing human chromosome 5 were very effectively sorted in a fluorescence-activated cell sorter (FACS) using monoclonal antibody 6G12. This method for sorting cells containing human chromosome 5 or an appropriate fragment of this chromosome from among human-rodent hybrid cells should be very useful in studies on gene expression, gene cloning and gene mapping.

Animals↗
PubMed1991

Characterization of secretin release in response to food and intraduodenal administration of fat and hydrochloric acid.

The development and validation of a radioimmunoassay that detects release of secretin in plasma in response to low doses of secretagogues [intraduodenal HCl (0.033 meq/min); intraduodenal sodium oleate (0.04 mmol/min)] or an oral mixed meal in conscious dogs is described. Plasma secretin levels increased significantly (P less than 0.05) in response to an oral mixed meal in conscious dogs from a basal level of 4.0 to a peak level of 12.3 pg/ml at 15 min. Infusion of graded doses of HCl (2, 4, 8, 16, meq/hr for 30 min) intraduodenally in six dogs resulted in significant elevation of plasma secretin levels in a dose-dependent manner. The pancreatic bicarbonate and volume outputs correlated with the dosage of HCl administered and with the elevations in plasma secretin concentrations. Intraduodenal infusion of increasing doses of sodium oleate (2.4, 4.8, 9.6, and 19.2 mmol in 15-min periods) resulted in a significant (P less than 0.05) elevation of plasma levels of secretin.

Animals↗