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Biomedical subjects

T Murase

Publications and source records attributed to T Murase.

At least 289 records · Page 16Linked to original sources
PubMed1990

[Tetanus antitoxin levels in various Japanese age groups in 1989].

The nationwide DPT vaccine program was started in 1969 for infants under 12 months of age. In order to estimate the tetanus immune status among the general population of various age groups, we measured the serum tetanus antibody level in randomly selected outpatients from Metropolitan Tokyo (n = 211, 6 months-60 years) and Hamamatsu, a city of 510 thousand population (n = 128, 3 years-80 years) between January 1987 and June 1989. Among the 211 subjects from Tokyo, the antibody value exceeding effective level of 0.01 HAU/ml was observed in 102 subjects (48.3%). The antibody positive rate was 90.8% in subjects of 3 to 21 years and was 27.7% in subjects of 22 years or older. The positive rate was significantly higher in subjects of 21 years or younger (p less than 0.005). Among 128 subjects from Hamamatsu, 60 (46.1%) had a positive antibody and the antibody positive rare was 96.9% in subjects of 3 to 21 years and was 29.5% in subjects of 21 years or younger (p less than 0.005). The above findings indicate that our DPT vaccination program has been functioning well for the last 20 years and that the immunized population is adequately protected against tetanus.

Adolescent↗
PubMed1990

Increased erythrophagocytic activity of macrophages in dogs with Babesia gibsoni infection.

To elucidate the mechanism of anemia caused by Babesia gibsoni infection in dogs, the erythrophagocytic activity of macrophages in infected dogs was investigated in vitro. In the present study, macrophages obtained from peripheral blood (PB-macrophages) and bone marrow (BM-macrophages) of splenectomized dogs with chronic B. gibsoni infection were examined. The BM-macrophages in the splenectomized dogs with chronic babesiosis exhibited an increased erythrophagocytic activity compared with those from splenectomized, non-infected dogs. In the infected dogs, erythrophagocytic activities of macrophages against both auto- and iso-erythorcytes from normal dogs were almost the same. Administration of an anti-protozoal drug, diminazene diaceturate, resulted in a decrease of the erythrophagocytic activity of BM-macrophages associated with an increase of the hematocrit value in splenectomized dogs with chronic babesiosis. In splenectomized dogs with acute babesiosis, erythrophagocytic activity of BM-macrophages was also elevated. Such a phenomenon was not, however, observed in splenectomized dogs with onion-induced hemolytic anemia. These results suggest that the erythrophagocytic ability of macrophages in the infected dogs might be accelerated by parasites per se through an unknown mechanism, resulting in severe anemia in spite of low parasitemia.

Anemia↗
PubMed1990

The release of hepatic triglyceride lipase from rat monolayered hepatocytes in primary culture.

The release of hepatic triglyceride lipase from cultured rat hepatocytes and its hormonal regulation were studied. The activity of lipase released into the medium in the presence of heparin was increasing for 24 hours on the 2nd day of culture. The activity in the absence of heparin was only 10% of that in the presence of heparin. When hepatocytes were cultured with anti-hepatic triglyceride lipase IgG, the lipase activity was suppressed by 92%. The results suggest that the enzyme released into the culture medium is identical to hepatic triglyceride lipase which can be released only in the presence of heparin, the mode of release being similar to that of lipoprotein lipase from adipocytes. The addition of colchicine and monensin to the medium resulted in the inhibition of lipase secretion by 20% and 61%, respectively. Insulin enhanced lipase activity only 20%, whereas dexamethasone suppressed the activity by 44%. These data indicated that hepatic triglyceride lipase is secreted and released from hepatocytes in the presence of heparin and its secretion is regulated by hormones.

Animals↗
PubMed1990

Increased accumulation of cytosine arabinoside in human leukemic cells and enhancement of its cell-killing activity by uridine.

The effects of uridine(UR) on the cell-killing activity of cytosine arabinoside(ara-C) against human leukemic cells, MOLT-4, and on ara-C accumulation in cells were studied. The 50% lethal dose(LD50) of ara-C as determined by clonogenic assay was decreased to 5.0 x 10(-8) mol from 9.0 x 10(-7) mol after 3 days exposure to 10(-3) mol of UR. The accumulation of 3H-ara-C at 24 and 48 h was significantly increased in culture medium containing 10(-8) mol of 3H-ara-C and 10(-3) mol of UR (5,129 +/- 123.5 vs 2,554 +/- 115.5 cpm/10(5) cells at 24 h, p less than 0.01, and 5,772 +/- 123.2 vs 1,372 +/- 51.8 cpm/10(5) cells at 48 h, p less than 0.01). It is noteworthy that cell-killing activity of ara-C against human leukemic cells was enhanced by the combination with a nucleoside(UR), but not with antileukemic agents.

Cell Survival↗
PubMed1990

Effect of a stromal cell derived hematopoietic factor on human bone marrow progenitor cells.

Conditioned media (KM-102CM and KM-103CM) obtained from two different human bone marrow stromal cell lines (KM-102 and KM-103) were analysed for their ability to stimulate human hematopoietic stem cells. Both KM-102CM and KM-103CM stimulate the formation of granulocyte-monocyte colony forming unit (CFU-C) and erythroid burst forming unit (BFU-E) colonies in the presence of erythropoietin, and also maintain the long term proliferation of stem cells in vitro. When KM-102CM and KM-103CM were fractionated by DEAE-cellulose chromatography and treated with antiserum against granulocyte-monocyte colony stimulating factor (GM-CSF) these colony stimulating activity (CSA) and burst promoting activity (BPA) contained in these media were neutralized by the antiserum and thus proved to be basically identical to GM-CSF. These results showed that the GM-CSF produced by the marrow stromal cells can maintain and proliferate the hematopoietic progenitor cells in the long term and thus gave us an evidence of one of the regulatory functions of the marrow stromal cells in hematopoiesis.

Cell Division↗
PubMed1990

[Statistical evaluation of determinants of progression of superficial bladder cancer by proportional hazards model].

To evaluate clinical and pathological factors present at the initial consultation which affect disease progression, we reviewed data from 223 patients with superficial bladder cancer (pTa and pT1) who were initially treated at Nagoya University Hospital between January 1973 and December 1987. The factors included in the present analysis were age, sex, symptoms, interval between initial symptoms and first consultation, location of tumor, size, number, endoscopic shape, histological pattern of growth, grade and stage. The median duration of the follow-up after initial treatment was 46 months. Of the 223 patients, 17 died: 8 (3.6%) of bladder cancer and the remaining 9 (4.0%) of unrelated causes. Disease progression developed in 12 patients (5.4%): muscle invasion of the bladder wall in 11 and lung metastasis in one. The interval between initial treatment and progression ranged from 4 to 108 months, with a median of 11.5 months. Of the 12 patients, 9 (75%) had disease progression within 2 years. Progression was significantly associated with poor prognosis (p less than 0.001): the 5-year actuarial survival rates were 47.1% and 92.8% in patients with and without progression, respectively. Univariate analysis by Cox's proportional hazards model demonstrated that characteristics such as irritative bladder symptoms, higher-grade tumors, invasion into lamina propria, and nonpapillary growth seen at initial consultation were significantly related to disease progression. Cox's proportional hazards model produced hazard ratios of 10.2 in irritative bladder symptoms (yes vs. no), 6.3 in histological grade (grade 3 vs. grades 0-2), 4.9 in stage (pT1 vs. pTa), and 4.7 in pattern of growth (papillary vs. nonpapillary).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

[Pure red cell aplasia with inhibitor to erythroid precursors in serum].

A patient with pure red cell aplasia (PRCA), who had the inhibitor to erythroid precursors in serum, is described. A 72-year-old female was referred to Nagoya National Hospital because of progressing anemia in April 1988. On admission, her hemoglobin was 4.8 g/dl, reticulocyte 0.8%, and bone marrow specimen contained only 1.2% erythroblast. On these bases, she was diagnosed as pure red cell aplasia. After small amount of blood was transfused, her hemoglobin and erythroblast in bone marrow (EBM) increased to 7.8 g/dl and 39.1%, respectively, and she was discharged. However, after a month, her hemoglobin dropped to 4.6 g/dl, reticulocyte to 0.1%, and EBM to 0%. Soon after corticosteroid therapy (prednisolone, 40 mg, daily) was started, a marked elevation of reticulocyte count was observed, and then her hemoglobin increased to 11.0 g/dl, and EBM to 31.6%. The reason for a transient spontaneous remission at the onset of her disease was occurred is unclear. The number of BFU-E in her bone marrow was within normal range, but it was suppressed significantly (65%) after the addition of her serum and the complement purified from rabbit plasma. This finding suggest the presence of inhibitor to erythroid precursors in her serum.

Aged↗
PubMed1989

Gene polymorphism identified by PvuII in familial lipoprotein lipase deficiency.

We previously demonstrated that the PvuII polymorphism is a useful marker to analyze the genetic defects in familial lipoprotein lipase (LPL) deficiency. In this study, we have mapped this polymorphic site and cloned the gene fragments containing this site from a patient and a normal subject. Comparative sequence analysis revealed that a C-T transition occurred in the gene of the patient at the PvuII site in the intron 6. Interestingly, the sequence near the PvuII site showed a significant homology to the consensus sequence of the 3' splice site. In addition, the insertional event into the human LPL gene, which was recently reported for a population of Caucasian patients, was not observed for eight unrelated Japanese patients, suggesting that genetic defects underlying familial LPL deficiency should be heterogeneous among races.

Base Sequence↗
PubMed1989

A facile, regio- and stereo-selective synthesis of ganglioside GM3.

Gangliosides GM3, containing three different fatty acyl groups at the ceramide moiety, have been synthesized. Coupling of 2-(trimethylsilyl)ethyl O-(6-O-benzoyl-beta-D-galactopyranosyl)-(1----4)- 2,6-di-O-benzoyl-beta-D-glucopyranoside (4), prepared from 2-(trimethylsilyl)ethyl beta-lactoside (1) by selective 3'-O-benzylation, O-benzoylation, and subsequent removal of the benzyl group, with methyl (methyl 5-acetamido-4,7,8,9-tetra-O-acetyl-3,5-dideoxy-2-thio-D-glycero-alpha-D- galacto - 2-nonulopyranosid)onate (5) using dimethyl(methylthio)sulfonium triflate as a glycosyl promoter, gave 2-(trimethylsilyl)ethyl O-(methyl 5-acetamido-4,7,8,9-tetra-O- acetyl-3,5-dideoxy-D-glycero-alpha-D-galacto-2-nonulopyranosylonate++ +)-(2----3)- O-(6-O- benzoyl-beta-D-galactopyranosyl)-(1----4)-2,6-di-O-benzoyl-beta-D- glucopyranoside (6), which was converted, via O-acetylation, selective removal of the 2-(trimethylsilyl)-ethyl group, and subsequent imidate formation, into the alpha-N-acetylneuraminyl-(2----3')-lactose trichloroacetimidate 9. Glycosylation of (2S,3R,4E)-2-azido-3-O-benzoyl-4-octadecene-1,3-diol (10) with 9 afforded the beta-glycoside 11, which was converted, via selective reduction of the azide group, coupling with fatty acids, O-deacetylation, and de-esterification, into the title compounds.

Carbohydrate Conformation↗
PubMed1989

Cachectin/TNF kills or inhibits the differentiation of 3T3-L1 cells according to developmental stage.

The effects of cachectin/tumor necrosis factor (TNF) on growth and differentiation of 3T3-L1 cells were examined. This fibroblastic cell line can be induced to differentiate into a mature cell type having the biochemical and morphological characteristics of normal adipocytes. At various stages of growth and differentiation, 3T3-L1 cells were exposed to 2.5 x 10(-16) to 2.5 x 10(-8) M (4.2 fg/ml to 420 ng/ml = ca. 1.2 x 10(-14) to 1.2 x 10(-16) U/ml) recombinant human cachectin/TNF for 24 hr, after which cytotoxicity or differentiation was evaluated. During log-phase cell growth, cachectin/TNF had no significant effect on cell viability, and the preadipocytic cells were also resistant to the cytotoxic effect of cachectin/TNF at the contact-inhibited confluent stage. However, when cachectin/TNF was added to the cells during induced differentiation, only 20% of the cells survived. After differentiation into adipocytes, cells regained their resistance to cachectin/TNF-induced cytotoxicity. Cachectin/TNF also markedly affected the differentiation of 3T3-L1 cells into adipocytes. When cells in the confluent phase of growth were exposed to cachectin/TNF for 24 hr, their subsequent hormone-induced differentiation to adipocytes was inhibited. Like cachectin/TNF, IL-1 also induces suppression of lipoprotein lipase and enhances lipolysis in differentiated 3T3-L1 adipocytes; however, in contrast to cachectin/TNF, IL-1 had no effect on the viability or differentiation of pre-adipocyte 3T3-L1 cells. These results indicate that the cytotoxic action of cachectin/TNF varies in the same cell type depending on the stage of growth or differentiation. The results also imply that cachectin/TNF may play a normal role in controlling the differentiation of certain types of cells in vivo including adipocyte lineages.

Animals↗
PubMed1989

A neonatal case of apolipoprotein C-II deficiency.

A neonatal case of apo C-II deficiency with hypertriglyceridaemia and xanthomas is presented. The patient responded well to a special diet formula containing medium-chain triglycerides (MCT). This is the first case of apo C-II deficiency to be discovered during the neonatal period.

Apolipoproteins C↗
PubMed1989

A rapid electrophoretic method for the detection of serum Lp(a) lipoprotein.

A rapid electrophoretic method detecting serum lipoprotein(a) (Lp(a)) was described. When serum lipoproteins were electrophoresed using an agarose gel film containing 0.6% agarose and 3% sucrose, a distinct extra-band was frequently detected between beta- and prebeta-bands. This lipoprotein band was identified as Lp(a) by immunoblotting technique using anti-Lp(a) serum. Using this electrophoretic method, we studied 1,353 subjects with a variety of diseases. The Lp(a)-positive subjects accounted for 8.4% of all. Neither sex nor age influenced the frequency of Lp(a) positivity. Frequencies of definite myocardial infarction in Lp(a)-positive subjects did not differ significantly from those in Lp(a)-negative ones. Those of cerebral infarction in Lp(a)-positive subjects were significantly higher than those in Lp(a)-negative ones. An electrophoretic method described herein is very useful for the rapid detection and screening of Lp(a), and hence for large-scale clinical studies of atherosclerotic risk assessment.

Adult↗
PubMed1989

Plasma apolipoproteins in patients with multi-infarct dementia.

We examined 27 elderly patients with multi-infarct dementia developed on the basis of cerebral arteriosclerosis. The levels of plasma cholesterol and triglyceride in the patients were 177 +/- 48 and 91 +/- 27 mg/dl (mean +/- SD), respectively. Despite normal plasma lipid levels, the patients had significantly higher plasma apo B (102 +/- 30 vs. 82 +/- 21 mg/dl for controls, P less than 0.01) and lower plasma apo A-I levels (104 +/- 25 vs. 130 +/- 22 mg/dl for controls, P less than 0.01) than the controls. Isoelectric focusing of apo E showed a 2-fold higher relative frequency for the epsilon 4 allele in patients than in Japanese controls (20.8 vs. 8.6-11.7% of total, P less than 0.05). The patients with phenotypes of E4/4 (n = 1) and E4/3 (n = 8) had higher plasma cholesterol levels than those with E3/3 (n = 15) (196 +/- 45 vs. 169 +/- 43 mg/dl). The results indicate that the patients had abnormalities in plasma lipoprotein metabolism and this may contribute to the development of cerebral arteriosclerosis.

Aged↗