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S Tarui

Publications and source records attributed to S Tarui.

At least 109 records · Page 6Linked to original sources

Lipopolysaccharide augments HLA-A,B,C molecule expression but inhibits interferon-gamma-induced HLA-DR molecule expression on cultured human endothelial cells.

The effect of bacterial lipopolysaccharide (LPS) on the expression of class I and II major histocompatibility complex (MHC) molecules on the surface of cultured human umbilical vein endothelial cells (HUVEC) was determined by indirect immunofluorescent staining followed by flow cytometric analysis. LPS at concentrations higher than 0.01 micrograms/ml augmented class I MHC (HLA-A,B,C) expression on HUVEC in a concentration-dependent manner. Optimal augmentation, approximately sixfold compared with control, was seen with 10 micrograms/ml of LPS. Time-course experiments indicated that the augmentation was maximal on Day 4. In contrast, LPS had no effect on the induction of class II MHC (HLA-DR) molecules and at concentrations higher than 0.01 micrograms/ml inhibited the interferon-gamma(IFN-gamma)-induced class II MHC expression. The inhibition was about 60% at the concentration of 100 micrograms/ml of LPS. Interleukin-1 (IL-1) had a similar effect as LPS on class I and II MHC expression. However, LPS appeared to affect MHC expression directly and not through production of IL-1 or cyclo-oxygenase pathway products, since anti-IL-1 antibodies or an inhibitor of cyclo-oxygenase pathway products, indomethacin, failed to reverse the effects of LPS. These data stress the role of LPS as a direct modulatory factor of class I and II MHC expression on endothelial cells during the development of immune and inflammatory response against Gram-negative bacteria.

Antibodies↗

Age-related changes in adrenergic alpha 1, alpha 2, and beta receptors of rat white fat cell membranes: an analysis using [3H]bunazosin as a novel ligand for the alpha 1 adrenoceptor.

Age-related changes in alpha 1-, alpha 2-, and beta-catecholamine receptors on membrane of rat epididymal fat cells were investigated. Both young (6 weeks old, weight about 190 g) and aged (20 weeks old, weight about 490 g) Sprague-Dawley male rats were used. For the alpha 1-adrenoceptor binding experiment, we developed a novel analytical method using the hydrophilic alpha 1-receptor selective antagonist, [3H]bunazosin. The binding of [3H]bunazosin to its binding sites was rapid, reversible, saturable, and stereospecific. Scatchard binding analysis showed a single class of binding site. The sites were characterized as alpha 1-adrenoceptors by inhibition experiments using various agonists and antagonists. The number of maximum binding sites (Bmax) of alpha 1-receptor binding was 37.0 +/- 6.5 (young) versus 24.0 +/- 3.2 (aged) fmol/mg protein (P less than 0.01). [3H]Rauwolscine and [3H]CGP-12177 were used for alpha 2- and beta-receptor binding, respectively. In alpha 2-receptor detection using [3H]rauwolscine as a ligand, Bmax increased markedly from 19.8 +/- 4.9 to 86.2 +/- 19.5 fmol/mg protein (P less than 0.01). In contrast, Bmax for beta-receptor decreased from 69.7 +/- 9.7 to 45.4 +/- 13.9 fmol/mg protein with increasing rat age (P less than 0.05). Kd showed no change in each of the binding experiments between young and aged rats. The cell volume increased from 0.07 +/- 0.02 to 0.15 +/- 0.06 nl. It is implied that anti-lipolytic activity strengthened on the whole mainly with the marked increase of alpha 2-receptor number and decrease of beta-receptor number.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

[DNA tests for mutant genes coding for transthyretins Gly42, Arg50 and Cys114 in Japanese cases of familial amyloid polyneuropathy].

Four different genes encoding variant transthyretins (TTR) have been known in Japanese cases with familial amyloidotic polyneuropathy (FAP); TTR Met30, Gly42, Arg50 and Cys114. First three mutant genes can be detected by restriction fragment length polymorphism using NsiI, Cfr13I and MvaI, respectively. Since a single base change responsible for TTR Cys114 produces no new restriction site, RFLP is not directly applicable for the detection of this gene. In this study, TTR Cys114 gene was amplified by polymerase chain reaction using mismatch primer to produce a new restriction site for HgiAI. The enzyme digestion of the product resulted in the appearance of extra fragments in the presence of the normal fragment. The accurate detections of all the four mutant genes are hereafter possible by these procedures.

Amyloidosis↗

Improvement of glucose and lipid metabolism associated with selective reduction of intra-abdominal visceral fat in premenopausal women with visceral fat obesity.

Visceral fat obesity (VFO) with predominant intra-abdominal fat accumulation has been shown to be more often associated with metabolic disorders than subcutaneous fat obesity (SFO). In the present study, changes in fat distribution and their effects on metabolic complications were investigated in forty premenopausal female obese patients in whom substantial weight reduction was obtained by means of a low calorie diet. Analysis of fat distribution by CT scanning demonstrated that visceral fat decreased to a greater extent than abdominal subcutaneous fat, which was particularly evident in VFO patients. On the other hand, change of fat distribution was small in SFO patients. That is, visceral to subcutaneous abdominal fat ratio (V/S ratio) decreased from 0.62 +/- 0.36 to 0.46 +/- 0.33 in VFO, whereas from 0.23 +/- 0.07 to 0.20 +/- 0.09 in SFO after weight reduction. Although obese patients, especially those with VFO, were frequently associated with glucose intolerance and hyperlipidemia, marked diminution was observed in the elevated levels of plasma glucose area on 75g OGTT, serum total cholesterol and triglyceride after weight reduction. By the examination of interrelationship between the changes in body weight, BMI, total and regional fat volume and changes in glucose and lipid metabolism, we found that the decrease in the V/S ratio and visceral fat volume were more strongly correlated with the improvement in plasma glucose and lipid metabolism compared to the decrease in body weight, BMI, total fat volume and abdominal subcutaneous fat volume. Furthermore, partial correlation analyses demonstrated that the metabolic improvements were associated with changes in visceral abdominal fat after control for changes in total adipose tissue volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗

Visceral fat obesity: anthropological and pathophysiological aspects.

Human obesity is a heterogeneous group from the aspect of topographical fat distribution. Our analyses using CT scan imaging indicated that human obesity should be classified into two categories: subcutaneous fat obesity and visceral fat obesity. Metabolic and circulatory disturbances are far more frequently associated with visceral fat obesity than with subcutaneous fat obesity. High sucrose diet might be one of the factors that increase visceral fat accumulation. On the other hand, visceral fat is rather sensitive to calorie restriction and exercise therapy, and can be reduced through these efforts of each subject with visceral fat obesity.

Abdomen↗

Bone marrow-derived cultured mast cells and peritoneal mast cells as targets of a growth activity secreted by BALB/3T3 fibroblasts.

When fibroblast cell lines were cultured in contact with bone marrow-derived cultured mast cells (CMC), both NIH/3T3 and BALB/3T3 cell lines supported the proliferation of CMC. In contrast, when contact between fibroblasts and CMC was prohibited by Biopore membranes or soft agar, only BALB/3T3 fibroblasts supported CMC proliferation, suggesting that BALB/3T3 but not NIH/3T3 cells secreted a significant amount of a mast cell growth activity. Moreover, the BALB/3T3-derived growth activity induced the incorporation of [3H]thymidine by CMC and the clonal growth of peritoneal mast cells in methylcellulose. The mast cell growth activity appeared to be different from interleukin 3 (IL-3) and interleukin 4 (IL-4), because mRNAs for these interleukins were not detectable in BALB/3T3 fibroblasts. Although mast cells are genetically deficient in tissues of W/Wv mice, CMC did develop when bone marrow cells of W/Wv mice were cultured with pokeweed mitogen-stimulated spleen cell-conditioned medium. Because BALB/3T3 fibroblast-conditioned medium (BALB-FCM) did not induce the incorporation of [3H]thymidine by W/Wv CMC, the growth activity in BALB-FCM appeared to be a ligand for the receptor encoded by the W (c-kit) locus. Because CMC and peritoneal mast cells are obtained as homogeneous suspensions rather easily, these cells may be potentially useful as targets for the fibroblast-derived mast cell growth activity.

Animals↗

Abnormalities of plasma lipoproteins in a new genetically obese rat with non-insulin-dependent diabetes mellitus (Wistar fatty rat).

We investigated plasma lipoprotein profiles and the activities of tissue cholesterol regulating enzymes in Wistar fatty rats, an animal model for non-insulin-dependent diabetes mellitus (NIDDM). Wistar fatty rats were made by transfer of the fa gene to the Wistar Kyoto rats by backcross-breeding. Wistar fatty and control non-diabetic littermates were given a laboratory chow or an atherogenic diet containing 1 percent (weight percent) cholesterol, 0.5 percent cholic acid, and 5 percent lard. Under the chow diet, plasma fasting glucose and immunoreactive insulin concentrations in Wistar fatty rats were 1.5- and 6-fold higher than controls, respectively. Plasma cholesterol was significantly increased in Wistar fatty rats compared with controls. Elevated plasma cholesterol levels in Wistar fatties was accounted for by the increases of cholesterol content in the d less than 1.006 g/ml lipoprotein and high-density lipoproteins. Under the atherogenic diet, plasma cholesterol levels in Wistar fatties were further increased by 129 percent compared with controls. The diet-induced increase of cholesterol contents was shown in all lipoprotein classes for Wistar fatty rats. The activities of regulatory enzymes for cholesterol biosynthesis or absorption were measured in Wistar fatty rats. Both hepatic and intestinal 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase activities were significantly higher in Wistar fatty rats than those in controls (P less than 0.05 and P less than 0.01, respectively). ACAT activities in Wistar fatties were significantly increased in the intestine (P less than 0.05) and decreased in the liver in comparison with controls (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

[A case of SSPE that showed watershed infarction like image on MRI initially, and progressed to whole brain atrophy].

We reported a 15-year-old male patient of subacute sclerosing panencephalitis (SSPE), progressed from stage I to stage IV. On his admission, his clinical state was stage I with disturbance of generalized attention, myoclonus of upper limbs and no focal cortical signs. After rapid progression to stage III in a month, his clinical state became fairly stable and gradually advanced to stage IV. We followed him with serial CT and MR images. On imagings we found initial lesion in left parietoocipital lobe and spread in right parietoocipital lobe, anterior lobe and then brain stem, showing low density on plain CT scans and high intensity of T2 weighed MR images. This initial lesion situated in watershed area was hardly distinguishable from watershed infarction. In addition, we found blood flow decrease in vertebral artery system with SPECT and Doppler flowmetry. These findings suggested vascular pathogenesis of SSPE. We showed the imaging processes of SSPE progression from formation of initial lesion to demyelination and gliosis of total brain.

Adolescent↗

Ideal body weight estimated from the body mass index with the lowest morbidity.

The ideal body weight (kg) of each individual can be calculated by the following formula: ideal body mass index x the height (m)2, since body mass index is expressed by the body weight in kilogram divided by the height squared in meters. We investigated an ideal body mass index with respect to morbidity in 4565 Japanese men and women aged 30-59 years. Ten medical problems served as indices of morbidity: lung disease, heart disease, upper gastrointestinal disease, hypertension, renal disease, liver disease, hyperlipidemia, hyperuricemia, diabetes mellitus and anemia. The value of body mass index associated with the lowest morbidity was 22.2 kg/m2 in men and 21.9 kg/m2 in women, according to the quadratic regression curves relating body mass index to morbidity. From these findings, we propose that the ideal body weight is 22 x height (m)2. Our recommendations apply to the age group studied, namely 30-59 years.

Adult↗

[Hemochromatosis].

Explore the source record for details and available documents.

Diabetes Mellitus↗

High sucrose diet increases visceral fat accumulation in VMH-lesioned obese rats.

We have previously reported that metabolic abnormalities in obese subjects are closely related to intraabdominal fat accumulation. In order to clarify the causal relationship between high sucrose intake and intraabdominal visceral fat accumulation, the effects of a high sucrose diet on mesenteric fat weight, fasting plasma glucose (FPG) and triglyceride (TG) levels were investigated in bilateral ventromedial hypothalamic-lesioned obese rats (VMH) and control rats (control). The mesenteric fat weight (g)/abdominal subcutaneous fat weight (g) (M/S ratio), a parameter of visceral fat accumulation, was significantly higher in a high sucrose diet fed group (HSD group) (VMH 1.94 +/- 0.71, control 1.63 +/- 0.28) than in a lab chow fed group (LC group) (VMH 1.30 +/- 0.31, control 1.27 +/- 0.33) (P less than 0.01). In addition, the fat cell volume of mesenteric fat deposits was significantly greater in the HSD group (VMH 1.17 +/- 0.26 nl, control 0.24 +/- 0.10 nl) than in the LC group (VMH 0.74 +/- 0.27 nl, control 0.14 +/- 0.07 nl) (P less than 0.001), although the fat cell number did not differ among any experimental rat groups. FPG and TG levels were higher in the HSD group than in the LC group in VMH-lesioned rats, and a significant correlation was observed between mesenteric fat volume and FPG levels (VMH r = 0.58, P less than 0.05; control r = 0.50, P less than 0.05) as well as between mesenteric fat volume and TG levels (VMH r = 0.49, P less than 0.05; control r = 0.56, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗

Selective increase in cytochrome P450 content in hepatic microsomes from rats with ventromedial hypothalamic lesions.

Changes in the components of hepatic microsomal electron transport systems and in drug hydroxylase activities were investigated in ventromedial hypothalamus (VMH) lesioned obese rats. Eight weeks after electrolysis of the bilateral VMH, the content of cytochrome P450 per mg microsomal protein (0.79 +/- 0.07 nmol/mg protein) was significantly higher (P less than 0.02) than that in the sham-operated rats (0.59 +/- 0.02). Cytochrome P450 per whole liver in the VMH-lesioned obese rats had also significantly increased (87 +/- 9 nmol vs 56 +/- 3, P less than 0.02). No significant differences were found in the cytochrome b5 contents, and the activities of NADPH- and NADH-cytochrome c reductases between the VMH-lesioned obese and sham-operated rats. The demethylation activities of aminopyrine (1.04 +/- 0.02 nmol/mg protein/min vs 0.94 +/- 0.02, P less than 0.05) and p-nitroanisole (0.96 +/- 0.02 vs 0.89 +/- 0.02 , p less than 0.02) and the aniline hydroxylase activity (0.22 +/- 0.01 vs 0.16 +/- 0.01, P less than 0.01) were enhanced, but 7-ethoxycoumarin O-deethylase activity was unchanged in the VMH-lesioned obese rats. These results indicate a selective increase in the content of cytochrome P450 among the components of the P450-dependent mixed function oxidase system in the liver of VMH-lesioned obese rats. Our observations suggest that drug metabolism may be enhanced in the hypothalamic obesity.

Animals↗

Tissue specificity in expression and alternative RNA splicing of human phosphofructokinase-M and -L genes.

Mode of the expression of phosphofructokinase (PFK) -M and -L genes was examined in various human tissues including muscle, placenta, liver, kidney, pancreas, stomach and reticulocytes. The gross level of mRNA expression of PFK-M and -L genes was estimated by Northern analysis. Polymerase chain reaction was used to detect mRNA expressed at low levels in these tissues. Tissue-specific expression of alternatively spliced PFK-M gene transcripts was also determined by polymerase chain reaction. The results indicated that alternative splicing of PFK-M gene transcripts was controlled in a tissue-specific manner.

Base Sequence↗

Human liver manganese superoxide dismutase. Purification and crystallization, subunit association and sulfhydryl reactivity.

Manganese superoxide dismutase (Mn-SOD) has been purified with a high yield (320 mg) from human liver (2 kg) and crystallized. Low-angle laser light scattering of the enzyme has shown that native enzyme is a tetrametic form. Four of the eight cysteine residues in the tetramer reacted with 5,5'-dithiobis(2-nitrobenzoic acid) or with iodoacetamide. The others were only reactive in protein heated with SDS or urea after reduction with dithiothreitol or 2-mercaptoethanol. The reactive sulfhydryl group was found to be located at Cys196 by amino acid sequence analysis of Nbs2-reactive peptides isolated by activated thiol-Sepharose covalent chromatography. Incubation of Mn-SOD in 1% SDS for 2 or 3 days at 25 degrees C or 5 min at 100 degrees C gave material showing two prominent components on polyacrylamide gel electrophoresis in the presence of 0.1% SDS. The major component had a molecular mass of 23 kDa; the other, 25 kDa. Reduction of the protein by dithiothreitol or 2-mercaptoethanol heated in SDS produced only the 25-kDa monomer species. Essentially, no thiol groups were detected in the 23-kDa form, in which two cysteine residues appear to have been oxidized to form an intrasubunit disulfide. This indicates that Cys196 has a reactive sulfhydryl and appears to be a likely candidate for a mixed disulfide formation in vivo.

Chromatography, Gel↗

A delayed-addition enzyme immunoassay for the relative cholesteryl ester transfer protein mass in patients with deficient plasma cholesteryl ester transfer activity.

The biochemical basis for the apparent deficiency of cholesteryl ester (CE) transfer activity was investigated in two unrelated subjects with markedly elevated high density lipoprotein-cholesterol (Atherosclerosis 1988; 70:7-12). Essentially no CE or triglyceride transfer activity was detected in the patients' plasma, utilizing four different lipid transfer assays. Using polyclonal antibodies raised against human plasma cholesteryl ester transfer protein (CETP), a delayed-addition enzyme immunoassay was developed to determine plasma CETP mass. CETP could not be detected with this assay in the plasma of the two subjects with transfer activity deficiency, indicating that the CE transfer activity deficiency in these subjects is due to the absence of plasma CETP. In addition, three hyperalphalipoproteinemic subjects with a partial deficiency of CE transfer activity had a reduced level of CETP mass. There was a good correlation between plasma CETP activity and mass levels. The principles of this immunoassay may be applicable to measure the mass levels of other proteins with catalytic activities.

Adult↗