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Biomedical subjects

S Tarui

Publications and source records attributed to S Tarui.

At least 145 records · Page 8Linked to original sources

Simple estimation of ideal body weight from body mass index with the lowest morbidity.

Body mass index (BMI) is expressed by the body weight (kg) divided by height (m) squared. Therefore, if we know ideal BMI, ideal body weight (kg) of each individual can be calculated by a formula: Ideal BMI x height (m)2. In order to estimate ideal BMI, we investigated average BMI with the lowest morbidity using 4565 Japanese men and women aged 30 to 59 years. Their BMI distributed widely with the highest frequency at 23 in men and 21 in women. The morbidity was evaluated by the number of medical problems that the subjects with each BMI have. The BMI associated with the lowest morbidity was calculated to be 22.2 kg/m2 in men and 21.9 kg/m2 in women according to the quadratic regression curves derived from the relation between BMI and morbidity. From these data, we propose that an ideal body weight in Japanese is 22 x height (m)2.

Adult↗

Laparoscopic findings of fatty liver using multiple regression analysis. "Spotty" and "diffuse" yellow color.

Laparoscopic features of fatty liver including the cases with fibrotic change were studied by multiple regression analysis. The coloration of the liver surface under laparoscopy was classified into three types: "spotty" yellow color (YC) type, "diffuse" YC type, and without YC type. The presence of YC on the liver surface depended on the amount of deposited lipid (standardized estimate = 0.606, p = 0.0001). However, the presence of YC and whether it appeared "spotty" or "diffuse" was independent of the intralobular distribution and size of the deposited lipid droplets. When YC was observed in cases without fibrotic change, 19 of the 23 with more than 30% lipid droplets in the biopsy specimens had "spotty" YC. When YC was found in cases with fibrotic change, all of the 14 cases with more than 30% lipid droplets were "diffuse" YC. A linear regression model showed that the yellow colored liver with fibrotic change had a "diffuse" appearance (yes = 1, no = 0) standardized estimate = 0.569, p = 0.0009). These data suggested that the amount of lipid deposited was responsible for the presence of YC on the liver surface both with and without fibrotic change, and that the co-existence of fibrotic change was a major factor for giving the yellow colored liver a "diffuse" appearance.

Biopsy↗

An enzyme-linked immunosorbent assay (ELISA) for adenosine 3',5'-cyclic monophosphate (cAMP) in human plasma and urine using monoclonal antibody.

A reliable and sensitive ELISA for cAMP in human plasma and urine is described, using a monoclonal antibody and a 96 well microtiter plate. Succinyl cAMP is conjugated to human serum albumin and adsorbed to the ELISA plate, giving an immobilized antigen approach which simplifies subsequent assay procedures. As low as 1.56 fmol/well of both plasma and urinary cAMP is measurable. Recoveries of added cAMP in plasma and urine were from 99% to 109%. Intra-assay coefficients of variation were less than 6.1% for plasma and 7.0% for urine samples. Inter-assay coefficients of variation for plasma and urine samples were less than 8.9% and 9.5%, respectively. There was a good correlation between the values obtained by ELISA and radioimmunoassay (RIA) (plasma: r = 0.94, n = 66; urine: r = 0.98, n = 64; nephrogenous cAMP: r = 0.96, n = 51).

Antibodies, Monoclonal↗

Modulation of c-myc expression by transforming growth factor beta 1 in human hepatoma cell lines.

The effects of transforming growth factor beta 1 (TGF-beta 1) on cell proliferation of human hepatoma cell lines, PLC/PRF/5 and Mahlavu, were investigated under serum-free conditions. DNA synthesis was strongly inhibited in the PLC/PRF/5 cells by addition of TGF-beta 1 (0.5 to 4.0 ng/ml), but remained unchanged in the Mahlavu cells. Also the expression of c-myc mRNA was suppressed by the addition of TGF-beta 1 in the PLC/PRF/5 cells but not in the Mahlavu cells. These results indicate that TGF-beta 1 might regulate cell growth, in part, by modulating c-myc expression, although there is no direct proof that c-myc expression is really relevant to DNA synthesis mediated by TGF-beta 1.

Carcinoma, Hepatocellular↗

Expression of transforming growth factor-beta 1 mRNA in human hepatocellular carcinoma.

We investigated the expression of transforming growth factor beta 1 (TGF-beta 1) mRNA in tumor tissues surgically removed from ten patients with hepatocellular carcinoma (HCC). All HCC tissues expressed TGF-beta 1 mRNA at different levels, indicating the presence of activated transcription of TGF-beta 1 gene in human HCC tissues in vivo. The level of TGF-beta 1 mRNA expression showed no relationship to main tumor size of plasma alpha-fetoprotein level. Some HCC tissues presenting a relatively low grade of histological differentiation showed the highest levels of TGF-beta 1 mRNA expression.

Aged↗

Demonstration of platelet antigens that bind platelet-associated autoantibodies in chronic ITP by direct immunoprecipitation procedure.

Platelet antigens that bind platelet-associated autoantibodies in chronic idiopathic thrombocytopenic purpura (ITP) were demonstrated using a direct immunoprecipitation procedure. ITP platelets, with bound autoantibodies, were radiolabelled and solubilized, and then platelet antigen-antibody complexes adsorbed to protein A-bearing Staphylococcus aureus were analysed by 7.5% sodium dodecyl sulphate, polyacrylamide gel electrophoresis (SDS-PAGE). Direct immunoprecipitation demonstrated the presence of platelet-associated autoantibodies against glycoprotein (GP) IIb/IIIa in four of six ITP patients with an intensive band corresponding to platelet-associated IgG. These results were confirmed by indirect immunoprecipitation using ether eluates from two ITP patients. In addition, only direct immunoprecipitation demonstrated the presence of autoantibodies against an unidentified protein having a molecular mass of 56 kDa in three of the six patients. These three ITP patients having autoantibodies against GP IIb/IIIa and against the 56 kDa protein were studied after splenectomy. Two patients, showing disappearance of autoantibodies against these antigens, attained a complete remission, and one patient, with autoantibodies against the 56 kDa protein despite splenectomy, attained only partial remission. These data suggest that autoantibodies against GP IIb/IIIa and against the 56 kDa protein may play a role in platelet destruction in some ITP patients.

Adult↗

Two human monoclonal antiplatelet autoantibodies established from patients with chronic idiopathic thrombocytopenic purpura.

Two human hybridomas secreting antiplatelet autoantibodies were established by somatic cell fusion using splenocytes from two patients with chronic idiopathic thrombocytopenic purpura (ITP). These monoclonal antibodies, HT7F and HT8C, were of the IgM isotype and reacted with autologous and allogeneic platelets fixed with paraformaldehyde (PFA). They also bound to fresh platelets. An elution study showed that eluates from allogeneic platelets reacted with autologous platelets. These results indicated that HT7F and HT8C were autoantibodies recognizing a site on the platelet surface. Both monoclonal antibodies were able to induce complement activation in vitro. HT7F was demonstrated to bind to a platelet protein having a molecular mass of 105 kDa under both nonreducing and reducing conditions. No human hybridoma synthesizing antibody against 105 kDa platelet protein has been reported to date. These antibodies may play a role in the pathogenesis of thrombocytopenia in some ITP patients.

Adult↗

Alteration of membrane oligosaccharides by castanospermine, an alpha glucosidase inhibitor, enhances immunoglobulin production in Staphylococcus aureus Cowan I-stimulated lymphocyte culture.

Castanospermine (CSP) inhibits alpha-glucosidase, which is involved in the initial step of N-linked oligosaccharide processing of secretory and membrane glycoproteins. In Staphylococcus aureus Cowan I (SAC)-stimulated human lymphocyte culture, CSP at a dose of 20 micrograms/ml caused a twofold increase in immunoglobulin G (IgG) release after 7 days. An initial 48-h exposure to CSP sufficed for this enhancing effect. Plaque-forming cell assays on the seventh day disclosed that CSP caused an increase in the number of IgG-, IgA- and IgM-secreting cells. In cross-culture experiments, only a mixture of B cells pretreated with CSP and untreated T cells showed an increase in IgG production. Tritiated thymidine incorporation studies revealed that CSP enhanced B-cell responses to T cell-derived soluble factor (TSF). When incubated with CSP for 18 h, B cells showed an increased surface binding on [3H]concanavalin A (Con A). These results indicate that the alteration in B-cell membrane oligosaccharides enhances the response to TSF at an early stage of SAC culture, leading to an increase in Ig-secreting cell number at later stages. The present study provides evidence that cell-surface oligosaccharides of B cells play an important role in the responses of B cells to lymphokines.

Alkaloids↗

Acid treatment of platelets as a simple procedure for distinguishing platelet-specific antibodies from anti-HLA antibodies: comparison with chloroquine treatment.

The identification of antibodies to platelet-specific antigens is important for correctly diagnosing neonatal alloimmune thrombocytopenia, posttransfusion purpura and refractoriness due to platelet-specific antibodies. However, the serologic identification of these platelet-specific antibodies is complicated by the presence of anti-HLA antibodies. We examined and compared the diagnostic usefulness of acid-treated and chloroquine-treated platelets for the discrimination of platelet-specific antibodies from anti-HLA antibodies. The viability of acid-treated platelets is 83.4%, which is better than that of chloroquine-treated platelets (52.6%). The antigenicity of HLA class I antigens of acid-treated platelets was significantly reduced compared with that of PBS- or chloroquine-treated platelets. On the other hand, platelet surface glycoprotein Ib and glycoprotein IIb/IIIa, and platelet-specific antigens were stable following acid or chloroquine treatment. Chloroquine-treated platelets were not suitable targets for analysis by immunofluorescence flow cytometry because of nonspecific fluorescence derived from platelet damage. We conclude that acid-treated platelets are more suitable targets than chloroquine-treated platelets for screening for platelet-specific antibodies and also for analyses of the specificity of platelet-specific antibodies.

Antibody Specificity↗

Close correlation of intra-abdominal fat accumulation to hypertension in obese women.

The relation between intra-abdominal visceral fat accumulation and blood pressure was investigated in 67 obese women (mean body mass index, 33.6 +/- 3.1; average age, 50 +/- 11 years). As an index of intra-abdominal fat accumulation, the ratio of the intra-abdominal visceral fat area to subcutaneous fat area was determined using a computed tomographic section at the level of the umbilicus. When the obese subjects were divided into a hypertensive group and a normotensive group, the ratio of the intra-abdominal visceral fat area to subcutaneous fat area in the hypertensive group was significantly higher (0.53 +/- 0.33 versus 0.29 +/- 0.12, p less than 0.01). Significant correlations between the ratio of intra-abdominal visceral fat area to subcutaneous fat area and systolic blood pressure (r = 0.62, p less than 0.001) and diastolic blood pressure (r = 0.53, p less than 0.001) also were found. However, no significant difference existed in either the body mass index or the waist-to-hip circumference ratio between the hypertensive and normotensive groups. Plasma renin activity, aldosterone, epinephrine, and norepinephrine levels were not significantly different between the two groups. Moreover, the correlation between the ratio of the intra-abdominal visceral fat area to subcutaneous fat area ratio and blood pressure was found independent of age and body mass index by multiple regression analyses. We conclude that intra-abdominal fat accumulation itself may play an important role in the pathogenesis of hypertension in obesity.

Abdomen↗

Accumulation of apolipoprotein E-rich high density lipoproteins in hyperalphalipoproteinemic human subjects with plasma cholesteryl ester transfer protein deficiency.

This study characterized the plasma lipoproteins of familial hyperalphalipoproteinemic patients with or without deficiency of cholesteryl ester transfer protein (CETP) activity. The subjects with CETP deficiency have increased levels of apolipoprotein (apo) E. The increased concentration of apo E in these subjects was correlated to the appearance of apo E-rich high density lipoproteins (HDL). Sodium dodecyl sulfate-polyacrylamide gel analysis revealed that these lipoproteins contained predominantly the apo E (82%) and little amount of apo A-I (18%). These apo E-rich HDL displayed a much higher affinity than human LDL in binding to LDL receptors on human fibroblasts. Furthermore, 3.5 times fewer apo E-rich HDL than LDL were required to saturate the receptors on fibroblasts. These data indicated that the apo E-rich HDL in CETP-deficient human subjects contained multiple copies of apo E and bound to the LDL receptor through multiple interactions. The apo E-rich HDL, with similar properties as cholesterol-induced apo E HDLc, were not detectable in normal human subjects or in hyperalphalipoproteinemic subjects with normal CETP activity. The apo E-containing HDL in the latter subjects were smaller and contained only small amounts of apo E (14%). The difference in apo E-containing HDL in these subjects suggests a correlation between CETP level and the appearance of apo E-rich HDL.

Apolipoprotein A-I↗

Inhibitory effect of somatomedin C/insulin-like growth factor I on adrenocorticotropin- or forskolin-induced steroidogenesis in isolated rat adrenocortical cells.

The effects of recombinant human somatomedin C/insulin-like growth factor (IGF-I) on the steroidogenic response of isolated rat adrenocortical cells to ACTH, forskolin, and (Bu)2cAMP were examined during short term incubations. The effect of IGF-I on cAMP production by cells stimulated with ACTH or forskolin was also examined. IGF-I inhibited ACTH-, forskolin-, and (Bu)2cAMP-induced corticosterone production in a concentration-dependent manner. IGF-I (30 ng/ml) also significantly inhibited ACTH-induced cAMP production. However, the peptide had no significant effect on forskolin-induced cAMP production. IGF-I suppressed ACTH-induced cAMP production both in the presence and absence of 3-isobutyl-1-methylxanthine, suggesting that IGF-I acts to inhibit the formation of cAMP rather than the stimulation of cAMP degradation. The observation that IGF-I inhibited steroidogenesis induced by (Bu)2cAMP strongly suggests that one site of inhibition is at some step(s) distal to cAMP formation. However, the inhibition of cAMP production after stimulation with ACTH also suggests a plasma membrane site of action for IGF-I in adrenocortical cells.

Adrenal Cortex↗

A patient with hypocortisolism and Cushing's syndrome-like manifestations: cortisol hyperreactive syndrome.

One patient is reported who has the manifestations of Cushing's syndrome in spite of persistent hypocortisolemia. His serum levels of cortisol and free cortisol were below normal, and 24-h urinary excretion of 17-hydroxycorticosteroids and cortisol were decreased. There was a rapid and substantial increase in serum cortisol in response to synthetic ACTH-(1-24). Plasma levels of ACTH were marginally increased by successive administration of CRH and vasopressin, which were followed by substantial increases in serum cortisol. Glucocorticoid activity of the patient's serum, as measured by a RRA was low. There were no responses of urinary 17-hydroxycorticosteroids after metyrapone treatment. These laboratory examinations ruled out any known clinical conditions resulting in hypocortisolemia. The clinical condition could also be explained by cortisol hyperreactivity of the patient's cells. In vitro hyperreactivity to glucocorticoids was demonstrated in cultured skin fibroblasts whose aromatase activity was increased 1.5- to 1.8-fold above that of normal cells, and [3H]thymidine incorporation was inhibited more effectively by the addition of cortisol or dexamethasone. The mechanism by which the patient is hyperreactive to glucocorticoids remains unexplained.

Adrenocorticotropic Hormone↗

Hypertension in obese children: fasting serum insulin levels are closely correlated with blood pressure.

The relationship between blood pressure and anthropometric or metabolic factors was studied in 324 obese children aged 9.5 +/- 1.8 years (mean +/- standard deviation). Obese children had a significantly higher blood pressure than non-obese children (systolic blood pressure: 121 +/- 14 mmHg in obese children vs 112 +/- 11 mmHg in non-obese children, P less than 0.001; diastolic blood pressure: 72 +/- 9 mmHg in obese children vs 66 +/- 7 mmHg in non-obese children, P less than 0.001). When the obese children were divided into hypertensive and normotensive groups, there was a significant difference in fasting serum insulin levels between the two groups (19.3 +/- 9.3 microU/ml in the hypertensive group vs 13.0 +/- 6.1 microU/ml in the normotensive group), and a close correlation between fasting serum insulin levels and systolic blood pressure was demonstrated (r = 0.63, P less than 0.001). However, there was no significant correlation between blood pressure and the degree of obesity itself or the waist-to-hip ratio in the obese children. There was no significant correlation between blood pressure and fasting plasma glucose, serum total cholesterol, or triglycerides levels in the obese children. Moreover, the correlation between fasting insulin levels and blood pressure was shown to be independent of the degree of obesity or waist-to-hip ratio and age by multiple regression analysis. These results indicate that hyperinsulinemia itself may play an important role in the pathogenesis of hypertension in obese children.

Anthropometry↗