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Biomedical subjects

M Tsuchiya

Publications and source records attributed to M Tsuchiya.

At least 433 records · Page 24Linked to original sources
PubMed1986

The mechanism of insulin-induced increase of the rate of de novo purine biosynthesis in primary cultured rat hepatocytes.

The effect of insulin on the rate of de novo purine biosynthesis was studied in freshly isolated hepatocytes from adult male rats. Insulin started to increase the rate of de novo purine biosynthesis at 1.5 X 10(-10) M and plateaued at 1.5 X 10(-8) M with the magnitude of increase of about 280%. Insulin at 1.5 X 10(-9) M or the higher concentration increased the 5-phosphoribosyl 1-pyrophosphate (PRPP) availability for purine ribonucleotide synthesis to about 230%. Insulin increased ATP concentration to 127% and decreased AMP, ADP, GMP and GDP concentration to 73, 69, 73 and 69% in association with the increased adenylate energy charge of 0.90 in comparison to the control level of 0.83. But the total adenine and guanine nucleotide concentration in the cell was not significantly changed. In addition insulin increased the specific activity of amidophosphoribosyltransferase (ATase) with the increased Vmax and the unchanged Km for PRPP.

Amidophosphoribosyltransferase↗
PubMed1986

Malabsorption of long-chain fatty acid in cholera toxin-induced secretory diarrhea.

The effects of cholera toxin-induced diarrhea on the absorption of fatty acids of different chain lengths were investigated using rat small intestine. In the study using isolated jejunal loops, the absorption of the long-chain fatty acid, linoleic acid, into the intestinal mucosa was significantly impaired 90 min after the administration of linoleic acid micelles in the cholera toxin-treated rats. This reduction of linoleic acid absorption in the cholera toxin-treated rats was not found at 180 min. We could not find any mucosal accumulation of labeled linoleic acid or disturbance of triglyceride formation in the intestinal mucosa as compared with that of controls. The amount of linoleic acid transported into the intestinal lymph was delayed and reduced in cholera toxin-treated rats. Furthermore, the absorption of the medium-chain-length fatty acid, octanoic acid, was unchanged in the cholera toxin-treated rats. These results suggest that intestinal secretion induced by cholera toxin may delay the mucosal uptake and lymphatic transport of long-chain fatty acids. Cholera toxin may not affect triglyceride formation in the epithelial cells.

Animals↗
PubMed1986

Earlobe crease and coronary heart disease in Japanese.

To evaluate whether a significant statistical correlation exists between earlobe crease (EC) and coronary heart disease (CHD), 1000 Japanese adult patients (573 males, 427 females) were examined for the presence or absence of EC, clinical or angiographic evidence of CHD, and the following coronary risk factors: male sex, age over 50 years, obesity, hypertension, diabetes mellitus, cigarette smoking, and hyperlipidemia. Patients were divided into two groups according to clinical evidence of CHD: 237 patients with angina pectoris and/or myocardial infarction (CHD+ group); 720 patients without evidence of CHD (CHD- group). Coronary angiography was performed on 200 patients from this sample population; these patients were also divided into two groups: 119 patients with greater than 50% luminal narrowing of at least one major coronary artery (stenosis+ group); 81 patients with no significant atherosclerotic changes in the coronary arteries (stenosis- group). EC was present in 58 of 237 CHD+ patients (24.5%) but in only 35 of 720 CHD- patients (4.8%; P less than 0.001); it was present in 31 of 199 stenosis+ patients (26.1%) but in only 3 of 81 stenosis- patients (3.7%; P less than 0.01). EC was also found to correlate significantly with some coronary risk factors; the correlations between the presence of EC and the presence of CHD and coronary risk factors were investigated by multivariate analysis. In a multivariate setting, the existence of CHD and an age of over 50 years was significantly related to the presence of EC. To investigate the relationship between EC and advancing age, all patients were separated into age-groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Pathological findings of lymphangiectasia of the large intestine in a patient with protein-losing enteropathy.

Lymphangiectasia of the large intestine associated with protein-losing enteropathy is reported. A 33-yr-old man suffered from diarrhea, sometimes mixed with blood. Colonoscopic study revealed reddish and edematous mucosa with multiple flat elevated lesions and giant folds in the localized segment of the rectosigmoid. An intestinal clearance test of alpha 1-antitrypsin revealed the association of protein-losing enteropathy. Operation was performed successfully, resulting in a marked improvement of symptoms and laboratory data, especially serum total protein, albumin, IgG, and Leu-2a-positive cells (suppressor/cytotoxic T cells). Giant folds consisted of the submucosal edema and hyperplasia of the epithelial glands with cystic dilatation of glands, and flat elevated lesions consisted of mucosal and submucosal edema associated with intestinal lymphangiectasia, adipose tissue, and blood capillaries. The population of the Leu-2a-positive cells in the lamina propria and intraepithelial layer was decreased and that of the Leu-3a-positive cells (helper/inducer T cells) in the lamina propria was increased.

Adult↗
PubMed1986

In vivo inhibition of the rate of de novo purine synthesis in rat liver by glucagon.

The rates of de novo purine and protein synthesis were assessed in vivo in rat liver after bolus administration of glucagon. The specific activity of hepatic purines and the specific activity ratio of hepatic purine/protein were used as an index of the rate of de novo purine synthesis and the rate relative to protein. Glucagon at doses of 0.01 mg to 0.1 mg/200 g body weight (BW), administered as an intravenous bolus, inhibited dose-dependently the rate of de novo purine synthesis and the rate relative to protein although it increased dose-dependently the hepatic concentration of 5-phosphoribosyl 1-pyrophosphate (PRPP). The inhibition of the rate of de novo purine synthesis recovered to control levels during the period between 60 and 90 minutes after glucagon administration. Dibutyryl cyclic AMP (Bt2 cAMP) partially mimicked this effect of glucagon in that it did not increase the rate of de novo purine synthesis in spite of increased concentrations of PRPP. These results suggest that an intravenous bolus of glucagon inhibits the rate of de novo purine synthesis through increasing cAMP concentration. The data are consistent with inhibition of amidophosphoribosyltransferase (ATase) in spite of increased PRPP concentrations.

Animals↗
PubMed1986

Circadian cycles in VIP content and VIP stimulation of cyclic AMP accumulation in the rat pineal gland.

VIP content in the rat pineal gland and cyclic AMP accumulation in response to VIP in the daily light and dark cycle were examined. VIP content in the pineal varied significantly during the day and night; the content decreased during exposure to light and was lowest at the onset of darkness, 6 p.m. (mean +/- SE, 23 +/- 5 pg/pineal), and increased during the night and was highest at the onset of light, 6 a.m. (72 +/- 12 pg/pineal). Response of cyclic AMP accumulation to VIP varied with a periodicity inversely related to the daily light and dark cycle of VIP content; cyclic AMP accumulation in response to 10(-7) M VIP increased in proportion to periods of exposure to light and peaked at 6 p.m., and decreased with the onset of darkness.

Animals↗
PubMed1986

Isolation and characterization of the cDNA for murine granulocyte colony-stimulating factor.

A cDNA sequence coding for murine granulocyte colony-stimulating factor (G-CSF) has been isolated from a cDNA library prepared with mRNA derived from murine fibrosarcoma NFSA cells, which produce G-CSF constitutively. Identification of murine G-CSF cDNA was based on the cross-hybridization with human G-CSF cDNA under a low-stringency condition. The cDNA can encode a polypeptide consisting of a 30-amino acid signal sequence, followed by a mature G-CSF sequence of 178 amino acids with a calculated Mr of 19,061. The nucleotide sequence and the deduced amino acid sequence of murine G-CSF cDNA were 69.3% and 72.6% homologous, respectively, to the corresponding sequences of human G-CSF cDNA. The murine G-CSF cDNA, when introduced into monkey COS cells under the simian virus 40 promoter, could direct the synthesis of a protein that can stimulate the granulocyte colony formation from mouse bone marrow cells and support the proliferation of murine NFS-60 myeloid leukemia cells.

Amino Acid Sequence↗
PubMed1986

Liquid ionization mass spectrometry of phospholipids.

Several phosphatidylcholines (PC) and a phosphatidylethanolamine (PE) were subjected to liquid ionization (LI) mass spectrometry, in which a sample is ionized through energy transfer from metastable argon atoms under atmospheric pressure. Commercially available and synthesized, saturated or unsaturated fatty acid containing phospholipids and their mixtures were studied. A sample either as a concentrated chloroform-methanol solution or with glycerol (matrix) gave characteristic peaks such as MH+ and four fragment ions. One of the fragment ions (e.g., m/z 551 of PC 16:0, 16:0) containing both fatty acid residues has been commonly observed with other ionization methods such as CI, FD, and FAB, but the other fragment ions have not been observed in other mass spectra with one exception on desorption CI. Ions b and d (e.g., m/z 464 and 328, respectively, for PC 16:0, 16:0) contain one fatty acyl residue and the other ion containing the phosphorylcholine moiety appears at m/z 196 for PC. Thus the masses of the MH+ ion and these fragment ions provide useful structural information even in the case of a mixture. The ion b (e.g., m/z 488 of PC 18:0, 18:2) observed during an early period of heating was formed mainly by the loss of one acyl group at sn-1 of the glycerol backbone and thus may be used to differentiate the positional specificities of the constituent fatty acids. The temperature of the sample, however, should be controlled precisely, because it has a significant effect on the mass spectrum. The present method (LI) also provided useful information for a mixture of PC and PE.

Mass Spectrometry↗
PubMed1986

Increased rate of de novo purine synthesis and its mechanism in regenerating rat liver.

In regenerating rat liver at 12 h after a 70% hepatectomy, [14C]glycine incorporation to hepatic acid-soluble purines increased by 2.4-fold with a 26% increase of the mean rapidly miscible glycine pool size and its comparable turnover rate. Amidophosphoribosyltransferase (EC 2.4.2.14, ATase) activity increased 1.8-fold at 18 h and 5-phosphoribosyl-1-pyrophosphate (PRPP) concentration increased 3.0-fold at 12 h after surgery. Decreases in ATP and GTP concentrations of 13 and 15%, respectively, in regenerating rat liver at 12 h after surgery were counterbalanced by increased AMP and GMP concentrations of 13 and 44%, respectively, with comparable inhibitory potentials on ATase. These results suggest than an increased rate of de novo purine synthesis in regenerating rat liver is mediated by the increased ATase activity and PRPP concentrations.

Adenosine Monophosphate↗
PubMed1986

[Effect of mazindol on glucose absorption in everted rat small intestine].

Effect of an anorexiant, mazindol, on glucose absorption was investigated. Ten weeks-old female Sprague-Dawley rats were divided into mazindol treated (fed on powder diet containing 100 mg/kg of mazindol) and control groups. Four weeks later, experiments of continuous observation of glucose absorption and glucose transport were performed in each group using the everted sac method. During 180 min of continuous observation of glucose absorption, significantly lowered glucose concentrations of the serosal medium were observed in the mazindol treated group at oral and caudal ends of the upper, caudal end of the middle, and caudal ends of the lower small intestine, whereas no significant differences in glucose concentrations of the mucosal medium were observed between the two groups. After 60 min incubation for monitoring the glucose transport, significantly decreased glucose concentrations of serosal medium were observed in mazindol treated group at oral and caudal ends of the upper, caudal ends of the middle and caudal ends of the lower small intestine, whereas no significant differences in glucose concentrations of mucosal medium were observed. The results suggested that there is little effect on glucose absorption, but the metabolism of glucose or the remaining glucose in the small intestinal wall is increased by mazindol treatment.

Animals↗
PubMed1986

Platelet dysfunction and alteration of prostaglandin metabolism after chronic alcohol consumption.

To study the effects of chronic alcohol consumption on platelet functions, the rate of arachidonate-induced platelet aggregation, the production of malondialdehyde in platelets, and plasma levels of prostaglandin endoperoxide metabolites were examined in 88 chronic alcoholics and 24 healthy controls. The rate of platelet aggregation and the production of malondialdehyde in platelets were greater in chronic alcoholics both on admission and 1 week after. However, these alterations returned to the level of healthy controls within 4 weeks of abstinence from alcohol and were independent of the number of circulating platelets. Furthermore, on admission, plasma levels of thromboxane B2 were significantly increased in chronic alcoholics when compared with those of healthy controls (400.8 +/- 36.5 versus 241.7 +/- 28.9 pg/ml plasma; p less than 0.025) and were also significantly correlated with malondialdehyde production in washed platelet debris (r = 0.6049; p less than 0.001). In contrast, plasma levels of 6-keto prostaglandin F1 alpha and prostaglandin E were not altered after chronic alcohol consumption. As a result, the ratio of 6-keto prostaglandin F1 alpha to thromboxane B2 was markedly decreased in chronic alcoholics (0.31 +/- 0.03 versus 0.62 +/- 0.13; p less than 0.001). These results strongly suggest that the imbalance in prostaglandin endoperoxide metabolites is produced by chronic alcohol ingestion. Moreover, a significant correlation was observed between platelet aggregation rate and malondialdehyde production during platelet aggregation (r = 0.559; p less than 0.005). Thus, we conclude that chronic alcohol consumption alters platelet thromboxane metabolism, which is likely associated with the increased ability of platelets to aggregate.

Adult↗
PubMed1986

Malotilate (diisopropyl 1,3-dithiol-2-ylidenemalonate) increases liver de novo purine synthesis and amidophosphoribosyltransferase activity.

The effect of malotilate (diisopropyl 1,3-dithiol-2-ylidenemalonate) on de novo purine synthesis was studied in rat liver in vivo and in primary cultured rat hepatocytes in vitro. In the in vivo system, malotilate increased [14C]glycine incorporation by 1.4- to 1.7-fold into acid soluble hepatic purines 4 to 18 hr and the rapidly miscible glycine pool size at least by 2.0-fold 12 hr after administration. Malotilate did not change 5-phosphoribosyl-1-pyrophosphate concentration but increased significantly amidophosphoribosyltransferase (E.C. 2.1.2.14) activity per unit of DNA or per unit of liver protein. Malotilate also increased significantly the hepatic cyclic AMP concentration 2 to 12 hr after administration. In the in vitro system, malotilate increased [14C] formate incorporation into acid soluble purines with accompanying increases in 5-phosphoribosyl-1-pyrophosphate availability and the specific activity of amidophosphoribosyltransferase. These results suggest that malotilate increases the rate of de novo purine synthesis in the liver by its direct action on hepatocytes, the mechanism of this increase is due to the combined increase of amidophosphoribosyltransferase activity and 5-phosphoribosyl-1-pyrophosphate supply and cyclic AMP may play a role for this response.

Adenosine Triphosphatases↗
PubMed1985

Amino acid sequence of histone H1 at the ADP-ribose-accepting site and ADP-ribose X histone-H1 adduct as an inhibitor of cyclic-AMP-dependent phosphorylation.

The ADP-ribosylation site of histone H1 from calf thymus by purified hen liver nuclear ADP-ribosyltransferase was determined and effects of the ADP-ribose X histone-H1 adduct on cAMP-dependent phosphorylation of the histone H1 were investigated. ADP-ribosylated histone H1 was prepared by incubation of histone H1, 1 mM [adenylate-32P]NAD and the purified ADP-ribosyltransferase. N-Bromosuccinimide-directed bisection of ADP-ribosylated histone H1 showed that the NH2-terminal fragment (Mr = 6000) was modified and contained serine residue 38, the site of phosphorylation by cAMP-dependent protein kinase. Digestion of the NH2-terminal fragment with cathepsin D and trypsin, and purification of this fragment, using high-performance liquid chromatography, yielded a radiolabelled single peptide corresponding to residues 29-34 of histone H1, containing the arginine residue as the ADP-ribosylation site. These results indicate that ADP-ribosylation of histone H1 occurs at the arginine residue 34, sequenced at the NH2-terminal side of the phosphate-accepting serine residue 38. Phosphorylation of histone H1 from calf thymus by cAMP-dependent protein kinase was markedly reduced when histone H1 was ADP-ribosylated. Kinetic studies of phosphorylation revealed that ADP-ribosylated histone H1 was a linear competitive inhibitor of histone H1 and a linear non-competitive inhibitor of ATP.

Adenosine Diphosphate Ribose↗
PubMed1985

ADP-ribosylation of phosphorylase kinase and block of phosphate incorporation into the enzyme.

Phosphorylase kinase purified from rabbit skeletal muscle was ADP-ribosylated by hen liver nuclear ADP-ribosyltransferase. This modification, as was seen in cAMP-dependent phosphorylation, was observed only in alpha and beta subunits of the phosphorylase kinase and the latter was more rapidly modified. Analysis of the ADP-ribosylated amino acid residue sequenced in alpha and beta subunits showed that both subunits were modified at the area of the arginine residue. The Km for NAD was 0.10 mM and the pH optimum was 9.0. When the ADP-ribosylated phosphorylase kinase was phosphorylated by cAMP-dependent protein kinase, a reduction in phosphate incorporation occurred with increase in the ADP-ribosylation. ADP-ribosylation also suppressed autophosphorylation, to a lesser degree than observed with cAMP-dependent phosphorylation. The ADP-ribosylation-dependent reduction of phosphorylation resulted in a suppression of the phosphorylation-dependent activation of the phosphorylase kinase. These results together with findings of ADP-ribosyltransferase activity in the rabbit skeletal muscle [Soman, G. et al. (1984) Biochem. Biophys. Res. Commun. 120, 973-980] suggest that ADP-ribosylation participates in the regulation of the phosphorylase kinase activity through changes in the rate of phosphorylation.

Adenosine Diphosphate Ribose↗