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Biomedical subjects

H Adachi

Publications and source records attributed to H Adachi.

At least 505 records · Page 28Linked to original sources
PubMed1984

[Clinical value of the sequential study of the uric acid in CSF in patients with cerebral diseases: Part I. Brain tumor and the effect of irradiation].

Uric acid is the end product of the purine metabolism in the human and is mainly excreted to the urine. The studies on cerebrospinal fluid (CSF) uric acid in patients with various neurological diseases were reported in the literature. In the present study the authors discussed the clinical value of the sequential study of the CSF uric acid content in patients with brain tumors. CSF was investigated for uric acid in 23 controls and 30 cases of brain tumor. The results were as follows: The mean value and standard deviation of the uric acid in CSF in controls was 0.23 +/- 0.13 mg/dl. The uric acid in CSF increased in patients with malignant brain tumor (0.49 +/- 0.22 mg/dl, p less than 0.005), but was in normal range in patients with benign brain tumor (0.32 +/- 0.13 mg/dl, 0.10 less than p less than 0.25). There was no significant correlation between CSF uric acid and CSF protein contents. Uric acid in the lumbar CSF was approximately 4 times higher than in the ventricular CSF in patients with brain tumor. The CSF uric acid had progressively increased during irradiation to the whole brain. The factors contributing to increase of the uric acid in CSF were thought to be increased permeability of blood-CSF barrier, global damage of brain tissue, increased nucleic acid catabolism in the central nervous system (CNS) for example in tumor, inflammation or immunoreaction, increased of xanthine, hypoxanthine or xanthine oxidase activity in the CNS, directly increased of plasma components into the CSF due to such as subarachnoid hemorrhage, intraventricular hemorrhage, bleeding in the tumor or surgical operation, dysfunction of the CSF dynamics.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1983

Effect of chloride ion on the oxygen affinity of hemoglobin York (alpha 2 beta 2(146)Pro) and S-York hybrid hemoglobin (alpha 2 beta S beta York). Role of the beta 82 lysyl and beta 146 histydyl residues in chloride binding to hemoglobin.

We estimated the relative role of various chloride binding sites in determining the oxygen affinity of hemoglobin using abnormal hemoglobins such as Hb York (Hb Y) (alpha 2 beta 2(146)Pro), Hb Malmö (Hb M) (alpha 2 beta 2(97)Gln), and Hb S and chemically modified hemoglobins such as cross-linked Hb S, Hb Y, and asymmetrical SY hemoglobin with bis(3,5-dibromosalicyl)fumarate. The chloride effect on the p50 values of Hb S and Hb M was identical to that of Hb A. In contrast, the effect of chloride on the p50 values of Hb Y was only 20% of that of Hb A. Cross-linking between the two beta 82 lysyl residues with fumarate decreased the chloride effect by 40%. The effect of chloride on cross-linked Hb Y, in which both beta 82 lysyl and beta 146 histidyl residues were modified, was unchanged from that on Hb Y (20% of Hb A). The effect of chloride on the p50 value of SY asymmetrical hybrid hemoglobin was 40% of that of Hb A or Hb S, which is midway between the values obtained for cross-linked Hb S and Hb Y. From these results, the contribution of beta 146 His and beta 82 Lys on oxygen affinity by binding of chloride was calculated to be 40% each; the remaining 20% chloride effect was attributed to alpha 1 Val.

Chlorides↗
PubMed1983

[The cellular mechanism of action of gastrin on the corporal mucosa of the canine stomach. (2) Ca2+-activated, phospholipid-dependent protein kinase and phospholipid turnover--possible mediator of gastrin action].

The existence of Ca2+-activated, phospholipid-dependent protein kinase (protein kinase C), the effect of gastrin on phospholipid metabolism and guanylate cyclase activity were investigated to elucidate the cellular mechanism of action of gastrin on the corporal mucosa of the canine stomach. Protein kinase activity was determined by measuring the incorporation of [32P] into calf thymus H1-histone from [32P]-ATP. One unit of protein kinase was defined as the amount of enzyme which incorporated 1 pmol of phosphate from ATP into H1-histone. Protein kinase C was found in 100,000xg supernatant of homogenate fractionated by a DEAE-cellulose column chromatography. Characteristics of further purified protein kinase C, such as dependency on divalent cations and phospholipids, were in agreement with those of previously reported protein kinase C in other tissues. Furthermore, the gastric corporal mucosa was found to contain protein kinase C in large quantities. The specific activity of protein kinase C was 26,000 units/mg protein. The phospholipid metabolism was evaluated by the incorporation of [14C]-glycerol-3-phosphate and the change of the radioactivity of [32P] in individual phospholipids. Each phospholipid was extracted from the gastric corporal mucosa and isolated by thin layer chromatography. Guanylate cyclase activity was determined by measuring the cGMP produced, using radioimmunoassay. Gastrin significantly increased the incorporation of [14C]-glycerol-3-phosphate into phosphatidylethanolamine in the presence of acetylcholine (Ach). Ach increased the uptake of the tracer into phosphatidylinositol significantly, and the increase was enhanced by the simultaneous addition of gastrin. In the experiments with [32P]-labeled phospholipids, gastrin increased the incorporation of [32P] into phosphatidylethanolamine significantly. The significant increase of the radioactivity in phosphatidylinositol by Ach failed to be enhanced by gastrin, but that of phosphatidylethanolamine by Ach was enhanced by gastrin. No stimulation of guanylate cyclase activity by gastrin was detected in the dispersed gastric corporal mucosal cells. These results indicate that gastric corporal mucosa was one of the most abundant tissues in which protein kinase C was contained, when compared with various mammalian tissues previously reported by Minakuchi, Nishizuka, et al. Nishizuka et al, recently proposed the novel hypothesis that phosphatidylinositol turnover activated by cAMP-independent agonists will be essentially required to activate protein kinase C. Our results suggest that gastrin can provoke phospholipids turnover including phosphatidylinositol turnover in gastric corporal mucosa. Therefore, our data indicate the possibility that the protein kinase C system plays an important role in the cellular mechanism of action of gastrin on gastric corporal mucosa.

Animals↗
PubMed1983

Use of 125I-secretin to identify and characterize high-affinity secretin receptors on pancreatic acini.

We prepared 125I-secretin and studied the kinetics, stoichiometry, and chemical specificity with which the labeled peptide binds to dispersed acini prepared from guinea pig pancreas. Iodinated secretin retained intrinsic biological activity in that it was as effective but 2.5-times less potent than native secretin in its ability to bind to pancreatic acini and to increase cellular cAMP. Scatchard analysis of binding of 125I-secretin indicated that each pancreatic acinar cell has approximately 93,000 binding sites, half of which are occupied by 11 nM iodinated secretin. Binding of 125I-secretin was rapid, reversible, saturable, specific, and temperature dependent. Binding of 125I-secretin was inhibited by secretin, vasoactive intestinal peptide, PHI, and Gila monster venom but not by glucagon, gastric inhibitory polypeptide, cholecystokinin, caerulein, gastrin, bovine pancreatic polypeptide, somatostatin, neurotensin, leucine-enkephalin, methionine-enkephalin, carbachol, bombesin, litorin, eledoisin, physalaemin, or substance P. With agonists (secretin, vasoactive intestinal peptide, PHI, or Gila monster venom), as well as antagonists (C-terminal fragments of secretin), there was a close correlation between their relative potencies for inhibiting binding of 125I-secretin and their relative potencies for increasing cAMP (agonists) or inhibiting the secretin-induced increase in cAMP (antagonists). For a given agonist, however, a 40-fold higher concentration was required for half-maximal inhibition of binding of 125I-secretin than was required to produce a half-maximal increase in cellular cAMP. Thus, maximal stimulation of cellular cAMP occurs when approximately one-third of the secretin receptors are occupied by an agonist.

Animals↗
PubMed1983

[Analysis of coronary hemodynamics in exercise by T1-201 scintigraphy: examination of rates of change of cardiac output, myocardial blood flow distribution, coronary blood flow and coronary vascular resistance].

From our observation that initial distribution of 201T1 in tissue is mainly dependent on blood flow distribution, we designed the method to obtain the rates of change of coronary blood flow and coronary vascular resistance and applied it to the analysis of coronary hemodynamics in patients with ischemic heart disease during submaximal exercise. We measured the rates of change of cardiac output (delta CO) and myocardial blood flow distribution (delta Fract ) in two occasions by the sequential two injections of T1, and obtained the rate of change of coronary blood flow (delta Flow) from delta CO and delta Fract . Using the rate of change of mean blood pressure, we calculated also the rate of change of coronary vascular resistance (delta CVR). The initial components of histograms of the right ventricle by the first and second injections of T1 were fitted into gamma function curve. S1 and S2 were the areas bounded by the curve and baseline of the first and second injections, and then the cardiac output ratio was estimated by R X S1/S2, where R was the dose ratio measured by another camera system. The five min count rates on the myocardium by the first (H1) and second (H2) injections of T1 were calculated five min after the injection. H2 was approximately H1 X R in the same condition of T1 injection but H2 was not equal to H1 X R, when the T1 injection was done in the different loading condition. Therefore the rate of change of myocardial blood flow distribution was calculated as delta Fract = (H1 X R-H2)/H2.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output↗
PubMed1982

Gastrin release from gastrinoma cells stimulated with secretin.

The secretin injection test has been proved to be useful in the diagnosis of gastrinoma in vivo. Fresh gastrinoma cells were cultured for a short time in vitro and then stimulated with secretin. A rise in the gastrin concentration in the culture medium was observed within 10 min after the addition of secretin. This fact may be evidence that gastrinoma cells have receptors which bind with secretin resulting in the release of gastrin.

Cells, Cultured↗