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Biomedical subjects

S Uchida

Publications and source records attributed to S Uchida.

At least 469 records · Page 26Linked to original sources
PubMed1987

Dissecting aneurysms of the anterior circle of Willis arteries. Report of two cases.

Two cases of spontaneous dissecting aneurysm extending from the supraclinoid portion of the internal carotid artery to the middle cerebral artery are reported in two teenaged patients. Both patients collapsed with a headache on the right side, left hemiparesis, and altered consciousness due to cerebral ischemia. One patient became alert in 2 days; however, his condition rapidly deteriorated 4 days later and he died on the 8th day from massive cerebral infarction. The other patient received a right superficial temporal artery (STA)-middle cerebral artery (MCA) anastomosis 50 hours after his initial symptoms. He improved gradually and is able to walk without help. Cerebral angiograms 3 months after the operation disclosed progressive attenuation of the MCA and dilatation of the anastomosed STA. Artificial collateral flow demonstrated in the postoperative angiogram may have been useful in preventing massive cerebral infarction.

Adolescent↗
PubMed1987

Surface antigens on hamster cells transformed by SV40, BK virus and JC virus.

We studied the surface antigens on hamster cells transformed by SV40, BK and JC viruses using a complement-dependent cytotoxicity test. Antiserum was obtained from guinea pigs immunized with an SV40-transformed hamster cell line, and used after appropriate absorption with a range of cell types. The cell lines transformed by these viruses were all found to possess the following surface antigens: 1) a unique set of organ antigens, 2) fetal antigen(s), and 3) an antigen tentatively named primate polyoma virus-transformed hamster cell antigen (PPH antigen-1). These antigens were not detected on other hamster cell lines, including those transformed by mouse polyoma-, adeno-, herpes-, or retro-viruses Neither could they be detected on mouse, rat or human cells transformed by SV40 or BK viruses. They were, thus, probably host-derived antigens specifically depressed or unmasked by the primate polyoma viruses. In addition, all hamster cell lines tested, including BHK21, carried an antigen(s) named hamster cell line antigen, which could not be detected on surfaces of normal cells, in primary or secondary culture.

Animals↗
PubMed1987

Phorbol ester inhibits bradykinin-stimulated inositol trisphosphate formation and calcium mobilization in neuroblastoma x glioma hybrid NG108-15 cells.

In neuroblastoma x glioma hybrid NG108-15 cells, bradykinin (BK) receptor stimulation leads to phosphoinositide hydrolysis, formation of inositol phosphates and mobilization of intracellular calcium. Treatment of the cells with 12-O-tetradecanoyl phorbol 13-acetate (TPA) suppressed the spike phase of increases in intracellular calcium concentration. In radioligand binding studies, TPA treatment did not interfere with [3H]BK specific binding to intact cells or to cell membranes. The ability of guanyl-5'-yl-imidodiphosphate to promote the conversion of the high affinity sites of the BK receptors into a low affinity sites was unaffected by TPA. TPA treatment showed the dose-dependent, noncompetitive inhibition of BK-stimulated formation of inositol trisphosphate. In the membrane preparations from TPA-treated cells, guanosine 5'-(3-O-thio)triphosphate-stimulated inositol trisphosphate formation was inhibited by 50%. These data indicate that TPA exerts its inhibitory action on BK responses at the sites of guanine nucleotide-binding protein or phospholipase C or both.

Bradykinin↗
PubMed1986

Bradykinin-induced intracellular Ca2+ elevation in neuroblastoma X glioma hybrid NG108-15 cells; relationship to the action of inositol phospholipids metabolites.

The effect of bradykinin on the intracellular Ca2+ concentration ([Ca2+]i) in NG108-15 cells was studied using a Ca2+ indicator quin 2. Bradykinin induced two phases of change in [Ca2+]i. Bradykinin induced a spike phase of [Ca2+]i increase which was detectable within 15 s and decayed to near-basal concentration in 3 min and then a prolonged plateau phase of [Ca2+]i increase which continued for 15 min. The bradykinin-induced spike phase was not diminished by decreasing extracellular Ca2+ concentration ([Ca2+]o) to 1 microM. On the contrary, the plateau phase was dependent on [Ca2+]o and inhibited by Ca2+ blockers, verapamil (50 microM), nifedipine (1 microM). The iontophoretic injection of inositol-trisphosphate (IP3) into the single cell induced the increase of [Ca2+]i, which was independent of [Ca2+]o. These results indicate that the bradykinin-induced spike phase is mediated by the release of intracellular Ca2+ stores induced by IP3, while the plateau phase is mediated by influx of extracellular Ca2+ probably through voltage-sensitive Ca2+ channels.

Animals↗
PubMed1986

1-Oleoyl-2-acetyl-glycerol and phorbol diester stimulate Ca2+ influx through Ca2+ channels in neuroblastoma x glioma hybrid NG108-15 cells.

The effect of 1-oleoyl-2-acetyl-glycerol (OAG) and the phorbol diester 12-O-tetradecanoyl-phorbol-acetate (TPA) on the intracellular Ca2+ concentration ([Ca2+]i) in NG108-15 cells was studied using a Ca2+ indicator, quin 2. OAG and TPA induced an increase in [Ca2+]i from 100 +/- 19 to 187 +/- 24 nM and 192 +/- 15 nM, respectively, within 15 min. The increase in [Ca2+]i induced by activators of protein kinase C was dependent on the extracellular Ca2+ concentration [Ca2+]o) and was inhibited by the Ca2+ blockers, verapamil and nifedipine. These results indicate that the OAG- and TPA-induced [Ca2+]i increase is mediated by the influx of extracellular Ca2+ through voltage-sensitive Ca2+ channels.

Calcium↗
PubMed1986

A thiol protease of peritoneal macrophages in the guinea pig.

Proteolytic enzymes of the guinea pig peritoneal exudate macrophages were investigated using synthetic fluorogenic peptide substrates. Among several enzymes, t-butyloxycarbonyl-phenylalanyl-seryl-arginine 4-methylcoumaryl-7-amide cleaving enzymes had the highest activity, and the activity in exudate macrophages was about 3 times stronger than that in resident macrophages. The molecular weight of the enzyme was around 35,000 and optimal pH around 6.5-7.0. It was inhibited by thiol-blocking reagents, suggesting a thiol protease.

Animals↗
PubMed1986

Isolation of glucagon-secreting cell lines by cloning insulinoma cells.

Six glucagon-secreting cell lines designated as In-R1-G1, -G3, -G7, -G9, -G10, and -G11 were isolated from insulinoma cells (In-111-R1) by single cell cloning. A small amount of insulin was also detectable in the incubation medium when hormone secretion was stimulated by the addition of arginine or theophylline. These cell lines grew as monolayers and the population doubling times varied from 16.8 to 28.8 h. Karyologically these clones were aneuploid and the modes of chromosome numbers were 61 to 70. Electron microscopic examination of one of these clones showed that these cells contained moderately developed Golgi apparatus and a few secretory granules, which more or less resembled alpha-cell granules. By gel filtration study of the incubation medium, glucagon and glucagonlike material were eluted. The molecular weight of the latter was approximately 9000, which suggested the concomitant secretion of proglucagon into the medium. The levels of secreted glucagon in basal state were 0.3 to 3.0 ng/10(6) cells/2 h. Glucagon secretion was markedly enhanced in the presence of amino acids. Glucagon secretion increased slightly in the presence of high concentration of glucose in Hanks' balanced salt solution; however it was not affected by the varying concentrations of glucose when the cells were incubated in complete media with amino acids. Glucagon secretion was also stimulated by the addition of theophylline. These clonal cell lines seem to provide a useful tool for investigating the mechanism of glucagon secretion.

Adenoma, Islet Cell↗
PubMed1986

A monoclonal antibody with broad reactivity to human interferon-alpha subtypes useful for purification of leukocyte-derived interferon.

A monoclonal antibody to human interferon-alpha, termed HT-1 antibody, with a broad reactivity to various subtypes of interferon-alpha was prepared. It bound and neutralized all of the four subtypes of E. coli-derived human recombinant interferon-alpha (alpha 1, alpha 2, alpha 4, and alpha 6) tested; it also neutralized human natural leukocyte interferon but only partially. Human interferon-beta and -gamma were not bound. The antibody conjugated to Sepharose beads retained over 90% of human leukocyte interferon induced by Sendai virus. The bound interferon was recovered by acid elution in good yields and in almost pure form (specific activity was about 2 X 10(8) international units/mg protein). The purified interferon showed, in SDS-polyacrylamide gel electrophoresis, an activity profile with major peaks in a mol. wt. range of 17,000-22,000, which completely agreed with the profile shown by polyclonal antibody-purified interferon. Such purified leukocyte interferon-alpha preparations containing most of the naturally occurring subtypes can be useful for clinical and other purposes.

Animals↗
PubMed1986

High Ca2+ inhibits AVP-dependent cAMP production in thick ascending limbs of Henle.

To further gain insights into the mechanisms underlying impaired urine concentration in hypercalcemia, effects of increasing Ca2+ concentrations in the incubation medium on cAMP production in response to 10(-8) M arginine vasopression (AVP) were examined in thick ascending limbs of Henle (MTAL) and collecting tubules (MCT) dissected from outer medulla of mouse kidney. Increasing Ca2+ in the incubation medium from 1.0 mM to either 2.0 mM or 5.0 mM inhibited AVP-dependent cAMP production in MTAL but not in MCT. This inhibition of AVP-dependent cAMP production by 2.0 mM Ca2+ in MTAL was not reversed by verapamil or diltiazem. Also, Ca2+ ionophore A23187 did not inhibit AVP-dependent cAMP production in MTAL in the presence of 1.0 mM Ca2+. Increasing medium Ca2+ from 1.0 to 5.0 mM inhibited cAMP production in MTAL in response to both glucagon and forskolin by the magnitude comparable to that seen in response to AVP. These results show that high Ca2+ inhibits AVP-dependent cAMP production only in MTAL and not in MCT. In addition, the lack of effects of Ca2+ channel blockers and Ca2+ ionophore suggests that high ambient Ca2+ per se may inhibit AVP-dependent cAMP production in MTAL. The fact that high Ca2+ also suppressed cAMP production in response to glucagon or forskolin suggests that Ca2+ may inhibit AVP-dependent adenylate cyclase at postreceptor site(s), one of which is the catalytic unit of the enzyme.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1986

Alterations in muscarinic receptors of ventricular muscle in carbachol-induced short-term desensitization.

The inhibitory action of a muscarinic agonist on the contractile response of cardiac muscle is transient due to short-term desensitization of muscarinic cholinergic receptors. Studies were made on the binding of the muscarinic antagonist L-[3H]-quinuclidinyl benzilate ([3H]QNB) to the muscarinic receptor in the membrane fraction of ventricular muscle of guinea pigs desensitized by perfusion with carbachol for 10 min. Desensitization did not change the maximum binding or equilibrium dissociation constant (Kd) of [3H]QNB, but shifted the inhibition curves of [3H]QNB binding by carbachol to the right both in the presence and absence of 5-guanylyl imidodiphosphate (GppNHp). Analysis of these inhibition curves with a multiple site model suggested that superhigh and high affinity agonist binding sites were converted to low affinity sites in the desensitized state. GppNHp has additive effects to the prior exposure to carbachol, suggesting a different site of action from short-term exposure of agonist. We conclude that agonist-induced short-term desensitization of the muscarinic receptor of ventricular muscle is caused by reduction in the affinity of the receptor for agonist without reduction in its amount or affinity for antagonist.

Animals↗
PubMed1986

Effect of calcitonin gene-related peptide on the cyclic AMP level of isolated mouse diaphragm.

The effect of calcitonin gene-related peptide (CGRP) on the cyclic nucleotide level in isolated mouse diaphragm was investigated. CGRP at concentrations of up to 1 microM caused dose-dependent increases in cyclic AMP levels but had no effect on cyclic GMP levels. At 1 microM, CGRP increased cyclic AMP levels by about 2.7-fold. Moreover, in the presence of phosphodiesterase inhibitor (Ro 20-1724), CGRP still caused even greater dose-dependent increases in cyclic AMP levels. Even in the presence of propranolol, a beta-adrenergic antagonist, CGRP stimulated increased cyclic AMP levels. In addition, specific binding of CGRP was observed in mouse diaphragm. All these results suggest that CGRP increases intracellular cyclic AMP levels via a CGRP receptor but not the beta-adrenergic receptor.

Animals↗