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Biomedical subjects

K Murakami

Publications and source records attributed to K Murakami.

At least 1,081 records · Page 60Linked to original sources
PubMed1985

Renal cell carcinoma with intracaval tumor thrombus extending to the diaphragm: ultrasonography and surgical management.

We describe the successful management of a patient with intracaval extension of renal cell carcinoma to the level of the diaphragm. Ultrasonography delineated clearly the upper extent of the tumor thrombus and revealed no invasion of the vena caval wall at or above the entrance of the main hepatic veins. To prevent severe hypotension caused by intrapericardial control of the inferior vena cava, the aorta was clamped temporarily just above the celiac axis. The tumor was removed completely en bloc with the thrombus. Blood loss was minimal and the patient recovered promptly.

Aged↗
PubMed1985

Effects of tris(hydroxymethyl)aminomethane on biosynthesis and release of insulin in the pancreatic Langerhans islets.

Tris(hydroxymethyl)aminomethane (Tris) has been shown to inhibit selectively the Golgi apparatus and Golgi-endoplasmic reticulum-lysosomal system (GERL system) of several kinds of cells including pancreatic B cells. This study was designed to assess the effect of Tris on insulin, glucagon and somatostatin release and insulin synthesis in pancreatic B cells by using isolated rat pancreatic islets. Tris suppressed glucose-induced insulin release, whereas it did not affect the glucagon and somatostatin release. Furthermore, the incorporation of [3H]leucine into the insulin fraction was suppressed by 10 mM Tris, but the sum of the radioactivity of both proinsulin and insulin fraction were not influenced. The present study suggests that the Golgi apparatus and GERL system may play a role in insulin secretion and biosynthesis in pancreatic B cells.

Animals↗
PubMed1985

The presence of essential histidine residues in manganese(III)-containing acid phosphatase from sweet potato.

Chemical modification studies of manganese(III)-containing acid phosphatase [EC 3.1.3.2] were carried out to investigate the contributions of specific amino-acid side-chains to the catalytic activity. Incubation of the enzyme with N-ethylmaleimide at pH 7.0 caused a significant loss of the enzyme activity. The inactivation followed pseudo-first-order kinetics. Double log plots of pseudo-first-order rate constant vs. concentration gave a straight line with a slope of 1.02, suggesting that the reaction of one molecule of reagent per active site is associated with activity loss. The enzyme was protected from inactivation by the presence of molybdate or phosphate ions. Amino acid analyses of the N-ethylmaleimide-modified enzyme showed that the 96%-inactivated enzyme had lost about one histidine and one-half lysine residue per enzyme subunit without any significant decrease in other amino acids, and also demonstrated that loss of catalytic activity occurred in parallel with the loss of histidine residue rather than that of lysine residue. Molybdate ions also protected the enzyme against modification of the histidine residue. The enzyme was inactivated by photooxidation mediated by methylene blue according to pseudo-first-order kinetics. The pH profile of the inactivation rates of the enzyme showed that an amino acid residue having a pKa value of approximately 7.2 was involved in the inactivation. These studies indicate that at least one histidine residue per enzyme subunit participates in the catalytic function of Mn(III)-acid phosphatase.

Acid Phosphatase↗
PubMed1985

Covalent binding of moxalactam to cephalosporinase of Citrobacter freundii.

The inhibition of Citrobacter freundii cephalosporinase activity by moxalactam is shown to be due to the formation of a transiently stable covalent complex, probably acyl enzyme. The covalent complex formed was identified by coelution of [14C] moxalactam with the enzyme by using Sephadex G-25 gel filtration in the presence of 5.7 M guanidine hydrochloride and by analytical isoelectric focusing. Both the side-chain carboxyl group and the 7 alpha-methoxy group of moxalactam were necessary to stabilize the complex. Moxalactam is racemic with respect to the alpha carbon of the 7 beta-acylamino side chain, and the complex with the R epimer (half-life, 4.6 min) decomposed much more rapidly than that formed with the S epimer (half-life, 130 min). For other beta-lactam antibiotics that were stable to beta-lactamase, the half-lives of enzyme-antibiotic complexes were less than 4 min.

Cephalosporinase↗
PubMed1985

Calmodulin inhibitors decrease the CRF-and AVP-induced ACTH release in vitro: interaction of calcium-calmodulin and the cyclic AMP system.

The effect of N-(6-aminohexyl)-5-chloro-naphthalene-1-sulfomide (W-7) and trifluoperazine (TFP) was examined on ACTH release from cultured rat anterior pituitary cells and pituitary halves. These drugs significantly inhibited the ACTH release induced by synthetic ovine corticotropin-releasing factor (CRF) in a dose-related manner. In pituitary halves, arginine vasopressin (AVP) at 10 and 100 ng/ml showed almost the same ACTH-releasing activity as CRF at the same concentrations. W-7 and TFP inhibited the CRF-and AVP-induced ACTH release from pituitary halves. The cyclic AMP levels in the pituitary halves were significantly increased by CRF, but not AVP. Although W-7 inhibited CRF-induced ACTH release, it did not have an effect in cyclic AMP accumulation. These results suggest that CRF exerts ACTH-releasing activity through both the calcium-calmodulin system and cyclic AMP system and that AVP stimulates ACTH release mainly through the calcium-calmodulin system.

Adrenocorticotropic Hormone↗
PubMed1985

Nonlinear parameter tomography system using counterpropagating probe and pump waves.

In this paper, a novel tomographic system for imaging the nonlinear parameter (B/A) of biological objects is described. This parameter is closely related to the detailed properties of tissue, and may well provide a new powerful tool for ultrasonic tissue characterization. In our new system, an impulsive, relatively high power (10 mW/cm2), low frequency pump wave is applied from the opposite direction of a cw low intensity probe wave of high frequency (5 MHz) so that the phase of the probe wave is modulated sequentially by the product of the nonlinear parameter (B/A) along the beam (x axis) and the pressure of the impulsive pump wave. This modulated probe wave is detected and demodulated to derive the distribution of (B/A) along the x axis. Many responses are averaged to increase the S/N ratio. Inverse or other filtering operations are applied to widen the frequency bandwidth of the pump wave. The entire system is realized in hardware. The counterbeam orientation makes the imaging system compact, with easy access to many parts of the human body. Its resolution is two times that of the perpendicular system proposed previously by us and the attenuation of the pump wave can also be compensated for easily. A practical system aimed at breast and liver diagnosis is described. The principle of the method and the system construction are described. B/A images of several objects are given.

Animals↗
PubMed1985

An antigen of Plasmodium yoelii that translocates into the mouse erythrocyte membrane upon entry into the host cell.

Monoclonal antibodies against the rodent malaria parasite, Plasmodium yoelii, have been prepared and characterized by indirect immunofluorescence on acetone-fixed infected mouse erythrocytes. The antibody of clone K2 reacted strongly with late trophozoites and schizonts, whereas it did so weakly and diffusely with ring forms and early trophozoites. Strong fluorescence was confined to granular structures in schizonts and merozoites. Parasites that invaded erythrocytes in vitro lost the strong fluorescence. Instead, immunofluorescence appeared in the membranes of erythrocytes infected in vitro with merozoites. Erythrocytes infected with more than one merozoite had intensified immunofluorescence in their membranes. Staining of the invaded erythrocytes with 4',6-diamidino-2-phenylindole (DAPI) hydrochloride demonstrated that membranes of all the invaded erythrocytes acquired the P. yoelii antigen. These results suggest that the P. yoelii antigen in merozoites is translocated into erythrocyte membranes upon entry into the host cell. Immunofluorescence continued to appear in membranes of infected erythrocytes throughout the intra-erythrocytic parasite growth. Staining of unfixed infected erythrocytes with the K2 antibody failed to detect the parasite antigen. In contrast, immunofluorescence was present in unfixed membranes of erythrocyte ghosts, which had been spontaneously formed after rupture of schizont-infected erythrocytes by merozoite release. No immunofluorescence appeared in either acetone-fixed or unfixed ghosts of normal erythrocytes. These results suggest the antigenic determinant of the P. yoelii antigen is exposed at the cytoplasmic surface of the infected erythrocyte membrane. Immunoprecipitation has revealed that the K2 antibody recognizes a 160 X 10(3) Mr P. yoelii antigen.

Animals↗
PubMed1985

Role of endothelium in the contractions induced by norepinephrine and clonidine in rat aorta.

The inhibitory effects of endothelium-derived relaxing factor (EDRF) on the contractions induced by norepinephrine and clonidine in rat aorta were examined. Carbachol induced a relaxation of norepinephrine-induced contraction in rat aorta with endothelium. Removal of endothelium inhibited the carbachol-induced relaxation and increased the magnitude of norepinephrine-induced contraction. Quinacrine, a phospholipase A2 inhibitor, methylene blue, a guanylate cyclase inhibitor and tetraethylammonium, a potassium permeability inhibitor, inhibited carbachol-induced relaxation and augmented the magnitude of norepinephrine-induced contraction only when endothelium was present. Clonidine induced a contraction when endothelium was removed or muscle was treated with methylene blue. The contractions induced by norepinephrine and clonidine were equally sensitive to prazosin and equally less sensitive to yohimbine. Clonidine inhibited the norepinephrine-induced contraction, whereas it potentiated the angiotensin 11- or 12 mM K-induced contractions in the aorta with endothelium. The inhibitory effect of clonidine on the norepinephrine-induced contraction was reduced by endothelium-removal and by methylene blue but not by yohimbine. These results suggest that norepinephrine has a strong direct stimulating action and clonidine has a weak one on vascular smooth muscle cells possibly mediated by alpha 1-adrenoceptors, and their contractile effects are inhibited by the spontaneously released EDRF.

Angiotensin II↗
PubMed1985

The effect of nifedipine on CRF-41 and AVP-induced ACTH release in vitro.

The effect of nifedipine on CRF-41- and AVP-induced ACTH release was examined using monolayer cultured rat anterior pituitary cells and pituitary halves. Nifedipine inhibited ACTH release induced by synthetic rat CRF-41 in two systems. In pituitary halves, CRF-41 significantly stimulated both ACTH release and cyclic AMP accumulation. Nifedipine inhibited CRF-41-induced ACTH release and the inhibitory effect of nifedipine on CRF-41-induced ACTH release was accompanied by parallel decrease of cyclic AMP levels in pituitary halves. Nifedipine did not inhibit AVP-induced ACTH release in pituitary halves, and AVP did not significantly affect cyclic AMP accumulation in pituitary halves. These results suggest that CRF-41 stimulates ACTH release through the intracellular cyclic AMP system and calcium-calmodulin system which are accelerated by the influx of extracellular calcium ions. Moreover, it is suggested that the calcium required for AVP-induced ACTH release is derived primarily from intracellular rather than extracellular sources.

Adrenocorticotropic Hormone↗
PubMed1985

Stability of rat (human) corticotropin-releasing factor in serum, urine and tissue incubation medium.

The stability of rat (human) CRF in serum, urine and tissue incubation medium was examined using Sephadex gel filtration and CRF radioimmunoassay with anti-rat (human) CRF serum. Human serum after incubation with rat (human) CRF for 1 h at 37 degrees C showed two peaks of CRF immunoreactivity on a Sephadex G-50 fine column. Most of the immunoreactivity coeluted with the rat (human) CRF marker. When rat (human) CRF was incubated with rat liver, kidney or hypothalamus, only 3.1-14.9% of the CRF was recovered at the rat (human) CRF position on gel filtration, and two to four CRF-immunoreactive peaks appeared after the rat (human) CRF marker. When rat (human) CRF was incubated with human urine (pH 6.0) for 24 h at room temperature, one peak of CRF immunoreactivity coeluted with the rat (human) CRF marker on Sephadex gel filtration. The urine extracts of normal rats showed some small peaks of CRF-like immunoreactivity on the Sephadex column, with the main peak appearing after authentic CRF. These results suggest that rat (human) CRF is relatively stable in serum and urine, but is easily degraded by tissue enzymes, with the degraded CRF fragments being excreted in the urine.

Animals↗
PubMed1985

Effects of antimycin A on vascular and intestinal smooth muscle contraction and calcium movements.

The effects of antimycin A on smooth muscle preparations of guinea-pig taenia coli and rabbit aorta were investigated. In guinea-pig taenia coli, antimycin A inhibited the sustained phase but had less effect on the transient phase of K-induced contraction. The inhibitory effect of antimycin A became less in the presence of high concentration (40 mM) of glucose under hypoxia whereas antimycin A strongly inhibited both transient and sustained phase of K-induced contraction in the absence of glucose. Antimycin A inhibited the K-induced increase in cellular Ca content but not the increased rate of Ca uptake at the concentration needed to inhibit the K-induced contraction in taenia coli. In rabbit aorta, antimycin A inhibited the K-induced contraction only in the absence of glucose. Antimycin A inhibited the norepinephrine-induced contraction in aorta and this inhibitory effect was not observed in the presence of 40 mM glucose under hypoxia. Antimycin A inhibited the K-induced increase in cellular Ca content at a concentration without any effect on the K-induced contraction in aorta. On the other hand, the K-induced increase in the rate of Ca uptake was not inhibited by antimycin A. Antimycin A reduced oxygen consumption of resting and K-stimulated muscle, and decreased tissue ATP content in high K solution in taenia coli and aorta. It is concluded that antimycin A inhibits mitochondrial function in both guinea-pig taenia coli and rabbit aorta, leading to an inhibition of the K-induced sustained contraction in taenia and norepinephrine-induced contraction in aorta. Antimycin A does not seem to inhibit K-stimulated Ca influx; this agent inhibits only K-induced increase in cellular Ca content, which may represent mitochondrial Ca accumulation.

Adenosine Triphosphate↗
PubMed1985

Stimulation of protein glycosylation in cultured hepatoma cells by polyprenyl phosphates.

The aim of this work was to selectively stimulate N-glycosylation of proteins in cultured AH 70Btc hepatoma cells. Dolichyl phosphate, alpha-dihydrodecaprenyl phosphate and solanesyl phosphate were entrapped in egg lecithin liposomes and supplied to the cells. After treatment with 0.6-15 nmol of the polyprenyl phosphates/3 ml/dish for 48 hr, the incorporations of [14C]glucosamine into N-linked saccharide chains of glycoproteins and into lipid intermediates were increased to various extents. The stimulation by alpha-dihydrodecaprenyl phosphate was most significant and 15 nmol of the lipid/dish increased the incorporation into N-linked saccharide chains of glycoproteins by about 80%. The incorporations of [14C]glucosamine into O-linked saccharide chains and of [14C]leucine into proteins were not changed significantly by alpha-dihydrodecaprenyl phosphate. When the N-linked glycopeptides prepared from the cells and those from the cells treated with the polyprenyl phosphate were compared by Sephadex G-50 column chromatography, no significant difference was observed. Analysis of reduced cellular glycoproteins by sodium dodecyl sulfate/polyacrylamide-gel electrophoresis showed that alpha-dihydrodecaprenyl phosphate increased the incorporation of [14C]glucosamine into N-linked saccharide chains of certain high-molecular-weight glycoproteins. In addition, the polyprenyl phosphate enhanced the adhesiveness of the cells to the substratum, probably as a result of the stimulation of N-glycosylation of proteins.

Animals↗