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Biomedical subjects

K Takeda

Publications and source records attributed to K Takeda.

At least 1,171 records · Page 65Linked to original sources
PubMed1985

Interaction of tyrosine residues with the chromophore in bacteriorhodopsin.

We previously reported that the absorption spectrum at low temperatures of iodinated bacteriorhodopsin can be separated into four components with maxima at shorter wavelengths than in native bacteriorhodopsin. In this study, the time course of the formation of each spectral component after iodination was analyzed, revealing that these four components correspond to four different iodinated states of tyrosine residues interacting with the retinal chromophore of bacteriorhodopsin. Therefore at least two tyrosine residues interact with the chromophore of bacteriorhodopsin.

Bacteriorhodopsins↗
PubMed1985

Kinetic aspects of the interaction of horse heart cytochrome c with sodium dodecyl sulfate.

The sodium dodecyl sulfate (SDS) concentration dependence of spectral changes in circular dichroism (CD) and in absorbance of cytochrome c were examined in the far-ultraviolet region, aromatic region, and the Soret band. The Soret peak obtained in 0.60 mM SDS was nine times greater than that of the native state. (The critical micelle concentration, CMC, of SDS was 2.2 mM in the phosphate buffer used.) The results indicated that the drastic change at the Soret band did not accompany the corresponding large-scale change in secondary structure of the protein. In the stopped-flow measurements, two and three processes were followed at 406 nm below and above the CMC, respectively. At 289 nm only one process was observed, and this corresponded to the second process at 406 nm. Therefore, the second process at 406 nm was considered to be a change in tertiary structure around the heme group. The first process and the third process seemed to reflect a change in the heme environment; the former appeared to be due to a solvent effect and the latter due to a binding effect of a large number of dodecyl sulfate ions.

Animals↗
PubMed1985

Lack of influence of the carbamoyl group on the stereochemistry of the acid-catalyzed opening of the aziridine ring of the mitomycins and of congeners.

The acid-catalyzed opening of the aziridine ring of mitomycins A and C is known to occur predominantly with cis stereochemistry. We have observed that the presence or absence of a carbamoyl group at C-10 of mitomycin C and in certain of its analogues does not have a significant influence on the stereochemistry of the opening of this ring. The trans product obtained from mitomycin C was shown to be stable when treated with acid under the conditions of its formation. Mitomycin B was also shown to yield predominantly the cis product when it was subjected to acid-catalyzed opening of its aziridine ring. The 1H NMR spectra of acetate derivatives prepared from mitomycin B show two sets of signals that are due to two populations of rotamers. The analysis of these spectra has substantiated several previous spectral assignments. This paper also presents some thoughts on acid-catalyzed bifunctional DNA alkylation by mitomycins and 10-decarbamoyloxy-9-dehydromitomycins.

Chemical Phenomena↗
PubMed1985

Effect of adenosine deaminase inhibitors on myocardial reactive hyperaemia following brief coronary occlusions.

Effect of two agents of adenosine deaminase inhibitor, 8-azaguanine and adenine, on myocardial reactive hyperaemia was tested in the anaesthetised open-chest dog. Reactive hyperaemic flow response of the circumflex coronary artery was observed following 5, 10, 15, 20 and 30 s coronary occlusions before, during and after infusion of 8-azaguanine and adenine, which are known as adenosine deaminase inhibitors. Intracoronary infusion of 8-azaguanine and adenine caused the minimum increase in the baseline coronary flow. Both the nucleic acids shifted the dose response curve of adenosine to the left. 8-azaguanine enhanced volume response of flow at all occlusion intervals tested. The infused dose of adenine also intensified volume response of flow after 5, 15, 20 and 30 s occlusions. Fifteen minutes after termination of the nucleic acid infusions, the reactive hyperaemia returned towards control levels. The results suggest that 8-azaguanine and adenine enhance myocardial reactive hyperaemia possibly by inhibiting adenosine deaminase to degradate myocardial interstitial adenosine to inosine.

Adenine↗
PubMed1985

Change of inhibitor sensitivities of Escherichia coli F1-ATPase due to a mutational substitution of Phe for Ser at residue 174 of the beta subunit.

The F1-ATPase from the uncD11 mutant of E. coli (Kanazawa, H., Horiuchi, Y., Takagi, M., Ishino, Y., & Futai, M. (1980) J. Biochem. 88, 695-703), showed different enzymological properties from the wild-type enzyme. The mutant F1-ATPase had biphasic kinetics and essentially the same Km values as the wild-type enzyme, although its Vmax values were lower. The mutant enzyme showed altered sensitivities to dicyclohexylcarbodiimide (DCCD), azide and quercetin; it was less sensitive than the wild-type to quercetin and DCCD, and its Mg2+-dependent ATPase activity was slightly more resistant to azide than that of the wild-type, whereas its Ca2+-dependent activity was more sensitive. On the other hand, the mutant and wild-type F1 were inhibited equally by 4-chloro-7-nitro-2,1,3-benzoxadiazole (NBD-Cl). The fact that the Mg2+- and Ca2+-dependent F1-ATPase activities of the wild-type and mutant responded differently to quercetin and azide suggested that their mechanisms of action were different. Previous studies (Noumi, T., Mosher, M.E., Natori, S., Futai, M., & Kanazawa, H. (1984) J. Biol. Chem. 259, 10071-10075) indicated that Ser is replaced by Phe at residue 174 of the beta subunit of the mutant. Thus the Ser residue or its neighboring area(s) may constitute the binding site of DCCD, quercetin and azide.

Amino Acid Sequence↗
PubMed1985

Centrally-induced vasodepressor responses to diltiazem, a calcium channel blocker, in rats.

The effects of a calcium channel blocker, diltiazem, on central cardiovascular regulation were investigated by injecting it intracerebroventricularly (i.c.v.) in urethane-anaesthetized rats. The blood pressure decreased immediately after the injection returning to baseline level 20-30 min later. Both heart rate and abdominal sympathetic nerve activity decreased correspondingly. Diltiazem injected intravenously (i.v.) decreased both blood pressure and heart rate without affecting sympathetic nerve firing. Although the central pressor responses to carbachol and prostaglandin E2 were not affected by i.c.v. pretreatment with diltiazem, diltiazem attenuated the pressor responses to angiotensin II. Furthermore, electrical lesioning of the anteroventral third ventricle (AV3V) area significantly attenuated the depressor responses to diltiazem injected i.c.v. These results suggest that diltiazem injected i.c.v. affects the central nervous system to decrease sympathetic outflow, and thereby to attenuate the central vasopressor effects of angiotensin II in the brain AV3V area.

Angiotensin II↗
PubMed1985

Growth of defective subacute sclerosing panencephalitis viruses in human neural cells and their neurovirulence in mice.

A defective subacute sclerosing panencephalitis (SSPE) virus which had been passaged in human embryonic lung cells was transferred to cultures of three neural cell types: neuroblastoma, oligodendroglioma and glioblastoma. The growth characteristics of the virus in these cells were essentially similar to those in non-neural cells. On the other hand, a marked difference in neurovirulence was noticed for the virus grown in neural cells when examined by intracerebral inoculation into mice. The virus passaged in neuroblastoma and oligodendroglioma cells showed high neurovirulence, inducing an acute encephalitis, whereas the virus passaged in human embryonic lung cells and that in glioblastoma cells did not show neurovirulence. These results suggest that the virus recovered its neurovirulence after passage in certain human neural cells.

Animals↗
PubMed1985

Effects of breathing therapy with a dead-space-resistance device on post-cardiac surgical patients.

The effects of a dead-space-resistance device (IDSEP breather) on Pao2, Paco2 and functional residual capacity (FRC) in 11 post-cardiac surgical patients were studied. There were no significant changes in Pao2, Paco2 and FRC after the IDSEP therapy. Changes in Pao2 between the pre- and post-IDSEP therapy correlated well with changes in FRC (r = 0.797, P less than 0.01). Breathing therapy with the dead-space-resistance device appeared not to bring any benefit in early post-cardiac surgical patients.

Adult↗
PubMed1985

Inhibitors of calcium buffering depress evoked transmitter release at the squid giant synapse.

Evoked release of transmitter at the squid giant synapse was examined under conditions where the calcium ion concentration in the presynaptic terminal was manipulated by inhibitors of calcium sequestration. Simultaneous intracellular recordings of presynaptic and post-synaptic resting and action potentials were made during bath application of one of the following metabolic inhibitors: sodium cyanide (NaCN), carbonyl cyanide-p-trifluoromethoxyphenyl hydrazone (FCCP); ruthenium red (RuR) and sodium-free (lithium) sea water. Cyanide and lithium sea water reversibly depressed the post-synaptic potential (p.s.p.) whilst RuR and FCCP blocked the evoked post-synaptic response irreversibly. The progressive reduction of p.s.p. amplitude was accompanied by a reversible increase in synaptic delay. The time course of block of the p.s.p. was similar for different agents and dependent on the rate of presynaptic activity (30-40 min at 0.01 Hz). Recovery of the post-synaptic action potential following block by cyanide and lithium sea water was obtained within 40 min and 5 min respectively. Synaptic depression by the metabolic inhibitors does not result from changes in presynaptic resting or action potentials, nor from a change in post-synaptic receptor sensitivity. The post-synaptic response to the local ionophoresis of L-glutamate was unchanged following inhibition of evoked release of transmitter by cyanide. Injections of EGTA into presynaptic terminals poisoned by cyanide produced transient increases in p.s.p. amplitude, suggesting that cyanide is having its effect through raising intracellular calcium rather than lowering ATP. Control experiments injecting EGTA into unpoisoned nerve terminals showed no apparent effect on evoked transmitter release.

Action Potentials↗
PubMed1985

Microbial degradation of natural rubber vulcanizates.

An actinomycete, Nocardia sp. strain 835A, grows well on unvulcanized natural rubber and synthetic isoprene rubber, but not on other types of synthetic rubber. Not only unvulcanized but also various kinds of vulcanized natural rubber products were more or less utilized by the organism as the sole source of carbon and energy. The thin film from a latex glove was rapidly degraded, and the weight loss reached 75% after a 2-week cultivation period. Oligomers with molecular weights from 10 to 10 were accumulated during microbial growth on the latex glove. The partially purified oligomers were examined by infrared and H nuclear magnetic resonance and C nuclear magnetic resonance spectroscopy, and the spectra were those expected of cis-1, 4-polyisoprene with the structure, OHC-CH(2)-[-CH(2)-C(-CH(3))=CH -CH(2)-](n)-CH(2)-C(=O)- CH(3), with average values of n of about 114 and 19 for the two oligomers.

Journal Article↗
PubMed1985

Intracoronary adenosine enhances myocardial reactive hyperemia after brief coronary occlusion.

Adenosine is a prime candidate for the role of mediator between myocardial metabolic state and coronary blood flow. However, there are few reports concerning the direct effects of exogenously added adenosine on coronary autoregulation. The present investigation in the open-chest dog studied the effects of a threshold dose of intracoronary adenosine infusion on reactive hyperemia following brief coronary occlusions. The infused dose did not increase nonocclusive flow by greater than 10%. Adenosine enhanced total hyperemic flow at all occlusions tested (5, 10, 15, 20, and 30 s). Aminophylline pretreatment reduced reactive hyperemia below the control level even in the presence of an intracoronary infusion of adenosine. Adenosine injected into the left atrium and intracoronarily infused papaverine did not affect hyperemic response to 5- and 15-s coronary occlusions. The results suggest that a minimum dose of exogenously added adenosine enhances myocardial reactive hyperemia, possibly by potentiating the effects of endogenous adenosine released during ischemia.

Adenosine↗
PubMed1985

Peripheral origin of plasma dopamine.

To clarify the peripheral origin of plasma dopamine (DA), we studied the changes in plasma levels of free and conjugated catecholamines after nephrectomy, adrenalectomy, chemical sympathectomy and renal denervation. Nephrectomy markedly increased conjugated DA levels, indicating that plasma DA is rapidly excreted through the kidney and originates outside the kidney. Adrenalectomy reduced plasma total epinephrine (E) to undetectable limits, whereas total norepinephrine (NE) and DA levels remained unchanged. In addition, the subsequent immobilization stress significantly increased both total NE and DA, but not E. Chemical sympathectomy with 6-hydroxydopamine decreased both NE and DA by 66% and 72%, respectively. E level, however, was not affected by sympathectomy. Although the following immobilization stress significantly increased all catecholamines levels, the magnitude of increase in concentrations of NE and DA were much less than that of E. These results suggest that plasma DA is mainly derived from the peripheral sympathetic nerve terminals. However, the renal nerve, one of the sympathetic nerves, did not serve as a source of plasma DA because renal denervation had no effect on plasma DA levels in spite of the marked depletion of free DA in the kidney.

Adrenalectomy↗
PubMed1985

Centrally induced vasodepressor and sympathetic nerve responses to taurine.

The effects of taurine on central cardiovascular regulation were investigated by intracerebroventricular (ICV) injection of taurine in urethane-anesthetized rats. Blood pressure fell gradually to attain the maximum level at 10 to 15 min after the injection of 50 micrograms taurine and returned to the basal level 20 min later. After injecting 200 micrograms of taurine, blood pressure began to fall within 30 seconds and attained the maximum level at 2 to 5 min and did not return to the basal level by 20 min. Both heart rate and abdominal sympathetic nerve activity decreased as the blood pressure fell, However, the similar amount of taurine injected intravenously did not affect the blood pressure, the heart rate or the abdominal sympathetic nerve activity. These results suggest that taurine causes the central nervous system to lower the blood pressure by decreasing the sympathetic nerve outflow.

Animals↗
PubMed1985

Studies on collagen in the experimental myocardial infarction.

The healing process of myocardial infarction was studied with special reference to the production of collagen by the determinations of prolylhydroxylase (PHase) activity and contents of hydroxyproline (Hyp) of the collagen subfractions, i.e., neutral salt soluble (NSC), acid soluble (ASC) and insoluble collagens (ISC) in comparison with histologic observation of the proliferation of connective tissue in the canine heart. The contents of Hyp in NSC and ASC increased in the infarcted tissue 5 days after coronary ligation prior to its increase in ISC. The content of Hyp in NSC, which is a precursor of ASC and ISC, reached the maximal value at 7 days and that reached the maximal value in ASC 7 to 14 days after coronary ligation. ISC increased markedly after 14 days. PHase activity increased on the second day and attained to the highest at 5 to 7 days. Proliferation of fibroblasts paralleled with the increases in PHase activity and NSC, and an increase in collagen fiber did with the contents of ISC. From these results it is concluded that in the healing stage of myocardial infarction, PHase was activated earlier than the increase in immature collagen in the infarcted area which was observed 5 to 7 days after coronary ligation and was followed by the production of mature collagen after 14 days.

Animals↗