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Biomedical subjects

M Naka

Publications and source records attributed to M Naka.

At least 91 records · Page 5Linked to original sources
PubMed1989

[Assessment of reproducibility of transcranial Doppler velocimetry].

In recent years, transcranial Doppler velocimetry has been widely used as a noninvasive method for measurement of blood flow velocity in basal cerebral arteries. As for the reproducibility of this method, however, there have been only few reports so far. In the present study, we attempted to evaluate the reproducibility of this method by changing the examiners and the timing of the examination. Fifteen healthy volunteers were investigated by using a pulsed wave Doppler ultrasound device with a 2 MHz transducer. Both peak and mean spatial frequencies calculated from the frequency spectrum of the Doppler signals from the middle cerebral artery (MCA) and the basilar artery (BA) were used as blood flow parameters for assessing the reproducibility. The arterial blood pressure and the end-tidal carbon dioxide partial pressure (PECO2) were also monitored during the ultrasonic examinations. The intra- and inter-observer reproducibilities were evaluated by obtaining the coefficient of variation (CV) of the differences and/or analyzing the correlation between the values from the two measurements by the same examiner and by two separate examiners, respectively. The intraobserver reproducibility in separate days was also evaluated. Both in the mean arterial blood pressure and in PECO2, no significant changes were observed between the two measurements in each subjects. In the present examination, the CV and r values ranged from 6.7 to 19.5% and from 0.69 to 0.95, respectively, showing good reproducibility of the transcranial Doppler method for measurement of blood flow velocity, though some differences were observed as follows. The intraobserver reproducibility was better than the interobserver reproducibility.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Long-term survival of a patient with pseudoaneurysm of the left ventricle following myocardial infarction].

A 76-year-old man had an extensively calcified left ventricular pseudoaneurysm which was a sequela of acute myocardial infarction suffered 22 years ago. He experienced acute anterolateral myocardial infarction in January 1964. In March 1964, the presence of a left ventricular aneurysm was suspected by chest radiography and fluoroscopy. He was, however, in good health since then. In April 1986, when he was admitted for treatment of acute bronchitis, a large calcified density was found in the left ventricular region on chest radiography. The electrocardiogram was compatible with an old anterolateral myocardial infarction. Two-dimensional echocardiography showed an immobile portion of the left ventricle which contained "moya-moya" (sluggish, smoky) echoes. A saccular aneurysm of the left ventricle was confirmed by radioisotope cardiac pool scans, reconstruction CT and left ventriculography. Due to the poor general condition of the patient, we followed his course without surgery. He died in October 1986. At autopsy, the pseudoaneurysm was markedly calcified, and its wall was adherent to the parietal pericardium. Histologically, the pseudoaneurysmal structure turned out to be a pseudoaneurysm since the saccular wall contained only scar tissue but no myocardial cells. This is a very rare case of a patient with a left ventricular pseudoaneurysm who survived for 22 years after its occurrence.

Aged↗
PubMed1988

Correlation of conformation and phosphorylation and dephosphorylation of smooth muscle myosin.

The rate of phosphorylation and dephosphorylation of smooth muscle myosin by myosin light chain kinase and by two myosin light chain phosphatases (gizzard phosphatase IV and aorta phosphatase) are measured in various conditions; the relationship between the rate of phosphorylation and dephosphorylation of myosin and the myosin conformation is also studied. The rate of dephosphorylation of myosin was completely inhibited in the presence of 1 mM MgCl2 and ATP at low ionic strength where phosphorylated myosin forms a folded conformation. The inhibition was released when myosin formed either an extended monomer or filaments. The rate of phosphorylation of myosin was also affected by the conformation of myosin. The rate for a folded myosin was slower than those for an extended monomer and filamentous myosin. The phosphorylation and dephosphorylation of heavy meromyosin, subfragment-1, and the isolated 20,000-dalton light chain are not inhibited at low ionic strength, and the rate of phosphorylation and dephosphorylation was decreased with increasing ionic strength. KCl dependence of the rate of phosphorylation and dephosphorylation of myosin was normalized by using KCl dependence of subfragment-1, and it was found that the marked inhibition of the rate of phosphorylation and dephosphorylation of myosin is closely related to the change from an extended to a folded conformation of myosin.

Animals↗
PubMed1988

Inhibition of human platelet secretion and of Ca2+, calmodulin-dependent protein phosphorylation by the antiallergic agent GMCHA.

Calcium ion-dependent interaction with purified calmodulin (CaM), of a potent inhibitor of histamine release from mast cells, trans-4-guanidinomethylcyclohexanecarboxylic acid p-tertbutylphenylester (GMCHA), was investigated using 5-(dimethylamino)-1-naphthalenesulfonyl-calmodulin (dansyl-CaM). GMCHA undergoes a fluorescence increase with the Ca2+-dansyl-CaM complex but there is no significant change in the dansyl-CaM fluorescence with GMCHA, up to a 10 microM in the absence of calcium ion. This suggests that binding of GMCHA to CaM is Ca2+-dependent on the apparent Kd is approximately 1 microM. GMCHA suppressed the fluorescence of the hydrophobic probe 8-anilino-1-naphthalenesulfonate (ANS), in the presence of the Ca2+-CaM complex, with an IC50 value of 3 microM. [3H]N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) bound to the purified CaM was displaced, in a concentration dependent manner by GMCHA, the Ki value of GMCHA against the binding of W-7 to CaM was 2.3 microM, and there was a selective inhibition of the Ca2+-CaM induced activation of enzymes such as myosin light chain kinase. Increasing the CaM concentration in the presence of Ca2+ overcame the GMCHA-induced inhibition of myosin light chain kinase activation, with a Ki value of 2.7 microM. GMCHA at these concentrations is effective in inhibiting the release of histamine from mast cells. Moreover, this compound suppresses platelet secretion and relaxes vascular strips, at concentrations similar to those seen with the CaM interacting action and characteristic of CaM antagonists such as W-7. GMCHA also inhibits the Ca2+, CaM-dependent myosin light chain phosphorylation of human platelets. These results suggest that GMCHA, a potent inhibitor of histamine release from mast cells, suppresses platelet secretion, relaxes vascular smooth muscle and inhibits Ca2+, CaM-dependent protein phosphorylation, all at similar concentrations.

Adenosine Triphosphate↗
PubMed1988

Two phosphorylated forms of myosin in thrombin-stimulated platelets.

Three forms of 20-kDa myosin light chain (MLC), unphosphorylated, monophosphorylated, and diphosphorylated MLC (designated 20K, 20K-P, and 20K-PP) were demonstrated in thrombin-stimulated human platelets by two different gel electrophoretic methods: in the presence of glycerol urea or in two dimensions (isoelectric and sodium dodecyl sulfate). The diphosphorylation of platelet 20-kDa MLC increased, dose dependently, up to 0.4 U/ml thrombin and reached 25% of platelet 20-kDa MLC. After mono- or diphosphorylated 20-kDa MLC from thrombin-stimulated platelets was digested with trypsin, the analysis using two-dimensional peptide mapping demonstrated that two different sites were phosphorylated by MLC kinase and protein kinase C, as noted in the case of 12-O-tetradecanoylphorbol-13-acetate-stimulated platelets (M. Naka, et al. (1983) Nature (London) 306, 490-492). The more rapid monophosphorylation was catalyzed preferentially by MLC kinase while the slower and additional phosphorylation was catalyzed mainly by protein kinase C. These results suggest the importance of distinguishing multiple site phosphorylation of 20-kDa MLC in thrombin-activated human platelets.

Binding Sites↗
PubMed1988

Denaturation of bacteriorhodopsin by organic solvents.

The denaturation of bacteriorhodopsin by various organic solvents was studied using absorption, circular dichroism (CD) and fluorescence measurements. Organic solvents with a hydrogen-bonding group caused the release of retinal. The CD measurements showed that the helical structure was maintained even in the denatured state, whereas its tertiary structure was destroyed. The change in fluorescence intensity of tryptophan and fluorescent retinal also confirmed that the tertiary structure was destroyed. Comparison of the denaturation efficiency of various organic solvents showed that the concentration at denaturation was inversely proportional to the partition coefficient of the denaturant. This inverse proportionality clearly indicated that denaturation was determined by the concentration of denaturants which partitioned into the hydrophobic region of the membrane. It was discussed from the experimental results that the tertiary structure of bacteriorhodopsin was stabilized by the hydrogen-bonding networks between side chains of the helices. The results obtained from analysis of the amino acid sequence were also consistent with the hydrogen-bonding mechanism for the formation of the tertiary structure.

Journal Article↗
PubMed1988

Serial myocardial lactate metabolic changes after intracoronary thrombolysis in evolving myocardial infarction.

To investigate whether early reperfusion (less than or equal to 3 hours) preserves aerobic myocardial metabolism in acute myocardial infarction, we examined serial changes in trans-cardiac lactate extraction after thrombolysis in 43 patients with acute antero-septal myocardial infarction. In the chronic phase, we also determined abnormally contracting segments as an index of infarct size and regional ejection fraction as an index of chronic regional cardiac function. In the early reperfusion group (less than or equal to 3 hours), positive lactate extraction was restored and there were small abnormally contracting segments and a high regional ejection fraction. The intermediate reperfusion group (3-5 hours), however, had sustained anaerobic lactate extraction, large abnormally contracting segments and a low regional ejection fraction. The late reperfusion (greater than 5 hours) group showed apparently aerobic lactate extraction, but had large abnormally contracting segments and a low regional ejection fraction. Thus, early reperfusion preserves aerobic lactate metabolism and good chronic ventricular function.

Adult↗
PubMed1987

Selective inhibition of catalytic activity of smooth muscle myosin light chain kinase.

Systematically synthesized derivatives of ML-9, 1-(5-chloronaphthalenesulfonyl)-1H-hexahydro-1,4-diazepine, were found to inhibit both Ca2+-calmodulin-dependent and -independent smooth muscle myosin light chain kinases with a similar concentration dependence, and their inhibitions were of the competitive type with respect to ATP. Moreover, ML-9 as well as ATP or ADP exhibited an effective protection to inactivation of smooth muscle myosin light chain kinase by the nucleotide affinity label 5'-p-fluorosulfonylbenzoyladenosine, suggesting that ML-9 binds at or near the ATP-binding site on the kinase molecule. These derivatives, which were structurally unrelated to ATP and exhibited more hydrophobic properties detected by reverse-phase high-performance liquid chromatography, exhibited more potent inhibition toward smooth muscle myosin light chain kinase, indicating that the hydrophobic properties of these derivatives positively correlated well with their potencies of inhibiting the catalytic activity for the enzyme. These findings suggest that the ATP-binding site at the active center of smooth muscle myosin light chain kinase is located in a hydrophobic environment. The potent vaso-relaxing effect of ML-9 on rabbit vascular strips and on saponin-treated skinned smooth muscle cells was discussed in relation to the in vivo inhibition by this drug of smooth muscle myosin light chain kinase.

Adenosine↗
PubMed1986

The modulatory role of myosin light chain phosphorylation in human platelet activation.

Myosin 20 K-Da light chain phosphorylation in human platelets was found to be catalyzed by MLCK in the early phase during collagen activation. The effect of newly synthesized selective inhibitor of MLCK, ML-9, on collagen induced platelet activation was investigated. ML-9 delayed the time course of the myosin 20 K-Da light chain phosphorylation, sequentially led to a delay in aggregation, secretion and phosphorylation of the 40K-Da peptide, in a dose-dependent fashion. It is proposed that the MLCK catalyzed phosphorylation of myosin 20 K-Da light chain may be an initial response and if so may influence the sequent reactions in the activation of platelets with collagen.

Blood Platelets↗
PubMed1986

Oral OPC-8212 for the treatment of congestive heart failure: hemodynamic improvement and increased exercise capacity.

The chronic effects of the oral administration of OPC-8212 (3,4-dihydro-6-[4-(3,4-dimethoxybenzoyl)-1-piperazinyl]-2(1H)-quinolinon e) on resting hemodynamics and exercise capacity were assessed in 15 patients with congestive heart failure (NYHA II-IV). Doses of 30 or 60 mg per day were given per os over 3.0 weeks on average (range 2-6 weeks). Multigated radionuclide ventriculography and multistage exercise testing were performed before and during OPC-8212 therapy to assess the changes in left ventricular volume and exercise capacity respectively. Systolic blood pressure showed a slight increase (from 123 +/- 3 to 129 +/- 4 mmHg) during OPC-8212 therapy, while heart rate was unchanged (69 +/- 3 vs 67 +/- 3 beats/min). The left ventricular end-diastolic volume index decreased from 127 +/- 9 to 107 +/- 7 ml/m2, and ejection fraction and the P/V index (the ratio of peak systolic pressure to left ventricular end-systolic volume index) increased during OPC-8212 therapy (from 27% +/- 3% to 30% +/- 4% and from 1.5 +/- 0.2 to 2.0 +/- 0.3 mmHg/ml/m2 respectively). NYHA functional class was improved in 9 of 15 patients, and the average peak work load achieved during exercise testing increased from 27 +/- 6 to 47 +/- 7 W. No significant adverse effect was observed in any patient. These results indicate that OPC-8212 enhances the inotropic state and, hence, reduces heart size with no change in heart rate. Moreover, it increases exercise capacity. Thus, OPC-8212 is an inotropic agent with promise for application in the long-term treatment of congestive heart failure.

Administration, Oral↗
PubMed1986

[Collateral circulation during exercise-induced angina: evaluation by coronary angiography].

The pathophysiological significance of coronary collateral vessels remains controversial, despite previous intensive studies. We performed the multistage supine ergometer stress test for 26 patients with effort angina and collaterals. The changes in the collaterals were observed during each anginal attack by coronary angiography before and after intravenous nitroglycerin. The collaterals of 21 patients disappeared or diminished during exercise-induced angina before nitroglycerin administration, and were unchanged in the remaining five cases. However, the collaterals of all patients after nitroglycerin administration were unchanged or increased during exercise-induced angina. Considering there were no significant changes in pulmonary arterial end-diastolic pressures during angina before and after nitroglycerin administration, a pressure gradient between the donor and recipient coronary arteries was suggested as being related to the patency of the collaterals. These results suggested the following: 1. It is not appropriate to postulate that the collaterals visualized at rest may remain unchanged during exercise-induced angina. 2. It is not reasonable to conclude that exercise accelerates the development of collateral circulation. 3. One favorable effect of nitroglycerin administration is the prevention of exercise-induced ischemia via collateral circulation.

Adult↗