[Diagnosis of myocardial infarction by percutaneous coronary angioscopy].
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Biomedical subjects
Publications and source records attributed to Y Uchida.
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To investigate possible developmental changes in the physiological effect of atrial natriuretic peptide (ANP) after birth, we studied the effect of ANP on the slice cGMP content and the particulate guanylate cyclase activity of aorta, kidney and lung in neonate, 2-week-old and adult rats of both sexes. Incubation with human ANP(99-126) (hANP) increased significantly the slice cGMP content of aorta, kidney and lung in three ages of rats. The hANP-stimulated fraction of cGMP contents of kidney decreased, that of lung increased with development, whereas that of aorta showed no significant change. Consistently, the hANP-responsive particulate guanylate cyclase activity decreased in kidney, increased in lung during development, without significant developmental change in aorta. These results indicate a differential change in the effect of hANP on the slice cGMP content among tissues during development. The developmental change in the effect of hANP on slice cGMP content is probably caused by the ontogenetic change in activation of ANP receptor-linked guanylate cyclase.
Intratracheally injected or aerosolized ET-1 induced quick and long-lasting bronchoconstriction of anesthetized mongrel dogs, thus increasing respiratory resistance(Rrs) with concomitantly decreasing dynamic compliance(Cdyn). As collateral resistance(Rcs) was measured postexposure to aerosolized ET-1 using wedged bronchoscope technique, ET-1 increased Rcs in a dose and time dependent manner. The increase attained maximal in 2 min and then, gradually declined. When the dogs were pretreated with the intravenous injection of 0.1 micrograms/kg ICI 198615, an inhibitor of lipoxygenase, the constrictive response was slowed down. Essentially similar results were also observed with the intravenous injection of 5 mg/kg indomethacin. Our observations suggest that the early phase of the ET-1 induced bronchoconstriction is mediated by eicosanoid metabolites.
Atomic steps on (111) and (100) crystal surfaces of Pt were observed using a commercial scanning electron microscope (SEM) in secondary electron mode. By comparing the SEM images and those by reflection electron microscopy (REM), the observed contrast was confirmed to be that from atomic steps on crystal surfaces. The contrast mechanism is briefly discussed. One application of this imaging technique is also shown.
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Freeze-thawed rat liver mitochondria were extensively washed with potassium phosphate, pH 7.5, and the residue was extracted with 10 mM potassium phosphate, pH 7.5, 1% (w/v) sodium cholate, 0.5 M KCl. The four beta-oxidation enzyme activities of the washes and the last extract were assayed with substrates of various carbon chain lengths. Our data suggest that the last extract contains a novel acyl-CoA dehydrogenase and long-chain 3-hydroxyacyl-CoA dehydrogenase. A novel acyl-CoA dehydrogenase was purified. The molecular masses of the native enzyme and the subunit were estimated to be 150 and 71 kDa, respectively. One mole of enzyme contained 2 mole of FAD. These properties and immunochemical properties of the enzyme differed from those of three other acyl-CoA dehydrogenases: short-, medium-, and long-chain acyl-CoA dehydrogenases. Carbon chain length specificity of the enzyme differed from that of other acyl-CoA dehydrogenases. The enzyme was active toward CoA esters of long- and very-long-chain fatty acids, but not toward those of medium- and short-chain fatty acids. The specific enzyme activity was greater than 10 times that of long-chain acyl-CoA dehydrogenase when palmitoyl-CoA was used as substrate. We propose the name "very-long-chain acyl-CoA dehydrogenase" for this enzyme.
Long-chain 3-hydroxyacyl-CoA dehydrogenase was extracted from the washed membrane fraction of frozen rat liver mitochondria with buffer containing detergent and then was purified. This enzyme is an oligomer with a molecular mass of 460 kDa and consisted of 4 mol of large polypeptide (79 kDa) and 4 mol of small polypeptides (51 and 49 kDa). The purified enzyme preparation was concluded to be free from the following enzymes based on marked differences in behavior of the enzyme during purification, molecular masses of the native enzyme and subunits, and immunochemical properties: enoyl-CoA hydratase, short-chain 3-hydroxyacyl-CoA dehydrogenase, peroxisomal enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase bifunctional protein, and mitochondrial and peroxisomal 3-ketoacyl-CoA thiolases. The purified enzyme exhibited activities toward enoyl-CoA hydratase and 3-ketoacyl-CoA thiolase together with the long-chain 3-hydroxyacyl-CoA dehydrogenase activity. The carbon chain length specificities of these three activities of this enzyme differed from those of the other enzymes. Therefore, it is concluded that this enzyme is not long-chain 3-hydroxyacyl-CoA dehydrogenase; rather, it is enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase/3-ketoacyl-CoA thiolase trifunctional protein.
In previous studies, we discovered a growth inhibitory factor (GIF) that was abundant in normal human brain, but greatly reduced in Alzheimer's disease (AD) brain. Molecular cloning of a full-length cDNA for human GIF revealed that the GIF had striking homology to metallothioneins. Furthermore, it was determined that the GIF gene was on chromosome 16, as are the metallothionein genes. GIF, in contrast to metallothioneins, was found to be expressed exclusively in the nervous system. The GIF protein produced by Escherichia coli harboring the GIF cDNA in a prokaryotic expression vector inhibited the growth of neonatal rat cortical neurons. These results indicate that GIF is a new member of the metallothionein family with distinct tissue-specific expression and functions. Northern blot analysis revealed that expression of the GIF mRNA is drastically decreased in AD brains. The result raises the possibility that down-regulation of the GIF gene in AD brain plays an important role in the pathogenesis of AD.
In rat carrageenin-induced pleurisy, bradykinin (BK) was hardly able to be detected (< 160 pg per rat) in the exudates. In contrast, des-Phe8-Arg9-BK (des-8,9-BK) level, determined by an enzyme immunoassay (EIA) newly developed, was larger in the exudate and the levels were kept throughout the entire course of this inflammation. Arg-Pro-Pro-Gly-Phe ([1-5] BK) level, measured by an EIA newly developed, was much higher than that of des-8,9-BK in the exudate. Intrapleural administration of soy bean trypsin inhibitor (0.3 mg per rat) reduced the levels of both des-8,9-BK and [1-5] BK in the exudates. Reduction in the residual levels of plasma prekallikrein (P-Kall) and high-molecular-weight-kininogen (HMW-K), not low-molecular-weight-kininogen (LMW-K), were accompanied with increase in these BK degradation products, indicating that plasma prekallikrein was activated in the pleural cavity. On the other hand, intravenous injection of acetaldehyde to rats pretreated with disulfiram resulted in the significant increase in the levels of [1-5] BK in the blood, which was accompanied with reduction in the residual levels of LMW-K, not of HMW-K and P-Kall in plasma. These results indicated that the detection of BK degradation products was a good marker for the kinin release in vivo and that the concomitant reduction of the precursor proteins allowed us to identify the type of kallikrein-kinin systems relevant to the kinin release.
The kinetics of somatostatin-producing cells (D-cells) in the rat antral mucosa after truncal vagotomy were studied using double immunostaining for bromodeoxyuridine (BrdU) and somatostatin. Both the concentration of somatostatin and D-cell density in the antral mucosa demonstrated a significant increase on the 3rd day after truncal vagotomy. With the single labeling of BrdU, a few D-cells showed positive immunostaining for BrdU throughout the experimental period in both vagotomized and sham operated rats. With cumulative labeling, the BrdU labeled cells demonstrated a linear increase in an identical number for each experimental time-point in both groups. The labeling index of BrdU in the D-cells increased significantly, beginning on the 3rd day and attaining a maximum level of 41.8% on the 10th day, in the vagotomized group after cumulative labeling. In this group, however, the density of D-cells with no immunoreactive BrdU also increased quickly on the 3rd day with cumulative labeling. The present study indicates that the most important factor involving D-cell hyperplasia observed after truncal vagotomy is the activation of pre-existing D-cells to synthesize and release hormones, together with the rapid replication of progenitor cells and their maturation to D-cells.
One hundred and forty-three workers exposed to one or more of toluene, xylene, ethylbenzene, styrene, n-hexane, and methanol at sub-occupational exposure limits were examined for the time-weighted average intensity of exposure by diffusive sampling, and for biological exposure indicators by means of analysis of shift-end blood for the solvent and analysis of shift-end urine for the corresponding metabolite(s). Urinalysis was also performed in 20 nonexposed control men to establish the "background level." Both solvent concentrations in blood and metabolite concentrations in urine correlated significantly with solvent concentrations in air. Comparison of blood analysis and urinalysis as regards sensitivity in identifying low solvent exposure showed that blood analysis is generally superior to urinalysis. It was also noted that estimation of exposure intensity on an individual basis is scarcely possible even with blood analysis. Solvent concentration in whole blood was the same as that in serum in the case of the aromatics, except for styrene. It was higher in blood than in serum in the case of n-hexane, and lower in the cases of styrene and methanol.
Exposure of 34 male workers to combined toluene, styrene and methanol was monitored by personal diffusive sampling of solvent vapours in breathing zone air, analysis of shift-end blood for the 3 solvents and analysis of shift-end urine for hippuric, mandelic and phenylglyoxylic acids and methanol. The exposure of most of the workers was below current occupational exposure limits. Regression analysis showed that a linear correlation exists for each of the 3 solvents between any pairs of the concentrations in air, blood and urine. Namely, toluene, styrene and methanol concentrations in blood obtained at the end of a shift are linearly related to the time-weighted average intensity of exposure to corresponding solvents, and also hippuric, mandelic and phenylglyoxylic acids as well as methanol in shift-end urine. The concentrations of hippuric, mandelic and phenylglyoxylic acids as well as methanol in urine correlated with the respiratory exposure intensity. Comparison of the present results with the exposure--excretion relationship after occupational exposure to the individual solvent showed that no modification in metabolism is induced by the combined exposure when exposure is low, as in the present case.
Angioscopy has been shown to provide more detailed information on lesion morphology before and after interventional procedures than angiography. Therefore to evaluate the effects of laser angioplasty, angioscopy was performed in five patients with peripheral or coronary vascular disease who underwent excimer laser angioplasty. The excimer laser was operated at 308 nm, 135 nsec, 25 Hz, and 40 to 60 mjoules/mm2 and was coupled into multifiber wire-guided catheters of 1.4 to 2.0 mm diameter for coronary lesions and into catheters of 2.2 mm diameter for peripheral lesions. There were three coronary (one left anterior descending, one circumflex, one right coronary artery) and two peripheral (one common iliac artery, one superficial femoral artery) lesions. Angioscopy was successfully performed before and after laser ablation without any complications in all five lesions. The characteristics of angioscopic findings after excimer laser angioplasty consisted of flaps, fractures of plaques, and abundant tissue remnants. There was no apparent thermal injury. Recanalized channels were small and irregular. These results indicate that (1) angioscopy is effective and safe for evaluation of lesion morphology after laser angioplasty; (2) laser ablation does not result in thermal injury; and (3) irregular channels after recanalization and abundant tissue remnants may explain the suboptimal results after laser angioplasty.
Matrix vesicles (MV) isolated from mineralizing tissues contain high alkaline phosphatase (ALPase) activities associated with the membrane; this may be because MV originate from the plasma membrane of chondrocytes. Previous studies in our laboratory demonstrated that lactate dehydrogenase (LDH) isoenzymes, which appeared to be derived from chondrocytes cytosol, were located in MV of the epiphyseal growth plate of young-rabbit leg bones [1]. In the epiphyseal cartilage, alkaline phosphatase (ALPase) is enriched in the growth zone, whereas it is rarely detected in the resting zone, suggesting that MV containing ALPase are not present in the resting zone. In recent study, we divided the epiphyseal cartilages of young-rat rib bones into the growth zone and the resting zone, followed by the isolation of MV after collagenase digestion. MV containing ALPase and LDH were found in the growth zone, and surprisingly, vesicles containing LDH without ALPase were found in the resting zone [2]. The function of LDH-containing vesicles without ALPase is unknown at the present. However, these findings might accelerate the studies on cell-mediated calcification, because (1) LDH could be a marker enzyme of these vesicles, (2) LDH is found to be a specific cytosolic enzyme which is enfolded in these vesicles, suggesting that an unknown mechanism for the specific uptake of the cytosolic enzyme might be present.
We propose new criteria for the electrodiagnosis of Martin-Gruber connection. Forty-seven patients with cubital tunnel syndrome were studied, and 8 (17%) were found to have a Martin-Gruber connection. Eighty-seven patients without cubital tunnel syndrome were also studied, and 14 (16%) had a Martin-Gruber connection. The rate of occurrence of the anastomosis in these two groups was approximately the same. No sensory communication was demonstrated, and the lateral intrinsic muscles received more innervation from the communicating branch than the hypothenar muscles. The entry point of the crossing fiber from the median nerve to the ulnar nerve was 3 to 10 cm distal to the medial humeral epicondyle, and there may be a significant risk of injury in ulnar nerve transposition.
This study was performed to examine the effect of naloxone on drinking behavior in a schizophrenic inpatient with psychosis, intermittent hyponatremia, and polydipsia (PIP syndrome). His body weight was checked five times daily, and the maximum and minimum weight gains during a day were chosen as an index of polydipsia. Both daily (0.6 mg) and repeated (0.6 mg for 6 days) injections of naloxone suppressed his weight gain significantly for 2 weeks. Withdrawal of the drug for 4 weeks resulted in weight gain recovering to control level. Thereafter, a second trial was performed to examine the long-term effect of this treatment. A daily naloxone (0.6 mg) injection series was performed once every 2 weeks for six series (12 weeks). This drug regimen also suppressed his weight gain in a continuous fashion. The study showed that naloxone seems to be a potential treatment for PIP syndrome and that endogenous opioid systems play a part in the compulsive drinking behavior of the PIP syndrome.
One acute and one tardive akathisia patients, respectively, and 10 neuroleptic-treated schizophrenic patients were injected with biperiden 5 mg or saline and the response to anticholinergics was monitored by microvibration (MV) as an indicator of muscle tonus. These data were subjected to the Fast Fourier Transform and an averaged power spectrum was computed. The biperiden injection markedly reduced the power spectral values of MV in acute akathisia. In contrast with acute akathisia, the biperiden injection significantly increased the power spectral values of MV in tardive akathisia. The subjective feelings of akathisia patients were parallel to the power spectral values of MV. Control patients were not affected by such treatment. The present findings show that the subjective symptoms of akathisia can be well defined by the objective, differential response to anticholinergics in a manner similar to the visible extrapyramidal symptoms (dystonia, dyskinesia) induced by neuroleptics.
The feasibility of an Nd:YAG laser system with automatic control of hot-tip probe temperature was examined in 15 segments (14.7 +/- 6 cm in length) of iliofemoral arteries from 13 patients. The hot-tip temperature to be attained and the upper limit temperature at which lasing was to be stopped were preset. A catheter with a 1.8-mm hot-tip probe was introduced into the obstructed segment and angioplasty (lasing time 5-10 sec) was performed under angioscopic guidance. Recanalization was observed in all segments without obvious complications. No thermal effects below 50 degrees C, coagulation at 100 degrees C, carbonization at 200 degrees C, or sticking of the hot-tip to the luminal surface at 300 degrees C or over, were observed by angioscopy. Rapid recanalization was obtained between 200 degrees C and 300 degrees C. The results indicate that this novel laser system is feasible and hot-tip temperature between 200 degrees C and 300 degrees C is ideal for treatment of chronic arterial obstruction in Japanese patients.