[A gold-silver-palladium Konus telescopic crown in a mandibular left quadrant 1st and 2nd molar defect].
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Biomedical subjects
Publications and source records attributed to H Asada.
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The organic acids in renal tissue biopsy (0.5-1 mg) obtained from chronic glomerulonephritis patients were analyzed capillary column gas chromatography--mass spectrometry. Some twenty compounds were identified in the renal tissue. The organic acid profile of renal tissue showed a marked difference from those of urine and serum. In particular, 4-hydroxybutyric acid and 4-hydroxy-2-butenoic acid, which are usually undetectable in urine and serum, were detected for the first time in renal tissue in considerably large amounts.
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1. In the guniea-pig mesenteric artery, E614 (less than 10(-6) g/ml) did not modify the membrane potential and resistance, but did suppress the spike evoked by outward current pulses in the presence of 3-5 mM TEA. This agent also suppressed the K-induced and noradrenaline-induced contractions. 2. In the mesenteric artery, E614 suppressed the amplitude of e.j.ps evoked by perivascular nerve stimulation. However, the facilitation process produced by repetitive stimulation was less affected. Miniature e.j.ps generated in the presence of 3 mM TEA were also suppressed by E614. 3. In the porcine coronary artery, E614 had little effect on the spike evoked by outward current pulses, in the presence of TEA. The mechanical response evoked by acetylcholine, excess [K]0 or electrical depolarization was hardly affected. 4. When the action of E614 was compared with that of diltiazem, a Ca channel blocker, this agent possesses properties which produce vasodilation of the peripheral vascular bed and thus may be considered as a hypotensive agent.
An antibody specific for puromycin (PU) was prepared by immunization of rabbits with a PU conjugate of bovine serum albumin, which was newly synthesized by coupling PU to mercaptosuccinylated bovine serum albumin via a cross-linker, N-(gamma-maleimidobutyryloxy)succinimide. Enzyme labeling of PU was performed using beta-D-galactosidase [EC 3.2.1.23] via N-(m-maleimidobenzoyloxy) succinimide. An ultrasensitive and specific enzyme immunoassay for PU was developed utilizing these reagents by a double antibody technique. The standard curve of the assay was linear in the range of 2 pg to 100 pg, and the lower limit of detection was 28.2 pm (2 pg/tube); so the enzyme immunoassay was found to be approximately 326,000 times more sensitive than a microbiological assay. Further, the enzyme immunoassay is free from interference by any purine or pyrimidine analogs, or by other drugs commonly used for the inhibition of protein synthesis. Using this assay, drug levels were easily determined in rat tissue following PU administration. Since PU is extensively available as an inhibitor of protein synthesis, the enzyme immunoassay should provide useful tool for developing biochemical and toxicity studies of PU.
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The effects of 3,4-dihydro-8-(2-hydroxy-3-isopropylaminopropoxy)-3-nitroxy-2H-1-benzopyran (K-351) on vascular smooth muscle cells and neuromuscular transmission were investigated by the microelectrode and mechanographic methods using intact and skinned smooth muscles from guinea pigs. K-351 markedly inhibited the norepinephrine-induced contraction and slightly reduced the K-induced contraction in the mesenteric artery, but did not affect the acetylcholine-induced contraction in the coronary artery. K-351 inhibited the contraction evoked by perivascular nerve stimulation to a greater extent than that evoked by exogenously applied norepinephrine in the pulmonary artery. However, these sequences were reversed in the mesenteric artery. In the mesenteric artery, K-351 (6 x 10(-7) M) suppressed and phentolamine (10(-6) M) enhanced the contraction evoked by perivascular nerve stimulation, at frequencies over 1.0 Hz. In the mesenteric artery, K-351 did not affect the spike evoked by an outward current pulse or the spike on the excitatory junction potential; in the portal vein, it did increase spontaneously generated spikes due to depolarization of the membrane. In the skinned mesenteric artery, K-351 did not modify the amplitude of Ca-induced contraction. The excitatory junction potential evoked by perivascular nerve stimulation (0.1-1.0 Hz) was markedly inhibited by K-351 with no effect on the facilitation process, whereas phentolamine enhanced both excitatory junction potentials and the facilitation process. These findings indicate that K-351 inhibited mainly intra- and extrajunctional alpha adrenoceptors and, as the former was not affected by phentolamine or prazosin, the action of this new agent differs from the actions of heretofore available alpha-1 and alpha-2 adrenoceptor antagonists.
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An analytical method for separation and identification of compounds in uremic ultrafiltrate has been developed using a glass capillary column gas chromatography-mass spectrometry-computer system. The ultrafiltrate samples of blood were obtained during hemodialysis treatment of chronic uremic patients and non-uremic patients using the extracorporeal ultrafiltration method. Sample preparation consisted of acidification, extraction, evaporation, and trimethylsilylation. Many compounds were newly identified in the uremic ultrafiltrate by electron impact ionization, chemical ionization, and high resolution mass spectrometry. Six toxic polyphenols, namely, catechol, resorcinol, hydroquinone, 2-methoxyresorcinol, 3-methoxycatechol, and methoxyhydroquinone were first detected in the uremic ultrafiltrate.
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Although activated charcoal and alumina have been used extensively as sorbents in uremic patients, the following problems remain to be solved: 1) elution of SO4--from activated charcoal which does not adsorb it; 2) production of methylguanidine from creatinine on the surface of activated charcoal; 3) production of lipoperoxide from fatty acids by chemical reaction of activated charcoal; 4) adsorption of Ca++ and Mg++ when alumina adsorbs inorganic phosphate. These problems are studied in vitro and clinically.
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Chlorophyllin a was conjugated with alpha-(3-aminopropyl)-omega-methoxypoly(oxyethylene), PEG-NH(2), to form the PEG-chlorophyllin conjugate through acid-amide bonds. The PEG-chlorophyllin conjugate was stable toward light illumination under anaerobic condition in comparison with chlorophyllin a. The conjugate catalyzed the reduction of methyl viologen in the presence of 2-mercaptoethanol and the evolution of hydrogen gas in the presence of methyl viologen (an electron carrier), 2-mercaptoethanol (an electron donor) and hydrogenase (Scheme 1). Furthermore, the PEG-chlorophyllin conjugate catalyzed the photoreduction of NADP(+) or NAD(+) in the presence of ascorbate as an electron donor and ferredoxin-NADP(+) reductase as the coupling enzyme. Utilizing the reducing power of NADPH generated by the PEG-chlorophyllin conjugate under the illumination, CO(2) fixation was accomplished by the synthesis of malate (C(4)) from pyruvate (C(3)) and CO(2) in the presence of malic enzyme (Scheme 2). These reactions mentioned above did never proceed in dark or without each enzyme.
Acute and persistent viral infection of the inner ear of rats was induced with hemorrhagic fever with renal syndrome (HFRS) virus following intraperitoneal inoculation. Newborn (within 24 h after birth) rats were inoculated intraperitoneally (i.p.) with HFRS virus (B-1 strain), and the cochlea was examined using an immunohistochemical technique for the localization of viral antigens 1 week (acute infection) and 1 year (persistent infection) after infection. Virus-specific antigens were detected in the inner ear structures of the rats suffering from both acute and persistent infection. Morphological changes in the inner ear structures of these rats were observed, with hemorrhage and infiltration of lymphocytes and macrophages. Moreover virus could be isolated from the blood of all infected rats. In the present study, we have proved that HFRS virus can infect the inner ear via the viremia.