[Surgical treatment of perivalvular leakage following mitral valve replacement with left atrial wall dissection--left thoracotomy approach].
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Biomedical subjects
Publications and source records attributed to T Shida.
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Observations of Raman spectra of various nucleic acids indicate that the guanine ring breathing frequency is sensitive to the internal rotation angle around the glycosidic bond and to the conformation of the five-membered ring of the ribose residue that is directly connected with the guanine residue in question. It is found that 682 cm-1 for C2'-endo-anti, at 665 cm-1 for C3'-endo-anti, and at 625 cm-1 for C3'-endo-syn. A DNA octamer d(GpGpApApTpTpCpC) shows, in its aqueous solution, a broad Raman band at 680 cm-1 with a tail at 670 cm-1. This fact suggests that the guanosine residues in this oligomer take primarily C2'-endo-anti conformation but an appreciable amount of fluctuation of the ribose ring structure towards C3'-endo is involved.
A purified allergen, antigen SBP, was obtained from the pollen of the Japanese cedar (Cryptomeria japonica, Sugi in Japanese) by ammonium sulfate precipitation, ion-exchange chromatography on diethylaminoethyl and carboxymethyl cellulose, and gel chromatography on Sephadex G-150. Antigen SBP was a heat-sensitive basic glycoprotein of approximately 40,000 molecular weight. By preparative isoelectric focusing and gel chromatography on Sephadex G-100, antigen SBP could be further separated into four subfractions, differing in both isoelectric point and molecular weight. By immunodiffusion analysis, direct skin testing, and radioallergosorbent test inhibition, it was shown that antigen SBP was the major allergen of Japanese cedar pollen, and the four subfractions were seen to be antigenically and allergenically identical.
Formoterol and salbutamol were compared for in vitro inhibition of allergen-induced histamine release from allergic leukocytes and human lung tissue passively sensitized with allergic serum. Formoterol inhibited the release of histamine from leukocytes but salbutamol showed little inhibiting effect. When combined with theophylline, formoterol was a more potent inhibitor of the release of histamine from leukocytes in allergic patients than salbutamol. In fragments of human lung sensitized with allergic serum, the concentration required to inhibit histamine release by 50% was 2 x 10(-11) M for formoterol and 8.5 x 10(-9) M for salbutamol. The potency of salbutamol and formoterol in blocking specific 3H-dihydroalprenolol binding to beta-adrenoceptors on guinea pig lung membranes revealed that formoterol had higher affinity for beta-adrenoceptors than salbutamol, and the concentration required for half-maximum stimulation of adenylate cyclase was approximately 200-fold higher for salbutamol than for formoterol.
The effect of immunization of guinea pigs with ovalbumin on the number and affinity of alpha 1- and beta-adrenergic and cholinergic muscarinic receptors was studied in lung membranes by direct binding techniques using 3H-prazosin, 1-3H-dihydroalprenolol and 1-3H-quinuclidinyl benzilate. After immunization by intraperitoneal injection of ovalbumin to guinea pigs, the number and affinity of each receptor in sensitized animals were not significantly different from those of control animals. Sensitization of guinea pigs by an aerosol exposure with the antigen resulted in a decreased number of beta-adrenergic receptor (458 +/- 29 vs. 687 +/- 56 fmol/mg protein; p less than 0.01), and an increased number of alpha 1-adrenergic receptor (36 +/- 2 vs. 25 +/- 2 fmol/mg protein; p less than 0.01), but no change was observed in the number of muscarinic receptors, as compared with control animals. On the other hand, following a prolonged sensitization of guinea pigs with a low dose of the aerosolized antigen, the number of muscarinic receptors was significantly increased in the lung of sensitized animals (50 +/- 2 vs. 42 +/- 2 fmol/mg protein; p less than 0.01); however, we found no significant differences between sensitized and normal animals in the number of alpha 1- and beta-adrenergic receptors. There were no different changes in the affinity of these receptors in all experiments.
After guinea pigs were exposed to histamine or acetylcholine aerosol for 1 week, alpha 1- and beta-adrenergic and cholinergic muscarinic receptors on the lung membranes were measured by direct binding techniques using 3H-prazosin, l-3H-dihydroalprenolol, and l-3H-quinuclidinyl benzilate, respectively, and adenylate cyclase responses to l-isoproterenol (10(-5) to 10(-8) M) and NaF (20 mM) were also examined on the membranes. After the inhalation, the number of beta-adrenergic receptors was decreased by about 25% without a significant change in binding affinity for l-3H-dihydroalprenolol, while the number and the affinity of alpha 1-adrenergic and muscarinic receptors on the membranes were not significantly different from those in the control animals. When compared with the control animals, the lung membranes showed a reduced adenylate cyclase response to l-isoproterenol, and the response to 10(-5) M of l-isoproterenol was significantly decreased by 11% in the lung membranes. The histamine inhalation showed no significant effect on basal adenylate cyclase activity and adenylate cyclase response to NaF.
FUT-175 is a new anti-complemental drug which strongly inhibits complement-mediated allergic reactions in animals. It was reported that FUT-175 does not affect both antibody formation and host defense to bacterial infection in mice. The present study was undertaken to examine the effects of FUT-175 on various immunological reactions in humans. FUT-175 dose-dependently decreased the antigen-induced anaphylactic histamine release from leukocytes of atopic patients. However, i.d. treatment of FUT-175 neither inhibited antigen- or compound 48/80-induced immediate type skin reactions in atopic patients nor antigen-induced early, late or delayed type skin reactions in Candida-sensitive patients. FUT-175 also did not inhibit the PPD-mediated delayed type skin reaction in healthy subjects. FUT-175 at a dose of 10(-4)M but not at 10(-8) to 10(-5)M significantly decreased the proliferation of human atopic peripheral blood lymphocytes (PBL) caused by mite antigen, concanavalin A or pokeweed mitogen. 51Cr release from human PBL was slightly enhanced by FUT-175 at a dose range of 10(-6) to 10(-4)M. FUT-175 did not change the number of SIg receptors or C3 receptors on human B cells. FUT-175 hardly affected the nitroblue tetrazolium reduction test and Escherichia coli-mediated chemotaxis in human neutrophils. These results strongly suggest that FUT-175 does not affect immunological functions and host defense in humans.
Since a first successful A-C bypass using saphenous vein graft was performed in 1970, eighty five patients with severe coronary heart disease were operated on in our clinic. Up to date, A-C bypass was carried out in sixty four cases, and aorto-coronary sinus bypass (Ao-Cs bypass) as an arterialization of the coronary venous system was done in one case in the group of angina pectoris. Three cases among sixty four patients who underwent A-C bypass and a case of Ao-Cs bypass died of low cardiac output syndrome postoperatively. Other two cases died of refractory arrhythmia and cardiomyopathy 6 years after surgery. The remaining fifty nine cases are doing well without any complications during follow up from ranging 2 months to 13 years (mean 3 years 4 months). Recently, no operative death was found during past 8 years with development of surgical technique and myocardial protection. Ventricular function (cardiac index, LVedp, Max LV dp/dt, EF, LVEDVI , double products at rest and during treadmill exercise test) disclosed good results especially in complete revascularization group. Graft patency had a close correlation between a diameter of the coronary artery at the anastomosis site and bypass graft flow after completion of bypass. Subsequently, a good patency rate (84%-86%) was obtained in cases with the coronary artery more than 1.5 mm in diameter. It could be concluded that A-C bypass was useful procedure to improve ventricular function as well as clinical symptoms and longevity of the life.
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FUT-175 is a new synthetic protease inhibitor which strongly inhibits complement-mediated hemolysis via the classical and alternative pathways. The present study was undertaken to examine the effects of FUT-175 on antibody formation and host defense in mice since the complement system participates in both immunological responses and host defense against bacterial infection. FUT-175 did not suppress the primary IgM and IgG antibody responses to sheep red blood cells, although FUT-175 was given at 10 to 100 mg/kg/day p.o. for 3 days before or after immunization. On the other hand, the primary anti-DNP IgE antibody response to DNP-conjugated ovalbumin was slightly suppressed only by post-administration of FUT-175 in a dose of 100 mg/kg/day p.o. for 5 days. However, the results of the adoptive transfer experiments indicate that FUT-175 did not affect either T cells or B cells participating in the secondary anti-DNP IgE antibody formation. FUT-175 in a dose of 10(-4)M but not at 10(-6) to 10(-5)M significantly decreased the proliferation of spleen cells caused by concanavalin A, lipopolysaccharide or the one-way mixed lymphocytes culture reaction using 1000 R-irradiated spleen cells from BDF1 mice as stimulator cells and those from C57BL/6 mice as responder cells. FUT-175 had an inhibitory rather than an enhancing effect on host defense to infection with Escherichia coli when administered at 10 to 100 mg/kg/day p.o. for 3 days before or after infection. These results strongly suggest that FUT-175 does not affect antibody formation and host defense in mice.
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Experimentally, we produced obstruction of the intestine in dogs, and the intraluminal pressure of the small intestine was measured without inducing anesthesia and with the abdominal wall closed. The maximum active intraluminal pressure reached 44.1 +/- 3.3 milligrams of mercury three days after the obstruction was produced. The pressure rose further to 95 millimeters of mercury, or higher, after an intravenous injection of physostigmine or during vomiting. When the intraluminal pressure is artificially increased and the vascular structure is observed by the resin-casting method, impairment of the villous circulation of the mucosa is already seen when the pressure reaches 20 millimeters of mercury. When the pressure was further increased, the circulation impairment spread toward the outer layer of the intestine. Mesenteric blood flow, peripheral vascular resistance and submucosal blood flow did not show significantly lower values than did the control group, unless the intraluminal pressure was 100 millimeters of mercury, or higher, but the oxygen consumption of the intestinal tissues was significantly lower than that for the control group when the intraluminal pressure was 40 millimeters of mercury, or higher. The resin-casting method showed that, at this pressure, a finding believed to indicate an arteriovenous shunt was already present at the mucosal villous base. The aforementioned results indicate that selective mucosal ischemia may occur when the intraluminal pressure increases to a range that is clinically possible when obstruction of the intestine occurs.
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