[Clinical hemodynamic evaluation of Omniscience tilting disc valves in aortic position].
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Biomedical subjects
Publications and source records attributed to M Okabe.
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A relatively simple, specific and sensitive radioimmunoassay system has been developed for the detection of heterophile Hanganutziu-Deicher (H-D) antigen(s) and antibodies. The 125I-labeled H-D antigen-active molecule used for the assay is a bovine erythrocyte major glycoprotein previously found to have a strong H-D antigen potency. The antigen-antibody complex was precipitated with normal human serum as the carrier protein, followed by the addition of rabbit anti-human IgG F(ab')2 serum. With this method, different H-D antigen-active molecules were compared for heterophile H-D antigen potency with reasonable sensitivity detecting about 0.3 ng of cold glycoprotein. 8 different lung cancer tissues were assayed for H-D antigen. The sera from the 8 lung cancer patients were also screened by ELISA and RIA in an attempt to correlate expression of H-D antigen on tissues with elevation of H-D antibodies. The results showed that all patients' tissues expressed the antigen(s) but only 3 of them had abnormal levels of H-D antibodies. This could have been due to excess antigens in circulation or immune complexes.
A sensitive and specific radioimmunoassay for antiarrhythmic peptide (AAP) has been developed, utilizing 3-(4-hydroxy, 5-[125I]iodophenyl)propionyl AAP and guinea pig anti-AAP serum. Synthetic AAP was used as a standard and the polyethylene glycol method was employed to separate free AAP from antibody-bound AAP. The minimum detectable dose of AAP was 0.2 pmol. In the assay system, immunoreactivity was shown not to be attributable to fragments derived from AAP, gelatin or collagen peptides, which sequences differ only by one amino acid from those of AAP. Immunoreactive (IR) AAP extracted from rat tissues and serum gave parallel dose-response curves to those of AAP. Thus, the AAP equivalents per g or ml of tissues measured in adult male rats were 203 pmol in heart, 166 pmol in kidney, 4 pmol in serum, and 2 to 6 pmol in the other tissues. IR-AAP was separated into two fractions by Sephadex G-25 chromatography. Fr. I was considered to have a larger molecular mass than AAP, while Fr. II appeared to have a molecular mass equal to AAP. Ratios of Fr. II in total IR-AAP were 50% in heart and 10% in kidney, while serum IR-AAP gave only Fr. II. The IR-AAP level in heart showed a positive correlation increase with age in rats.
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The Lung is capable of the synthesis and the release of prostaglandins responded to a number of pathophysiological stimuli, which may impair myocardial performance. Present study was undertaken to determine the release of circulating negative inotropic substance(s) from the lung and whether or not blockage of prostanoid synthesis, or infusion of prostaglandin are related to the production of this substance(s). Sixteen isolated left lower lobes were divided into 3 groups: (1) untreated, isolated blood-perfused lungs (n = 5), (2) prostaglandin I2, 1 microgram/min, continuously added to the perfusate (n = 6), and (3) five lobes pretreated with ibuprofen (12.5 mg/kg) in addition to 1 microgram/min prostaglandin I2. Perfusion of an isolated lobe with heparinized whole blood caused thrombocytopenia. The plasma 4 hours after perfusion led to the generation of a humoral agent(s) that reduced developed tension (Tpd) of a papillary muscle (p less than 0.05), and Ca++ -and Mg++-ATPase of sarcoplasmic reticulum (SR) (p less than 0.01). With prostaglandin I2, thromboxane B2 rose from 0.076 to 0.362 ng/ml at a level higher than control (p less than 0.05). The plasma significantly lowered SR-ATPase and myofibril-Mg++-ATPase activities and further reduced papillary muscle Tpd. By pretreatment with ibuprofen, adverse prostaglandin I2 effects were eliminated. The observation suggests that the lung produces prostaglandin related negative inotropic substance(s) that may reduced contractility, affected by energy availability.
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Right ventricular (RV) function in terms of hemodynamics and RV wall motion was studied in 14 mongrel dogs during left heart bypass (LHB) using a centrifugal blood pump. The wall motion was analyzed by two-dimensional echocardiography (2D-echo). Incremental changes in LHB flow ratios of 0% (controls), 25%, 50%, 75% and a maximum 85-100% were accompanied by decrements of segmental shortening of the interventricular septum (IVS) by 54 +/- 12%, 43 +/- 5%, 42 +/- 2%, 35 +/- 0% and 0%, respectively. In addition to akinesis of the IVS during maximum flow, a specific part of the RV free wall adjacent to the IVS also had marked depression of contractions and overall RV contraction was nearly dependent on the RV free wall opposite to the IVS. Maximum LHB flow induced complete depression of the left ventricular cavity, a marked increase in RV volume, and depression of the RV ejection fraction on 2D-echo. Excessive or prolonged LHB reduces the RV wall motion capability and may lead to right heart failure. Our results suggest that an LHB ratio of about 75% is optimum to maintain normal cardiac function, particularly that of the right heart.
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Highly purified recombinant human interferon-gamma produced by Escherichia coli (ReIFN-gamma) was examined for ability to stimulate natural killer (NK) cell cytotoxic activity and antibody-dependent cell-mediated cytotoxicity in human peripheral blood lymphocytes (PBLs) in comparison with natural human interferon-gamma (IFN-gamma) and with recombinant human interferon-beta produced by E. coli (ReIFN-beta). The activity of ReIFN-gamma to stimulate NK cell cytotoxicity was about 10 times greater than that of ReIFN-beta and similar to that of IFN-gamma when PBLs were pretreated with each interferon for 16 hr. The effects of ReIFN-gamma were completely neutralized by a rabbit anti-ReIFN-gamma antibody, but not by a rabbit anti-ReIFN-beta. ReIFN-gamma did not show any significant NK-enhancing effect when it was added directly to the killing phase of standard 51Cr-release assay for 4 hr, while ReIFN-beta showed a marked effect. The time course study showed that the NK-activating effect of ReIFN-gamma was not expressed until 2 hr after the start of incubation, while that of ReIFN-beta was expressed rapidly and sufficiently within 15 min. This kinetic difference between ReIFN-gamma and ReIFN-beta was confirmed by an experiment using the Ca2+-pulse method, in which the killing rate in the Ca2+-dependent stage of NK cytolysis was increased by ReIFN-gamma, but only after 6 hr of preincubation, while the effect by ReIFN-beta was expressed rapidly at 30 min. These findings suggest that ReIFN-gamma and ReIFN-beta may stimulate NK cell cytotoxicity through different intracellular events after they bind to their receptors on the surface of NK cells.
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This study details improvements in the intubation of a long intestinal decompression tube by use of a new flexible tip guide wire and a new intestinal decompression tube. The intubation route of the endoscope was changed from the oral to the nasal cavity. Although the guide wire formerly used (TGBD-65-345) could be inserted into the descending part of the duodenum by passing it through the biopsy channel of the endoscope, with this new method, the guide wire (TGBD-65-450) could be inserted into the upper jejunum. The endoscope could also be left in the stomach, when this method was used. The long tube was introduced along this guide wire into the upper jejunum. As a result of these improvements, the intubation rate for long intestinal decompression tubes was significantly more rapid and the time reduced. Intubation rate to the jejunum was 96 percent successful, as compared with a former success rate of 75 percent. The intubation time was decreased to 11.3 +/- 5.6 min. to the duodenum and 18.6 +/- 8.6 min. to the upper jejunum. This differs markedly from the former method which required 16.0 +/- 5.3 min. and 39.6 +/- 22.7 min, respectively.
Based on the working hypothesis that the OA-6129 group of carbapenem compounds might be the direct precursors for PS-5, epithienamycins A and C and MM 17880, Streptomyces fulvoviridis A933 17M9, a producer of PS-5, PS-6, PS-7, PS-8, epithienamycins A, B, C and D, MM 17880, MM 13902 and MM 4550, was subjected to NTG-mutation to provide a blocked mutant numbered 1501 which was found to produce OA-6129 A, OA-6129B1, OA-6129B2 and OA-6129C instead of PS-5, epithienamycins A and C and MM 17880, respectively. In a cell-free system, the parent strain demonstrated an ability to convert OA-6129A to NS-5, whereas the mutant did not. The L- and D-amino acid acylases were also shown to depantothenylate the OA-6129 group of carbapenems.
The structures and stereochemistry of OA- 6129D and E, new carbapenam compounds produced by Streptomyces sp. OA-6129, were determined by spectroscopic analysis and chemical transformation.
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