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Biomedical subjects

M Okada

Publications and source records attributed to M Okada.

At least 1,207 records · Page 67Linked to original sources
PubMed1990

[Improvement in the mechanical properties of artificial blood vessel suitable for the extracranial cerebral artery].

Saphenous vein interposition grafts have been commonly used for the reconstruction of occlusive lesions in the extracranial cerebral vessels, such as carotid or vertebral arteries. In contrast, cerebral revascularization using an artificial blood vessel has not been so common. This is due to the fact that conventional artificial blood vessels have been too firm or too rigid for use in the neurosurgery. Another reason is that the long term patency rate of small caliber artificial blood vessels has usually been inferior to that found in autologous vein grafts. The purpose of this study was to develop a soft and compliant artificial blood vessel suitable for cerebrovascular surgery. This new artificial blood vessel is made of polyurethane, porous in structure (porous polyurethane). Thus, multiple small-sized pores exist both in the inner and outer surfaces, and in the wall of the porous polyurethane graft. To test its mechanical properties, we evaluated stress-strain curves and compliance. In comparison to expanded polytetrafluoroethylene graft (Goretex), which has been one of the most commonly used artificial blood vessels in the cardiovascular surgery, the mechanical properties of the porous polyurethane graft more closely resembled those of the common carotid artery in dogs. Thus, porous polyurethane graft was shown to be a soft and compliant new artificial blood vessel. This means not only that it can be maneuvered with technical ease for anastomosis but also that there is a reduction of compliance-mismatch between the host vessel and the artificial vessel. Compliance mismatch has been documented as a major factor in the inducement of intimal hyperplasia, which causes a delayed occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Large subcutaneous calcification in systemic lupus erythematosus.

A 42-year-old woman first received the diagnosis of systemic lupus erythematosus at our hospital in 1986. Thereafter, she noticed a small subcutaneous nodule on her left leg. This nodule became larger, and many new nodules appeared. Some of these were amassed to form large, flat, platelike tumors. Roentgenographic and histological examination revealed that they were calcium deposits. To our knowledge, this is the first report of very large, hard tumors resulting from calcium deposition in the skin.

Adult↗
PubMed1990

[Modern trends in the field of the coronary artery surgery: clinical experience of laser application].

In the recent years, laser has been widely utilized in the field of medicine. But, there are few application in the cardiovascular surgery. Since 1980, we have applied lasers in the following three categories in the field of cardiovascular surgery. That is, Group 1: laser angioplasty for occlusive arterial disease, Group 2: laser vascular anastomosis especially for small caliber vessels, Group 3: new myocardial revascularization. Consequently, effects of laser application could be clearly recognized in these fields. On the basis of excellent results of our experimental studies, laser was clinically employed for 135 patients with anginal pain, intermittent claudication or renal failure. Optimal conditions for laser angioplasty were 6 watts in output and 3 sec in irradiation time for each shot. Laser irradiation was carefully repeated according to the grade of atherosclerotic changes. Angioscope was useful for keeping safe procedures. On the other hand, optimal conditions of vascular anastomosis were 20-40 mW in output and 6-12 sec/mm in irradiation time. They consisted of laser angioplasty with 6 cases of intraoperative coronary laser angioplasty in 37 cases, and vascular anastomosis including 8 cases of coronary artery bypass surgery in 97 cases, new myocardial revascularization in one case. These patients are doing well without any complications throughout laser. Our clinical experience of laser application in the cardiovascular surgery are presented.

Adult↗
PubMed1989

A protein tyrosine kinase involved in regulation of pp60c-src function.

We recently identified a novel protein tyrosine kinase that specifically phosphorylates truncated pp60c-src (Mr = 53,000) at a tyrosine residue(s) distinct from its autophosphorylation site. In this study, we examined whether this enzyme phosphorylates intact pp60c-src (Mr = 60,000) and determined its phosphorylation site. Non-neuronal and neuronal forms of intact pp60c-src were separately purified from the membrane fraction of neonatal rat brain by sequential column chromatographies. The novel kinase phosphorylated tyrosine residues of both forms of intact pp60c-src. The phosphorylation occurred in parallel with autophosphorylation of pp60c-src, and in both forms the final stoichiometry estimated was quite similar to that of autophosphorylation (about 5%). The enzyme also phosphorylated pp60c-src in which the kinase activity had been destroyed by an ATP analogue, p-fluorosulfonylbenzoyl 5'-adenosine. The phosphorylation site of the non-neuronal form was analyzed by sequential peptide mapping with tosylphenylalanyl chloromethyl ketone-treated trypsin and alpha-chymotrypsin. Tryptic digestion of the phosphorylated pp60c-src yielded a unique phosphopeptide that cross-reacted with an antibody specific for the carboxyl-terminal sequence of chicken pp60c-src. Digestion of the phosphopeptide with chymotrypsin yielded a product that comigrated with a synthetic phosphopeptide corresponding to the carboxyl-terminal 15 residues of chicken pp60c-src. These results clearly indicate that the carboxyl-terminal sequence of rat pp60c-src is identical to that of chicken pp60c-src, and a tyrosine residue corresponding to chicken Tyr527 is the phosphorylation site. This phosphorylation resulted in a decrease in the enolase phosphorylating activity of pp60c-src. Kinetic experiments indicated that this decrease in activity was due to a decrease in the Vmax value of pp60c-src. These findings support our previous proposal that the novel tyrosine kinase acts as a specific regulator of pp60c-src in cells.

Animals↗
PubMed1989

Ascorbic acid suppresses the deconjugation of noradrenaline but not dopamine in plasma.

The characteristics of hydrolysis of sulfoconjugated noradrenaline (NA) and dopamine (DA) in plasma using sulfatase were investigated. Ascorbic acid has been used as an antioxidant during the hydrolysis of conjugated NA or DA. Hydrolysis of NA sulfates was considerably inhibited by adding ascorbic acid (0.5-10 mM), and slightly inhibited by adding dithiothreitol (1-10 mM). In contrast, the hydrolysis of DA sulfates was not affected after either ascorbic acid or DTT treatment. On the basis of these findings, the levels of NA sulfates previously reported are found to be markedly lower than the actual levels of NA sulfates in human plasma.

Ascorbic Acid↗
PubMed1989

Relationship of calcium and adenylate cyclase messenger systems in rat brain synaptosomes.

The effects of cyclic AMP on the rise in cytosolic free calcium concentration, [Ca2+]i, after stimulation with 15 mM K+ in rat brain synaptosomes were investigated. The fluorescent chelating agent Quin-2 was employed to monitor alterations of K+-evoked [Ca2+]i. Under normoxic conditions, clonidine (1, 10 microM), an alpha 2-adrenoceptor agonist, decreased the 15 mM K+-evoked [Ca2+]i. Although yohimbine (1, 10 microM), an alpha 2-adrenoceptor antagonist, had little or no effect on K+-evoked [Ca2+]i, the inhibitory effects of clonidine were blocked by yohimbine. 8-Bromo cyclic AMP, a cyclic AMP analogue, (50-500 microM), increased K+-evoked [Ca2+]i in a dose-dependent manner. The addition of cyclic AMP analogues subsequent to clonidine treatment reversed the clonidine-induced suppression of K+-evoked [Ca2+]i. On the other hand, under hypoxic conditions, K+-evoked [Ca2+]i was reduced by about 50-60%. 8-Bromo cyclic AMP and the adenylate cyclase activators, yohimbine (1-10 microM) and isoproterenol, a beta-adrenoceptor agonist, (0.1-10 microM), transiently reversed the reduction of the K+-evoked [Ca2+]i caused by hypoxia. These results indicate that the activation of alpha 2-adrenoceptor produces a rapid, sustained decrease in [Ca2+]i which may be due to a decrease in the levels of intracellular cyclic AMP. In addition, the increase in cellular levels of cyclic AMP reversed the reduction of the Ca2+ response to high K+ stimulation caused by hypoxia. If this is so, there is the possibility that increased cyclic AMP might improve the hypoxic damage.

Adenylyl Cyclases↗
PubMed1989

[Clinical analysis of renal cell carcinoma with extension into the inferior vena cava].

We performed clinical analysis of 12 patients with renal cell carcinomas associated with tumor thrombosis in the inferior vena cava. Eleven cases were men, and one was a woman; their ages range from 48 to 76 years old with a mean of 58 years. Nine tumors were observed on the right side, the other 3 tumors were observed on the left side. In five cases, the distant metastases of the disease were noticed at the first visiting to our hospital. Lung metastases were found in five and bone or liver in each one. Chief complaints were macroscopic hematuria in 8 cases (67%), and were weight loss or general fatigue. The symptoms of obstruction of the inferior vena cava, such as venous dilatation of abdominal wall, edema of lower extremities and varicocele of the testes, were seen in 6 cases. The level of the tumor thrombosis was preoperatively determined by CT, echography, cavography or MRI. The level was near the right atrium in one, near the hepatic vein in 8 and near the renal vein in 3, although there was no case extending into the right atrium. Transperitoneal nephrectomy and thrombectomy in the inferior vena cava were performed in 9 cases. Surgery could not be performed in the other 3 patients of their poor general condition or severe heart disease. One patient died because of massive hemorrhage during the operation. The other complications were transient renal failure in 3 cases and postoperative bleeding in one case. In 4 patients without distant metastases or regional lymph nodes metastasis, two died of multiple metastasis of renal cell carcinomas and diabetic coma. The other two cases are alive without disease for 4 and 40 months after operation. For renal cell carcinoma extending into the inferior vena cava without metastasis, nephrectomy and thrombectomy should be performed using the extracorporeal circulation.

Aged↗
PubMed1989

[Effects of anti-platelet aggregating agents on peplomycin induced pulmonary toxicity in mice].

In order to find a method to ameliorate pulmonary toxicity of peplomycin (PEP), microscopic changes of the lung following PEP administration and effect of anti-platelet aggregating agents on the toxicity was investigated in mice. When PEP was administered intravenously once a day for 7 days, microthrombi mainly composed of aggregated platelets and fibrin appeared in the capillaries of the lung in an early phase before severe pulmonary edematous lesions and fibrosis occurred. Combination therapy of anti-platelet aggregating agents such as phthalazinol, dipyridamole, ticlopidine and indomethacin suppressed these toxic changes. Especially, ticlopidine was the most effective and superior to prednisolone used clinically for amelioration of the toxicity. Microthrombi, preceding edematous lesions, were considered to be attributed to damages of endothelium by PEP, because PEP itself did not develop platelet aggregation in vitro and ex vivo. Therefore, the microthrombi are likely to produce congestion of pulmonary microcirculation leading to edematous lesions by increase of permeability, and to play significant roles in the development of pulmonary fibrosis in a late phase. Anti-platelet aggregating agents such as ticlopidine are concluded to ameliorate the lung toxicity by preventing microcirculation impairment with the microthrombus.

Animals↗
PubMed1989

Role for the third constant domain of the IgG H chain in activation of complement in the presence of C1 inhibitor.

The multidomain architecture of Ig H chains was initially implicated in the variety of functions imposed on each species of Ig. However, the activation of C by IgG is the only function that has been attributed to a single domain of C gamma 2, whereas most of other functions of IgG require both C gamma 2 and C gamma 3 domains. This one domain-one function relationship in the C activation by IgG, too, was questioned recently by the fact that a C gamma 3-less fragment of rabbit IgG, F(acb)2, is definitely less capable of activating C than intact IgG. Here we reexamined capacities of F(acb)2 to bind and activate C1 in the presence and absence of C1 inhibitor (C1-In) in comparison with intact IgG, by using SRBC sensitized with these proteins (EFacb, EIgG). At an ionic strength of 0.065 and 37 degrees C, where C1q was bound equally well by these cells and the dissociation was limited, C1s, presumably in the form of C1r2C1s2, dissociated from EFacb at a rate 7-fold greater than that from EIgG, irrespective of the presence or absence of C1-In. A physiologic concentration of C1-In reduced the rate of C1 activation by EFacb to 5% that by EIgG. The results present evidence that the C gamma 3 domain, too, plays a crucial part in the C1 activation process by stabilizing the zymogenic conformation of C1 and protecting it from the attack by C1 inhibitor.

Animals↗
PubMed1989

Disseminated infection of Pneumocystis carinii in a patient with the acquired immunodeficiency syndrome.

This report describes the histopathology of a disseminated Pneumocystis carinii infection in a 24-year-old Japanese male haemophiliac diagnosed as having the acquired immunodeficiency syndrome. He developed respiratory symptoms, and Pneumocystis carinii pneumonia was confirmed by transbronchial lung biopsy. On the 70th day of hospitalization the patient died. Autopsy findings revealed Pneumocystis carinii not only in the lungs but also in the stomach, jejunum, ileum, colon, mesoappendix, abdominal lymph nodes, diaphragm, and thyroid gland.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Role of prostaglandin deficiency in pathogenetic mechanism of gastric lesions induced by indomethacin in rats.

The present study was undertaken in rats using 2-deoxy-D-glucose (2DG) as a stimulator of gastric motility and a low dose of indomethacin as a prostaglandin (PG) synthesis inhibitor to investigate the roles of gastric motility and PG deficiency in the pathogenesis of indomethacin-induced gastric lesions. Subcutaneously administered indomethacin at 5 mg/kg did not induce any visible damage in the mucosa within 4 hr, but at 25 mg/kg produced linear hemorrhagic lesions along the long axis of the stomach. 2DG (100 mg/kg/hr), given intravenously, produced linear nonhemorrhagic lesions along the mucosal folds and, in the presence of 5 mg/kg of indomethacin, caused severe hemorrhagic lesions in the same areas of the stomach. Gastric motility was markedly enhanced by both indomethacin (25 mg/kg) and 2DG, while acid output and mucosal blood flow were increased only by the latter. Mucosal PGE2 levels were significantly reduced by indomethacin (25 mg/kg) but not by 2DG. Indomethacin at 5 mg/kg alone had no or little effect on any parameter except PG levels, which were reduced to similar degrees as caused by 25 mg/kg of the agent. Time-course development of the lesions was closely associated with those changes in gastric motility after administration of indomethacin (25 mg/kg) and 2DG. These results suggest that the enhanced gastric motility is, by itself, sufficient to induce damage (nonhemorrhagic) in the mucosa and that a PG deficiency alone does not induce any damage but is required for further extension to hemorrhagic lesions of nonhemorrhagic ones that are initially induced by enhanced gastric motility.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Augmentative effect of Nocardia rubra cell-wall skeleton on the induction of human lymphokine-activated killer (LAK) cells by the production of LAK cell helper factor(s).

Nocardia rubra cell wall skeleton (N-CWS) was found to synergistically augment lymphokine-activated killer (LAK) cell generation from human peripheral blood mononuclear cells (PBMC) in the presence of a suboptimal dose of recombinant interleukin-2 (rIL-2). N-CWS increased the number of PBMC expressing IL-2 receptor on their surfaces, and the presence of N-CWS at the early stage of the culture period was essential for the exertion of its augmentative activity on the LAK induction. The predominant phenotype of LAK precursor cells responding to N-CWS and rIL-2 was CD3- CD16+. Culture supernatant from N-CWS-stimulated PBMC was found to act as a substitute for N-CWS in the induction of LAK generation in the presence of rIL-2, suggesting that these cells produced a factor capable of augmenting LAK cell induction (LAK helper factor, LHF). LHF was found to have a molecular mass of 29 kDa by gel filtration, and could also function as a killer helper factor to augment allo-antigen-specific cytotoxic T lymphocyte generation from human peripheral blood T cells as well as murine thymocytes. LHF showed no species specificity, indicating that it is different from IL-4. The enhancing activity of LHF was not neutralized with anti-TNF alpha, anti-IL-1 alpha, or anti-IL-1 beta antibodies. Furthermore, no tumor necrosis factor-alpha (TNF alpha), TNF beta, IL-1 alpha, beta, IL-2, IL-5, IL-6 or interferon activity was detected in semi-purified LHF during enzyme-linked immunosorbant assay and biological assays. The present findings indicate that LHF produced from N-CWS-stimulated PBMC is a molecule distinct from TNF alpha, TNF beta, interferon, IL-1, -2, -4, -5, and -6, and suggest that LHF might be a novel lymphokine involved in LAK generation.

Adjuvants, Immunologic↗