Biomedical subjects

A Sumiyoshi

Publications and source records attributed to A Sumiyoshi.

At least 73 records · Page 4Linked to original sources

PubMed1992

Effects of antithrombotic drug, Y-20811 on mural thrombus formation and intimal thickening following intimal injury.

Inhibitory effect of Y-20811 on platelet thrombus formation induced by mechanical intimal injury and subsequent intimal fibrous thickening was studied. In the short term experiment, polyethylene tubing was inserted into the rabbit aorta and was drawn out one hour after with or without Y-20811 administration, then the rabbits were sacrificed. In the experiment for the quantitative analysis of platelet adhesion, 51Cr-labeled platelets were used. Radioactivities of 2cm length of the injured segment of the thoracic aorta and the proximal 2cm of the normal segment were measured. Radioactivity of the injured segment was significantly lower in rabbits treated with Y-20811 than the control ones. The mean thickness (area of thrombi/length of injured intima) and the maximal thickness of the mural thrombi in the Y-20811-treated rabbits were significantly lower than those in control rabbits. De-endothelialized area showed raised platelet thrombi in the control group and diffuse thin-layered platelet sheets in Y-20811-treated rabbits. In the long term experiment, polyethylene tubing was indwelled for 24 hours. Rabbits were sacrificed 10 days after drawing out the tubing. Through the experiment Y-20811 was injected intravenously every 24 hours. There was no significant difference between the control group and the Y-20811-treated one in both mean thickness and maximal thickness of the intimal fibromuscular thickening. The experiments indicate that Y-20811 has an inhibitory effect on platelet thrombus formation following intimal injury, but subsequent myointimal thickening is not inhibited by the drug.

Animals↗

PubMed1992

The content of urokinase-type plasminogen activator antigen as a prognostic factor in urinary bladder cancer.

Urokinase-type plasminogen activator (u-PA) is thought to be implicated in cancer invasion and metastasis. The aim of this study was to determine whether the u-PA content of cancer tissue is a prognostic factor in bladder cancer. Tissue samples from 46 patients with bladder cancer were assessed for u-PA antigen by a highly sensitive enzyme immunoassay. The relationships between the u-PA level in extracts of bladder cancer and the survival rates of the bladder-cancer patients were examined. Patients with a high u-PA level (8 ng/mg of protein and more) showed a statistically significantly higher rate of survival than those with a low u-PA level (p less than 0.005). The u-PA antigen level in cancer tissue was significantly lower in low-graded and non-invasive cancers than in others (p less than 0.01).

Aged↗

PubMed1992

Replication of endothelial cells and smooth muscle cells induced in vivo by hypercholesterolaemia and materials released from platelet-rich white thrombus.

Endothelial cell injury is considered to be the primary event in atherogenesis. In this study, we investigated the effects of hypercholesterolaemia, and substances released from platelet-rich thrombi, individually and together on endothelial cells and the wall of the rabbit in vivo. We divided 24 rabbits into four groups: I was a control group on a normal diet; II was a tubing group on a normal diet, in which polyethylene tubing was inserted into the ascending aorta; III was a group being fed a cholesterol diet; and IV was a combined group being fed a cholesterol diet with polyethylene tubing in the ascending aorta. Segments from the descending thoracic and abdominal aortas which were not injured directly by tubing were examined morphologically and for [3H] thymidine incorporation into endothelial cells and smooth muscle cells. The descending aortas of groups II, III, and IV showed various degrees of endothelial cell damage. [3H]Thymidine incorporation into endothelial cells and aortic wall was increased in groups II, III, and IV (most in group IV) as compared with group I. These data indicate that hypercholesterolaemia and substances released from activated platelets and/or white mural thrombi can cause endothelial damage which may result in endothelial and smooth muscle cell proliferation. In addition, a combination of these two factors showed an additive effect on the endothelial injury and regeneration in vivo.

Animals↗

PubMed1992

The relationship between cardiovascular complications of estrogen therapy and fibrinolysis in patients with prostatic cancer.

To determine the relationship between cardiovascular complications of estrogen therapy and fibrinolysis, fibrinolysis parameters plasminogen, urokinase-type plasminogen activator (u-PA), tissue-type plasminogen activator (t-PA), and plasminogen activator inhibitor-1 (PAI-1), were assessed in 12 prostatic cancer patients before and 6 weeks after the onset of estrogen therapy. The levels of plasminogen, u-PA, and PAI-1 in the patients treated with the estrogen therapy were significantly higher than those in the patients before the therapy. The t-PA level in the patients during the therapy was significantly lower than that before the treatment. Cardiovascular complications were found in two patients (16.7%) during estrogen therapy. In the two patients, marked elevation of PAI-1 and decreased level of t-PA were observed during the therapy. These results indicate that cardiovascular complications of estrogen therapy in patients with prostatic cancer may be related to hypofibrinolysis resulting from changes of PAI-1 and t-PA.

Aged↗

PubMed1992

Vascular contraction in perfused carotid arteries of cholesterol-fed rabbits.

The purpose of the present study was to investigate the effects of hypercholesterolemia on sympathetic vascular responsiveness in the perfused rabbit carotid artery. Two groups of rabbit carotid arteries were evaluated for the simultaneous measurement of noradrenaline (NA) release and vasoconstrictor response induced by electric nerve stimulation and for exogenous NA-induced vasoconstriction in vitro. One group of rabbits was fed a diet containing 0.5% cholesterol for 2 weeks and the other group was fed standard rabbit chow. By scanning electron microscopy, monocytes adhering to the endothelial cells and penetrating into the subendothelium were observed. Neither endothelial denudation nor platelet adhesion could be detected. Rabbit carotid arteries were cannulated and perfused with a physiological solution at a constant flow rate. The vessels were subjected to both transmural field stimulation (TFS; 1.5-24 Hz) and exogenous NA administration. TFS caused a frequency-dependent increase in endogenous NA release with subsequent pressor responses in both groups. Exogenous NA also induced a dose-dependent pressor response, but a significant reduction was observed in the cholesterol-fed group. Methoxamine induced a similar response in both groups. It was concluded that hypercholesterolemia decreased the sensitivity of extrajunctional alpha-receptors in the perfused rabbit carotid artery.

Animals↗

PubMed1992

Contribution of the endothelium to intimal thickening in normocholesterolemic and hypercholesterolemic rabbits.

Endothelial cell injury is considered to be a primary event in the pathogenesis of atherosclerosis. In this study, we investigated the aortic intimal lesion after balloon catheterization in hypercholesterolemic and normocholesterolemic rabbits with or without probucol, an antioxidant. After deendothelialization, the rabbits were divided into four groups: 1) a control group fed a standard diet; 2) a probucol-treated group; 3) a cholesterol-fed group; and 4) a group fed a mixed cholesterol and probucol diet. Four animals from each group were killed at 2, 4, and 8 weeks after deendothelialization. The aortic segments of nonendothelialized areas, borderline areas, and uninjured areas were histologically and immunohistochemically examined. Deendothelialized areas showed various degrees of intimal thickening, which was mainly composed of smooth muscle cells in rabbits from groups 1 and 2. The intimal thickness of group 3 was significantly larger than that of other groups in any area examined. The intimal thickness of group 4 was less than that of group 3 despite the hypercholesterolemic state in the former group. The intima of borderline areas was generally thicker than that of nonendothelialized areas. Although the borderline lesions of groups 3 and 4 contained numerous macrophages, the number of macrophages was lower in the nonendothelialized compared with the reendothelized lesion. These data indicate that endothelial cell injuries can cause intimal thickening. The regenerated endothelial covering is favorable for monocyte migration and attachment. This process, together with the proliferation of smooth muscle cells, greatly contributes to the progression of atherosclerosis, which appears to involve lipid oxidation. Probucol prevented intimal thickening to a certain degree in this experiment in the normocholesterolemic as well as the hypercholesterolemic state.

Animals↗

PubMed1992

Horseshoe kidney and membranous glomerulonephritis with cold activation of complement.

A 48-year-old woman was admitted to our hospital because of proteinuria associated with persistent hypocomplementemia. Intravenous pyelography indicated the presence of horseshoe kidney without other abnormalities. Hypocomplementemia was caused by cold activation of complement. There were some findings suggestive of chronic liver disease (positive HCV antibody, hypergammaglobulinemia, low cholinesterase, etc.). Percutaneous renal biopsy showed the features of multiple evolutional phases of membranous glomerulonephritis.

Cold Temperature↗

PubMed1992

Liver tissue injury secondary to iron overload in beta-thalassemia/hemoglobin E disease.

Liver tissues from 17 patients with advanced stages of beta-thal/Hb E disease were examined by light and electron microscopy, with emphasis on cellular damage due to excess iron overload. Various histochemical stains were performed to grade degrees of iron deposition and fibrosis, and to demonstrate hepatitis B surface antigen, in Kupffer cells as well as macrophages. The results of light and electron microscopic studies were correlated. There was a variation in the distribution of hepatic iron and the severity of fibrosis. In most of the cases ballooning degeneration of the hepatocytes, increase in number of lysosomes, hemosiderin and ferritin in hepatocytes as well as in the sinusoidal lining cells were found. The ferro-acidophilic body, representing another important form of hepatocellular necrosis also occurred. So far no precise mechanisms can be concluded.

Adolescent↗

PubMed1992

Cytoprotective effect of dilazep on hydrogen peroxide-perturbed vascular endothelial cells.

The effect of dilazep and dimethyl thiourea (DMTU) on the hydrogen peroxide-derived injury of culture pulmonary artery epithelial cells (CPAEC) was assessed by colorimetric assay of MTT formazan (MTT formazan assay). When CPAEC were treated with hydrogen peroxide, neither cell lysis nor detachment of the cells from surface of the well was observed. However, the MTT formazan formation was decreased in a time and dose dependent manner. The decrease in the formation was significantly suppressed in the presence of dilazep (0.1 to 10 microM) or DMTU (0.01 to 0.3 microM). CPAEC treated with hydrogen peroxide in the same way enhanced an activation of prothrombin, and this enhancement was significantly inhibited in the presence of dilazep (1 to 3 microM). These data indicate that dilazep exerts a cytoprotective effect against challenges of intracellular oxidant produced by hydrogen peroxide and suppresses augmented procoagulant activity of injured cells.

Animals↗

PubMed1992

Pulmonary microthromboemboli in thalassemic cases.

Lung specimens obtained from wet materials were reviewed for detection of microthrombi. Multiple microthrombi, which were composed mainly of platelets, were seen in the pulmonary arteriole and microcirculation in two autopsy cases with splenectomized thalassemic disease. These findings provide a rational explanation for the increased spontaneous platelet aggregation in the whole blood, and may be an additional factor to the progress of pulmonary dysfunction and hypoxemia seen in splenectomized thalassemic patients.

Adult↗

PubMed1992

Cavitating Pneumocystis pneumonia in an autopsied case of adult T-cell leukemia.

Cavitating necrosis is rare in Pneumocystis carinii pneumonia. In this report, we describe an autopsy patient with adult T-cell leukemia associated with cavitating Pneumocystis carinii pneumonia. The patient, a 61-year-old woman, died of an acute crisis of adult T-cell leukemia associated with diffuse pulmonary infection of Pneumocystis carinii. Postmortem examination revealed necrotic foci in both lungs, one of which, in the left lower lobe, had a central cavitation. Microscopically, leukemic cell infiltration was abundant in the lung parenchyma but not in the necrotic lesions. Pneumocystis carinii organisms were distributed diffusely in the alveoli and also in the cavity wall. Intranuclear and intracytoplasmic inclusion bodies were scattered in the lung indicating cytomegalovirus infection. However, no bacterial or fungal infection was detected in the lungs, even in the necrotic lesions. Cavitating Pneumocystis carinii pneumonia occurs in other immunodeficiency diseases apart from AIDS. To our knowledge, this report is the first case of cavitating Pneumocystis carinii pneumonia in adult T-cell leukemia.

Blast Crisis↗

PubMed1992

[Arterial intimal thickening].

Disturbances in the integrity of the arterial endothelium are considered to be a primary event in the pathogenesis of atherosclerosis. Platelets do not adhere to the intact endothelium but with removal of the endothelium, a thrombotic response to the exposed thrombotic subendothelium occurs. With time, proliferation of smooth muscle cells occurs in the inner-most part of the media beneath the thrombus, and the proliferated smooth muscle cells migrate beyond the internal elastic lamina to invade the thrombus and organize it. A growth factor released from activated platelets (PDGF) stimulates smooth muscle cell proliferation. At the same time, the endothelium, adjacent to the thrombus, proliferates and covers the organizing thrombus from its margin. Thus, localized flat or raised intimal thickenings are formed from organization of mural thrombus or repair of intimal injury. There is much evidence that the release of platelet constituents can damage the vessel wall. Our study clearly demonstrated that material released from situ platelet-rich mural thrombi into the arterial circulation can cause endothelial damage and promote the proliferation of smooth muscle cells in the intima, downstream, and in remote segments of the arterial wall, without apparent endothelial denudation. PDGF, together with other growth factors, is also considered to be involved in smooth muscle cell proliferation in this case.

Arteries↗

PubMed1991

Comparative immunohistochemistry of malignant fibrous histiocytoma and sarcomatoid carcinoma of the urinary tract.

An immunohistochemical analysis using antibodies to cytokeratin, epithelial membrane antigen, alpha-1-antitrypsin, alpha-1-antichymotrypsin and factor XIIIa was performed in four cases of malignant fibrous histiocytoma and five cases of sarcomatoid carcinoma in the urinary tract. All cases of malignant fibrous histiocytoma showed positive staining for factor XIIIa, alpha-1-antitrypsin and alpha-1-antichymotrypsin. No case was positive for factor XIIIa, but one case with sarcomatoid carcinoma stained positive for alpha-1-antitrypsin and alpha-1-antichymotrypsin. All cases showed positive staining for cytokeratin and 4 cases with sarcomatoid carcinoma were positive for epithelial membrane antigen, but no cases with malignant fibrous histiocytoma were positive. Immunohistochemical analysis would thus help to distinguish malignant fibrous histiocytoma from sarcomatoid carcinoma of the urinary tract.

Aged↗

PubMed1991

Tertiary hyperparathyroidism associated with metastatic cardiac calcification in a haemodialyzed patient.

A 32-year-old man undergoing haemodialysis treatment for 10 years was referred to our hospital because of intractable heart failure with atrioventricular block. On the 5th hospital day he was found dead in bed. Autopsy revealed extensive metastatic calcification involving the myocardium and the cardiac conduction system, and a parathyroid adenoma with hyperplastic parathyroid glands. Retrospectively, first-degree heart block developed 14 months before death, and was subsequently associated with intraventricular conduction defect and atrioventricular block (Wenckebach type). Throughout the 3 years the patient received 1 alpha-hydroxycholecalciferol (1 alpha-OH-D3) and the calcium-phosphorus product (Ca X P) exceeded 70. 1 alpha-OH-D3 should not be prescribed when patients develop an increase in Ca X P and exploration of the parathyroid glands should not be delayed if heart block presents in long-term haemodialyzed patients.

Adenoma↗

PubMed1991

Miliary tuberculosis presenting as fever and jaundice with hepatic failure.

A 58-year-old male patient with miliary tuberculosis presenting as jaundice and hepatic dysfunction was reported. He was admitted to the Miyazaki Medical College Hospital, Miyazaki, Japan, because of fever and jaundice. Chest x-ray revealed a calcified primary affect of tuberculosis in the left upper lung field and miliary shadows throughout both lung fields. Liver function tests showed indications of obstructive jaundice and hepatic dysfunction. He rapidly deteriorated and died 3 days after admission. Autopsy revealed disseminated miliary tuberculosis in all major organs. Many miliary tubercles were densely distributed in the liver, especially in and near the portal tracts. The intestine was free from tuberculous lesions. Miliary tuberculosis with jaundice is rare and its pathogenesis is discussed.

Fever↗

PubMed1991

An autopsy case of necrotizing ventriculo-encephalitis caused by cytomegalovirus in Hodgkin's disease.

A 59-year-old Japanese woman with Hodgkin's disease developed progressive dementia and died of pneumonia. The autopsy revealed necrotizing ventriculo-encephalitis caused by cytomegalovirus (CMV) infection, which was confirmed by immunohistochemical and electron microscopic examinations. It is suggested that CMV ventriculo-encephalitis could occur not only in patients with acquired immunodeficiency syndrome, but also in other immunocompromised hosts.

Autopsy↗

PubMed1991

Immunoreactive endothelin in human kidney.

Using a sensitive and specific radioimmunoassay for endothelin, we examined immunoreactive endothelin in human kidney tissue obtained from three necropsy and three nephrectomy cases. Immunoreactive endothelin was present in high concentrations in human kidney inner medulla (necropsy cases: 1.08 +/- 0.47 pg/mg wet weight:mean +/- SE)(nephrectomy cases: 2.77 +/- 0.46). Characterization by reverse phase high performance liquid chromatography indicated that the only immunoreactive endothelin in human kidney inner medulla is endothelin-1, although immunoreactive endothelin in rat and pig kidney inner medulla comprises both isopeptides endothelin-1 and -3, suggesting that the genetic expression of endothelin differs according to species.

Aged↗

PubMed1991

Correlation between urokinase-type plasminogen activator production and the metastatic ability of human rectal cancer cells.

The correlation between the production of plasminogen activators (PA), especially urokinase-type PA (u-PA), by cancer cells and their metastatic potential was studied. For this purpose, cells from the human rectal adenocarcinoma tumor line (RCM-l/nu) originally maintained by serial passage in nude mice as the solid subcutaneous tumor, were injected into the spleen. Cancer cells from liver metastatic foci were suspended and then injected into the spleen. After 10 cycles of this selection, a highly metastatic liver tumor line termed L-10 was obtained. The amount of u-PA in the supernatant of the tumor homogenate of L-10 was larger than that of RCM-l/nu. Using an in vitro culture system, the media conditioned by L-10 cells had a higher PA activity and a higher u-PA antigen level than by RCM-l/nu cells. The apparent difference in u-PA activity and antigen levels of these two lines was not due to the difference in the production of plasminogen activator inhibitor (PAI), because PAI antigen level and PAI activity in the culture media were almost equal between them. No tissue-type PA production was detectable in these tumor lines. From these results we deduce that u-PA may play an important role in tumor metastasis.

Adenocarcinoma↗