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H Kunii

Publications and source records attributed to H Kunii.

8 recordsLinked to original sources
PubMed2001

Increased plasminogen activator inhibitor-1 and apolipoprotein (a) in coronary atherectomy specimens in acute coronary syndromes.

BACKGROUND: Although increased tissue factor expression is known in vulnerable plaques, there is no reported study to compare plaque fibrinolysis in stable and unstable plaques. This study investigates the extent of plasminogen activator inhibitor-1 (PAI-1) and apolipoprotein (a) [apo(a)] in the plaques of different types of coronary artery disease as well as the correlation between these molecules and infiltration of macrophages to plaques. METHODS: Using immunohistochemical staining, we examined PAI-1 expression and apo(a) deposition in coronary atherosclerotic specimens obtained by directional coronary atherectomy from 19 patients with acute myocardial infarction (AMI), 12 with unstable angina pectoris (UAP), and 13 with stable angina pectoris (SAP). The percentages of the total areas of specimens stained with PAI-1 or apo(a) were estimated by an NIH image program. The proportion of macrophages as a percentage of all cells in plaques was calculated as the macrophage density. RESULTS: We found significantly higher percentages of total areas of specimens stained with PAI-1 in AMI (25.5 +/- 8.6%, P < 0.001) and UAP (22.2 +/- 10.4%, P < 0.005) than in SAP (9.5 +/- 5.0%), as well as with apo(a) (AMI; 11.7 +/- 7.1%, P < 0.005, UAP; 11.1 +/- 5.5%, P < 0.01 versus SAP; 3.9 +/- 1.5%). Linear regression analysis of all the samples showed a correlation between PAI-1 or apo(a) and macrophage density (PAI-1: r = 0.75, P < 0.001 and apo(a): r = 0.56, P < 0.001). CONCLUSIONS: Our results suggest a possible contribution of increased PAI-1 and apo(a) in plaques to the pathogenesis of acute coronary syndromes including impaired fibrinolysis.

Aged↗
PubMed2000

Lipoprotein(a) is a potential coronary risk factor.

Lipoprotein(a) (Lp(a)) is recognized as a new coronary risk factor, but few studies have quantitatively assessed the relationship of serum Lp(a) levels with other coronary risk factors in many patients undergoing coronary cineangiography. Seventeen coronary risk factors were quantified (i.e., age, gender, hypertension, impaired glucose tolerance, cerebrovascular accident, hyperuricemia, smoking, family history of ischemic heart disease (IHD), history of hyperlipidemia, Lp(a), total cholesterol, high density lipoprotein (HDL)-cholesterol, triglyceride, low density lipoprotein-cholesterol, apolipoproteins(apo)A-I,B, E) to determine their relationship with the numbers of involved coronary vessels using multiple regression test in 1,006 patients who underwent coronary cineangiogram (280 non-IHD patients: 144 men, 136 women; 726 IHD patients: 460 men, 266 women; age 16-84 years, mean 60.5+/-0.3). Multiple regression test indicated R = 0.506 and items that showed high beta weight and significant p level were age, Lp(a), impaired glucose tolerance, total cholesterol, cerebrovascular accidents, HDL-cholesterol, smoking, gender, family history of IHD, and apo-A-I (0.221, p<0.001; 0.174, p<0.001; 0.616, p<0.001; 0.138, p<0.001; 0.122, p<0.001; -0.12, p<0.001; 0.092, p<0.01; 0.091, p<0.01; 0.067, p<0.05; -0.065, p<0.05; respectively). It was concluded that Lp(a) is an independent, potential, and modifiable coronary risk factor, and that reduction of serum Lp(a) is important in the clinical management of patients with IHD.

Adolescent↗
PubMed1998

Surface expression of complement regulatory proteins, decay-accelerating factor (DAF) and CD59, on cultured human endothelial cells.

To clarify the response of endothelial cells to complement, we studied not only the reaction of endothelial cells against complement lysis sensitivity (CLS) test, but also the expression of complement regulatory proteins by two-color flow cytometric analysis and backscattered scanning immunoelectron microscopic analysis using monoclonal antibodies to decay-accelerating factor (DAF) and/or CD59. Complement activation didn't lead to the cell death of human aortic endothelial cells (HAECs) and human umbilical vein endothelial cells (HUVECs). In control, two-color flow cytometric analysis indicated that HAECs consisted of a single double-positive population for these proteins as well as HUVECs. Then, HUVECs and HAECs after the CLS test resulted in having same distribution by flow cytometry. Moreover, the microscopic analysis showed that DAF or CD59 was expressed with a diffuse distribution. However, DAF on HUVECs and CD59 on HAECs were present at the margin of cell surfaces more than at the other places. These findings suggest that endothelial cells have a defense mechanism for complement activation in vitro by the changes of expression of complement regulatory proteins on the membrane surface, and that the mechanism of HAECs to complement is the same as that of HUVECs.

Antibodies, Monoclonal↗
PubMed1996

Histological effect of intranodal injection of the streptococcal preparation OK-432 for cervical lymph node metastases of malignant head and neck tumors.

To investigate the histological effect of intranodal injection of the streptococcal preparation OK-432, we performed intranodal injection in 4 patients with cervical lymph node (CLN) metastases of malignant head and neck tumors (squamous cell carcinoma (SCC) of the oropharynx, SCC of the parotid gland, malignant lymphoma, and rhabdomyosarcoma of the nasal cavity). An initial dose of 5 klinische Einheit (KE) and a maintenance dose of 10 KE of OK-432 were administered into each metastatic or residually involved CLN twice a week. The total dose of OK-432 ranged from 105 KE to 395 KE and the number of administrations ranged from 11 to 40. Post treatment histological examination of excised tissue specimens revealed no tumor cells; there was only fibrosis and inflammatory cell infiltration. These findings suggest that intranodal injection of OK-432 can be utilized for treatment of relatively small CLN metastases of malignant head and neck tumors.

Aged↗
PubMed1995

Involvement of von Willebrand factor and PGI2 in platelet binding to a partially denuded endothelial monolayer.

Platelet binding to an endothelial monolayer was examined after denudation. The binding increased for up to 10 min and thereafter declined gradually. Antibodies against von Willebrand factor (vWF) inhibited the binding. Production of prostacyclin (PGI2) occurred 10 min after endothelial denudation. This study suggests that vWF is involved in the binding during the first 10 min and that PGI2 suppresses the binding thereafter.

Blood Platelets↗