Search PubMed⌕ Search

Biomedical subjects

A Nishio

Publications and source records attributed to A Nishio.

At least 55 records · Page 3Linked to original sources
PubMed2000

Vasopressin receptor subtypes on mesenteric and cremasteric arterioles in rat.

We studied the effects of a selective vasopressin V(1A) receptor antagonist [1-(1-(4-(3-acetylaminopropoxy)benzoyl)-4-piperidyl)-3, 4-dihydro-2(1H)-quinolinone (OPC-21268)] and a selective vasopressin V(2) receptor antagonist [5-dimethylamino-1(4-(2-methylbenzoylamino)benzoyl)-2,3,4, 5-tetrahydro-1H-benzazepine (OPC-31260)] on vasopressin-induced contraction of mesenteric and cremasteric arterioles in urethane-anaesthetized rats. Vasopressin was infused intravenously for 60 min or applied topically to arterioles directly. Vasopressin infusion (50, 100 or 500 ng/kg/min) decreased the diameter of both mesenteric and cremasteric arterioles. Vasopressin (500 ng/kg/min)-induced vasoconstriction was antagonized by OPC-21268 (0. 2, 1.0 and 5.0 mg/kg, i.v.), dose-dependently, but not by OPC-31260. Topically applied vasopressin (4.6x10(-10)-4.6x10(-8) M) dose-dependently constricted both microvessels. Pre-administration of OPC-21268 (5.0 mg/kg, i.v.) completely inhibited topically applied vasopressin-induced vasoconstriction in both microvessels, and OPC-31260 partially inhibited it in cremasteric arterioles. These results suggest that vasopressin induces vasoconstriction in rat mesenteric and cremasteric arterioles mainly by stimulating vasopressin V(1A) receptors, while vasoconstriction in cremasteric arterioles is partly associated with stimulation of vasopressin V(2) receptors.

Animals↗
PubMed2000

Expression of membrane-type 1 matrix metalloproteinase in coronary vessels of allotransplanted primate hearts.

BACKGROUND: The mechanisms of intimal thickening in cardiac allograft vasculopathy (CAV) remain controversial after heart transplantation. Matrix metalloproteinase-2 (MMP-2) plays a crucial role in degrading extracellular matrix (ECM) during neointimal formation. Recently, it has been revealed that MMP-2 is activated by membrane-type 1 matrix metalloproteinase (MT1-MMP). This process involves tissue inhibitor of MMP-2 (TIMP-2), forming an MT1-MMP/TIMP-2/pro-MMP-2 complex. In this study, we hypothesize that these components contribute to the pathogenesis of CAV. METHODS: Heterotopic cardiac allografting was performed in randomly paired Japanese monkeys with an immunosuppressive regimen of intravenous administration of antihuman CD18 monoclonal antibody. The donor hearts were harvested at Days 22, 28, 40, 41, and 95 posttransplantation. We examined expression of MMP-2, MT1-MMP, and TIMP-2 of graft vessels using immunohistochemistry and protein level by western blot analysis. RESULTS: Pathologically, various degrees of neointimal formation were observed. In the allografts harvested at Days 22, 28, 40, and 41, MT1-MMP was expressed in the endothelial cells and smooth muscle cells (SMCs) in media of some arteries without histological change, accompanied by expression of MMP-2 and TIMP-2. In the severely thickened neointima of the allograft harvested at Day 95, MMP-2 and faint MT1-MMP were expressed in SMCs of severely thickened neointima and media; TIMP-2 expression was seen only in noncollagenous tissue of severely thickened neointima. MMP-2 protein was more intensely expressed in the allograft harvested at Day 95 than in the allograft harvest at Day 41, while TIMP-2 protein level was almost same in the 2 samples. CONCLUSION: We observed the simultaneous expression of MMP-2, MT1-MMP, and TIMP-2. Thus, ECM degradation triggered by MT1-MMP/TIMP-2/pro-MMP-2 complex could be a novel mechanism of CAV.

Animals↗
PubMed2000

Alcohol sclerotherapy of hepatic cysts: its effect in relation to ethanol concentration.

While ultrasonically guided percutaneous aspiration and ethanol injection therapy has proved useful for non-neoplastic giant hepatic cysts that cause symptoms, the optimum quantity of ethanol injected into hepatic cysts has not been established. In eight patients with non-neoplastic giant hepatic cysts who were treated by ethanol injection, ethanol concentration in cystic fluid after treatment was estimated. Ethanol concentrations ranged from 5.9 to 47.6%. Hepatic cyst regressed almost completely in five cases; in all of which, the estimated ethanol concentrations were more than 40%. Our results suggest that it is desirable to drain cystic fluid as much as possible and to inject ethanol as little as possible, so that the estimated ethanol concentration in the cyst exceeds 40% for maximal effect and minimal side effects.

Journal Article↗
PubMed2000

Primary biliary cirrhosis: an orchestrated immune response against epithelial cells.

Primary biliary cirrhosis (PBC) is an organ-specific autoimmune disease that predominantly affects women and is characterized by chronic progressive destruction of small intrahepatic bile ducts with portal inflammation and ultimately fibrosis. The serologic hallmark of PBC is the presence of antibodies to mitochondria, especially to the E2 component of the pyruvate dehydrogenase complex. The mechanisms by which (and if) such antibodies produce liver tissue injury are unknown. However, the presence of these antibodies has allowed detailed immunological definition of the antigenic epitopes, the nature of reactive autoantibodies and the characterization of T-cell responses. Several mechanisms may now be proposed regarding the immune-mediated bile duct damage in PBC, including the possible role of T-cell-mediated cytotoxicity and intracellular interaction between the IgA class of antimitochondrial antibodies and mitochondrial autoantigens. There are major questions which remain unanswered, including, of course, etiology, but also the reasons for female predominance, the absence of PBC in children, the relative ineffectiveness of immunosuppressive drugs, and the specific role of mitochondrial antigens. The data so far provide suggestive evidence that PBC is a mucosal disease; this thesis provides a basis for discussion of etiology via the enterohepatic circulation of toxins and/or infection.

Acyltransferases↗
PubMed2000

Histochemical study of angiogenesis in basaloid squamous carcinoma of the esophagus.

Angiogenesis of esophageal basaloid squamous carcinoma (BSC) was studied immunohistochemically and compared with that of squamous cell carcinoma (SCC). In tissues taken from six patients with esophageal BSC and 35 with esophageal SCC, angiogenesis was evaluated by measuring microvessel density (MVD), defined as the microvessel count determined using factor VIII-related antigen immunostaining, and by measuring immunoreactivity of vascular endothelial growth factor (VEGF) and thymidine phosphorylase (dThdPase). Three of the six patients with BSC had distant metastases. There was no difference of MVD between BSC and SCC (22.0 +/- 4.6 vs. 27.6 +/- 9.4). VEGF expression tended to be more frequently observed in BSC than in SCC (100% vs. 60.0%; p = 0.066). Strong expression of VEGF was detected in three BSC with distant metastases; however, there was no difference in the rate of strong VEGF expression between BSC and SCC. The MVD in the cases of BSC with strong VEGF expression, i.e. in the cases with distant metastases, was higher than that in the cases of BSC with weak VEGF expression (p=0.049). There was no difference in dThdPase expression of the cancer cells between BSC and SCC (50.0% vs. 54.3%), whereas the infiltrating stromal cells of all the BSC expressed dThdPase. Strong dThdPase expression in the cancer cells or in the infiltrating stromal cells was observed in two and three BSC, respectively. However, there were no differences in the rate of cancer cells or stromal cells with strong dThdPase expression between BSC and SCC. In one BSC with high MVD and distant metastases, VEGF and dThdPase were both strongly expressed. The vascularity of esophageal BSC was not different from that of SCC. VEGF may participate in angiogenesis of esophageal BSC and may influence the rate of metastasis in esophageal BSC patients. dThdPase may play a partial rule in angiogenesis and metastasis in some cases of BSC.

Aged↗
PubMed2000

The pyruvate dehydrogenase complex as a target autoantigen in primary biliary cirrhosis.

Mitochondrial autoantigens and their B and T cell autoepitopes have been well defined in primary biliary cirrhosis (PBC). However, the relationships of the antimitochondrial antibodies and the mechanisms of bile duct destruction in PBC remain an enigma. The serological hallmark of PBC remains the presence of antibodies to mitochondria, particularly to the E2 component of the pyruvate dehydrogenase complex (PDC-E2). However, several mechanisms may now be proposed which may explain the immune-mediated bile duct damage in PBC. These include the possible role of T cell-mediated cytotoxicity as well as the interaction between the IgA class of antimitochondrial antibodies and the mitochondrial autoantigens. A prominent feature in this discussion is the highly directed and specific immune response to the mitochondrial antigens, including PDC-E2 as well as other members of the 2-oxo-acid dehydrogenase complexes. Ultimately, the mechanisms that lead to this immune reaction should provide data on other questions in PBC, including the reasons for female predominance, the absence of PBC in children and the relative ineffectiveness of immunosuppressive agents.

Autoantigens↗
PubMed2000

Captopril increases the affinity of bradykinin receptor binding sites in bovine coronary arterial endothelial cells.

In a radioligand binding study using bovine coronary artery endothelial cell membranes, captopril changed a single bradykinin (BK) binding site (Kd = 1.77 nM, Bmax = 60.2 fmol/mg protein) to high- (Kd = 0.68 pM, Bmax = 17.7 fmol/mg protein) and low- (Kd = 1.00 nM, Bmax = 72.5 fmol/mg protein) affinity binding sites. This effect was reversed by GppNHp. Captopril also enhanced BK-induced endothelium-dependent relaxation in saponin-treated coronary rings, and GppNHp partially suppressed this enhancement. These results suggest that captopril may affect BK receptors that couple to G-proteins.

Angiotensin-Converting Enzyme Inhibitors↗