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T Maeba

Publications and source records attributed to T Maeba.

At least 55 records · Page 3Linked to original sources
PubMed1996

Impact of adhesion molecules of the selectin family on liver microcirculation at reperfusion following cold ischemia.

We investigated the role of adhesion molecules in the early phase of reperfusion following cold ischemia. Livers of male Lewis rats were preserved for 0 h (group A) or 24 h in University of Wisconsin (UW) solution without additives (group B) or in UW solution with anti-ICAM-1 antibody (group C) or anti-E-selectin-1, SLe(x) and SLe(a) antibodies (group D). The livers were then reperfused with diluted rat whole blood (DWB; groups A and B). DWB containing anti-ICAM-1 and LFA-1 antibodies (group C) or DWB containing anti-L-selectin, SLe(x) and SLe(a) antibodies (group D). The reperfusion was performed at 37 degrees C for 1 h at 5 cm H2O of perfusion pressure. During reperfusion, hepatic microcirculation was assessed by monitoring portal and peripheral tissue blood flow. Bile production was significantly reduced in group B livers compared with those in group A. Anti-ICAM-1 and LFA-1 antibodies failed to improve hepatic microcirculation, whereas anti-LECAM-1, SLe(x) and SLe(a) antibodies significantly improved the microcirculation. Bile production in group C and D livers was comparable to that in group B livers. Preservation for 24 h significantly increased the release of TNF-alpha from 0.207 to 43.7 pg/g per hour during reperfusion. Monoclonal antibodies to the adhesion molecules did not suppress the release of TNF-alpha in groups C and D. Histological examination demonstrated a lack of leukocyte infiltration or thrombus in hetapic microvessels. The extent of hepatocyte necrosis did not differ among groups B, C, and D. We conclude that the microcirculatory disturbance in the early phase of reperfusion occurs as a result of the tethering of leukocytes through the interaction of the selectin family and their ligands, and that the ICAM-1-LFA-1 pathway is not involved in this step. The lack of improvement in bile production with antibodies to the selectin family and their ligands strongly suggests that other mechanisms participate in the deterioration of hepatic function.

Adenosine↗
PubMed1996

Combination immunotherapy with OK-432, recombinant granulocyte-colony-stimulating factor and recombinant interleukin-2 for human hepatocellular carcinoma.

The antitumor effects of immunotherapy using streptococcal preparations (OK-432), recombinant granulocyte-colony-stimulating factor (rG-CSF) and recombinant interleukin-2 (rIL-2) were examined for human hepatocellular carcinoma (HCC). Following subcutaneous injection of OK-432 (2 KE) and rG-CSF (50-60 microg), low-dose intratumoral administration of OK-432 (3-12 KE) was performed. Thereafter, 2 x 10(5) JRU of rIL-2 was subcutaneously injected. This therapeutic regimen was repeated twice. Serum alpha-fetoprotein levels were markedly decreased in three of seven patients with HCC by this treatment. Post-therapeutic histological examination revealed that trabecular cords or pseudoglandular arrangements of tumor cells were completely disordered in all cases and that extensive infiltration of lymphocytes into the tumor stroma was present in five cases. The number of CD4- and CD57-positive cells among tumor-infiltrating lymphocytes after immunotherapy was significantly higher than that in patients without immunotherapy (P <0.01). These findings suggest that even a small intratumoral injection of OK-432 can induce extensive infiltration of helper/inducer and natural killer cells into the tumor stroma when combined with subcutaneous injection of OK-432, rG-CSF and rIL-2 and that these cells might play important roles in tumor cytotoxicity.

Aged↗
PubMed1996

Protective effects of antithrombin III supplementation on warm ischemia and reperfusion injury in rat liver.

The effect of antithrombin III (AT III) supplementation on energy status, microcirculation, cytoprotection, and prostacyclin (PGI2) production during and after a period of warm ischemia of the rat liver was investigated. AT III supplementation (250 units/kg) stimulate prostaglandin I2 (PGI2) production from 1 hour after administration, with maximal production observed at 3 hours. Ischemia was induced by occluding the hepatoduodenal ligament for 30 minutes, and experiments were continued for 60 minutes after reperfusion. The rats received AT III (250 units/kg IC) 30 minutes before induction of liver ischemia (AT III group). In the AT III group, recovery of the beta-ATP/inorganic phosphate ratio measured by 31P nuclear magnetic resonance showed significant improvement (p < 0.01), and the recovery of tissue blood flow markedly improved (p < 0.01) compared to the saline-treated group (control group). Leakages of aspartame aminotransferase, alanine aminotransferase, and lactate dehydrogenase were mitigated in the AT III group (p < 0. 05). Ultrastructural alterations of sinusoidal endothelial cells were markedly reduced in the AT III group. The PGI2 level at the end of reperfusion was significantly elevated (p < 0.01) in the AT III group compared to the control group. The results of this study indicated that pretreatment with AT III significantly improved the energy status and microcirculation, as well as histologic damage, after liver ischemia and reperfusion. One of the fundamental effects of AT III might be mediated through the production of prostacyclin.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Enhanced expression of the protein kinase substrate annexin in human hepatocellular carcinoma.

Annexin (AX) constitutes a new family of Ca2+-dependent membrane-binding proteins; 13 of them have been described. Among these, annexin-1 (AX-I) has displayed many biological functions in vitro. Its actual role in vivo, however, remains unknown. We already reported that AX-I was expressed in proliferating (regenerating) hepatocytes at both protein and messenger RNA (mRNA) levels. The role of AX-I in human hepatocellular carcinoma (HCC) remains obscure. In this study, the amounts of AX-I at protein and mRNA levels, as well as its localization, have been determined in the normal human liver, chronic hepatitis liver, and nontumorous and tumorous portions of HCC. AX-I was rarely found in normal and chronic liver tissues, whereas it is overexpressed at both the transcriptional and translational levels in tumorous and nontumorous regions of HCC. In addition, more AX-I was expressed in the tumorous portion than the nontumorous portion of HCC. AX-I was present in the hepatocytes and HCC cells, localized mainly in the cytoplasm. AX-I was expressed in poorly differentiated cancer cells. Furthermore, AX-I was tyrosine-phosphorylated in HCC. We also found that some of the AX-I- positive hepatocytes in the nontumorous tissues were derived from a particular subset of parenchymal cells (stem or oval cells). These results indicate that AX-I plays an important role in the malignant transformation process leading to HCC and that it is closely related to the histological grade of HCC. HCC would offer a novel tool with which to study the function of AX-I in malignant transformation.

Annexin A1↗
PubMed1996

[Chemotherapy for two patients with non-Hodgkin's lymphoma in hemodialysis].

There are few reports on chemotherapy of non-Hodgkin's lymphoma (NHL) in patients with chronic renal failure. Two long-term hemodialysis patients were treated for NHL with modified CHOP therapy. The plasma pharmacokinetics of adriamycin (ADR) and etoposide (VP-16) were investigated in these patients. In the first case, NHL was diagnosed in a 37-year-old male (diffuse pleomorphic, T cell type, stage I E). After 4 courses of chemotherapy, he achieved complete remission. The second case, was a 56-year-old male who was admitted to our hospital with melena and abdominal pain. A diagnosis of NHL (diffuse mixed, B cell type, stage III E) was made. Complete remission was achieved with 2 courses of chemotherapy. Levels of hematological and neurological toxicity were moderately severe but tolerable. Pharmacokinetics of ADR and VP-16 in these patients were similar to those in patients with normal renal function. These results suggested that ADR and VP-16 were effective drugs for hemodialysis patients with NHL.

Adult↗
PubMed1995

Surgical treatment of an enormous aneurysmal portahepatic venous fistula: report of a case.

We report herein the case of a 20-year-old woman in whom an enormous aneurysmal portahepatic venous fistula was found. The portal aneurysm developed in the anterior inferior segment of the right hepatic lobe, and communicated with the right portal vein and the right hepatic vein. Due to the enormous size of the shunt, and because the patient's venous blood ammonia level increased by about twofold after eating, a right lobectomy of the liver was performed. A review of the available literature and a discussion of the most appropriate treatment follows the presentation of this case.

Adolescent↗
PubMed1995

Prediction of the early prognosis of the hepatectomized patient with hepatocellular carcinoma with a neural network.

The early prognosis of the hepatectomized patients with hepatocellular carcinoma was determined preoperatively with a perceptron-type neural network. The neural network was trained with the preoperative data of 54 example cases with the early prognosis, successful or died of hepatic dysfunction, as teaching signals. After learning these examples, the neural network came to give a precise prediction to the example data except for one case. With the learned neural network, the outcomes of the hepatectomy of 11 patients (10 successful; 1 died) were predicted prospectively with 100% precision. The usefulness of the neural network for the prediction was determined.

Adult↗
PubMed1995

Comparison of warm and cold ischemia of the canine small intestine.

Warm and cold ischemia-reperfusion injuries to canine small intestine was compared. In the warm ischemic model, the superior mesenteric artery of mongrel dogs was clamped for 2 h and then released (group A). As a cold ischemia model, canine small intestines were harvested with cold lactated Ringer solution, preserved for 24 h in cold LR solution and then autotransplanted (group B). After ischemia and during reperfusion, activities of maltase (MAL), myeloperoxides (MPO), xanthine dehydrogenase (XD) and xanthine oxidase (XO) were measured as well as hypoxanthine (HX) concentration. MAL activities were not changed during warm or cold ischemia, whereas it was remarkably decreased after revascularization in both the groups. Neutrophil infiltration after reperfusion was shown by the increase of MPO activities to 8 and 1.5 U/mg protein in groups A and B respectively from a normal value of 0.35 U/mg protein. During warm ischemia, %XO (XO/XD + XO) was increased from 18.4 to 84.9% for 2 h. In contrast, %XO was not changed for 24 h of cold ischemia. Tissue accumulation of HX was increased 2.8 times from a normal value of 1.06, 2 h after warm ischemia, but there was almost neither accumulation of HX nor the conversion of XD to XO in 24 h cold ischemia. It was observed that warm and cold ischemia caused similar injury after reperfusion in spite of the striking difference in the conversion of XD to XO and accumulation of HX. Thus, it is suggested that the XO system is not always necessary for ischemia-reperfusion injury.

Animals↗
PubMed1994

The effect of FK506 on warm ischemia and reperfusion injury in the rat liver.

The protective effect of FK506 on hepatocytes against ischemia and reperfusion injury was examined by evaluating the following: the high energy phosphorus metabolism obtained using 31P magnetic resonance spectroscopy (31P-MRS) and the tissue blood flow of the liver in ischemia and the reperfusion process, mitochondrial glutamic oxaloacetic transaminase (m-GOT) and glutamic pyruvic transaminase (GPT), the survival rates of the animals, a histological study and immunohistological staining for intercellular adhesion molecule-1 (ICAM-1) in the liver after ischemia. The rats were treated with FK506 1 mg/kg/day i.m. for 4 days before testing. Ischemia was induced by clamping the hepatoduodenal ligament for 30 min. In 31P-MRS, the recovery of the hepatic energy status after ischemia, evaluated by beta-ATP/inorganic phosphate (Pi), was significantly better in the FK506 group. It also coincided with the recovery of tissue blood flow monitored with a laser Doppler flowmeter. In the histological examination, the congestion observed in the periportal region of the control group was mild, while there was less induction of ICAM-1 in the endothelial cells of the portal veins and hepatic veins in the FK506 group. From these findings, we concluded that FK506 had a protective effect on hepatocytes against warm ischemia and reperfusion injury, and the mechanism for this could partially be attributed to improved tissue blood flow after ischemia by the modulation of immunological events.

Alanine Transaminase↗