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Biomedical subjects

F Ishida

Publications and source records attributed to F Ishida.

At least 73 records · Page 4Linked to original sources
PubMed1993

Reconstruction of jugular and portal blood flows using remodeled great saphenous vein grafts.

Remodeled great saphenous vein grafts were used to reconstruct both jugular and portal veins. The great saphenous vein was split longitudinally and sutured side-to-side to construct a vessel twice the diameter and one half the length of the original vessel. This graft was used with good results for reconstruction of the jugular veins in a patient after a bilateral neck dissection for tongue cancer and for a portal vein in a patient after resection for cancer in the head of the pancreas.

Adult↗
PubMed1993

Aplastic anemia and idiopathic thrombocytopenic purpura with antibody to platelet glycoprotein IIb/IIIa following resection of malignant thymoma.

A case of a 64-year-old Japanese woman who developed aplastic anemia and idiopathic thrombocytopenic purpura with antibody to platelet glycoprotein IIb/IIIa 4 years following a resection of malignant thymoma is reported. Bone marrow was hypocellular and ferrokinetics revealed the prolongation of the half-time of plasma iron disappearance and a decrease in red cell utilization, findings compatible with a diagnosis of aplastic anemia. The life span of platelets was markedly decreased to 3.07 h, and the test for antiplatelet glycoprotein IIb/IIIa antibody was positive. The patient's serum had a suppressive effect on the formation of colonies of burst-forming unit-erythroid and colony-forming unit-granulocyte using normal bone marrow cells. These results suggest that the aplastic anemia in this patient may have been induced by some suppressive activity in the serum. Splenectomy followed by an administration of cyclosporine effectively restored the peripheral blood count.

Anemia, Aplastic↗
PubMed1993

[Cell kinetics of colorectal tumors with assessment by K-ras mutation and PCNA labeling index].

K-ras mutations in colorectal tumors (53 carcinomas, 21 adenomas) were investigated using oligonucleotide probes specific for mutations at codon 12, 13, or 61 of the K-ras gene by polymerase chain reaction and oligonucleotide hybridization techniques, and the proliferative activities were assessed immunohistochemically by using anti-proliferating cell nuclear antigen (PCNA), counting PCNA labeling index (LI). Point mutations were observed 18.8% in the adenomas, 40.0% in the intramucosal carcinomas and 27.0% in the invasive carcinomas. Fewer incidences of K-ras mutations in the invasive carcinoma suggested carcinomas without K-ras mutation invade rapidly. Clinicopathologically, K-ras mutation-positive carcinomas tended to show the presence of venous invasion (p < 0.005). There were many distant metastases in the K-ras mutation-positive cases (p = 0.07). Moreover, among adenocarcinomas a significant correlation was demonstrated between PCNA LI and the pattern of infiltrating growth (p < 0.05). Our data imply that the K-ras mutation gains access to invasion and metastasis, as well as the ras mutation occurs at the initiation of the carcinoma. The present data suggest that K-ras mutations in colorectal carcinomas are correlated with venous invasion, while cell proliferative activities are related to stromal invasion, and these factors are independent markers for invasion of colorectal carcinomas.

Adenoma↗
PubMed1993

[Clinical efficacy of cis-diamminedichloroplatinum [II] and 5-fluorouracil (UFT) in advanced cancer of the alimentary tract].

A clinical study of the combination of cis-diamminedichloroplatinum [II] (CDDP) and 5-fluorouracil derivatives was conducted in advanced cancer of the alimentary tract. The regimen consisted of CDDP 50 mg/body/day (day 1-2, continuous infusion), 5-fluorouracil 500-750 mg/body/day (day 2-7, continuous infusion) and UFT 400 mg/day (day 8-28) on 1-3 courses. Thirty patients could be evaluated. The response rate was 25% (2/8) in cases of esophageal cancer, 31% (4/13) in gastric cancer and 33% (3/9) in colorectal cancer, with an overall response rate of 30% (9/30). A comparatively higher response rate was obtained in lymph node metastases (46%) and liver metastases (50%). Anorexia, nausea/vomiting and leukocytopenia were frequently observed, but almost all were well tolerated and recovered except two cases with severe leukocytopenia and nephrotoxicity. Based on these results, this combination chemotherapy seems to be useful for advanced cancer of the alimentary tract.

Adult↗
PubMed1992

Suppressive effects of the endothelin receptor (ETA) antagonist BQ-123 on ET-1-induced reduction of lipoprotein lipase activity in 3T3-L1 adipocytes.

Endothelin (ET)-1 reduced heparin-releasable lipoprotein lipase (LPL) activity in 3T3-L1 adipocytes in a concentration-dependent manner. However, a selective ETB receptor agonist, [Ala1,3,11,15]ET-1, did not act like ET-1. The ET-1-induced decrease in LPL activity was suppressed by a selective ETA receptor antagonist, BQ-123: the concentration-response curve for the ET-1 reduction of LPL activity was shifted to the right in the presence of BQ-123 in a concentration-dependent manner. This antagonistic effect of BQ-123 clarifies that the ETA receptor is responsible for the ET-1-induced reduction of LPL activity in 3T3-L1 adipocytes, which suggests that there is therapeutic potential for ETA antagonists in LPL-related lipoprotein disorders.

3T3 Cells↗
PubMed1992

Genetic and structural characterization of an amino acid dimorphism in glycoprotein Ib alpha involved in platelet transfusion refractoriness.

The platelet-specific alloantigen, Siba, located within the alpha-subunit of the glycoprotein (GP) Ib-IX membrane receptor, has been found to be involved in the pathogenesis of platelet transfusion refractoriness. We have identified the existence of a naturally occurring threonine/methionine dimorphism at position 145 of the GPIb alpha sequence, and determined that the Siba antigen corresponds to the molecule containing methionine145. The diallelic codons can be detected by restriction enzyme analysis of amplified genomic DNA fragments from the GPIb alpha gene. Evaluation of 61 healthy blood donors showed that the allele frequencies are 89% and 11% for the threonine145 and methionine145 codons, respectively. A positive correlation exists between platelet reactivity with the anti-Siba antibody and the presence of a methionine145-encoding allele. Moreover, recombinant expression of two soluble GPIb alpha fragments differing only at residue 145, provided definitive evidence that the human anti-Siba antibody reacts only with the molecule containing methionine145. These results explain the structural basis of the Siba human alloantigen system and define screening methodologies useful in transfusion medicine to match donor and recipient platelets accordingly.

Amino Acids↗
PubMed1992

Effect of bacteriohopane-32-ol on lipid metabolism in Hep G2 cells.

To investigate the biological activity of the hopane group of pentacyclic triterpenes, the effect of bacteriohopane-32-old (Monol) on lipid synthesis and secretion was determined using Hep G2 cells. Despite its structural similarity to 25-hydroxycholesterol, Monol did not affect free and esterified cholesterol synthesis determined by the incorporation from [14C]acetate. Monol reduced the phospholipid secretion from Hep G2 cells without affecting cellular phospholipid synthesis from [3H]glycerol. It also decreased the secretion of apolipoprotein B. These results suggest that the Monol-induced reduction in phospholipid secretion is due to a decrease in the number of lipoprotein particles secreted from Hep G2 cells.

Animals↗
PubMed1992

Effect of an inhibitor of squalene epoxidase, NB-598, on lipid metabolism in Hep G2 cells.

NB-598, a potent inhibitor of squalene epoxidase, inhibited cholesterol synthesis from [14C]acetate and induced intracellular squalene accumulation in Hep G2 cells. NB-598 inhibited cholesterol synthesis from [14C]acetate, [3H]mevalonate, and [3H]squalene, but not from [3H]2,3-oxidosqualene in Hep G2 cells. It reduced cholesterol ester synthesis remarkably in the absence of exogenous cholesterol. This compound did not have any effect on the synthesis of ubiquinone and dolichol. When Hep G2 cells were prelabeled with micellar [3H]cholesterol, NB-598 did not affect the excretion of bile acid incorporated from [3H]cholesterol. However, NB-598 decreased the secretion of free and esterified cholesterol, triacylglycerol, and phospholipids, and increased the secretion of squalene. NB-598 is thought not only to inhibit cholesterol synthesis, but also to inhibit the secretion of lipids.

Anticholesteremic Agents↗
PubMed1992

[Case report of a successful stage reduction of gastric carcinoma preoperatively treated by combined chemotherapy of 5-FU(UFT) and cisplatin].

A 52-year-old woman was diagnosed to have IIc+IIa-like advanced gastric carcinoma in the upper stomach by X-ray and endoscopic examination with biopsy. CT scan revealed swelling of the para-aortic lymph nodes which was taken to be evidence of metastases of the gastric carcinoma. The patient was considered to have surgically non-curative gastric carcinoma (Stage IV), and preoperative chemotherapy was initiated. The regimen consisted of CDDP 50 mg (day 1-2, drip), 5-FU 750 mg (day 2-7, drip) and UFT 400 mg (from day 8 to the day before operation, oral). About one month after initiating treatment, total gastrectomy with lymph node dissection was performed. Histopathological examination of the section of the primary tumor revealed that only a few cancer cell nests (poorly differentiated adenocarcinoma) remained in the muscle and subserosal layer. In all of the lymph nodes which were suspected to have metastases preoperatively, cancer cells completely degenerated into mucinous lakes or foam cell nests. No liver metastasis nor peritoneal dissemination was detected, and this case was judged to be stage II after chemotherapy.

Adenocarcinoma↗
PubMed1991

Human platelet-specific antigen, Siba, is associated with the molecular weight polymorphism of glycoprotein Ib alpha.

Platelet-specific antigen Sib(a) has been highly implicated in the pathogenesis of refractoriness to human leukocyte antigen (HLA)-matched platelet transfusions in Japan. We provide evidence that the Sib(a) antigen is located on the glycoprotein (GP) Ib alpha and has a close association with the molecular weight (mol wt) polymorphism of GPIb. In modified antigen-capture ELISA (MACE), anti-Sib(a) antibody reacted only with GPIb/IX held by a murine anti-GPIb/IX monoclonal antibody (MoAb). The reactivity of anti-Sib(a) antibody to Sib(a)-positive (Sib(a+)) platelets was abolished after they were treated with Serratia marcescens protease. Platelets from 50 healthy volunteers were semiquantitatively phenotyped for Sib(a) antigen by MACE and divided into three distinct groups: strongly positive, positive, and negative. They were also analyzed by sodium dodeyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and periodic acid-silver staining for mol wt polymorphism of GPIb, phenotyped as A, B, C, or D. Without exception, Sib(a+) platelets showed larger phenotypes (A or B). Removal of sialic acid from Sib(a+) platelets did not reduce the binding of anti-Sib(a). Finally, anti-Sib(a) antibody specifically immunoprecipitated A and B phenotypes of GPIb from Sib(a+) platelets. Thus, Sib(a) antigen evidently is located in the region of glycocalicin that is present only on the A and B phenotypes of GPIb.

Antigens, Human Platelet↗
PubMed1991

Effect of simvastatin (MK-733) on plasma triacylglycerol levels in rats.

The effect of simvastatin (MK-733), an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, on plasma triacylglycerol (TG) levels was studied in rats. Dietary administration of MK-733 (0.055%, w/w) for 7 days significantly (P less than 0.05) reduced plasma TG levels by 30.6% associated with a 44.3% significant (P less than 0.01) reduction in very low density lipoprotein TG (VLDL-TG) as compared to those in the concurrent control rats. Clofibrate (0.08%, w/w) also significantly (P less than 0.05) decreased plasma TG levels by 26.1%. MK-733 did not affect the triacylglycerol secretion rate (TGSR) during 0-1.5 hr after administration of Triton WR-1339, but reduced it by 33.9% during 1.5-3.0 hr. Clofibrate also decreased TGSR during 1.5-3.0 hr. MK-733 increased lipoprotein lipase (LPL) activity in epididymal adipose tissue and thigh muscle by 36.3 and 55.0% respectively. MK-733 significantly (P less than 0.05) increased LPL activity in the post-heparin plasma by 21.5%, although it did not affect hepatic triacylglycerol lipase (H-TGL) activity. Clofibrate did not affect LPL activity in the tissues or LPL and H-TGL activities in the post-heparin plasma. It is considered that the mechanism of plasma TG-lowering effect of MK-733 is the removal of VLDL-TG by an increase in LPL activity in the tissues as well as a decrease in the TGSR.

Adipose Tissue↗
PubMed1991

[Primary plasma cell leukemia associated with hypercalcemia].

A 34-year-old male was admitted to our hospital because of anorexia and nausea in September, 1987. On admission, anemia, thrombocytopenia and hypercalcemia were observed, and the peripheral blood showed leukocytosis with atypical plasma cells (50%). Bone marrow aspiration showed hypercellularity, with a presence of atypical plasma cells (82%). The M-type protein in the serum and urine was identified as lambda Bence Jones protein by immunoelectrophoresis. On systemic skeletal X-rays, osteolytic lesions were not detected. Thus, a diagnosis of plasma cell leukemia associated with hypercalcemia was made. Hypercalcemia was treated successfully with overhydration. However the disease was refractory to combination chemotherapy, and at 10 months after diagnosis, he died of septic candidiasis. Hypercalcemia associated with plasma cell leukemia in its initial stage is rare.

Adult↗
PubMed1990

Effect of simvastatin (MK-733) on the regulation of cholesterol synthesis in Hep G2 cells.

A new antihypercholesterolemic drug, simvastatin (MK-733), which is a prodrug of a potent 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, inhibited cholesterol synthesis from [14C]acetate concentration dependently without inhibiting it from [3H]mevalonate in Hep G2 cells. Therefore, MK-733 is thought to be converted to L-654,969, the active beta-hydroxy acid form of MK-733 in the cells and/or medium. MK-733 inhibited cholesterol ester synthesis, but did not affect phospholipid, free fatty acid and triacylglycerol synthesis. This compound increased HMG-CoA reductase activity concentration dependently and raised the specific binding, internalization and degradation of 125I-labeled low density lipoprotein by Hep G2 cells. Another HMG-CoA reductase inhibitor, pravastatin (CS-514), also behaved like MK-733. However, its potency was far less than that of MK-733.

Anticholesteremic Agents↗
PubMed1990

Comparative effects of simvastatin (MK-733) and pravastatin (CS-514) on hypercholesterolemia induced by cholesterol feeding in rabbits.

The preventive effects of simvastatin (MK-733) and pravastatin (CS-514), 3-hydroxy-3-methylglutarylcoenzyme A (HMG-CoA) reductase inhibitors, on hypercholesterolemia induced by 0.25% cholesterol feeding were compared in rabbits. MK-733 (6, 2 and 0.7 mg/kg) was found to prevent the increase in serum total cholesterol levels dose-dependently. High dose CS-514 (18 mg/kg) also limited the increase in the cholesterol levels, but medium (6 mg/kg) and low doses (2 mg/kg) of CS-514 were ineffective in preventing it. MK-733 inhibited the increase in VLDL and LDL cholesterol levels dose-dependently. MK-733 suppressed the increase in serum phospholipid levels. MK-733 inhibited the accumulation of cholesterol in the liver. The high dose of CS-514 also limited it. High dose MK-733 (6 mg/kg) reduced the cholesterol concentration in gallbladder bile. Neither MK-733 nor CS-514 affected bile acid excretion in the gallbladder bile. High dose MK-733 decreased the lithogenic index. MK-733 increased the number of LDL receptors, and high dose CS-514 also increased it. The suppressive effect of CS-514 on serum cholesterol levels at 18 mg/kg was found to be less than that of MK-733 at 0.7 mg/kg.

Animals↗
PubMed1990

Target cell of leukemic transformation in acute megakaryoblastic leukemia.

Acute megakaryoblastic leukemia (AMkL) is a newly defined acute leukemia in which the differentiation of proliferating blasts is arrested at the megakaryocytic precursor stage. In order to clarify whether a target cell of leukemic transformation in AMkL is a cell committed to megakaryocytic lineage, or a multipotential stem cell, we examined AMkL patients with regard to: a) the presence of myelodyplastic features in residual erythroid and granulocytic cells, b) coexistence of myeloperoxidase (MPO)-positive blasts with megakaryoblasts, and c) the presence of the same chromosomal abnormality in erythroid and granuloid colony-forming cells as seen in megakaryoblasts. Regarding the former two items, results were compared with those from megakaryoblastic crisis of chronic myelocytic leukemia (CML-MkBC) and transient myeloproliferative disorder in Down syndrome (DS-TMD), which are thought to be multipotential stem cell disorders. Among 18 patients with AMkL, three, all complicating myelofibrosis, had marked myelodysplastic changes of erythroid series and/or granulocytic series. In 4 out of 7 patients with CML-MkBC, 5 out of 8 patients with DS-TMD, and 7 out of 18 patients with AMkL, MPO-positive blasts, even though rare, were observed in addition to PPO-positive blasts. All except one of these patients with AMkL also showed complicating myelofibrosis. In one case of AMkL with myelofibrosis, chromosomal analysis of cultured cells of individual colonies revealed that all the analysable metaphases from both CFU-GM and BFU-E had the same chromosomal abnormality as megakaryoblasts. This study has clarified that a considerable proportion of AMkL cases, particularly those with complicating myelofibrosis or showing acute myelofibrosis, arise against the background of a multipotential stem cell disorder, even if blasts are exclusively megakaryocytic in phenotype.

Cell Transformation, Neoplastic↗