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Biomedical subjects

T Kikuchi

Publications and source records attributed to T Kikuchi.

At least 307 records · Page 17Linked to original sources
PubMed1996

Improvement of erythroid toxicity by lentinan and erythropoietin in mice treated with chemotherapeutic agents.

Lentinan, an antitumor polysaccharide, has been assessed for its potential in vivo to augment erythroid progenitor cells and protect them from the cytotoxic effects of antitumor chemotherapeutics. Lentinan augmented the level of burst-forming units-erythroid (BFU-E) and accelerated the recovery of the reduced number of BFU-E in mice treated with 5-fluorouracil (5-FU); lentinan did not influence red blood cell counts or colony-forming unit-erythroid (CFU-E) numbers in the femoral marrow. A significant decrease in stem cell inhibitory factor (SCIF) activities in bone marrow and an increase in colony-forming unit-spleen (CFU-S) formation were observed in the lentinan-treated mice. The mechanism of augmented BFU-E formation may be partly due to augmented production of stem cells, giving rise to both CFU-GM and BFU-E. Furthermore, when lentinan administration was followed by administration of erythropoietin (Epo) in 5-FU-treated mice, increases in femoral marrow and splenic CFU-E formation and augmentation of reticulocyte counts were observed beyond the level observed in mice treated with Epo alone. These results suggest that lentinan may augment the effects of Epo on erythropoiesis in the course of anemia and the decreased erythropoiesis in cancer patients receiving chemotherapy.

Animals↗
PubMed1996

[Therapy-related AML(M2) with t(8;21) that developed three years after chemotherapy for hepatocellular carcinoma].

A 60-year-old male with hepatocellular carcinoma was treated by repeated intra-arterial injection of epirubicin, carboplatin and doxorubicin. Subsequently, radiotherapy and intravenous administration of etoposide were also carried out. Thirty-three months later he developed AML (M2). The chromosome analysis revealed 45, X, -Y, t (8;21) (q22;q22), which suggested that this leukemia was induced by topoisomerase II targeting agents. He was treated with low dose BHAC and G-CSF and achieved complete remission. This leukemia may be caused by synergic effect of topoisomerase II inhibitors and carboplatin together with radiotherapy. This may be the first report of therapy-related leukemia following chemotherapy for hepatocellular carcinoma.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1996

[Axillo-iliac bypass grafting for reoperation of graft stenosis after aortic arch reconstruction of type B interruption of the aortic arch: two cases report].

Right axillo-iliac bypass grafting was performed in two females (10 and 14 years old) who had stenosis or obstruction of grafts after reconstruction of the aortic arch in type B interruption. The initial bypass operations were carried out at the age of 5 months and 5 years, with the use of a 5-mm EPTFE graft and a 10-mm Dacron graft. Nine years later, the EPTFE graft was completely obstructed, and the Dacron bypass has stenosis, kink and calcification. To minimize surgical invasion, axillo-iliac extra-anatomical bypass was employed in both patients. 8-mm or 10-mm Hemashield grafts were implanted between the right axillar artery and the right common iliac artery through the intrapleural-preperitoneal route, and favourable results were obtained in both patients. The axillo-iliac bypass is considered to be a beneficial conservative method of reoperation for stenosis after graft reconstruction of the aortic arch in the younger age patients.

Adolescent↗
PubMed1996

Pathomechanism of spontaneous regression of the herniated lumbar disc: histologic and immunohistochemical study.

To ascertain the pathomechanism of spontaneous regression of lumbar disc herniation, histological and immunohistochemical studies on 100 herniated discs were performed. Inflammatory findings such as cell infiltration, neovascularization, and granulation were observed in 16.9% of the protruded discs, 81.8% of the subligamentously extruded discs, 100% of the transligamentously extruded disks, and 80% of the sequestrated discs. The infiltrated cells were composed mainly of macrophages and a small number of T lymphocytes. Furthermore, the cell infiltration was more prominent in the nucleus pulposus (NP) than in the annulus fibrosus (AF). There was no correlation between the occurrence rate of inflammatory response and the length of the period from onset to operation. Based on these findings, it is considered that an extruded or sequestrated disc has a potential to be resorbed by phagocytes.

Adolescent↗
PubMed1996

[Open heart surgery with bloodless priming for cyanotic congenital heart diseases--the role of autologous blood donation after induction of anesthesia].

In 50 patients with cyanotic congenital heart diseases, open heart surgery was conducted with bloodless priming from January 1994 to August 1995. Surgical procedures included the Rastelli procedure (n = 14), the modified Fontan procedure (n = 10), and intracardiac repair of TOF (n = 26). The non-transfusion rate from January 1994 to August 1994 was 17% (1/6) in the Rastelli group, 67% (2/3) in the Fontan group, and 67% (8/12) in the TOF group. Autologous blood donation immediately after induction of anesthesia was carried out from September 1994 because post-operative hemorrhage and severe hemolysis of residual blood of the pump required conventional blood transfusions up to August. Autologous blood of 12 +/- 2 ml/kg could be collected, and the non-transfusion rate from September 1994 to August 1995 was increased to 75% (6/8) in the Rastelli group, 86% (6/7) in the Fontan group, and 93% (13/14) in the TOF group. There were no complications due to asanguineous extracorporeal circulation or autologous blood donation, and the post-operative hemodynamic and respiratory status were uneventful in almost all cases. We conclude that open heart surgery without blood transfusion is feasible in more than 70-80% patients who undergo the Rastelli procedure, the modified Fontan procedure or intracardiac repair of TOF. Autologous blood donation after induction of anesthesia proved to be highly effective method for reducing conventional blood transfusion.

Blood Transfusion, Autologous↗
PubMed1996

[Regulation of secretory leukoprotease inhibitor gene expression].

Secretory leukoprotease inhibitor (SLPI), also called antileukoprotease (ALP) or mucous proteinase inhibitor (MPI), is a 12-kDa, nonglycosylated serine protease inhibitor present in mucous secretions. It is thought to play a role in protecting the mucosae from injury associated with inflammation. SLPI is locally produced by serous cells, including bronchial submucosal glands. Previous papers have suggested that its gene expression in the airway epithelial cells shows cell-type specificity and is modulated at the mRNA level under normal and pathological conditions. To characterize the mechanism of this regulation, cis-acting elements which confer transcriptional activity on the SLPI gene were evaluated by luciferase assay, using human epithelial cell lines. Serial deletion of the promoter region from the 5' end showed that different cis-acting elements were responsible for the promoter function in A549 and HeLa cells.

Amino Acid Sequence↗
PubMed1996

[Sarcoidosis representing multiple splenic nodules in a patient with IgA nephropathy].

We have encountered a 49-year-old female with persistent proteinuria and hematuria. Blood pressure, renal function, physical findings and chest X-p showed no abnormality, but blood tests disclosed mild thrombocytopenia, elevated serum ACE activity, serum lysozyme activity and serum IgA concentration. Abdominal echography and CT revealed multiple nodules in her spleen. In order to make a definite diagnosis and exclude the possibilities of malignant lymphoma or metastatic malignant tumor, splenectomy, and open renal biopsy were performed at the same time. On histological examinations, light microscopic appearance of the spleen was characterized by non-caseating granulomas compatible with sarcoidosis. Renal biopsy specimen showed diffuse proliferative glomerulonephritis with positive staining of IgA predominantly located in the mesangial area, compatible with IgA nephropathy. The present case may provide suggestive evidence for a link between sarcoidosis and IgA nephropathy in the pathogenesis. IgA nephropathy complicated by sarcoidosis is rare, and thus is of particular interest because common immunological abnormalities might be considered in the disease process of both diseases. We feel that despite a low index of suspicion, physicians must be alert to the possibility of IgA nephritis associated with sarcoidosis. The literature is reviewed regarding the relationship between IgA nephropathy and sarcoidosis.

Female↗
PubMed1996

Effects of indomethacin on the production of matrix metalloproteinase-3 and tissue inhibitor of metalloproteinases-1 by human articular chondrocytes.

OBJECTIVE: To study the action of indomethacin on cartilage catabolic activity by comparing the production of a matrix degrading proteinase and its inhibitor in human articular chondrocyte cultures. METHODS: Matrix metalloproteinase-3 (MMP-3) and tissue inhibitor of metalloproteinases-1 (TIMP-1) in conditioned medium from human articular chondrocyte cultures were measured using a one-step sandwich enzyme immunoassay. TIMP-1 mRNA expression was analyzed by Northern blotting using a 0.6 kb cDNA probe for human TIMP-1. RESULTS: Human recombinant interleukin 1 beta (IL-1 beta) increased MMP-3 levels in primary chondrocyte cultures. Indomethacin at 10(-5) M inhibited this IL-1 beta stimulation, but had no effect in the therapeutic range (10(-6)-10(-7) M). Low levels of indomethacin (10(-7) M) significantly increased the production of TIMP-1 by chondrocytes. Synthesis of TIMP-1 appeared to be inhibited by prostaglandin E2 (PGE2), since exogenously added PGE2 reversed the stimulating effect of indomethacin on TIMP-1 production. Northern blot analysis showed that 10(-7) M indomethacin increased TIMP-1 mRNA levels in chondrocytes. CONCLUSION: Our findings indicate that low levels of indomethacin can benefit matrix metabolism by affecting the balance of proteinases to their inhibitors in human articular cartilage.

Blotting, Northern↗
PubMed1996

[Surgical resection of pulmonary metastases from colorectal cancer].

Pulmonary resection of metastatic lesions from colorectal cancer was performed in 19 patients. The cumulative 5-year survival after thoracotomy was 39%. Patients with either one or two metastases has a significantly better survival, with a 5-year survival of 55%, than did those with a greater degree of metastases. Other factors had no apparent influence on postthoracotomy survival. Therefore, the number of metastases should be carefully considered when pulmonary resection is considered for metastatic colorectal cancer.

Aged↗
PubMed1996

Receptor binding and antagonist properties of a novel endothelin receptor antagonist, TAK-044 [cyclo[D-alpha-aspartyl-3-[(4-phenylpiperazin-1-yl) carbonyl]-L-alanyl-L-alpha-aspartyl-D-2-(2-thienyl) glycyl-L-leucyl-D-tryptophyl]disodium salt], in human endothelinA and endothelinB receptors.

Receptor binding and antagonist properties of an endothelin (ET) receptor antagonist, TAK-044 ¿cyclo[D-alpha-aspartyl-3-[(4-phenylpiperazin-1-yl) carbonyl]-L-alanyl-L-alpha-aspartylD-2-(2-thienyl) glycyl-L-leucyl-D-tryptophyl]disodium salt¿, were investigated using recombinant human ETA and ETB receptors expressed in Chinese hamster ovary cells. The membranous ETA receptor was shown to be heterogeneous in ET-3 binding affinity (Hill coefficient = 0.54, Kd1 = 390 pM and Kd2 = 8.1 nM). This heterogeneity disappeared upon the addition of guanosine-5'-O-3-thiotriphosphate (Hill coefficient = 0.95, Kd = 7.8 nM). The Kd (from a computer program LIGAND analysis) and Ki (from Dixon plot analysis) values of TAK-044 were 95 and 120 pM for the membranous ETA receptor and 41 and 60 nM for the ETB receptor, respectively. The Kd values of TAK-044 for the ETA receptor was comparable to that of ET-1. The Ki values of TAK-044 for the cellular ETA and ETB receptors were 130 pM and 130 nM at 5,000 cells/well and 1.3 and 590 nM at 50,000 cells/well, respectively. Dixon plot analysis indicated that TAK-044 is a competitive inhibitor of ET-1 binding. TAK-044 inhibited ET-1-induced phosphatidylinositol hydrolysis and arachidonic acid release at 50,000 cells/well in a competitive manner with respective pA2 values of 8.5 and 8.7 in the ETA-expressing cells and 7.4 and 6.6 in the ETB-expressing cells. TAK-044 suppressed ET-1-induced transient increase in intracellular Ca+2 concentration in the ETA- and ETB-expressing cells with respective IC50 values of 2.8 and 230 nM. TAK-044 is a potent and competitive ETA receptor antagonist which simultaneously exhibits definite antagonist activity at the ETB receptor.

Animals↗
PubMed1996

[Significance of 5'-deoxy-5-fluorouridine (5'-DFUR) administration before surgery for advanced gastric and colonic cancers--activity of pyrimidine nucleoside phosphorylase (PyNPase) and serum immunosuppressive acidic protein (IAP)].

We administered preoperatively 5'-deoxy-5-fluorouridine (5'-DFUR) for treatment of advanced gastric and colonic cancers, and measured pyrimidine nucleoside phosphorylase (PyNPase) in the excised tumor sample and serum immunosuppressive acidic protein (serum IAP), which is an index of the immunity of host-bearing cancer, while studying its direct antitumor effect and improved immunity. Patients with 24 advanced gastric cancers and 36 colonic cancers were randomly divided into a preoperatively administered group and a non-administered group. In the preoperatively administered group, 5'-DFUR (1,200 mg/day) was orally administered on preoperative days 7 approximately 14. After collecting samples (about 0.5 g) from adjacent normal tissues with tumor within 30 minutes after extirpation of tumor and freezing those less than -20 degrees C, the PyNPase level was measured as soon as possible. Moreever, serum IAP levels at pre-administration in the administered group and on admission in the non-administered group were measured. Those in the administered group were measured again on the operative day. No decreasing tendency of PyNPase was generally found in cases with gastric colonic cancers, and no significant difference in stage-II was not either. However, a decreasing tendency in tumor activity was found by pre-administration. Moreover, there was significant improvement in the serum IAP level in cases with gastric and colonic cancers by pre-operative administration of 5'-DFUR. This tendency was also found in advanced colonic cancer with Dukes-C by Dukes's classification. In conclusion, it was suggested that the pre-operative administration of 5'-DFUR for treatment of advanced gastric and colonic cancers has a favorable influence for prognosis because the tumor region was retarded by the high PyNPase activity according to the severity of tumors and elevating tendency of the immune response in host.

Administration, Oral↗
PubMed1996

Effects of hyaluronan on cell proliferation and proteoglycan synthesis in rabbit ligamental cells.

The effect of hyaluronan (HA) on cell proliferation and synthesis of proteoglycan (PG) in rabbit ligamental cells was examined in vitro. HA promoted the incorporation of 35S-sulfate in a concentration-dependent manner, significantly at 100 micrograms/ml and upward, without effect on cell proliferation. The chromatographic profile of the 35S-labelled materials extracted with 4 M guanidine hydrochloride by Sepharose CL-2B was different in the HA-treated cells as compared with untreated cells. Although the radioactivities of the low-molecular fraction peaked at Kav 0.71 did not change, those of the high-molecular fraction (Kav 0.30-0.50) increased with treatment of HA. Ligamental cells expressed the mRNA of the PG family's versican and aggrecan (large-molecular weight PGs), biglycan and decorin (small-molecular weight PGs) in dot blot analysis. Although the mRNA expression of aggrecan, biglycan and decorin did not change, that of versican increased upon treatment with HA. These findings suggest that HA is involved in promoting production of the large-molecular-weight PG versican, and in facilitating extracellular matrix formation.

Animals↗
PubMed1995

Axonal degeneration promotes abnormal accumulation of amyloid beta-protein in ascending gracile tract of gracile axonal dystrophy (GAD) mouse.

The GAD mouse is a spontaneous neurological mutant with axonal dystrophy in the gracile tract of the medulla oblongata and spinal cord. The immunoreactivity of amyloid precursor protein (APP-IR) and amyloid beta-protein (A beta P-IR) was examined in the gracile tract and the dorsal root ganglia of normal and GAD mice. The mice were studied at 4, 9, 18, and 32 weeks of age. These periods correspond clinically to the initial, progressive, critical, and terminal stages of the disease, respectively. The APP-IR in both axons and glial cells was already accentuated to a higher level as early as 4 weeks of age in the gracile nucleus of GAD mouse. Similarly there was increase in APP-IR of GAD mouse in the dorsal root ganglia. Almost all of the primary neurons in the dorsal root ganglia at the lumbar cord level of GAD mouse revealed stronger APP-IR than those of normal mouse throughout all stages. The cells showing immunoreactivity for amyloid beta-protein became positive in axons and glial cells in the gracile nucleus by approximately the 9th week, and followed by an increase of A beta P-IR in order of the cervical, thoracic and lumbar spinal cords. These results suggest that the initial feature in GAD mouse is an accumulation of amyloid precursor protein induced by axonal dystrophy which then leads to a deposition of amyloid beta-protein within the cytoplasm of both axons and glial cells in the gracile tract.

Amyloid beta-Protein Precursor↗
PubMed1995

Long amyloid beta-protein secreted from wild-type human neuroblastoma IMR-32 cells.

The 39- to 43-amino acid amyloid beta-protein (A beta) is deposited as amyloid in Alzheimer's disease. Recent studies have suggested that short A beta (A beta 39 or A beta 40) and long A beta (A beta 42 or A beta 43) play different roles in Alzheimer-type pathology. However, little attempt has been made to investigate the cellular mechanisms underlying the generation of short and long A beta individually. In the present report, we first measured the amount of short and long A beta that are secreted from wild-type human and rodent cells with neuron- or glia-like properties using highly sensitive sandwich-ELISAs that discriminate long A beta from short A beta. The results showed that long A beta secreted by all cells constitutes approximately 10% of the total A beta. To identify the molecular species of long A beta, we next isolated the A beta species secreted from human neuroblastoma IMR-32 cells by affinity chromatography, gel-filtration HPLC, and reverse-phase HPLC. Mass spectrometric analysis demonstrated unequivocally that IMR-32 cells produce A beta 1-42 together with A beta 1-37, A beta 1-38, A beta 1-39, and most predominantly, A beta 1-40. Finally, to investigate the cellular mechanisms that generate A beta 1-42, we studied the effects of brefeldin A and monensin on the production of A beta 1-40 and A beta 1-42 in IMR-32 cells. These reagents reduced the production of both A beta 1-40 and A beta 1-42 simultaneously in a concentration-dependent manner.(ABSTRACT TRUNCATED AT 250 WORDS)

Amyloid beta-Peptides↗
PubMed1995

Autoantibodies against beta-crystallins induce lens epithelial cell damage and cataract formation in mice.

One-year-old B6C3/f mice, injected with beta-crystallins emulsified with CFA, developed lens epithelial cell damage. Both serum transfer and mAb transfer studies clearly established that the autoimmune insult is induced by humoral immunity. Older mice were more susceptible to autoimmune insult than younger animals. Lens epithelial cell damage invariably proceeded to cortical and posterior subcapsular cataract formation. This mouse model of experimental autoimmune cataract formation will facilitate the exploration of the relation between immune phenomena and human age-related cataract.

Age Factors↗
PubMed1995

Elucidation of the region responsible for EDTA tolerance in PQQ glucose dehydrogenases by constructing Escherichia coli and Acinetobacter calcoaceticus chimeric enzymes.

We constructed various chimeric PQQ glucose dehydrogenases (PQQGDHs) from an EDTA-sensitive PQQGDH from Escherichia coli and an EDTA-tolerant PQQGDH from Acinetobacter calcoaceticus by homologous recombination of their structural genes. The EDTA tolerance of the resulting chimeric enzymes was investigated. Our results demonstrated that EDTA tolerance of PQQGDHs can be completely altered by substituting each corresponding region. The EDTA tolerance of A. calcoaceticus PQQGDH is mostly within a region composed of about 90 amino acid residues located between 45 and 56% of the distance from the N-terminal region.

Acinetobacter calcoaceticus↗