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H Kikuchi

Publications and source records attributed to H Kikuchi.

At least 271 records · Page 15Linked to original sources
PubMed1997

[A case report of choroid plexus carcinoma].

Choroid plexus carcinoma (CPC) is a rare tumor with poor prognosis, whose optimal treatment has not yet been established. We report a case of a one-year-old infant who has been treated with successive combined therapy. The therapy involved two operations for partial removal, interrupted radiotherapy up to 12Gy, 2 cycles of salvage chemotherapy, followed by an operation for total removal, and then a further 3 cycles of chemotherapy. CT scan after the preoperative salvage chemotherapy showed remarkable shrinkage of the residual tumor, which made operative procedure easier. The patient was disease-free for ten months after the last operation. Patients with combined preoperative chemotherapy and total resection seem to enjoy prolonged progression-free survival, so preoperative chemotherapy for choroid plexus carcinoma seems to be of benefit, despite the fact that its optimal recipe has not yet been established.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1997

[Quantitative determination of serum anti ribosomal-P protein antibody by enzyme immunoassay].

An enzyme immunoassay for serum anti-ribosomal P protein antibodies (anti-P) is developed, using highly purified synthetic ribosomal P peptides of the carboxyl terminal 22 amino acid sequence conjugated to human serum albumin (HSA) as an antigen. Anti-P levels were determined by subtracting the nonspecific binding activities to HSA. The concentration of anti-P which produced half of the maximal absorbance at 492 nm (OD492) given by saturating concentrations of anti-P in the ELISA plate was defined as 1 U/ml. The anti-P values in the samples were determined by referring to a standard curve made from a standard serum containing anti-P. Serum anti-P levels in 34 normal individuals were 5.52 +/- 8.39 U/ml (mean +/- SD). Anti-P in sera from 45 patients with systemic lupus erythematosus (SLE), 24 patients with rheumatoid arthritis (RA) and 27 patients with Behçet's disease were also analyzed. The values for serum anti-P in SLE, RA and Behçet's disease groups were 251.04 +/- 843.07 U/ml, 5.97 +/- 15.18 U/ml, and 2.62 +/- 3.35 U/ml (mean +/- SD) respectively. The positive ratio for serum anti-P in SLE patients was significantly higher than that in patients with RA or Behçet's disease (p < 0.05 as determined by chi-square test). These results indicate that quantitative determination of serum anti-P by our enzyme immunoassay is a successful tool for the diagnosis of SLE.

Adult↗
PubMed1996

Differences in inducibility of CYP1A1-mRNA by benzimidazole compounds between human and mouse cells: evidences of a human-specific signal transduction pathway for CYP1A1 induction.

Three benzimidazole compounds, omeprazole (OP), thiabendazole (TBZ), and lansoprazole (LP), were compared with respect to the induction of CYP1A1-mRNA in human hepatoma cells, HepG2. OP was the most potent inducer among the three compounds, but LP was found to be a weak inducer. Induction by TBZ was at an intermediate level. None of these compounds induced CYP1A1-mRNA in a mouse hepatoma cell line, Hepa-1. The transient expression of mouse Cyp1a1-CAT gene into HepG2 cells showed that OP treatment of the transfectants induced CAT activity to the same degree as 2,3,7,8-tetrachlorodibenzo-p-dioxin treatment. Therefore, the cellular factors in human cells were able to work on the mouse regulatory element. The expression of human aryl hydrocarbon (Ah) receptor in the mouse Hepa-1 mutant cell line cl-19, which is defective in Ah receptor, did not increase the induction level of CYP1A1-mRNA by OP treatment. When the cultured medium of HepG2 cells in the presence of OP was added to the mouse Hepa-1 cell culture medium, CYP1A1-mRNA was not induced in Hepa-1 cells. It is thus concluded that metabolites of OP in human cells are not the ligands for the human Ah receptor. Therefore, in human cells, but not mouse cells, there must be an OP-sensitive activation factor for the human Ah receptor.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1996

Natural resistance against tumors grafted into the brain in association with histocompatibility-class-I-antigen expression.

The role of MHC-class-I-antigen expression in intracerebral anti-tumor natural resistance was examined using MHC-positive Lym+ and MHC-negative Lym- lymphoma cell lines. Lym+ was sensitive to MHC-class-I-restricted CTL-mediated lysis, while lym- was resistant. Both lines were susceptible to NK-cell-mediated lysis. There was no difference in in vitro growth rate of in vivo intraperitoneal tumorigenicity between them. Inoculation of Lym+ cells into the brain caused upregulation of the intracellular MHC mRNA to the same level as after treatment with interferon-gamma, resulting in an increase in cell-surface MHC expression. Although inoculated Lym- cells also underwent an increase in cytosolic MHC mRNA, the cell-surface MHC expression remained negative. Immunoprecipitation revealed that the terminal glycosylation did not occur normally in Lym-. An in vivo intracerebral tumorigenicity assay, using 2 groups of untreated and NK-cell-depleted syngeneic mice, showed that Lym+ was less tumorigenic than Lym-. In T-cell-depleted mice, however, no difference was detected between them. In addition, when Lym+ and Lym- cells were inoculated into the brain of allogeneic or syngeneic preimmunized mice (immunized with tumor cells), Lym+ was rejected, while Lym- was accepted. When allogeneic mice had received treatment for T-cell depletion before intracerebral inoculation, no rejection was observed in Lym+. On the other hand, Lym- cells, when injected i.p. into NK-depleted mice, had greater killing activity than Lym+ cells, while in T-cell-depleted mice Lym- was less tumorigenic than Lym+. These results suggest that MHC-positive tumor cells grafted into the brain may be rejected by CTL in an MHC-dependent manner, whereas MHC-negative tumor cells can escape from T-cell-mediated immunosurveillance and grow progressively in the brain, due to absence of intracerebral natural resistance mediated by NK cells.

Animals↗
PubMed1996

An intensive chemotherapy of adult T-cell leukemia/lymphoma: CHOP followed by etoposide, vindesine, ranimustine, and mitoxantrone with granulocyte colony-stimulating factor support.

SUMMARY: An intensive combination chemotherapy regimen supported by granulocyte colony-stimulating factor (G-CSF) was evaluated in adult T-cell leukemia/lymphoma (ATLL) patients in a multiinstitutional, cooperative study. Vincristine 1 mg/m2 i.v. day 1, Adriamycin 40 mg/m2 i.v. day 1, cyclophosphamide 400 mg/m2 i.v. day 1, prednisolone 40 mg/m2 i.v. days 1 to 3 and 8 to 10, etoposide 35 mg/m2 i.v. days 1 to 8, vindesine 2 mg/m2 i.v. day 8, ranimustine 50 mg/m2 i.v. day 8, mitoxantrone 7 mg/m2 i.v. day 8, and G-CSF 50 mg/m2 s.c. days 9 to 21 were given for 2 to 4 courses every 3 weeks to 83 patients with ATLL. Complete remission (CR) and partial remission (PR) were achieved in 35.8 and 38.3 percent, respectively, of 81 evaluable patients. The median survival of all patients was 8.5 months, with a predicted 3-year survival of 13.5 percent by the Kaplan-Meier method. The median duration of response was 7.6 months (range 0.2-42.7), and 13 patients were alive. Their median survival time was 29.1 months (range 19.2-44.7). In 67.6 percent of courses, white blood cell (WBC) nadirs were < 1.0 x 10(9)/L. Days required for the recovery of WBC from the nadir to > 1.0 x 10(9)/L were <5 days in 71.4 percent of the treatment courses. The G-CSF supported an intensified chemotherapy regimen for ATLL and yielded better response rate and longer survival compared to previous reports in Japan. Because duration of remission is still short, further studies of postremission therapy or other strategies are warranted.

Adult↗
PubMed1996

Hydroxylforms of p-boronophenylalanine as potential boron carriers on boron neutron capture therapy for malignant brain tumors.

Hydroxylforms of boronophenylalanine (BPA) were synthesized by conjugation with a cascade of polyols to decrease the BPA uptake of normal parenchyma without affecting uptake into the tumor. We determined their tumor cell killing effect on boron neutron capture therapy (BNCT) against BPA using the human glioma cell line T98G. The thermal neutron doses yielding the D37 (dose used to inhibit 63% colony formation) values of dl-p-BPA(OH)n were 1.45 x 10(12)nvt (n = 1), 1.33 x 10(12)nvt (n = 2), 3.37 x 10(12)nvt (n = 4), and 1.72 x 10(12)nvt (n = 0). The relative tumor cell killing effect on BNCT of dl-p-BPA(OH)n against dl-p-BPA, which was defined as the ratio of D37-BPA to D37-BPA(OH)n, was 1.18 (n = 1) 1.29 (n = 2), and 0.51 (n = 4). The tumor:normal brain ratio of dl-p-BPA(OH)n in 9L rat brain tumor models was improved 1.2- (n = 1) and 1.4-fold (n = 2) against that of dl-p-BPA without a decrease of its uptake into the tumor. The water solubility of BPA(OH)n increased against BPA, and the toxicity represented as the IC50 value of dl-p-BPA(OH)2 was nearly one half that of dl-p-BPA, being established in our previous works. Hydroxylforms of BPA, especially dl-p-BPA(OH)2, might be more suitable boron carriers of BNCT to malignant brain tumors since the radiation injury to the normal parenchyma surrounding the tumor is reduced.

Animals↗
PubMed1996

Heat shock induces differentiation of human embryonal carcinoma cells into trophectoderm lineages.

NCR-G3 cells were established from a testicular embryonal carcinoma and are highly multipotential, differentiating into trophectoderm cells upon exposure to retinoic acid. Differentiated NCR-G3 cells begin to produce human chorionic gonadotropin (hCG), a trophectoderm-specific hormone. We have previously isolated the up-regulated genes at the early stage of differentiation. One of them was found to be a heat shock protein gene. The heat shock protein gene (HSP90) is induced at the early stage of differentiation and decreases to the basal level or under the basal level at the later stage. We speculate that heat shock per se induces the differentiation of human EC cells. With exposure to heat, NCR-G3 cells began to express a series of differentiation markers such as cytokeratin and hCG. Heat, which is classically known to induce heat shock proteins, is able to differentiate an embryonal cell line into trophectoderm lineages, implying a new recognized function of a heat-like event in early differentiation.

Carcinoma, Embryonal↗
PubMed1996

Neuroprotective effect of FK506, an immunosuppressant, on transient global ischemia in gerbil.

Delayed neuronal death (DND) in CA1 region after transient global ischemia is a well-known phenomenon, but its mechanism has not been clarified. In order to examine the involvement of nitric oxide (NO) in DND, 7-nitro indazole (7NI), a selective neuronal NO synthase (nNOS) inhibitor, and FK506, an immunosuppressant which also inhibits nNOS, were administered intraperitoneally during and after transient global ischemia in gerbil. FK506 moderately ameliorated DND in a dose-dependent manner. However, 7NI showed only minor neuroprotective effects. These results show that DND is not mainly mediated by NO production via nNOS, and FK506 acts as a neuroprotective agent via unknown pathways other than nNOS inhibition.

Animals↗
PubMed1996

Expression of heat shock proteins in the developing rat retina.

Expression of three heat shock proteins (HSPs), HSP70, HSP90, and immunoglobulin heavy chain binding protein (Bip) was examined in the developing rat retina using Northern blot analysis. The expression of the inducible form of HSP70 remained uniformly low throughout the perinatal period until P5 and increased rapidly at P7. On the other hand, the constitutive form of HSP70, HSP90, and Bip were expressed constitutively in the rat retina throughout the developmental stage except P3-P5, at which a transient decrease of the expression was observed. The increase of inducible HSP70 mRNA at P7 may correspond to the functional maturation of photoreception in the visual nervous system and may be one of the stress responses to photostimulation. The potential roles of each HSP during development of the rat visual system are discussed.

Animals↗
PubMed1996

A novel chimera gene between EWS and E1A-F, encoding the adenovirus E1A enhancer-binding protein, in extraosseous Ewing's sarcoma.

Ewing's sarcoma/PNET, a tumor of the bone and soft tissue, is one of the most common causes of tumor death among youths. This tumor does not have specific phenotypes, but does have characteristic chromosomal translocations. Furthermore, the expression of EWS/FLI-1 or EWS/ERG chimeric genes was found to be generated through a t(11;22)(q24;q12) or a t(21;22)(q22;q12) translocation. In this study, we identified a new chimera gene between the transactivation domain of EWS and E1A-F, encoding the adenovirus E1A enhancer-binding protein. Since E1A-F is known to activate matrix metalloproteinase genes, the chimera gene may possibly be involved in tumor progression and could be a novel tumor marker for Ewing's sarcoma/PNET.

Adenovirus E1A Proteins↗
PubMed1996

Biopharmaceutical evaluation of the liposomes prepared by rehydration of freeze-dried empty liposomes (FDELs) with an aqueous solution of a drug.

We have evaluated a method for preparation of a dispersion of liposomes encapsulating a drug, namely rehydration of freeze-dried empty (not containing drug) liposomes with an aqueous drug solution (FDEL method). In the present study, we characterized and compared this method with the conventional method using a lipid composition of DPPC-DPPG-cholesterol in a molar ratio of 27:3:20. Two hydrophilic compounds, [3H]-inulin and [3H]-mannitol, were used as model drugs. Liposomal preparations by the FDEL method had an encapsulation efficiency of 2.9 and 6.7% for [3H]-inulin and [3H]-mannitol, respectively, when rehydrated and incubated at 70 degrees C. Since non-specific adsorption of these markers to liposomal membrane is negligible, this method produces liposomes which encapsulate a drug in the intravesicular space. One-tenth of the marker encapsulated in the liposomes prepared by the FDEL method (F-liposomes) was released very rapidly on incubation with rat plasma, followed by the slow release of the remaining fraction thereafter. No such rapid-release phase was observed for the liposomes prepared by the conventional method (C-liposomes). This suggests the existence of two types of encapsulation, loose encapsulation and tight encapsulation, in F-liposomes at least. Pharmacokinetic parameters of marker encapsulated tightly in F-liposomes were comparable to those in C-liposomes. It is likely that amphipathic drugs such as doxorubicin are incorporated into liposomes more easily than inulin and mannitol when formulated by the FDEL method. These results therefore suggest that the FDEL method is useful in the preparation of a liposomal formulation of a drug.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1996

The effect of adriamycin against a liver metastatic model by encapsulation in liposomes.

Antitumor activities of liposomes containing adriamycin (L-ADM) and their distribution process into tumour cells were analysed. The lipid composition of the liposomes was dimyristoylphosphatidylglycerol (DMPG)/egg phosphatidylcholine/cholesterol/adriamycin (ADM) in a molar ratio of 11.4:2:12:1.3. Liver-metastasizing murine tumour models, M5076 and L5178Y-ML, were used. In vivo antitumour effect against these tumour models was assessed from increase in life span (ILS). The survival prolongation effect of L-ADM in mice with liver failure caused by M5076 was significantly higher than that of F-ADM. In contrast, significant enhancement of the effects by encapsulation in liposomes was not observed in L5178Y-ML-bearing mice. In vitro cytostatic activities of L-ADM against M5076 cells as well as against other tumour cell lines were lower than those of F-ADM. The in vitro kinetic study on the distribution of L-ADM to the tumour cells revealed that ADM in L-ADM was taken up into the tumour cells mainly after it was released from the liposomes rather than taken up as the liposomal form. Among the cell lines tested, M5076 cells had the highest phagocytic activity and therefore the highest uptake activity of ADM during incubation with L-ADM. These findings suggest that the augmented antitumour activity of L-ADM in M5076-bearing mice was the result of phagocytosis of L-ADM by M5076 cells as well as the reduction of toxicity, prolonged retention of ADM in systemic circulation, and liver accumulation of ADM after administration of L-ADM.

Animals↗
PubMed1996

Monocytic differentiation modulates apoptotic response to cytotoxic anti-Fas antibody and tumor necrosis factor alpha in human monoblast U937 cells.

Interferon-gamma (IFN-gamma), vitamin D3 (VD), and retinoic acid (RA) induce differentiation of human monoblastic leukemia U937 cells to macrophage-like cells with potential superoxide anion-generating activity upon further stimulation. Here we report that U937 cells thus differentiated show various responses to apoptotic induction with a cytotoxic anti-Fas antibody and tumor necrosis factor (TNF). VD-or RA-treated U937 cells acquired resistance against Fas- or TNF receptor (TNFR)-mediated apoptosis, whereas apoptotic cell death was accelerated in IFN-gamma-treated cells. By flow cytometric analyses, no decrease in expression of surface Fas antigen or p55 TNFR was observed in differentiated U937 cells. Cell surface expression of CD11b was seen only when differentiation was induced with VD or RA but not with IFN-gamma. The growth of VD- or RA-treated cells was retarded but IFN-gamma-treated cells were prolific. These findings suggest that the differentiation state differs with the inducer and that the cellular response to apoptotic induction is closely related to the state including the cell cycle.

Antigen-Antibody Reactions↗
PubMed1996

Embolization of cerebral aneurysms with a liquid embolus, EVAL mixture: report of three cases.

Embolization of three surgically difficult cerebral aneurysms was performed using our newly developed non-adhesive embolic material, EVAL mixture (ethylene vinyl alcohol copolymer). Conventional embolic materials such as detachable balloons or microcoils were not used because of a large or irregular aneurysmal neck. After temporary occlusion of the parent artery with a superselective balloon catheter, the EVAL mixture was slowly injected through a microcatheter placed in the aneurysm or parent artery. The locations of the aneurysms were anterior communicating artery, basilar artery-posterior cerebral artery and basilar artery-anterior inferior cerebellar artery (BA-AICA). One aneurysmal occlusion and 2 parent artery occlusions were performed. Patients had no persistent deficits. The patient with the BA-AICA aneurysm associated with an arteriovenous malformation died of rupture of the residual AVM due to haemodynamic change 2 weeks after embolization. In selected and limited cases, embolization of surgically difficult cerebral aneurysms using EVAL mixture was more effective and safer than embolization using conventional embolic materials such as balloons and microcoils.

Adult↗
PubMed1996

A cationic polymer, Eudragit-E, as a new liquid embolic material for arteriovenous malformations.

We have developed a new liquid material for embolisation of arteriovenous malformations: a mixture of methyl and butyl methacrylate, plus dimethylaminoethyl methacrylate copolymer (Eudragit-E) in a solvent consisting of ethanol and iopamidol. Upon contact with aqueous substances, Eudragit-E precipitates rapidly and forms a soft elastic sponge within 3 s, as the ethanol diffuses. In blood, the positively charged Eudragit-E aggregates the negatively charged blood elements. Transcatheter embolisation of 4 canine and 52 rat renal arteries was feasible. Histological studies revealed no acute inflammatory reaction within 1 week, but mild to moderate reactions in the subacute and chronic stages. No recanalisation was seen. Because of its unique properties and excellent thrombogenicity the Eudragit-E, mixture seems a promising embolic material.

Analysis of Variance↗
PubMed1996

Apoptosis induced by selenium in human glioma cell lines.

Several studies have shown that selenium can inhibit tumorigenesis in tissues. However, little is known about the mechanism and the effect of selenium on DNA, especially in brain tumor cells. In this study we examined the biological effect of selenium on human glioma cell lines (A172 and T98G). Selenium exhibited an antiproliferative effect on these cell lines (and induced the typical ladder pattern of DNA fragmentation commonly found in apoptosis), which were prevented by catalase. Few effects of selenium on NT14 fibroblasts were found. These findings demonstrate that selenium may induce, by apoptosis, cell death of human glioma cell lines, which are resulting from free radical oxygen forming.

Apoptosis↗