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Biomedical subjects

J Hirata

Publications and source records attributed to J Hirata.

At least 55 records · Page 3Linked to original sources
PubMed1993

Recurrent appearance of 14q+ chromosome associated with lymphoid crisis of Ph-positive chronic myelogenous leukemia.

The 14q+ chromosomal anomaly commonly found in cases of lymphoid neoplasm recurrently occurred during the lymphoid crisis of a patient with Philadelphia chromosome (Ph) positive chronic myelogenous leukemia (CML). At presentation lymphoblasts, with pre-B phenotype increased, and both the Ph and 14q+ were found in the same metaphases. After treatment with vincristine and prednisolone, the patient entered into the chronic phase, and only a Ph was detected in 100% of the cells examined. The 14q+ reappeared at the recurrence of the lymphoid crisis, and then disappeared in the second chronic phase. The BCR/ABL mRNA, which is specific for CML, was detected in the blastic cells by a method using reverse transcriptase and polymerase chain reaction. The rearrangement of the immunoglobulin heavy chain gene (JH gene) was also detected in the blastic cells. These results suggest that the 14q+ was closely associated with the lymphoid crisis of the CML patient.

Chromosome Aberrations↗
PubMed1993

PML/RAR alpha fusion gene is expressed in both granuloid/macrophage and erythroid colonies in acute promyelocytic leukaemia.

Acute promyelocytic leukaemia (APL) associated with a t(15;17) translocation generates a PML/RAR alpha chimaeric gene which is transcribed as a fusion PML/RAR alpha mRNA. To clarify the pathophysiologic role of PML/RAR alpha in APL patients, we examined the expression of PML/RAR alpha in haemopoietic colonies in five patients with APL by reverse transcriptase polymerase chain reaction (RT-PCR) analysis. By the two-step RT-PCR method, we demonstrated that PML/RAR alpha positive clones were present in progenitor cells including both CFU-GM and BFU-E in two cases. This result suggests that the translocation of PML/RAR alpha occurred in a pluripotent stem cell in some APL patients. In four patients we detected two amplified cDNA fragments of 780 and 640 bp which presumably arose by alternative splicing of the PML gene. Interestingly, of CFU-GM and BFU-E colonies examined in four patients, there were three different types of colonies: those expressing only the 780 bp fragment, those expressing only the 640 bp fragment, and those expressing both fragments. This suggests that alternative splicing was clonally determined in each colony. We describe a useful RT-PCR technique for the study of gene expression in a limited number of haemopoietic precursor cells.

Adult↗
PubMed1993

Changes of peripheral blood lymphocyte subsets before and after operation of patients with endometriosis.

This study was performed to elucidate whether endometriotic lesions can affect peripheral blood lymphocyte-subsets. Changes of lymphocyte-subsets of normal healthy women and patients with uterine myoma or endometriosis before and after operation were also examined by using two-color assay methods. The percentage and absolute number of CD57+CD16+ cells [moderately differentiated natural killer (NK) cells] of NK cell subsets in peripheral blood from patients with endometriosis were significantly lower than values from normal healthy women and patients with uterine myoma, while there was no difference in CD4+ and CD8+ lymphocyte-subsets between normal healthy women and patients with uterine myoma or endometriosis. In patients with endometriosis the percentage and absolute number of CD8+CD11+ cells (suppressor T-cells) was significantly increased after operation, while those in patients with urine myoma did not change. On the other hand, resection of endometriotic lesions resulted in a significant decrease of the percentage of CD57+CD16- cells (immature NK cells) and a significant increase of not only the percentage but also the absolute number of CD57+CD16+ cells (moderately differentiated NK cells), suggesting that existence of endometriotic lesions disturbs differentiation of the NK cells. Furthermore, suppressor inducer T-cells as shown by measuring CD4+2H4+ and CD4+4B4- cells were significantly increased after operation of endometriosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Establishment and characterization of a CA125-producing human ovarian clear cell carcinoma cell line].

A human ovarian cancer cell line designated "KK" was established from ascites of a patient with ovarian clear cell carcinoma. This cell line was grown for more than 2 years and over 140 passages in medium RPMI1640 containing 10% FCS. Doubling time of this cell line at passage 70 was approximately 4 days and saturation density was 1.1 x 10(5)/cm2. Plating efficiency was approximately 23%. Chromosome analysis revealed aneuploidy with a model number of 67. PAS-positive substances were present in the cytoplasm. CA125 and SLX were detected in both the original tumor and the cultured cells. This cell line is less sensitive to cisplatin than KF cells and IC50 was 0.95 microM.

Adenocarcinoma, Clear Cell↗
PubMed1993

[Establishment of a cisplatin-resistant human ovarian cancer cell line].

A human ovarian cancer cell line designated "MH" was established from ascites of a patient with ovarian serous cystadenocarcinoma treated with cisplatin. This cell line was grown for more than 2 years and over 100 passages in medium RPMI1640 containing 10% FCS. The cell doubling time, saturation density and plating efficiency was approximately 6.3 days, 5.5 x 10(4)/cm2, and 42%, respectively. Chromosomal analysis revealed aneuploidy with a modal number of 72 and 14-19 types of marker chromosomes. CA125 was detected in both the original tumor and the cultured cells. This cell line is cisplatin-resistant (IC50: 3.28 microM) and has high protein kinase C activity.

Adult↗
PubMed1993

[Inhibitory effects of oral administration of ginsenoside Rh2 on tumor growth in nude mice bearing serous cyst adenocarcinoma of the human ovary].

We examined the inhibitory effect of the oral administration of ginsenoside Rh2 (Rh2) on tumor growth in nude mice bearing human ovarian cancer cells (HRA). In the first experiment, it was revealed that daily administration of 30 microM Rh2 significantly inhibited tumor growth. In the second experiment, therefore, various concentration of Rh2 (1, 15, 30, 60, 120 microM) were administered every day for 91 days, beginning the day after tumor inoculation. Treatment with Rh2 resulted in a remarkable retardation of the HRA cell tumor growth. In particular, tumor growth in mice treated with 15, 30 and 120 microM Rh2 was significantly inhibited, compared to that in CDDP treated mice as well as in untreated mice. Consequently, 50% survival in nude mice treated with 15, 30 and 120 microM Rh2 was significantly prolonged, compared to that not only in untreated mice but also in CDDP treated mice. No side effect was observed in any mice treated with Rh2. Red ginseng containing Rh2 has been used exclusively, orally administered. In the present study, we considered that oral administration of Rh2, which is a component of red ginseng, has strong inhibitory effects on human ovarian cancer cell growth in nude mice.

Administration, Oral↗
PubMed1993

[Interleukin-6 production in endometriosis].

The purpose of this study was to assess whether endometriotic implants of endometriosis could produce Interleukin (IL)-6. IL-6 was measured by means of an enzyme-linked immunosorbent assay (ELISA) in 21 patients with endometriosis of stage IV according to R-AFS classification of endometriosis. The tissues obtained from endometriotic implants were incubated for 24 hours and all their supernatants (n = 8) were positive for IL-6 and the mean level of IL-6 was approximately 30pg/ml per 1mg tissue dry weight. The level of IL-6 in the supernatant did not correlate with the serum estradiol level or with positivity against autoimmune antibodies in patients with endometriosis before surgery. The cultured stromal cells obtained from endometriotic implants were immunohistochemically positive for rabbit antihuman IL-6 polyclonal antibodies. IL-1 alpha (0.5ng/ml) and lipopolysaccharide (LPS) (10 micrograms/ml) caused a 50% and a 130% increase respectively, in IL-6 production in untreated cells (p < 0.01) of 24-hour culture (n = 3). On the other hand, estradiol, progesterone and danazol apparently had no effect on IL-6 production. The serum IL-6 levels of patients with myoma uteri (n = 10) were significantly (p < 0.05) enhanced after surgery, while those of patients with endometriosis (n = 14) declined after surgery. The anti IL-6 antibodies between 10ng/ml and 100ng/ml inhibited cell growth 20% (p < 0.05), while IL-1 alpha (0.5ng/ml) inhibited cell growth 50% (p < 0.01) in a 5 day cell culture (n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)

Autoantibodies↗
PubMed1993

[Antitumor effect of PSK and its combined effect with CDDP on ovarian serous adenocarcinoma-bearing nude mice].

Although the antitumor effect of PSK can be increased by potentiating the immune functions of PSK in tumor-bearing hosts, the mechanisms of its action are not fully understood. In this study, we examined the antitumor effect and CDDP combined effect of oral administration of PSK on nude mice bearing a human ovarian cancer cell line (KF cells). 1. PSK was observed to have a significant antitumor effect in tumor-bearing nude mice and subsequently to bring about an increase in the survival rate and prolongation of the life span. 2. The antitumor effect of CDDP was (but not significantly) enhanced by oral administration of PSK and the prolongation of the life span of the tumor-bearing nude mice was obtained. 3. Six weeks after tumor inoculation, no significant natural killer (NK) cell activity in spleen cells from untreated nude mice was observed. However, when PSK (100 mg/kg but not 500 mg/kg) was given every other day, significant NK activity was induced. 4. The serum immunosuppressive acid protein (IAP) value in nude mice treated with PSK alone was significantly higher than that in nude mice treated with a combination of PSK (100 mg/kg) and CDDP. These results suggest that CDDP prevents the increase in serum IAP that occurs when PSK is used and that consequently combinations of PSK and CDDP result in augmentation of antitumor effects.

Animals↗
PubMed1992

Fate of ciliated epidermal cells during early development of Xenopus laevis using whole-mount immunostaining with an antibody against chondroitin 6-sulfate proteoglycan and anti-tubulin: transdifferentiation or metaplasia of amphibian epidermis.

Xenopus embryonic epidermis changes its cellular composition during development: the appearance of ciliated epidermal cells before hatching is a remarkable characteristic. In this study, the functional change of ciliated cells to mucus-secreting cells was examined with immunocytochemistry using anti-tubulin and anti-chondroitin 6-sulfate (C6S). Before hatching, most epidermal cells were labeled with anti-C6S in a granular fashion. Immunoelectron microscopy revealed that the anti-C6S-positive structure was the mucus granule. Ciliated epidermal cells lacked anti-C6S staining, but were strongly labeled with anti-tubulin. After hatching, most ciliated cells in the surface of the embryo disappeared. During their disappearance, some ciliated cells exhibited anti-C6S-positive granular labeling. This strongly suggests that the disappearance of ciliated cells is a functional conversion to mucus-secreting cells instead of shedding through cell death.

Actins↗
PubMed1992

Adjuvant effects of antineoplastic prostaglandins to cisplatin in nude mice bearing human ovarian cancer cells.

Effects of antineoplastic prostaglandins (PG) on human ovarian cancer cell growth were examined by using HR cells derived from ascites of a patient with serous cystadenocarcinoma of the ovary. With regard to inhibition of cancer cell proliferation in vitro, the effects of delta 7-PGA1 was most marked, followed by that of delta 12-PGJ2, PGJ2 and PGD2. When antineoplastic prostaglandins were administered to nude mice bearing HR cells, tumor growth in groups treated with PGJ2 and delta 12-PGJ2 alone was significantly inhibited 63 days after tumor inoculation, compared to that in an untreated group. Consequently, a significant prolongation of median survival was obtained with delta 12-PGJ2, compared to that in untreated groups and in groups with cisplatin alone. In addition, when prostaglandins were administered together with cisplatin, adjuvant inhibitory effects on the tumor growth were obtained 35, 56 and 63 days after tumor inoculation. Subsequently a significant prolongation of median survival was observed when cisplatin was combined with PGD2 or delta 7-PGA1, compared to the results in groups treated with PGD2 alone, delta 7-PGA1 alone or cisplatin alone. Combination of PGJ2 or delta 12-PGJ2 and cisplatin resulted in a significant decrease of hematocrit and body weight 63 days after tumor inoculation, suggesting a deterioration of the median survival. These results suggest that combination of PGD2 or delta 7-PGA1 with cisplatin may be of clinical use for ovarian cancer resistant to cisplatin.

Animals↗
PubMed1992

Analysis of clonality at the level of progenitors in chronic myelogenous leukaemia using the polymerase chain reaction.

The Philadelphia (Ph1) chromosome is a specific structural abnormality in which the abl oncogene is activated due to the formation of the novel chimeric gene, bcr/abl. To investigate the clinicopathological role of bcr/abl in Ph1-positive chronic myelogenous leukaemia (CML), we studied the clonal origin of haematopoietic progenitors by detecting bcr/abl mRNA in a single haematopoietic colony using the polymerase chain reaction (PCR). Nine patients with CML were examined. In 5 chronic phase patients, all granulocyte/macrophage (CFU-GM) and erythroid (BFU-E) progenitor-derived colonies were positive for bcr/abl mRNA. Colonies in which the transcripts were not detectable were observed in 4 patients. These 4 patients included one patient with a normal karyotype and without splenomegaly, a patient with cyclic oscillation of her white blood cell level, a patient treated with busulfan and interferon-alpha (INF-alpha), and a patient relapsing after allogenic bone marrow transplantation (BMT). Our observations indicate that detection of Ph1-positive clones by PCR may be used to evaluate clinical stages and the effects of treatment in CML.

Adolescent↗
PubMed1992

Deletion of chromosome 6q in two cases of acute myeloblastic leukemia and a review of the literature.

Two cases of acute myeloblastic leukemia (AML M2) associated with a deletion of chromosome 6q are described. One was a 38-year-old man with constitutional inversion of chromosome 9, and another was a 57-year-old female atomic-bomb survivor. The karyotype of these patients were 46,XY,del(6)(q12q14),inv(9)(p11q13), and 47,XX,6q-,+min, respectively. In both cases c-myb protooncogene, which is located in chromosome 6q, was neither deleted nor rearranged, and c-myb messenger RNA level was not elevated. These results suggest that c-myb is not involved in the leukemogenesis of AML with 6q- as well as lymphoid malignancies with 6q-. Out of 23 AML cases with 6q- reviewed, 6 cases had erythroleukemia, and 4 developed in Down syndrome patients.

Adult↗
PubMed1992

Modulation of human lymphocyte response to phytohemagglutinin by antineoplastic prostaglandins.

The effects of antineoplstic prostaglandins (PGs) (PGE1, PGE2, PGA1, PGA2, delta 7-PGA1, PGD2, PGJ2 and delta 12-PGJ2) on human peripheral blood lymphocyte (PBL) responses to phytohemagglutinin (PHA) were studied in vitro. All PGs used in this study alone had no mitogenic effect on the PBL. The PBL response to PHA was significantly stimulated at low concentrations (10(-7) and 10(-8) M) of the PGE series while the high concentration (10(-5) M) markedly inhibited the PHA response. PGA1 and PGA2, metabolites of the PGE series, and also delta 7-PGA1 stimulated the PHA response in a dose-dependent manner between 10(-6) and 10(-8) M, and showed a significant stimulatory effect at 10(-6) M while significantly inhibiting the PHA response at 10(-5) M. Similarly, 10(-6) and 10(-7) M (but not 10(-8) M) of PGD2 stimulated significantly the PHA response. PGJ2 and delta 12-PGJ2, which are metabolites of PGD2, also stimulated the PHA response in a dose-dependent manner between 10(-6) and 10(-8) M, and had a significant stimulatory effect at 10(-6) and 10(-7) M. The degree of the stimulatory effect was most marked with the PGD2 series among the antineoplastic PGs examined in this study. On the other hand, PGs (PGF1 alpha and PGF2 alpha) having no antineoplastic effect did not show such effects on the PHA response. These results suggest that antineoplastic PGs may have immunoregulatory effects through negative and positive feedback.

Antineoplastic Agents↗
PubMed1992

Urinary coagulation-fibrinolysis, kallirein-kinin systems and kininase in cases of preclampsia.

Urinary kallikrein and kallikrein activity significantly decreased in cases of preeclampsia (u-kall./CRE.index 42.39 +/- 9.66 ng/mg, u-kall. act./CRE.index 0.26 +/- 0.06 ng/min/mg), and urinary kininase II and kininase activity significantly increased (u-kininase/CRE.index 10.91 +/- 1.26 x 10(-3) IU/min/mg, u-kininase act./CRE.index 506.37 +/- 178.45 pg/min/mg) when compared with those of normal gravidas from 28 weeks to 42 weeks of gestation (u-kall./CRE.index 189.31 +/- 14.17 ng/mg, u-kall. act./CRE index 1.08 +/- 0.10 ng/min/mg, u-kininase/CRE.index 6.24 +/- 0.31 x 10(-3) IU/min/mg, u-kininase act./CRE.index 15.64 +/- 0.10 pg/min/mg). Urinary FPA, B beta 5-42, alpha 2-PI, and alpha 2PI-plasmin-complex (PIC) significantly increased in preeclampsia (u-FPA/CRE.index 23.59 +/- 8.47 ng/mg, u-B beta/CRE.index 105.26 +/- 29.30 ng/mg, u-alpha 2PI/CRE.index 121.53 +/- 43.57 ng/mg, u-PIC/CRE index 278.39 +/- 60.50 ng/mg) when compared with those of normal control group (u-FPA/CRE.index 0.92 +/- 0.04 ng/mg, u-B beta/CRE.index 12.15 +/- 0.44 ng/mg, u-alpha 2PI/CRE.index 4.18 +/- 0.33 ng/mg, u-PIC/CRE.index 5.98 +/- 1.15 ng/mg). Urinary urokinase markedly increased and urinary D-dimer was detected in severe cases of preeclampsia (u-UK/CRE.index 58.20 +/- 43.69 ng/mg, u-D-dimer 54.76 +/- 9.89 ng/ml) when compared with those of normal control group. These findings suggest that deficiency in urinary kinin excretion may induce hypertension in addition to the changes of urinary coagulation-fibrinolysis system that represents the occurrence of either the endothelial cell injury in the glomerulus or the renal tulbular damage in mild cases of preeclampsia, eventually resulting in the intra-renal vascular coagulation.

Female↗
PubMed1992

Differences in tyrosine phosphorylated proteins between cells expressing P210bcr/abl and P190bcr/abl.

We analysed differences between the populations of tyrosine phosphorylated proteins in two cell lines, K-562 and MR-87, which express two different bcr-abl fusion gene products, using both immunoprecipitation and Western blotting with an anti-phosphotyrosine antibody. K-562 cells preferentially expressed P210bcr/abl (P210), while MR-87 expressed P190bcr/abl (P190). Tyrosine phosphorylated proteins with a molecular mass of 150 kDa (p150) and 115 kDa (p110) were found in both K-562 and MR-87. A 36 kDa protein (p36) was tyrosine phosphorylated in vivo only in K-562 cells, while proteins with a molecular mass of 140 kDa (p140) and 62 kDa (p62) were found only in MR-87 cells. Moreover, several proteins in the detergent-insoluble cell fraction were differently tyrosine phosphorylated in vitro in K-562 and MR-87 lysates. These results suggest that P210 and P190 may have different substrates, and thus, different signal transduction pathways for cell proliferation, although the differential association of such cellular proteins with the two bcr/abl products remains to be clarified.

Fusion Proteins, bcr-abl↗
PubMed1992

[CD7 (+) stem cell leukemia presenting different phenotypes in lymph node and bone marrow].

A 27-year-old male with systemic lymphadenopathy was diagnosed as lymphoblastic-type lymphoma by inguinal lymph node biopsy in September, 1990. Bone marrow at the initial diagnosis contained 55.4% lymphoblasts with a phenotype of peroxidase (-), CD7 (+), CD4 (-), CD8 (-). Lymphadenopathy and lymphoblasts in bone marrow disappeared after MACOP-B therapy. In December, 1990, however, the patient again noticed swelling of cervical lymph nodes. At this time, the bone marrow contained 36.4% myeloblasts with a peroxidase (+), CD7 (+), CD13 (+), CD33 (+) phenotype. Cytogenetic and genetic study revealed that the lymphoblasts at the initial diagnosis and the myeloblasts at relapse shared an common abnormal karyotype, 11p-, and the same rearranged band of T-cell receptor delta, gamma, beta genes, suggesting that these two blasts originated from the same clone. The blasts obtained from the cervical lymph node at relapse were still negative for peroxidase, in contrast to the blasts from bone marrow. These findings suggest that this leukemia originated from a stem cell and differentiated along multilineage pathways.

Adult↗
PubMed1992

Studies on blood coagulation-fibrinolysis system regarding kallikrein-kinin system in the utero-placental circulation during normal pregnancy, labor and puerperium.

In our previous study (Adv. Exp. Med & Biol., 247B. 569. 1989, 198B. 41. 1986, blood & vessel, 17: 51. 1986), we reported on the mechanism of coagulation-fibrinolysis system and kallikrein-kinin system in the utero-placental circulation during normal pregnancy, labor and puerperium. The samples were collected from the uterine artery (UA), uterine vein (UV) and peripheral vein (PV). In this study, we tried to elucidate the mechanism of coagulation-fibrinolysis with relation to kks by measuring of Thrombin/Antithrombin III complex (TAT), tissue plasminogen activator (tPA), plasminogen activator inhibitor 1 (PAI) complex (tPA.PAI.C), active plasminogen activator inhibitor 1 (active PAI), alpha 2-plasmin inhibitor/plasmin complex (PIC). In 20 normal pregnant women, the levels of TAT, tPA.PAI.C and active PAI significantly increased the first trimester (TAT 4.31 +/- 2.05 ng/ml, tPA.PAI.C 39.52 +/- 17.34 ng/ml, active PAI 39.58 +/- 15.29 ng/ml, n = 20 M +/- SD P < 0.001) to the third trimester (TAT 6.39 +/- 1.93 ng/ml, tPA.PAI.C 57.94 +/- 30.80 ng/ml, active PAI 304.24 +/- 148.64 ng/ml, n = 20 M +/- SD P < 0.001) as compared with those of non-pregnant women (TAT 1.60 +/- 0.89 ng/mg, tPA.PAI.C 11.72 +/- 4.59 ng/ml, active PAI 11.53 +/- 7.48 ng/ml, n = 16 M +/- SD). In utero-placental circulation, the levels of TAT significantly increased (TAT 22.12 +/- 20.03 ng/ml n = 20 M +/- SD P < 0.001) in UV, and tPA.PAI.C and PIC. markedly increased (tPA.PAI.C 93.38 +/- 56.05 ng/ml, PIC 1.03 +/- 0.94 micrograms/ml n = 20 M +/- SD P < 0.02) in UV, but active PAI markedly decreased (active PAI 244.18 +/- 87.55 ng/ml n = 20 M +/- SD P < 0.02) as compared with those in PV (TAT 6.1 +/- 2.09 ng/ml, tPA.PAI.C 59.34 +/- 18.99 ng/ml, PIC 0.49 +/- 0.24 micrograms/ml, active PAI 349.14 +/- 157.34 ng/ml, n = 20 M +/- SD). These findings suggest that the significant increase in those complexes in UA has produced a deposition of fibrin clots in the area in contact with utero-placental blood vessel, although the marked increase in tPA.PAI.C and PIC incompletely inhibited the fibrinolytic activity of tPA by the active PAI. The kks shows a consumption of prekallikrein, LMW-kininogen and HMW-kininogen, and an overproduction of kinin in UV.

Antithrombin III↗