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Biomedical subjects

J Hirata

Publications and source records attributed to J Hirata.

At least 19 recordsLinked to original sources
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↗
PubMed1992

Studies of blood coagulation-fibrinolysis regarding kallikrein-kinin system in severe preeclampsia.

UNLABELLED: In our previous study 1), 2), 3) we reported the changes of coagulation-fibrinolysis, kallikrein-kinin system and kininase in preclampsis. In this study, we tried to obtain systemic information of chronic DIC status with regard to kallikrein-kinin system in severe preeclampsia. This systemic information was evaluated in 20 cases of normal gravidas from 28 to 42 weeks of gestation as a control by measuring plasma Thrombin/Antithrombin III complex (TAT), tissue plasminogen activator (tPA) plasminogen activator inhibitor (PAI) complex, active plasminogen inhibitor-1 (active PAI), 2PI plasmin complex (PIC). RESULTS: The levels of plasma TAT and tPA significantly increased (TAT = 10.9 +/- 8.3 ng/ml n = 24 M +/- SD P < 0.02, tPA = 6.1 +/- 3.2 ng/ml n = 10 M +/- SD P < 0.01), tPA PAI C and active PAI markedly increased (tPA PAI C = 85.07 +/- 50.01 ng/ml n = 24 P < 0.05, active PAI = 407.4 +/- 166.0 ng/ml n = 24 P < 0.205), and PIC and D-dimer = 435.1 +/- 145.2 ng/ml n = 8 M +/- SD P < 0.001) in severe preeclampsia as compared with those of normal values (TAT = 6.1 2.0 ng/ml, tPA = 3.6 +/- 1.5 ng/ml, tPA PAI C = 57.9 +/- 30.8 ng/ml, active PAI = 304.2 +/- 148.6 ng/ml, PIC = 0.49 +/- 0.24 mg/ml, D-dimer = 282.9 +/- 75.3 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Antithrombin III↗
PubMed1992

Hypo-triploid acute myeloid leukemia with isochromosome 11q.

A 78-year-old male developed acute myeloid leukemia (AML, M2) with an isochromosome 11q (i(11q)) in hypo-triploid populations. He died 2 months later from the leukemia without having responded to chemotherapy. We reviewed 12 cases in the literature with i(11q) in hematopoietic neoplasms and found that the i(11q) is associated with complex chromosome abnormalities and with elderly patients. Ten out of the 13 patients had an AML phenotype, and they had poor response to chemotherapy and a short survival. The i(11q) may be a non-random chromosome aberration in hematopoietic neoplasms.

Aged↗
PubMed1992

[In vitro and in vivo effects of ginsenoside Rh2 on the proliferation of serous cystadenocarcinoma of the human ovary].

Inhibition of human ovarian cancer cell proliferation in vitro and in vivo by Ginsenoside Rh2(Rh2) isolated from Red Ginseng was examined by using a cell line (HRA) derived from ascites of a patient with serous cystadenocarcinoma of the ovary. The HRA cell proliferation in vitro was inhibited in a dose-dependent manner with between 10 and 100 microM of Rh2. The uptake of radiolabeled precursors (3H-thymidine, 3H-uridine, and 3H-varine) by HRA cells was also inhibited in a dose-dependent manner with between 30 and 100 microM of Rh2. The growth of HRA cells transplanted into nude mice was not significantly inhibited by Rh2 alone. On the other hand, when cisplatin was administered together with 10 microM, 30 microM, or 50 microM Rh2, the growth of HRA cells was inhibited 31 and 35 days after tumor inoculation. Survival was also prolonged when cisplatin was administered with 10 microM and 30 microM Rh2. These results suggest that there is a synergistic effect between cisplatin and Rh2.

Animals↗
PubMed1992

P190-type bcr/abl expressed in myeloid colonies in a patient with Ph1-positive acute lymphoblastic leukemia.

In Philadelphia chromosome (Ph1)-positive acute lymphoblastic leukemia (ALL), some cytogenetic studies have suggested clonal derivation from a multipotential stem cell. The role of the product of the chimeric gene, P190, is not, however, well understood. We examined the expression of P190-type bcr/abl in single hematopoietic colonies obtained at various clinical stages of a patient with Ph1-positive ALL, using the polymerase chain reaction (PCR). Seven out of 58 colonies examined expressed P190-type bcr/abl. Five out of seven colonies were granulocyte/macrophage (GM) colonies and two were erythroid colonies. The cell lineages of these colonies were confirmed by testing for the expressions of the myeloperoxidase (MPO) gene in the GM colonies and the beta-globin gene in the erythroid colonies. These results suggest transformation of multipotential stem cell in this patient and confirm that expression of the P190-type bcr/abl fusion gene permits stem cell differentiation leading to Ph1-positive ALL.

Adult↗
PubMed1991

Polyneuropathy in acute megakaryoblastic leukemia.

Peripheral neuropathy is a rare complication in leukemia. The authors report a patient with acute megakaryoblastic leukemia (AMKL) and progressive symmetric polyneuropathy. Intense infiltration of leukemic cells in a peripheral nerve was observed at autopsy. This is the first report of AMKL with peripheral nerve involvement to the knowledge of the authors.

Extremities↗
PubMed1991

Calcium-regulating hormones and osteocalcin levels during pregnancy: a longitudinal study.

We measured serum concentrations of calcium-regulating hormones and osteocalcin in 20 women longitudinally throughout pregnancy, 1,25-Dihydroxyvitamin D levels were high early in pregnancy and increased with advancing gestation. Parathyroid hormone and osteocalcin levels were low in early pregnancy. They declined toward the middle of pregnancy, but increased in late pregnancy. The serum osteocalcin level correlated with the parathyroid hormone level. The synthesis of osteocalcin by osteoblasts is stimulated by the action of 1,25-dihydroxyvitamin D, and serum osteocalcin levels are also related to the levels of parathyroid hormone. During early and mid pregnancy, the stimulatory effect of 1,25-dihydroxyvitamin D on the synthesis of osteocalcin may be overridden by the inhibitory effect of declining parathyroid hormone levels. The increase in osteocalcin level in late pregnancy may be a consequence of increasing levels of both parathyroid hormone and 1,25-dihydroxyvitamin D.

Adult↗
PubMed1991

Inhibition of human ovarian cancer cell proliferation in vitro by ginsenoside Rh2 and adjuvant effects to cisplatin in vivo.

In vitro and in vivo effects of ginsenoside Rh2 on human ovarian tumor growth were examined by using a cell line (HRA) derived from ascites of a patient with serous cystadenocarcinoma of the ovary. The HRA cell proliferation in vitro was inhibited in a dose-dependent manner with dosages of 10-100 microM of ginsenoside RH2. DNA, RNA and protein synthesis by the HRA cells was inhibited in a dose-dependent manner at more than 15 microM of ginsenoside RH2. However, the growth of HRA cells transplanted in nude mice was not significantly inhibited by ginsenoside RH2. On the contrary, when cisplatin was administered together with 10 microM (but not 1 microM or 100 microM) ginsenoside RH2, the tumor growth was significantly inhibited 31 days after inoculation and the survival was also significantly prolonged, compared with not only the untreated group but also the groups given cisplatin alone or ginsenoside RH2 alone. This indicates synergistic effects between cisplatin and ginsenoside RH2. From monitoring of body weight and hematocrit, concentrations of ginsenoside RH2 used in this study did not seem to cause any adverse effect.

Animals↗
PubMed1991

Identification and mapping of neutralizing epitopes of human parvovirus B19 by using human antibodies.

We identified and mapped the regions responsible for neutralization in the human parvovirus B19 structural protein by using region-specific human antibodies derived from seropositive blood donors. The region-specific antibodies were purified by using affinity columns coupled with synthetic peptides of the hydrophilic regions including the beta-turn structure deduced by the predicted secondary structure of VP2. Fifteen highly specific antibodies against the synthetic peptides were obtained. Ten of them were able to precipitate the radiolabeled virus. Six of them proved to be able to protect the colony-forming unit erythroid cells in human bone marrow cell cultures from injury by the virus. The sequences recognized by the six neutralizing antibodies were sites corresponding to amino acids 253 to 272, 309 to 330, 325 to 346, 359 to 382, 449 to 468, and 491 to 515 from the amino-terminal portion of VP2. These observations suggest that the neutralizing epitopes were distributed in the region from amino acid 253 in the amino-terminal portion of VP2 to the carboxyl terminus of VP2.

Amino Acid Sequence↗