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Biomedical subjects

F Nakajima

Publications and source records attributed to F Nakajima.

At least 109 records · Page 6Linked to original sources
PubMed1984

Distribution and properties of type I and type II binding proteins in the cyclic adenosine 3':5'-monophosphate-dependent protein kinase system in Wilms' tumor.

We compared the relative amounts and properties of cyclic adenosine 3':5'-monophosphate (cAMP)-binding proteins in surgical specimens of Wilms' tumor and normal kidney. Cytosolic fractions of both tissues contained type I and type II isozymes of cAMP-dependent protein kinase (adenosine triphosphate: protein phosphotransferase, EC 2.7.1.37). Among tumor samples, the mean ratio of type I to type II cAMP-binding activity was 2.76 +/- 0.52 (S.D.) contrasted with 1.36 +/- 0.23 for normal kidney (p less than 0.001). The total soluble cAMP-binding activities in normal and malignant tissues differed only slightly. Photoaffinity labeling of cytosol from either tissue, using cyclic adenosine 3':5'-[8-azido-32P]monophosphate, disclosed three cAMP-binding proteins (Mr 47,000, 51,000, and 55,000) that were identified as regulatory subunits of the holoenzyme. Three lower-molecular-weight proteins with unknown function were considered to be proteolytic products of the larger proteins. The Mr 47,000 protein, a monomeric regulatory subunit of type I kinase, was clearly the dominant protein in tumor specimens, but it was much less abundant in normal kidney. The temperature sensitivities of the cAMP-binding proteins and their dissociation constants for cyclic adenosine 3':5'-[8-azido-32P]monophosphate incorporation did not differ appreciably between tumor and normal tissues. Wilms' tumor appears to have a full complement of regulatory subunits of cAMP-dependent protein kinase that are capable of normal cellular function.

Carcinoma, Hepatocellular↗
PubMed1984

[Differentiation induction and potentiation of chemotherapy by PGE1 infusion in patients with neuroblastoma--effect of PGE1 on metastatic potential of neuroblastoma].

Combination of dibutyryl adenosine 3', 5'-cyclic monophosphate or prostaglandin E1 (PGE1) and papaverine effectively induced differentiation of neuroblastoma in mice. Two cases of human neuroblastoma with stage III and IV were administered intraaortic PGE1 infusion combined with oral papaverine and conventional chemotherapy. There were no noticeable side effects and the treatment was effective in decreasing tumor size and promoting tumor maturation in the infused area. However, distant osseous metastases were developed in both cases, during and after the PGE1 administration. They survived 30 and 17 months, respectively, from the initiation of therapy. (Jpn J Cancer Chemother 10(9): 1936-1943, 1983) These results prompted us to study the metastatic potentials of neuroblastoma. In vitro studies demonstrated that cultured human neuroblastoma cells (NB-1, GOTO, SK-N-DZ, SJ-N-KP, SJ-N-CG and SK-N-FI) aggregate human platelets with maximum aggregation ranging from 28% to 51%. Addition of PGE1 or PGD2 to PRP effectively inhibited the tumor-cell-platelet interaction, with IC50 approximately 100 nM for PGE1 and 10 nM for PGD2, respectively. In addition, 50 microM PGE1 or PGD2, 5 microM PGI2 reversed neuroblastoma-induced platelet aggregation in 4 out of 5 cell lines were studied. These findings indicate a the possible role of PGs in effective inhibition of neuroblastoma metastases in vivo. However, two cell lines (SK-N-DZ and SJ-N-CG), which had been exposed to 8.5 microM PGE1 or PGD2 for 90 min and 72 hr, respectively, retained the platelet aggregating activity which was not significantly different from that of untreated cells. We conclude that clinical application of intraaortic PGE1 in the treatment of advanced neuroblastoma has advantage in potentiation of tumor cell kill and in inducing maturation. Administered PGE1 may exert its action in two ways: in preventing tumor metastasis or possibly in enhancing the metastatic potential of neuroblastoma cells. Further refinement of these modalities including other PGs such as PGD2 or PGI2 and more detailed studies on optimal PG administration to prevent metastasis should be evaluated in future.

Alprostadil↗
PubMed1983

[Intra-aortic prostaglandin E1 infusion in the treatment of advanced neuroblastoma].

Neuroblastoma, one of the commonest malignant childhood tumors, arises from the adrenal glands and/or sympathetic ganglia, and metastases into lymph nodes, bone marrow, bones, etc. Patients with advanced stages of neuroblastoma are poorly responsive to current combined chemo-radiotherapy. However, neuroblastoma is known to maturate into benign ganglioneuroma spontaneously or induced by certain chemicals. In our previous studies, adenosine 3', 5'-monophosphate (cAMP) was found to play an important role in this maturational process. It was also demonstrated that long-term continuous infusion of dibutyryl cAMP and papaverine caused significant growth-inhibition and tumor differentiation of C 1300 neuroblastoma in mice. These results prompted us to apply intra-aortic PGE1 infusion to two cases of abdominal neuroblastomas with stages III and IV.PGE1 infusion (0.25-3.0 ng/kg/min, over the period of 3 to 32 weeks), combined with oral papaverine and conventional chemotherapy, was effective in decreasing tumor size and promoting tumor maturation in the infused area. However, distant osseous metastases occurred in both cases, during and after the PGE1 administration. Similar modalities should be further evaluated in order to potentiate anti-metastatic effect on neuroblastoma cells.

Adrenal Gland Neoplasms↗
PubMed1983

[Rabbit brain tumor model].

We have established the rabbit brain tumor model. The domestic rabbits (Japanese White) inplanted the VX2 rabbit epidermoid carcinoma cell were died within three weeks after the inplantation. These brains showed massive brain tumor remarkably infiltrating into the surrounding brain. The flowcytometry of intracerebral VX2 tumor revealed a monopeak at the 2C and relatively large amount of S-phase cells. We think that this brain tumor model is more convenient for the combination treatment with operation and chemotherapy, because the rabbit brain is larger and intravenous injection is more easy than the rat or mouse.

Animals↗
PubMed1982

Characterization and activation of cyclic adenosine 3':5'-monophosphate-dependent protein kinase in C1300 murine neuroblastoma clones growing in vivo.

Cyclic adenosine 3':5'-monophosphate (cAMP)-dependent protein kinases from three clones of C1300 neuroblastoma, established as growing tumors in A/jax mice, were identified and characterized. Mean (+/- SD) intratumor concentrations of cAMP ranged from 5.0 +/- 2.4 to 6.8 +/- 1.9 pmol/mg protein; cytosolic protein kinase activity ratios, calculated from the -cAMP/+cAMP value, ranged from 0.12 +/- 0.02 to 0.18 +/- 0.02. The total amount of cytosolic cAMP-binding activity was highest in the NBA2 clone and nearly equal in N-18 and NBP2. By DEAE chromatography, two peaks of cAMP-binding activity eluting at ionic strengths of 0.09 and 0.15 M of NaCl were resolved from each clone. The latter peak was associated with catalytic activity (type II cAMP-dependent protein kinase), whereas the former was not (free type I cAMP-binding protein). Photoaffinity labeling with 8-azido (N3)-[32P]cAMP, followed by sodium-dodecyl-sulfate:polyacrylamide gel electrophoresis, resolved four major cAMP-binding proteins with molecular weights ranging from 39,000 to 56,000 in each clone. The mol. wt 47,000 protein was judged to be a free regulatory subunit of type I kinase, and the mol. wt 39,000 protein a cleavage product. The mol. wt 54,000 and 56,000 proteins were both endogenously phosphorylated and both had a lower affinity for 8-N3-[32P]cAMP, characteristic of type II kinase. Selected properties of the cAMP-binding proteins (kinetic and autophosphorylating features, response to tryptic hydrolysis, specificity for cAMP and temperature sensitivity) did not differ appreciably among clones. Despite initially low intratumor concentrations of cAMP, it was possible to activate the protein kinase system by simultaneous injection of N6, O2'-dibutyryl-cAMP and papaverine. This indicates that mouse C1300 neuroblastoma can be used profitably to study cAMP-induced neuroblast differentiation.

Animals↗
PubMed1982

Cerebrospinal fluid edema: a rare complication of shunt operations for hydrocephalus. Report of three cases.

Three cases are presented in which a rare complication occurred after a shunt operation for hydrocephalus. On postoperative computerized tomography (CT) scans, extensive low-density areas appeared in the white matter along the ventricular catheter. After shunt revision, gradual resolution or disappearance of the low-density area was clearly demonstrated on CT. In one patient, a collection of cerebrospinal fluid (CSF) was confirmed at operation and appeared to lie in the extracellular spaces of the white matter. The phenomenon is considered to be localized CSF edema, different from porencephaly.

Cerebrospinal Fluid↗
PubMed1982

[Astroblastoma in newborn baby (author's transl)].

A case of astroblastoma in a male newborn baby was reported. He has been suffered from convulsive seizures from six hours later after the birth, not controlled by the anticonvulsants, and lumbar tap revealed bloody cerebrospinal fluid. He had no response against the noxious stimuli and left clonic hemiconvulsion, and showed anisocoria, left pupil was dilated. Right BAG showed a large space occupying lesion in the right frontal lobe. Operation was performed eighteen hours after the birth. Right frontotemporal craniotomy revealed reddish-grey, soft tumor in the right frontal lobe infiltrating into the parietal and temporal lobe of the same side and frontal lobe of the left side. Right frontal lobectomy was performed. He had cardiac arrhythmia after the operation and died next day. Autopsy was not permitted. Histologically tumor tissue showed abundant vessels and perivascular pseudorosettes, and electron micrograph revealed glial filaments in the tumor cells. Histological diagnosis was astroblastoma.

Astrocytoma↗
PubMed1981

[A case of alpha-fetoprotein producing primary intracranial embryonal carcinoma treated with combination chemotherapy with cis-platinum, vinblastine and bleomycin (author's transl)].

A case of alpha-fetoprotein (AFP) producing primary intracranial embryonal carcinoma was reported with special reference to the chemotherapy. The patient was a 14-year-old male who had suffered from vomiting and disturbance of consciousness. CT scan revealed a tumor originating in the anterior part of the third ventricle and expanding into both lateral ventricles. Right frontotemporal craniotomy was performed and the tumor was totally removed under the microscope. The histological diagnosis was embryonal carcinoma. Inspite of the elevated amount of AFP in the serum, we could not verify the yolk sac element in the surgical specimen. Three months later, he became drowsy and another CT scan revealed recurrence of the tumor. Ommaya's reservoir was placed and CSF was drained to control the intracranial hypertension. But the disturbance of consciousness did not improve. We then started a combination chemotherapy with cis-platinum, vinblastine and bleomycin. Cis-platinum was given in a dosage of 20 mg/m2 body surface area as a 15 min. intravenous infusion for 5 consecutive days every 3 weeks for three courses. Vinblastine was given in a dosage of 0.4 mg/kg body weight intravenously for 2 consecutive days every 3 weeks for three courses. Bleomycin was given in a dosage of 30 mg intravenously 6 hours after vinblastine weekly for a total of 12 weeks. The AFP level of the serum and CSF was monitored every several days. After the chemotherapy, the AFP level of the serum and CSF decreased. Repeated CT scan revealed no evidence of tumor. His clinical condition improved remarkably. Toxicity was vomiting, proteinuria and leukopenia, but not so severe. Proteinuria continued after the chemotherapy, but BUN and creatinine did not elevate. It was emphasized that the combination chemotherapy with cis-platinum, vinblastine and bleomycin is effective remission-induction treatment for AFP producing primary intracranial embryonal carcinoma.

Adolescent↗