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T Dan'ura

Publications and source records attributed to T Dan'ura.

18 recordsLinked to original sources
PubMed2000

A reverse transcriptase-polymerase chain reaction assay in the diagnosis of soft tissue sarcomas.

BACKGROUND: Many types of sarcomas are characterized by specific chromosomal translocations that result in the production of novel chimeric genes. Detection of these fusion genes could be a sensitive molecular diagnostic assay. However, to the authors' knowledge there have been few systemic comparisons between the current histopathologic diagnosis and the presence or absence of particular fusion genes in patients with adult soft tissue sarcomas (STSs). METHODS: Total RNA was extracted from 75 cases of STS and analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) assay for the detection of a variety of fusion transcripts. The results of the molecular assay were compared with standard histopathologic diagnoses. RESULTS: Of the 18 tumors diagnosed as synovial sarcoma, 17 (94%) expressed SYT-SSX chimeric transcripts. All nine myxoid liposarcomas were positive for FUS-CHOP fusion transcripts. Of the four cases of Ewing sarcoma, two had an EWS-FLI1 fusion transcript and one had an EWS-ERG fusion transcript. A clear cell sarcoma had a EWS-ATF1 fusion transcript. None of 19 cases of malignant fibrous histiocytoma nor 3 leiomyosarcomas contained a fusion transcript. Three cases with an initial diagnosis other than synovial sarcoma expressed a SYT-SSX fusion transcript. A review of the slides and additional examination showed that a diagnosis of synovial sarcoma was appropriate for these cases. There was a trend for biphasic synovial sarcoma to contain the SYT-SSX1 fusion. CONCLUSIONS: The authors believe RT-PCR assay for the detection of a specific fusion gene provides a useful tool for confirmation of the diagnosis of adult STS in diagnostically difficult cases and in retrospective studies.

DNA Primers↗
PubMed2000

Synovial sarcoma with a large hematoma in the inguinal region.

We report the case of a patient with synovial sarcoma and a large hematoma of the inguinal region. The patient underwent tumor resection of the lower 2/3 of the acetabulum after preoperative chemotherapy. Twenty-four months after surgery, she is alive without any relapse and can walk without support.

Acetabulum↗
PubMed1998

High complication rate of reconstruction using Ilizarov bone transport method in patients with bone sarcomas.

We performed five reconstructions by bone transport in patients with bone sarcoma: three osteosarcomas, one Ewing's sarcoma and one chondrosarcoma. Four sarcomas were in the distal femur and one in the shaft of the tibia. Four patients received multidrug chemotherapy. The average length of the skeletal defect after tumour resection was 17 (range 10-25) cm. All patients underwent double elongation from both proximal and distal sites of the bone defect. The average follow-up period was 48 (range 40-66) months, and the average duration of external fixation was 32 months (range 579-1340 days). In one case, bone formation was satisfactory, but in the other cases, it was poor and slow. The average treatment index was 95 (range 53-191) days per 1 cm of elongation. In one case, the bone fragment disappeared during the bone transport. In one case, the end of the bone protruded from the skin, and osteomyelitis set in. This patient underwent above-knee amputation due to failure of infection control. Three patients suffered talipes equinus. One patient died of pulmonary metastasis. Two patients had fair and three had poor function. This method is not recommended for patients with bone sarcoma who may have a poor prognosis, as it has an unacceptably high complication rate.

Adolescent↗
PubMed1998

Vancomycin-impregnated polymethylmethacrylate beads for methicillin-resistant Staphylococcus aureus (MRSA) infection: report of two cases.

Two patients with methicillin-resistant Staphylococcus aureus (MRSA) infection were treated with vancomycin (VCM)-impregnated polymethylmethacrylate (PMMA) beads. One patient, who had a history of polycystic kidney and diabetes mellitus, who was receiving hemodialysis due because of non-functional kidney, underwent resection of an intermediate grade chondrosarcoma in the pelvis. MRSA infection developed and curettage of the lesion was performed, but MRSA infection recurred. During the second revision surgery, VCM-impregnated PMMA beads were implanted. MRSA infection has not recurred for 16 months since the implantation of the VCM beads. The second patient had a history of total hip arthroplasty (THA) performed because of coxarthrosis. After the initial surgery, MRSA infection developed, recurring after the second revision surgery for THA. After curettage following removal of the prosthesis, VCM beads were implanted with a spacer composed of VCM-PMMA and a Luque rod. Infection did not recur and THA revision was performed 3 months after the VCM beads implantation. Fifteen months after the last revision surgery, infection has not recurred.

Anti-Bacterial Agents↗
PubMed1989

Effective inhibition by pentobarbital of forskolin-stimulated adenylate cyclase activity in rat brain.

The effect of pentobarbital on the adenylate cyclase system was examined in synaptosomal membranes from rat brain. Pentobarbital inhibited forskolin-stimulated enzyme activity more effectively than the basal and Mn2(+)-stimulated enzyme activities. The degree of inhibition of the enzyme activity by pentobarbital was increased by the presence of forskolin in a concentration-dependent manner. No significant difference is observed in the degree of the inhibition by pentobarbital between the basal and forskolin-stimulated activities in the membranes prepared from the peripheral tissues.

Adenylyl Cyclases↗
PubMed1988

Inhibition of rat brain adenylate cyclase activity by benzodiazepine through the effects on Gi and catalytic proteins.

The effect of benzodiazepines on adenylate cyclase system was examined in rat brain. Micromolar concentrations of diazepam inhibited the enzyme activity in synaptic membranes in dose- and time-dependent manners. The inhibitory effect of diazepam was more evident on the enzyme activity in the presence of guanylyl-5'-imidodiphosphate (GppNHp) or NaF-AlCl3 than on that in the basal state. In the pertussis toxin-treated membranes, the effect of diazepam in the presence of GppNHp or NaF-AlCl3 was markedly suppressed. In addition, other benzodiazepines, such as medazepam, flurazepam, flunitrazepam, and clonazepam, had similar effects to those of diazepam, whereas Ro15-1788, an antagonist of a high affinity receptor in the central nervous system, had no effect on adenylate cyclase activity and did not antagonize the effect of diazepam. These findings indicate that benzodiazepines inhibit rat brain adenylate cyclase activity through the effects on both a low affinity benzodiazepine receptor coupled with the inhibitory GTP-binding regulatory protein (Gi) and catalytic protein.

Adenylyl Cyclase Inhibitors↗
PubMed1988

Involvement of the inhibitory GTP-binding regulatory protein and a low-affinity benzodiazepine receptor in the inhibitory effect of diazepam on rat brain adenylate cyclase system.

The effect of diazepam on the adenylate cyclase system was studied in rat synaptosomal membranes. Micromolar concentrations of diazepam inhibited the cyclase activities in the presence or absence of guanylyl-5'-imidodiphosphate (GppNHp). The inhibitory effect of diazepam was greater on the cyclase activity in the presence of GppNHp than on that in the basal state. This effect of diazepam was not antagonized by Ro15-1788, an antagonist of a high affinity benzodiazepine receptor in the central nervous system. Furthermore, micromolar concentrations of Ro15-1788 had no inhibitory effect on cyclase activities in the presence or absence of GppNHp. In addition, the bromide ion enhanced the inhibition by diazepam of the cyclase activity in the presence of GppNHp, but not the basal activity, although the bromide ion had no effect on both activities in the absence of diazepam. On the other hand, the pretreatment of synaptosomal membranes with GppNHp increased the KD value for [3H]diazepam binding from 98 microM to 198 microM. These data led us to conclude that diazepam inhibits rat brain adenylate cyclase through the effects on both a low affinity benzodiazepine receptor coupled with the inhibitory GTP-binding regulatory protein (Gi) and the catalytic protein.

Adenylyl Cyclase Inhibitors↗
PubMed1987

Protein kinases induce isoproterenol desensitization of beta-adrenoceptor-coupled adenylate cyclase system: significance of receptor occupancy.

Treatment of rat reticulocytes with isoproterenol resulted in dose- and time-dependent desensitization of adenylate cyclase to beta-adrenoceptor agonist stimulation. Cyclic AMP-dependent protein kinase was possibly involved in this desensitization. Treatment of rat reticulocytes with a phorbol ester, tetradecanoyl phorbol acetate (TPA), also induced desensitization to beta-adrenoceptor agonists, indicating the possible involvement of protein kinase C. The addition of a beta-adrenoceptor agonist enhanced the desensitizing effect of dibutyryl cyclic AMP or TPA. T1/2 (time for induction of half maximal desensitization) was decreased from 30 to 2.5 min in accordance with an increase in the concentration of the agonist. The extent of the desensitization was also increased by addition of the agonist. The potency with which the increase was induced was compatible with the potency for binding of the agonist to beta-adrenoceptors (KD values). These results suggest that cyclic AMP- or phorbol ester-induced desensitization is enhanced by receptor occupation by beta-adrenoceptor agonists.

Adenylyl Cyclase Inhibitors↗
PubMed1987

Characterization of heterologous desensitization of rat reticulocyte adenylate cyclase system.

Treatment of rat reticulocytes with isoproterenol caused about 50, 25, and 25% decreases in beta-adrenergic agonist-, fluoride-, and guanine nucleotide-stimulated adenylate cyclase activities, respectively. The desensitization was also induced by dibutyryl adenosine 3',5'-cyclic monophosphate (cyclic AMP) and 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) prevented the isoproterenol-induced desensitization, suggesting the involvement of cyclic AMP in the desensitization. Time course studies revealed that the desensitization to NaF-AlCl3 occurred faster than that to isoproterenol. Furthermore, the rate of the resensitization to NaF-AlCl3 by removal of isoproterenol was also faster than that to isoproterenol. Thus, it is likely that both guanine nucleotide-binding stimulatory regulatory protein, Ns, and beta-adrenergic receptor are sequentially involved in both desensitization and resensitization of the adenylate cyclase system in rat reticulocytes to isoproterenol.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1987

Inhibition of brain adenylate cyclase by barbiturates through the effect on the interaction between guanine nucleotide-binding stimulatory regulatory protein and catalitic unit.

The effect of barbiturates on an adenylate cyclase system in rat brain was examined. The activity of the catalytic unit of this system isolated from the synaptic membrane was inhibited by phenobarbital in dose- and time-dependent manners. The mode of the inhibition was non-competitive with respect to Mg-adenosine triphosphate (ATP). The activity of the synaptic membrane-bound adenylate cyclase was also inhibited by phenobarbital in a similar manner. The inhibitory effect of phenobarbital was more potent on the activation of the enzyme by 5'-guanylylimidodiphosphate (GppNHp) than on the basal enzyme activity. The inhibitory effect, however, was not observed in the synaptic membrane preparation in which the guanine nucleotide-binding stimulatory regulatory protein (Ns) and the catalytic unit of adenylate cyclase system had been functionally coupled by pretreatment with GppNHp. Similar results were obtained with other pharmacologically active barbiturates. These findings indicate that barbiturates primarily affect the activation of the catalytic unit by an interaction with Ns resulting in the inhibition of the enzyme activity.

Adenylyl Cyclase Inhibitors↗
PubMed1986

Relationship between the inhibition of adenylate cyclase by pentobarbital and the functional coupling of Ns and the catalytic unit.

The effect of barbiturate on adenylate cyclase system was examined in rat brain. Pentobarbital inhibited the enzyme activities in both synaptic membrane and solubilized catalytic unit of the system in dose and time-dependent manners. The inhibitory effect of pentobarbital was more potent on the activation of the system by NaF-AlCl3 than on the basal activity. The inhibitory effect, however, was less in the synaptic membrane in which the catalytic unit was prestimulated through coupling with Ns by the treatment with NaF-AlCl3. Similar results were obtained with the solubilized preparation which was pretreated with guanylyl-5'-imidodiphosphate before solubilization. On the other hand, the effect of pentobarbital was not modified by the treatment of the synaptic membrane with pertussis toxin. These findings indicate that barbiturates suppress primarily the activation of the catalytic unit through the coupling with guanine nucleotide-binding stimulatory protein (Ns) without affecting the inhibitory protein (Ni).

Adenylyl Cyclase Inhibitors↗
PubMed1986

Induction of desensitization by phorbol ester to beta-adrenergic agonist stimulation in adenylate cyclase system of rat reticulocytes.

Treatment of rat reticulocytes with a phorbol ester, tetradecanoyl phorbol acetate (TPA), resulted in the desensitization of adenylate cyclase to the beta-adrenergic agonist stimulation depending on the dose and period of the TPA treatment. Treatment of the reticulocytes with TPA caused approximately 40% reduction in the stimulation by beta-adrenergic agonists of adenylate cyclase activity, whereas the treatment had little effect on the basal activity and the activation by fluoride and guanine nucleotide of the enzyme system. No change in the number of beta-adrenergic receptors was observed after the TPA treatment. Treatment with 1-oleoyl-2-acetyl-glycerol (OAG), an activator of protein kinase C, also caused the desensitization of reticulocyte adenylate cyclase to isoproterenol. On the other hand, 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7), a potent inhibitor of protein kinase C, prevented the desensitization induced by TPA. These results suggest the involvement of protein kinase C in a process of desensitization of adenylate cyclase system to beta-adrenergic agonists in rat reticulocytes.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1986

Forskolin stabilizes a functionally coupled state between activated guanine nucleotide-binding stimulatory regulatory protein, Ns, and catalytic protein of adenylate cyclase system in rat erythrocytes.

Guanine nucleotide-binding stimulatory regulatory protein of adenylate cyclase system, Ns, in rat erythrocytes was activated by the treatment with guanylyl 5'-imidodiphosphate or NaF-AlCl3 in the presence of Mg2+. The activation was counterbalanced to the basal state either by the removal of Mg2+ or by the addition of beta(gamma)-subunit of N protein of this system. The depression from the activated state was markedly protected by the coexistence of forskolin at the time of the deactivation depending on the dose of forskolin. EC50 of forskolin for the stabilizing effect was much lower than that for the stimulation of adenylate cyclase activity. These data indicate that forskolin has an effect on the interaction between Ns and catalytic unit of adenylate cyclase system in addition to the direct effect on the catalytic unit.

Adenylyl Cyclases↗
PubMed1984

Mode of interaction between forskolin and manganese ion in activating catalytic unit of adenylate cyclase from rat brain.

Rat brain adenylate cyclase was solubilized with a combination of 0.7% sodium cholate and 0.6 M ammonium sulfate, and fractionated by addition of solid ammonium sulfate. The precipitate at 35% ammonium sulfate saturation contained neither guanine nucleotide-binding regulatory protein (G protein) nor calmodulin, and was used as the catalytic unit of the enzyme system. This catalytic unit was activated synergistically by forskolin and Mn2+. An apparent Km value for Mg-adenosine triphosphate (ATP) of the catalytic unit was about 80 microM in the basal state, while it increased in concurrence with the increase in the enzyme activity when forskolin was added to the assay system. The increase in the Km value depended on the forskolin concentration up to 1 microM, above which the value converged on ca. 200 microM. Furthermore, activation of the catalytic unit by forskolin was more marked at higher concentration of Mg-ATP. On the other hand, Mn2+ suppressed the increase in the Km value for Mg-ATP by forskolin, though the value in the basal state was not changed by Mn2+ alone. These findings indicate that the activation of the catalytic unit by forskolin is accompanied by the change in the affinity for Mg-ATP and Mn2+ modifies the change.

Adenylyl Cyclases↗