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T Fujimoto

Publications and source records attributed to T Fujimoto.

At least 523 records · Page 29Linked to original sources
PubMed1989

[A prognostic factor in childhood acute lymphoblastic leukemia: implication of cellular DNA contents. Children's Cancer and Leukemia Study Group].

The cellular DNA content of marrow blasts were measured by flow cytometry in 250 children with acute lymphoblastic leukemia (ALL). Abnormal DNA stemlines were detected in 51 cases (26%) of 196 children with untreated ALL and in 10 cases (18.5%) of 54 children with relapsed ALL. In untreated cases, the distribution of cellular DNA content for DNA aneuploidy showed that all except one hypodiploid case, had hyperdiploid DNA contents (DI greater than 1.0). Children with hyperdiploid DNA stemline had significantly better prognosis than did those with diploid DNA stemline (DI = 1.0) in both low-and high risk groups; risk assignment was based on an initial WBC count and age at diagnosis. The relative risk of failure to treatment for the hyperdiploid group was one third that of the diploid group in low-risk ALL and one fifth that of the diploid group in high-risk ALL. In relapsed ALL, there was no significant correlation between the cellular DNA contents and their prognosis after relapse. DNA aneuploidy was detected more frequently in late relapsed cases (40%) than in early relapsed cases (6.2%). These results show that cellular DNA content before treatment is an important prognostic factor in childhood ALL.

Adolescent↗
PubMed1989

[Childhood leukemia].

Explore the source record for details and available documents.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1988

Autoradiographic observation of platelets in cerebrovascular injuries induced by arachidonic acid and its prevention by ticlopidine.

The behavior of circulating 111In-labeled platelets in cerebrovascular injuries induced by arachidonic acid injection was studied. Fourteen rabbits were pretreated with the antiplatelet agent ticlopidine, and 10 rabbits were used for controls. Arachidonic acid (AA, 0.7 mg/kg) was injected into the internal carotid artery. Prior to the injection, platelets labeled with 111Inoxine were injected for autoradiography of the brain. Evans blue was injected as an indicator of blood-brain barrier disturbance. Nine control animals showed marked blue staining, and one showed slight blue staining. Seven out of the 14 pretreated animals showed slight or no staining, while 7 showed intensive staining. The distributions of the blue staining and the radioactivity showed high correlation. In the rabbits whose platelet aggregability was depressed by ticlopidine, lower blue staining as well as lower radioactivity was observed. Our findings suggest that activated platelets have an important role in the genesis of cerebrovascular injuries.

Animals↗
PubMed1988

Flow cytometric analysis by bromodeoxyuridine/DNA assay of cell cycle perturbation of methotrexate-treated mouse L1210 leukemia cells.

The in vitro effects of methotrexate (MTX) on cell cycle progression and DNA synthesis of L1210 leukemia cells were studied by the bromodeoxyuridine (BrdUrd)/DNA analysis technique. Low dose (10(-8) M) MTX, which slightly inhibits clonal replication of the cells, delays progress across the S phase, and treatment for 24 h results in a slight increase of the S-phase population. Much higher doses (10(-7) M and 10(-6) M) of MTX, which strongly reduce the clonogenicity, prevented the progression of cells at the G1-S boundary and across the S phase, but not in the other phases. The cells arrested at the G1-S boundary were able to incorporate BrdUrd in the medium for 6-12 h after the start of treatment and then lost the ability to incorporate BrdUrd. By determining the colony inhibitory activity of MTX, it could be shown that not only S-phase cells but non-S-phase cells are susceptible to cytotoxicity of MTX. MTX-induced S-phase arrest is closely associated with an alteration in the distribution of BrdUrd-labeled cells, and MTX apparently inhibits BrdUrd incorporation into L1210 cells as the dose and duration of treatment increase. These results suggest that MTX-induced cell cycle perturbation is related to inhibition of DNA synthesis.

Animals↗
PubMed1988

Comparison of intermittent or continuous methotrexate plus 6-mercaptopurine in regimens for standard-risk acute lymphoblastic leukemia in childhood (JCCLSG-S811). The Japanese Children's Cancer and Leukemia Study Group.

From 1981 to 1983, 131 previously untreated patients with acute lymphoblastic leukemia (ALL) standard-risk group were entered to the protocol JCCLSG-S811. Of 119 eligible patients, 115 (96.6%) attained complete remission by treatment with prednisone (PRD) plus vincristine (VCR) or vindesine (VDS). After preventive central nervous system (CNS) therapy including 18 Gy cranial irradiation and three doses of intrathecal methotrexate (MTX), the patients were assigned randomly to the two maintenance chemotherapies, Regimen A and Regimen B. Regimen A (intermittent regimen) consisted of PRD (120 mg/m2/day by mouth for 5 days) plus 6-mercaptopurine (6MP) (175 mg/m2/day by mouth for 5 days) plus VCR (2.0 mg/m2 intravenously) alternating biweekly with MTX (225 mg/m2 intravenously). Regimen B (continuous regimen) consisted of 6MP (50 mg/m2/day by mouth) plus MTX (20 mg/m2/week by mouth) combined with pulses of PRD and VCR (the same dosages as Regimen A) every 4 weeks. As the late intensification therapy (LIT), five courses of high-dose MTX (2000 mg/m2 per dose per week intravenously for three doses every 12 weeks) with leucovorin rescue were administered to all patients who were in continuous complete remission (CCR) for more than 2 years. Sixty and 55 patients, respectively, were registered in Regimen A and B. The CCR rates in Regimen A and B were 75.1% +/- 5.8% (mean +/- 1 SE) and 49.7% +/- 7.3% (P less than 0.01) at 4 years, and 72.1% +/- 6.3% and 49.7% +/- 7.3% (P less than 0.05) at 5 years, respectively. In Regimen B, CNS and testicular relapses increased after 3 years of CCR. In addition, the patients in Regimen B had a much higher incidence of infections than Regimen A. The LIT did not seem to have important effects on the duration of CCR. From these data we conclude that the intermittent cyclic regimen of 6MP and MTX may be more effective as compared to the continuous administration of these drugs in the maintenance chemotherapy.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1988

Pre-column derivatization of sisomicin with o-phthalaldehyde-beta-mercaptopropionic acid and its application to sensitive high-performance liquid chromatographic determination with fluorimetric detection.

The stability of the o-phthalaldehyde (OPA) derivatives of sisomicin obtained using beta-mercaptopropionic acid was investigated by reversed-phase high-performance liquid chromatography. One of the fluorescent derivatives of sisomicin was stable at least for 6 h in 50% methanol under the optimal conditions used (OPA concentration, pH and temperature). When plasma samples spiked with sisomicin were analysed, the response was linear in the calibration range 136-900 pg of sisomicin per injected volume (40 microliters). As little as 0.06 micrograms of sisomicin per 1 ml of plasma could be detected with signal-to-noise ratio greater than or equal to 2. For plasma samples spiked with 0.2 micrograms/ml sisomicin, the recovery was 97.1 +/- 6.6% (mean +/- S.D., n = 5) with a within-run coefficient of variation of 6.8% and a day-to-day coefficient of variation of 7.2%. The method was also applied to plasma samples from rabbit after a subcutaneous injection of 1 mg/kg sisomicin.

3-Mercaptopropionic Acid↗
PubMed1988

Extragonadal distribution of primordial germ cells in the early chick embryo.

Chick primordial germ cells (PGCs), after separation from the endoderm in early embryonic development, temporarily circulate via the blood vascular system and finally migrate into the gonadal anlagen. It has been noted by some authors that some PGCs are present in extragonadal sites in some vertebrates. In the present study, we examined the distribution and localization of PGCs in extragonadal sites in the chick embryo. PGCs were identified by periodic acid-Schiff staining with light microscopy. In embryos at stages 20-24 (PGCs are in the settlement stage in the gonadal primordium), approximately 20% of the total number of PGCs were observed in extragonadal regions. Approximately 90% of these ectopic PGCs were found in the head, mainly in the mesenchyme surrounding the neural tube. Even at stage 14 when PGCs were usually circulating in the blood vessels, some of the PGCs had emerged from the blood vessels and were detected in the extragonadal site. This pattern of distribution of ectopic PGCs in the head area is probably attributed to the earlier, dominant development of the capillary network, and to the sluggish capillary blood flow in that region, which allows intravascular PGCs to escape into the tissue.

Animals↗
PubMed1988

Smooth muscle cells of the chicken aortic arch differ from those in the gizzard and the femoral artery in the distribution of F-actin, alpha-actinin and filamin.

The distribution of F-actin, alpha-actinin and filamin in smooth muscle cells of the chicken was examined by immunofluorescent and immunoelectron microscopy. Those from the gizzard, the femoral artery and the aortic arch were compared. F-Actin labeled by NBD-phallacidin was seen diffusely distributed in the sarcoplasm in the gizzard and the femoral artery, but in the aorta it was observed as streaks and spots, with unstained areas in between. Epon sections of the aortic arch showed that bundles of thin myofilaments run in various directions interspersed with areas mostly occupied by intermediate filaments. alpha-Actinin labelling occurred in dense plaques along the sarcolemma in all the muscles examined. While dense bodies in the sarcoplasm were common and labelled for alpha-actinin in the gizzard and the femoral artery, hardly any were seen in the aortic arch and little labelling for alpha-actinin was observed in the sarcoplasm. Filamin was concentrated along the periphery of dense bodies and plaques in the gizzard and the femoral artery, but it was seen diffusely in the sarcoplasm of the aortic muscle. After chemical skinning of the latter, filamin labelling persisted only in the F-actin bundles, and other areas became negative. The present results show that smooth muscle cells of the aortic arch contrast with those of the gizzard and even with those of the femoral artery in the distribution of F-actin, alpha-actinin and filamin. The mechanisms of contraction and/or stress maintenance in the aortic smooth muscle may be different from those in other smooth muscles.

Actinin↗
PubMed1988

QS pattern in the right precordial leads of a child with extensive myocardial fibrosis following myocarditis.

A QS pattern in the right precordial leads of the electrocardiogram was noted in a 9-year-old asymptomatic boy. Echocardiography revealed paradoxical movement of the interventricular septum, which showed interstitial myocardial fibrosis in the biopsy specimen and a defective uptake of thallium-201. Extensive myocardial fibrosis was probably a sequela of an attack of myocarditis in infancy.

Child↗
PubMed1988

Interspecific melanocyte chimaeras made by introducing rat cells into postimplantation mouse embryos in utero.

Dissociated cells of whole midgestation rat embryos were injected into implanted albino mouse embryos on Day 8.5 of gestation in utero. This successfully produced viable interspecific chimaeras which were found to have pigmented hairs. Two of them had many pigmented hairs covering a large area of their bodies, including a forelimb and a hindlimb. The fact that some of the introduced rat cells differentiated into functional melanocytes suggests that embryonic cells of both species were able to interact with each other normally and that the foreign cells were kept from maternal immunological assault.

Animals↗
PubMed1988

Electrical oscillation and fluctuation in phospholipid membranes. Phospholipids can form a channel without protein.

Fluctuations and/or step-wise changes in membrane potential and electrical current were observed in bilayer membranes of dioleoylphosphatidylcholine (DOPC) in the absence of any channel protein. The DOPC membranes consisted of three types: black lipid membranes, pipette-clamp membranes and lipid membranes transferred to porous filter paper by conventional Langmuir-Blodgett techniques. This finding is significant since phospholipids are the main constituents of biomembranes. Lipid molecules with a cis double bond in their carbon skeleton are suggested to be important in the gating or excitation of biomembranes.

Electric Conductivity↗
PubMed1988

Diagnosis of allied functional bowel disorders using monoclonal antibodies and electronmicroscopy.

There are a number of conditions that clinically resemble Hirschsprung's disease despite the presence of ganglion cells on rectal biopsies. These conditions have been described under various names. There have been no systematic studies to date to distinguish these conditions from one another. We examined biopsy and surgical specimens from 19 cases of allied functional bowel disorders in an attempt to establish the most appropriate diagnostic procedure. Suction rectal biopsy and full thickness surgical biopsy specimens were examined by enzyme histochemistry (AChE), immunocytochemistry (monoclonal antibody D7), silver impregnation, and electronmicroscopy. Monoclonal antibody D7, which was produced in our own laboratory, is a good marker of autonomic nervous system. This unique antibody allowed us to distinguish various neuronal abnormalities of the bowel except the abnormalities of the argyrophil plexus, which were diagnosed by silver staining. Eight of the 19 cases had a smooth muscle disorder that was only diagnosed on electronmicroscopy. Our data suggest that the vast majority of allied functional bowel disorders can be diagnosed by examining a full thickness rectal biopsy by immunocytochemistry (D7 monoclonal antibody), silver impregnation, and electronmicroscopy.

Acetylcholinesterase↗
PubMed1988

New observations on the pathogenesis of multiple intestinal atresias.

It has been suggested that multiple intestinal atresias result from multiple ischemic infarctions of the intestinal tract. We have studied surgical material from 59 neonates with intestinal atresias seen at our hospital between 1975 and 1986. Forty (68%) patients had single intestinal atresias and 19 (32%) had multiple atresias. There were seven cases of hereditary multiple atresias seen in three families and 12 cases of nonhereditary multiple atresias. All hereditary cases had numerous type I or type II gastrointestinal atresias but none had type IIIa atresia. Six of the seven hereditary cases had multiple atresias in the small as well as large bowel. The 12 patients with nonhereditary atresias had various types of atresias but mesenteric or intestinal interruption was observed in only two patients. All patients with hereditary multiple intestinal atresias showed identical microscopic appearances in the small and large intestine, consisting of sieve-like multiple lumina, each surrounded by its own mucosa and muscularis mucosae but sharing a common muscle coat. There was no evidence of lanugo, bile pigments, or squames within the lumen distal to atretic segments in any of these patients. Six nonhereditary cases who had multiple septal atresias affecting only the small bowel demonstrated essentially similar lesions on microscopic examination as seen in hereditary cases. There was no evidence of arterial occlusion in the mesentery and lanugo, bile pigments, and squames could not be found distally in the intestinal contents in any of these cases. These pathologic findings suggest that all cases of hereditary multiple intestinal atresias and some cases of nonhereditary multiple intestinal atresias are a consequence of a malformative process of the gastrointestinal tract rather than an ischemic process.

Abnormalities, Multiple↗
PubMed1988

Natural history and pathophysiology of enterocolitis in the piebald lethal mouse model of Hirschsprung's disease.

A breeding colony of piebald lethal mice was established in order to study the natural history of congenital megacolon in a mouse model of Hirschsprung's disease and to investigate mucosal defense mechanisms and secretory functions in enterocolitis complicating congenital megacolon. In experiment 1, 214 mice were studied, 53 of which had congenital megacolon. All piebald lethal mice with congenital megacolon (S1/S1) died at 3 to 11 weeks of age. Two distinct patterns of mortality were identified. A majority of mice (64%) became acutely ill at 3 to 4 weeks of age and died, whereas the remainder died between 9 and 11 weeks of age. The former group of mice exhibited clinical and histologic evidence of severe enterocolitis while the latter group had massive abdominal distension and classical megacolon. In experiment 2, piebald mice with congenital megacolon were killed at the time of acute illness. Significant histologic and immunohistochemical differences were seen in the ganglionic colon between piebald mice with early clinical onset of acute illness and piebald mice with the classical clinical picture of congenital megacolon. In the former group of mice the number of immunocytes in the lamina propria was significantly higher than in control mice (P less than .001), immunoglobulin-producing cells were equally distributed throughout the lamina propria and IgA-containing cells were by far the most abundant cell type identified in the colon. In the latter group of mice, immunocyte responses were significantly low and the distribution of immunocytes markedly different, with the immunoglobulin-producing cells being located only at the deep layer of lamina propria.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗