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Biomedical subjects

S Koizumi

Publications and source records attributed to S Koizumi.

At least 109 records · Page 6Linked to original sources
PubMed1998

Diffuse brain damage caused by acute twin-twin transfusion during late pregnancy.

BACKGROUND: Monoamniotic twinning is a relatively rare event with increased antenatal and perinatal mortality. We describe a brain damage detected in a surviving monoamniotic twin after intrauterine death of the co-twin at 37 weeks of gestation. RESULTS: Severe entanglement and knotting of the umbilical cords was apparent at the time of delivery and a portion of the cord to the dead twin was narrowed significantly. It was suggested that transfer of blood occurred across placental anastomoses from the survivor to the dead fetus, resulting in transient but severe hypovolemia in the survivor. It is difficult to prevent this type of brain damage because the course of acute twin-twin transfusion is very rapid and the damage has already occurred by the time the death of the twin is diagnosed. CONCLUSIONS: We suggest that elective delivery should be considered in cases of monoamniotic twin pregnancies with additional risk factors.

Adult↗
PubMed1998

Yolk sac tumor with a unique uniform hepatoid pattern histology.

BACKGROUND: Yolk sac tumors (YST) exhibit several different histological subtypes and the mechanisms of cellular differentiation and prognosis of each subtype remain unknown. RESULTS: We report two infants with sacrococcygeal YST; one represented a typical histological subtype and the other showed a hepatoid subtype with uniform histology. The isoform of alpha-fetoprotein (AFP) in the patient with the hepatoid pattern was examined by lectin-affinity immunoelectrophoresis and represented as a YST, but not hepatocellular, subtype. The patient with typical YST responded well to VAB-6 combination chemotherapy. However, this regimen was only partially effective to the patient with the pure hepatoid histological subtype, and an etoposide with ifosfamide and cisplatin (VIP) regimen as a salvage chemotherapy combined with complete tumor resection was useful to achieve complete remission (CR). Both of the patients have been in CR for more than four years.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1998

[Signal transduction through ATP receptors in brain and the development of new drugs].

The possible involvement of adenosine 5'-triphosphate (ATP) receptors in the function of the hippocampus and of pain transmission is discussed. Involvement of these receptors in the function of the hippocampus has been suggested by several reports. In the paper we presented the data that ATP inhibits the glutamate release in cultured hippocampal neurons. This and the report revealing that ATP protected against cell death by glutamate suggest that ATP may be playing a role in the protection of the hippocampus from over-stimulation. Microglia cells are activated by the stimulation of ATP and releases plasminogen which is well known to promote the development of mesencephalic dopaminergic neurons and enhance neurite outgrowth from explants of neocortical tissue. Therefore, ATP may have a role in repairing the damaged neuronal networks as well as protection.

Adenosine Triphosphate↗
PubMed1998

[Usefulness of magnetic resonance imaging for the diagnosis of sigmoidovesical fistula: report of a case].

A 70-year-old man was given a diagnosis of sigmoidovesical fistula due to diverticulitis through the combination of examinations including cystoscopy, sigmoidoscopy, barium enema, urogram, computed tomography (CT), and magnetic resonance imaging (MRI). Among these, MRI was the most useful for the direct detection of the fistula in T1 weighted images and the confirmation of the lesion in T2 weighted images.

Aged↗
PubMed1998

[Treatment of children with non-Hodgkin's lymphoma with CCLSG NHL 855/890 protocols long-term outcome and incidence of secondary malignancies].

We report here on treatment results of consecutive CCLSG NHL studies (NHL855, 1985-1989; NHL890, 1989-1996). The NHL855 protocol consisted of an induction phase of five drugs (VCR, PRD, CPM, DXR, and high-dose MTX) and a maintenance phase of 7 drugs. The probabilities of EFS at 7 years were 78% (SE, 10%) for the patients with localized disease, and 38% (SE, 7%) for those with advanced disease. In the NHL 890 protocol, the patients were assigned to two different treatment groups according to their histology and received different consolidation therapy; non-lymphoblastic subtype was treated almost identically to NHL855 while LASP and VP-16 were newly added for the lymphoblastic subtype. The 7-year EFS improved to 91% (SE, 6%) for localized disease, and 61% (SE, 6%) for advanced disease. A remarkable improvement was particularly evident for lymphoblastic type with mediastinal mass. Optional trial of high-dose sequential chemotherapy and peripheral blood progenitor cell auto grafting resulted in an unfavorable outcome. The 7-year EFS according to main histological subgroups were as follows: 84% (10%) for large cell type, 67% (11%) for Burkitt's-type, 58% (10%) for lymphoblastic type. Secondary cancer occurred in two of the 163 patients studied. Both patients were AML (M0/M4) and MLL rearrangement was detected in the M4 case.

Adolescent↗
PubMed1998

[Bone marrow relapse in high-risk pediatric patients with acute lymphoblastic leukemia: a comparison of relapse times and initial clinical features of patients on different protocols. Children's Cancer and Leukemia Study group (CCLSG)].

To clarify the efficacy of modern intensive chemotherapy for ALL patients with unfavorable features, we compared the time to failure and initial clinical features of children who relapsed in the bone marrow or combined sites, as documented by early CCLSG studies (H811 and H851; 1981-1987) and later studies (H874 and H/HH911; 1987-1993) concerning high-risk ALL patients. In the later studies patients outcomes with new intensive regimens employing early intensification and reinduction therapy were apparently better than those of patients in the early studies with conventional regimens. When we compared the number of relapsed patients based on duration of first remission, we found that the improved outcomes for patients in the later studies were due to a decrease in the number who relapsed 7-36 months after the start of treatment (intermediate relapse), and that the percentage of those who relapsed within the first 6 months of therapy (early relapse) was higher. Patients with high initial WBC counts tended to relapse much earlier than those with low initial WBC counts. However, in the later studies, patients with high WBC counts often relapsed after the termination of therapy (late relapse). These results suggest that the intensive chemotherapy regimens used in the later studies can prevent the development of drug resistant leukemic clones, except in extremely high-risk patients likely to relapse within the first 6 months of therapy.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1998

[Studies of childhood non-Hodgkin's lymphoma--treatment results with the CCLSG NHL 960 protocol. Children's Cancer and Leukemia Study Group (CCLSG)].

We report here on the preliminary treatment findings of a CCLSG NHL 960 study that was initiated in March 1996. In this study, 37 patients with non-Hodgkin's lymphoma were assigned to 4 different treatment groups according to disease stage and histology: (1) localized disease; (2) advanced disease, lymphoblastic type; (3) advanced disease, large cell type; and (4) advanced disease, Burkitt type. The first three groups received the modified protocols of the NHL 890 study. Groups 1 and 3 received COPADM induction therapy (CPM, VCR, PRD, ADR, and MTX). After achieving remission, Group 1 received only maintenance therapy consisting of alternate administration of 7 drugs, while Group 3 received additional intensification therapy with combination chemotherapy consisting of MTX and Ara-C, followed by a maintenance phase involving the administration of 9 drugs. Group 2 received COPADL induction therapy (CPM, VCR, PRD, ADR, and LASP) and consolidation/intensification therapies followed by a maintenance phase. Group 4 received short-term intensive COPADM polychemotherapy. Twelve patients with localized with localized disease (stage I-II) and 25 patients with advanced disease (stage III-IV) were enrolled in this study. Except for 2 patients in the advanced disease stages who died earlier in the course of the study, all patients remained in remission.

Adolescent↗
PubMed1997

BDNF prevents NO mediated glutamate cytotoxicity in cultured cortical neurons.

The effects of brain-derived neurotrophic factor (BDNF) on glutamate-induced cytotoxicity were examined using primary cultures of rat cortical neurons. BDNF induced TrkB tyrosine phosphorylation in rat cultured cortical neurons. The cell viability was significantly reduced when cultures were briefly exposed to glutamate and incubated with normal medium for 24 h. Glutamate cytotoxicity was prevented by MK-801, which is a non-competitive blocker of N-methyl-D-aspartate and N(omega)-nitro-L-arginine, which is a blocker of nitric oxide synthetase. Delayed neurotoxicity was also induced by ionomycin, a calcium ionophore, and nitric oxide (NO) donors such as S-nitrosocysteine (SNOC) and 3-morpholinosydnonimine (SIN-1). Incubating cultures with BDNF for 10 min to 24 h protected cortical neurons against glutamate neurotoxicity. The protective effects of BDNF against glutamate cytotoxicity were dependent on both its concentrations and incubation time. BDNF also prevented the ionomycin-, SNOC-, and SIN-1 induced cytotoxicity. These results indicate that BDNF protects cultured cortical neurons from NMDA receptor-mediated glutamate neurotoxicity by reducing cytotoxic action of NO.

Animals↗
PubMed1997

Sequential cis/trans autophosphorylation in TrkB tyrosine kinase.

TrkB, a member of the tyrosine kinase family of growth factor receptors, is activated by binding of brain-derived neurotrophic factor or neurotrophin 4/5. The intracellular kinase domain of TrkB (ICD-TrkB) was prepared by an insect cell expression system and characterized to identify the mechanism of autophosphorylation. The time course of autophosphorylation, which shows a biphasic progression with a slow nonlinear phase followed by a fast linear phase, indicates the existence of autophosphorylation-induced activation in ICD-TrkB. This is also supported by the finding that phosphorylated ICD-TrkB shows significantly higher activity than control naive ICD-TrkB. Interestingly, the autophosphorylation rate in the linear phase clearly depends on the ICD-TrkB concentration, whereas the rate of initial autophosphorylation is independent of the concentration of ICD-TrkB in the reaction mixture. This observation suggests a two-step autophosphorylation, first an intramolecular activating step and then an intermolecular step. This mechanism is confirmed by the result that only the later phase of autophos-phorylation is inhibited by addition of glycerol which interferes with intermolecular interactions. Therefore, we propose the mechanism of ICD-TrkB autophosphorylation as a sequential cis/trans phosphorylation.

Animals↗
PubMed1997

Tyrosine phosphorylation of ErbB4 is stimulated by aurintricarboxylic acid in human neuroblastoma SH-SY5Y cells.

Aurintricarboxylic acid (ATA) has been reported to protect PC12 cells and cultured neuronal cells from serum starvation-induced cell death, and hippocampal neurons from N-methyl D-aspartate- or ischemia-induced cell death in vivo. We have found that ATA activated tyrosine phosphorylation cascade in PC12 cells as growth factors. Here, we report that ATA prevents cell death under serum starvation and induces tyrosine phosphorylation also in human neuroblastoma SH-SY5Y cells. Furthermore, it was found that erbB4, a member of epidermal growth factor receptor family, is tyrosine-phosphorylated in response to ATA. Both, erbB4 and its ligand, neu differentiation factor (NDF)/ heregulin family, have been reported to be expressed abundantly in nervous system. Thus, tyrosine phosphorylation of erbB4 might explain the neuro-protective activity of ATA.

Aurintricarboxylic Acid↗
PubMed1997

Continuous haemodiafiltration during and after cardiopulmonary bypass in renal failure patients.

PURPOSE: Continuous haemodiafiltration (CHDF) is a technique enhancing the efficiency of solute clearance of haemofiltration by infusing dialysis fluid through the haemofilter. It has been reported to control water and electrolyte balance continuously without haemodynamic instability in critically ill patients with renal failure, Therefore, we used CHDF during and after cardiopulmonary bypass (CPB) in two renal failure patients, and discuss its efficacy. CLINICAL FEATURES: The first patient undergoing aortic valve replacement had dialysis-dependent renal failure. Chronic renal failure in the second patient undergoing mitral valve replacement and coronary revascularization was controlled preoperatively with diuretics. In both cases, CHDF was performed not only during CPB but also in the post-CPB period. Serum concentrations of potassium, urea and creatinine were well-controlled in spite of large amount of blood transfused in the post-CPB period (1000 ml fresh blood and 400 ml fresh frozen plasma in the fist patient, and 1400 ml fresh blood in the second patient). There was no difficulty in haemostasis during the use of nafamostat mesilate as an anticoagulant to keep activated clotting time at about 150 sec for CHDF in the post-CPB period. CONCLUSION: Our initial experiences of CHDF during and after CPB suggest that the technique provides excellent electrolyte, metabolite and fluid management for the cardiac patients with chronic renal failure. Combined with nafamostat mesilate for anticoagulation, CHDF was simple and safe and did not increase the risk of bleeding.

Adult↗
PubMed1997

Nitric oxide participates in the stimulatory and neurotoxic action of endothelin on rat striatal dopaminergic neurons.

1. Our method of real-time monitoring of dopamine release from rat striatal slices revealed that endothelin (ET)-3-induced dopamine release was inhibited by NG-methyl-L-arginine (L-NMMA; 1 mM), an inhibitor of nitric oxide (NO) synthase, while NG-methyl-D-arginine (D-NMMA; 1 mM), an inactive isomer of L-NMMA, had no effect. 2. The inhibition of L-NMMA (0.1 mM) became apparent when tissues were pretreated with tetrodotoxin (1 microM) for 30 min and subsequently exposed to ET-3 (4 microM). 3. L-NMMA (0.1 and 1 mM) dose dependently protected against ET-3-triggered hypoxic/hypoglycemic impairment of striatal responses to high K+. 4. Thus, NO may work as a promoter in mediation of the stimulatory and neurotoxic action of ET-3 on the striatal dopaminergic system, presumably by interacting with interneurons in the striatum.

Animals↗
PubMed1997

Inhibition by ATP of calcium oscillations in rat cultured hippocampal neurones.

1 The effect of adenosine 5'-triphosphate (ATP) on glutamatergic synaptic transmission in hippocampus was examined by an indicator of intracellular Ca2+ oscillations. These oscillations were postsynaptic responses by glutamate released from presynaptic sites. ATP completely inhibited the oscillations in a concentration-dependent manner. 2 The ATP-induced inhibition was mediated via P2-purinoceptors since ATP exhibited the inhibitory action even in the presence of P1-purinoceptor antagonists. Also non-hydrolysable ATP analogues and uridine 5'-triphosphate (UTP) inhibited the oscillation. 3 The rank order of agonist potency of ATP analogues for inhibition of the Ca2+ oscillation was as follows: 2-methyl-thio-adenosine 5'-triphosphate > or = ATP > adenosine 5'-O-(3-thiotriphosphate)>UTP> alpha, beta-methylene-adenosine 5'-triphosphate. These inhibitory effects were insensitive to suramin. Judging from this rank order of potency, the inhibitory P2-purinoceptor could be assigned to a subclass of GTP-binding protein coupled-type receptors. 4 The site of action of ATP was thought to be presynaptic since ATP did not affect the postsynaptic Ca2+ responses by glutamate. These results suggest the existence of a presynaptic inhibitory P2-receptor that inhibits glutamate release in the hippocampus.

Adenosine Triphosphate↗
PubMed1997

Minimal residual disease with TEL-AML1 fusion transcript in childhood acute lymphoblastic leukaemia with t(12;21).

We analysed the TEL-AML1 transcript using reverse transcription-polymerase chain reaction (RT-PCR) in order to detect minimal residual disease (MRD) in seven children with t(12;21)-associated B-lineage ALL. Leukaemic cells with the TEL-AML1 transcript appear to be very sensitive to chemotherapy, and may be eradicated in most patients if adequate chemotherapy is given. However, a small number of patients with t(12;21) ALL may relapse under the currently used chemotherapy, and we believe that RT-PCR for detecting MRD with the transcript is a suitable tool for monitoring the efficacy of chemotherapy or impending relapse in these patients. We analysed the TEL-AML1 transcript using reverse transcription-polymerase chain reaction (RT-PCR) in order to detect minimal residual disease (MRD) in seven children with t(12;21)-associated B-lineage ALL. Two sets of primers, TEL exon 5 and AML1 exon 3 or 4, detected two types of transcript in four patients and two other types in two other patients. The two different translocation breakpoints in the AML1 gene with or without splicing out of AML1 exon 3 seemed to result in these four types of transcript in leukaemia samples.

Child↗
PubMed1997

Induction of a distinct morphology and signal transduction in TrkB/PC12 cells by nerve growth factor and brain-derived neurotrophic factor.

A clonal cell line stably expressing trkB (TrkB/ PC12) was established from rat pheochromocytoma PC12 cells. Brain-derived neurotrophic factor (BDNF), as well as nerve growth factor (NGF), stimulates neurite outgrowth in TrkB/PC12 cells. However, the morphology of BDNF-differentiated cells was clearly different from NGF-differentiated cells. BDNF treatment brought about longer and thicker neurites and induced a flattened soma and an increase in somatic size. This is not explained enough by the quantitative difference in the strength between TrkA and TrkB stimulation, because the level of BDNF-stimulated tyrosine phosphorylation of TrkB was similar to that of TrkA stimulated with NGF in PC12/TrkB cells. There was no difference in major tyrosine phosphorylated proteins induced by NGF and BDNF. Signal proteins such as phosphatidylinositol 3-kinase, phospholipase C-gamma 1, Shc, and mitogen-activated protein kinase seem to be involved in both TrkA- and TrkB-mediated signaling pathways. However, a tyrosine-phosphorylated 38-kDa protein (pp38) was detected in anti-pan-Trk immunoprecipitation only after NGF stimulation. Immunoprecipitation using three distinct anti-pan-Trk antibodies suggests that pp38 is not a fragment of TrkA. These data indicate that TrkA has a unique signal transduction pathway that is not stimulated through TrkB in TrkB/PC12 cells and suggest distinct functions among neurotrophin receptors.

Animals↗