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Biomedical subjects

T Koike

Publications and source records attributed to T Koike.

At least 415 records · Page 23Linked to original sources
PubMed1995

Proliferation and differentiation of myelodysplastic CD34+ cells: phenotypic subpopulations of marrow CD34+ cells.

In a search for a mechanism to explain the impaired growth of progenitor cells in patients with myelodysplastic syndromes (MDS), marrow CD34+ cells were purified up to 94.9% +/- 4.2% for normal individuals and 88.1% +/- 17.6% for MDS patients, using monoclonal antibodies and immunomagnetic microspheres (MDS CD34+ cells). Phenotypic subpopulations of these CD34+ cells were analyzed for CD38, HLA-DR, CD33, CD13, CD14, CD41 and CD3 plus CD19, in association with proliferative and differentiative capacities. The 15 studies performed included 12 MDS patients. Coexpression rate of CD13 significantly increased in the MDS CD34+ cell population with a value of 91.4% +/- 11.6% and ranging from 60.3% to 100%, and exceeded 99% in four studies, whereas that of normal CD34+ cells was 49.9% +/- 15.8%, ranging from 28.2% to 70.1% (P < .001). Coexpression rate of CD38, HLA-DR, CD33, CD14, and CD3 plus CD19 in MDS CD34+ cells did not significantly differ from that of normal CD34+ cells. The total number of colonies and clusters grown from 100 normal marrow CD34+ cells was 40.4 +/- 8.6, the range being from 27.2 to 50.3; this varied in MDS marrow CD34+ cells with a value of 34.0 +/- 28.7, the range being 0 to 95.9. The lineage of colonies and clusters promoted by MDS marrow CD34+ cells was predominantly committed to nonerythroid with impaired differentiation in 13 of 15 studies (87%). CD13 is first expressed during hematopoiesis by colony-forming unit granulocyte-macrophage and is absent in erythroid progenitors. Therefore, this study provides direct evidence for the lineage commitment of MDS CD34+ cells to nonerythroid with impaired differentiation and explains the mechanism of nil or low colony expression of MDS progenitor cells to erythroid lineage.

Aged↗
PubMed1995

Serum concentrations of IL-5, GM-CSF, and IL-3 and the production by lymphocytes in various eosinophilia.

The concentrations of interleukin-5 (IL-5), granulocyte-macrophage colony-stimulating factor GM-CSF, and interleukin-3 (IL-3) in serum and in IL-2-stimulated lymphocyte culture medium (L-IL2-CM) prepared from patients with reactive eosinophilia were measured by enzyme-linked immunosorbent assay (ELISA). Serum IL-5 levels were increased in 16 out of 42 cases. GM-CSF and IL-3 were below the detectable levels in all sera examined. The concentrations of IL-5 and GM-CSF in L-IL2-CM were increased in 10 out of 29 patients. IL-3 was below the detectable levels in all L-IL2-CM.

Angioedema↗
PubMed1995

Up-regulation of L-type Ca2+ channel associated with the development of elevated K(+)-mediated survival of superior cervical ganglion cells in vitro.

We have previously shown that elevated K(+)-mediated neuronal survival correlates well with a sustained increase in cytoplasmic Ca2+ ([Ca2+]i) through the opening of L-type Ca2+ channels. Elevated K+ (40 mM), however, failed to support the survival of superior cervical ganglion (SCG) cells freshly isolated from newborn rats, while another depolarizing agent, veratridine, was able to do so, suggesting that elevated K(+)-mediated Ca2+ influx occurs in a stage-dependent manner. Indeed, sustained levels of [Ca2+]i in response to high K+ remained low (91 nM) in these neurons, but became elevated (238 nM) in SCG neurons which had been exposed to nerve growth factor (NGF) for 5-7 days and were capable of responding to elevated K+ by survival. Semiquantitative PCR measurements of L-type Ca2+ channel mRNA revealed that this transcript increased dramatically during incubation with NGF for 3 days and reached a plateau level at Day 5 (seven-fold per surface area or nine-fold per total volume compared to that at Day 1). These findings show that NGF-mediated up-regulation of the expression of L-type Ca2+ channel mRNA correlates with the development of elevated K(+)-mediated neuronal survival in vitro and suggest its involvement in coordinate strengthening of pre- and postganglionic synapses in rat SCG neurons.

Animals↗
PubMed1995

Surgical experience with massive lobar haemorrhage caused by cerebral amyloid angiopathy.

Nineteen patients with massive lobar haemorrhage without angiographic lesions received direct or stereotactic surgery, and biopsy specimens were examined histologically. Ten patients (53%) were found to have vessels positive for Congo-red staining, and demonstrating amyloid angiopathy. In the patients with amyloid angiopathy, CT scan and surgical findings were investigated. Subarachnoid haemorrhage (9/10), irregularly shaped haematoma (9/10) and fluid-blood density level in the haematoma cavity (7/10) were frequently found on CT scan. The characteristic surgical findings in patients treated by direct surgery were subarachnoid haemorrhage adjacent to intracerebral haematoma (8/8) and the existence of a tangle of vessels in the haematoma cavity (4/8). Evacuation of haematomas was relatively easy, and difficulty of haemostasis was not encountered during surgery.

Aged↗
PubMed1995

Frequent TIA in the territory fed by the anastomosed STA after combined therapeutic ICA occlusion and extracranial-intracranial bypass: case report.

Frequent transient ischaemic attacks (TIAs) in the territory fed by the anastomosed superficial temporal artery (STA) after combined therapeutic internal carotid artery (ICA) occlusion and extracranial-intracranial bypass is described in a 52-year-old woman with a giant aneurysm in the supraclinoid portion of the left ICA showing impairment of visual acuity in the left eye and right upper quadrantanopia. After the balloon test occlusion of the left ICA which was tolerated, the left STA-middle cerebral artery anastomosis was performed and occlusion of the left ICA using detachable balloons was carried out a day later. TIAs corresponding to the territory fed by the anastomosed STA occurred nine times two to four days and five times eight to nine days after the ICA occlusion without new infarction on computed tomography (CT) scan. Single-photon emission computed tomography showed no hypoperfusion immediately after the initial TIA. CT scan revealed thrombosis of half of the aneurysm a day after the ICA occlusion. The patient developed the same TIA as previously by compression of the left anastomosed STA at the time of follow-up angiography which was carried out eight days after the occlusion. Although heparin was continuously administered after the ICA occlusion for two days, the initial TIA occurred during heparinization. Anticoagulation seemed to be inadequate judging from activated coagulation time and incomplete thrombosis of the aneurysm occurred during heparinization. It is likely that the TIAs are caused by embolism via the STA, which is a rare ischaemic complication.

Anastomosis, Surgical↗
PubMed1995

Relationship of microparticles with beta 2-glycoprotein I and P-selectin positivity to anticardiolipin antibodies in immune thrombocytopenic purpura.

We investigated the association of beta 2-glycoprotein I and P-selectin with platelet-derived microparticles in 48 patients with immune thrombocytopenic purpura and 20 normal controls using two-color flow cytometric analysis. In addition, anticardiolipin antibodies were detected by an enzyme-linked immunosorbent assay. Platelet microparticles from the patients showed a higher positivity for beta 2-glycoprotein I than those from the normal controls (23.1 +/- 15.4% vs. 5.3 +/- 3.1%, p < 0.01), but this positivity was not related to the presence of platelet-associated IgG or to the severity of thrombocytopenia. In the 18 patients with more than 20% P-selectin-positive microparticles, beta 2-glycoprotein I positivity was significantly higher than in the 30 patients with less than 20% P-selectin-positive microparticles (37.1 +/- 20.5% vs. 21.5 +/- 17.3%, p < 0.01). In addition, anticardiolipin antibodies were detected in eight patients, and they had a significantly higher level of beta 2-glycoprotein I-positive microparticles than the patients without such antibodies (42.0 +/- 22.9% vs. 22.6 +/- 18.9%, p < 0.05). Our results suggest that anticardiolipin antibodies activate platelets in immune thrombocytopenic purpura and cause the generation of microparticles rich in beta 2-glycoprotein I and P-selectin. These microparticles may then act to regulate coagulation abnormalities in patients with anticardiolipin antibodies.

Adolescent↗
PubMed1995

The ability of bovine mitochondrial transfer RNAMet to decode AUG and AUA codons.

The ability of bovine mitochondrial tRNA(Met) with the anticodon f5CAU (where f5C is 5-formylcytidine) to decode AUG and AUA codons was examined in a codon-dependent ribosomal binding assay. The AUG codon stimulated the binding of Met-tRNA(Met) to mitochondrial ribosomes in the presence of EF-Tu/TSmt. In contrast, the AUA codon did not promote the binding to mitochondrial Met-tRNA to the ribosome. To investigate the translation of the AUG and AUA codons more fully, an in vitro translation system from bovine liver mitochondria was developed. The activity of this system was greatly enhanced by the addition of 1 mM spermine and reached about half the activity observed with a comparable translational system from E coli. Two types of mRNA containing either AUG or AUA codons were synthesized using T7 RNA polymerase to transcribe their chemically synthesized genes. In the E coli system, the AUG-containing mRNA was translated as Met and the AUA-containing mRNA was translated as Ile. The AUG-containing mRNA but not the AUA-containing mRNA was translated as Met by the mitochondrial translational system. The process by which the AUA codon is translated as Met in the mitochondrial system remains to be clarified.

Animals↗
PubMed1995

Improvement in blood flow and diabetic neuropathy by thromboxane A2 dual blocker KDI-792.

We studied the effect of a thromboxane A2 (TXA2) dual blocker KDI-792 on skin blood flow as well as on the peripheral nerve function of nine diabetics with neuropathy. After administration of KDI-792, there was no change in urinary TXB2; however, urinary 6-keto-prostaglandin (PG) F1 alpha increased significantly. Nerve conduction velocity (NCV) and vibration perception threshold (VT) in the four extremities improved significantly, as did deep skin temperature and skin blood flow. The degree of improvement in sensory NCV in the lower extremities correlated significantly with that of deep skin temperature in the toes and the degree of improvement of VT in the lower extremities correlated well with that of deep skin temperature in the soles and of skin blood flow in the toes. Based on these findings, treatment of diabetic neuropathy with a TXA2 dual blocker appears to increase PGI2 production, improving blood flow, and resulting in improvement of nerve functions.

6-Ketoprostaglandin F1 alpha↗
PubMed1995

Thy-1 induced on rat endothelium regulates vascular permeability at sites of inflammation.

We investigated the role of surface adhesion molecules on endothelial cells in regulating vascular permeability, in vitro and in vivo. Cultured rat endothelial cells (REC) express Thy-1, intercellular adhesion molecule-1 (ICAM-1), CD44 and RT1A. Permeability of albumin across the REC monolayer increased through the interaction of Thy-1 and anti-Thy-1 mAb, but not through ICAM-1 and anti-ICAM-1, CD44 and anti-CD44, and RT1A and anti-RT1A mAb. This anti-Thy-1-effect was completely inhibited when the calmodulin antagonist W-7 and the protein kinase inhibitor H-7 was combined, while the IL-6-mediated increase in REC permeability was blocked by either W-7 or H-7, independently. The anti-Thy-1-mediated permeability increase was additively augmented when IL-6 was admixed. These data suggest that intracellular signaling pathways of anti-Thy-1- and IL-6-mediated permeability regulation may be overlapping to some extent but are largely independent. As anti-Thy-1-treatment generated rearrangement of vimentin filaments within REC, alteration of the cytoskeleton distribution may possibly correlate with the regulation of permeability. Although Thy-1-expression on rat vascular endothelium in vivo was not evident, it was induced at sites of Freund's complete adjuvant-induced dermatitis. The administered anti-Thy-1 mAb exclusively located on vascular endothelial surface at the sites of inflammation. Vascular permeability in inflamed skin tissues was significantly augmented when anti-Thy-1 but not anti-ICAM-1, anti-CD44 or anti-RT1A mAb was administered i.v., without affecting populations of inflammatory cells. The collective evidence suggests that Thy-1 induced on rat endothelium is one important regulatory event in vascular permeability at sites of inflammation.

Animals↗
PubMed1995

A 35 kDa mannose-binding lectin with hemagglutinating and mitogenic activities from "Kidachi Aloe" (Aloe arborescens Miller var. natalensis Berger).

A novel lectin was isolated from the leaf skin of "Kidachi Aloe" (Aloe arborescens Miller var. natalensis Berger) by sequential chromatographies on Sephadex G-25 gel filtration, DEAE ion exchange, and Superdex 75 gel filtration columns. The native lectin exhibited a molecular mass of about 35 kDa on both gel filtration on a Superdex 75 column and native-PAGE under nonreducing conditions. SDS-PAGE in the presence or absence of beta-mercaptoethanol revealed two distinct peptides with molecular masses of about 5.5 and 2.3 kDa, respectively, in addition to a major 9.2 kDa subunit, indicating the presence of a partially processed subunit. The N-terminal amino acid sequence of the intact subunit showed homology with that of snowdrop lectin. The native lectin showed hemagglutinating activity toward rabbit but not human and sheep erythrocytes, and specifically bound to mannose like snowdrop lectin did, indicating that the Aloe and snowdrop lectins are structurally and functionally similar proteins. In addition, the native lectin showed strong mitogenic activity toward mouse lymphocytes.

Aloe↗
PubMed1995

Autoimmune-prone (NZW x BXSB)F1 (W/BF1) mice escape severe thrombocytopenia after treatment with deoxyspergualin, an immunosuppressant.

Male (NZW x BXSB)F1 mice spontaneously develop a disease which closely resembles human systemic autoimmune disease, involving idiopathic thrombocytopenic purpura and glomerulonephritis. We investigated whether autoimmune thrombocytopenia in the mice responded to deoxyspergualin, as immunosuppressant. Deoxyspergualin completely prevented the development of thrombocytopenia and suppressed the increase in circulating autoantibodies against platelets. This agent also ameliorated lupus nephritis. These findings suggest that deoxyspergualin may be effective in the prevention of idiopathic thrombocytopenic purpura.

Animals↗
PubMed1995

Up-regulated expression of Fas antigen (CD95) by peripheral naive and memory T cell subsets in patients with systemic lupus erythematosus (SLE): a possible mechanism for lymphopenia.

Fas antigen (CD95) is a membrane-associated molecule that mediates apoptotic cell death and may play a role in the induction and maintenance of T cell tolerance. To elucidate the involvement of Fas antigen in human autoimmune diseases, we analysed Fas antigen expression by peripheral T cells from patients with SLE and rheumatoid arthritis (RA), using three-colour flow cytometry. Both CD4+ and CD8+ T cells from SLE patients expressed Fas antigen in a higher density than did these cells from healthy donors and from RA patients. Enhancement of Fas antigen density was noted in Fas+CD45RO+ memory T cells from SLE patients. More remarkably, a significant expression of Fas antigen was observed in CD45RO- naive T cells from SLE patients. CD4+CD45RO- T cells from SLE patients co-expressed Fas antigen and early to intermediate activation antigens such as CD25 and CD71, and late activation antigen HLA-DR in only FashiCD4+ naive T cells. Such up-regulation of Fas antigen expression in SLE patients seems to be clinically meaningful, because mean fluorescence intensity (MFI) of Fas antigen on CD4+ T cell subsets inversely correlates with the absolute size of CD4+ T cell subsets in peripheral blood of SLE patients. These results suggest that T cells with increased Fas antigen expression may be highly susceptible to apoptotic cell death, in vivo. A putative mechanism for lymphopenia in SLE patients is discussed.

Adult↗
PubMed1995

Proliferation and differentiation of myelodysplastic CD34+ cells in serum-free medium: II. Response to combined colony-stimulating factors.

To investigate the role of colony stimulating factors (CSFs) in the proliferation and differentiation of progenitor cells from myelodysplastic syndromes (MDS), marrow progenitor cells from 18 MDS patients were highly purified using CD34 monoclonal antibody and immunomagnetic microspheres (MDS CD34+ cells). These cells were cultured in serum-free medium with various combinations of five colony stimulating factors (CSFs): recombinant human interleukin-3 (rIL-3), granulocyte/macrophage-CSF (rGM-CSF), granulocyte-CSF (rG-CSF), macrophage-CSF (rM-CSF), and erythropoietin (rEP). Among the tested CSFs, such as rM-CSF, rG-CSF, rGM-CSF and rIL-3, a combination of the first three CSFs was the most effective stimulus for the proliferation of non-erythroid MDS progenitor cells. An increase of undifferentiated "blast" cell colonies in 5/18 MDS patients occurred and these 5 patients belonged to the high-risk group. In the presence of these three CSFs, rIL-3 had no effect on the proliferation and differentiation of MDS CD34+ cells; however, IL-3 was efficient for the proliferation of MDS CD34+ cells to the erythroid lineage. rGM-CSF or rIL-3 alone did not efficiently support proliferation and differentiation of CD34+ cells. M-CSF is present in normal human serum at a concentration of 550 +/- 110 U/ml, a concentration exceeding that used in this study (100 U/ml). Therefore, in vivo administration of G-CSF combined with GM-CSF to MDS patients may be one of the most effective CSF combinations for proliferation of MDS progenitor cells to the non-erythroid lineage. However, the effect on the capacity for differentiation was minimal, especially in patients belonging to the high-risk group.

Adult↗