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J Tanaka

Publications and source records attributed to J Tanaka.

At least 163 records · Page 9Linked to original sources
PubMed2000

Sequential analysis of HLA-C-specific killer cell inhibitory receptor (CD158b) expressing peripheral blood mononuclear cells during chronic graft-versus-host disease.

We have sequentially investigated the expression of natural killer cell inhibitory receptors (KIRs) for HLA-C (CD158b) on peripheral blood mononuclear cells (PBMC) in three patients with extensive chronic graft-versus-host disease (cGVHD) after allogeneic bone marrow transplantation (alloBMT). Clinical symptoms of cGVHD were not cured and worsened in the first patient whose CD158b-positive cells increased to 18.5% during cGVHD and decreased to 9.4% at 8 months after transplantation. On the other hand, cGVHD was cured and did not relapse in the second patient whose CD158b-positive cells increased up to 45.9% during cGVHD and sustained 19.4% at 8 months after transplantation. In contrast, CD158b-positive cells were less than 10% during the course of cGVHD in the third patient, and her cGVHD did not respond to treatment. Therefore, it appears that chronic allostimulation augments the expansion of CD158b-positive cells and these expanded CD158b-positive cells may have some role in the control of alloresponse in some patients.

Adult↗
PubMed2000

Expression of HLA-C-specific natural killer cell receptors (CD158a and CD158b) on peripheral blood mononuclear cells after allogeneic bone marrow transplantation.

We investigated the expression of natural killer cell receptors (NKRs) for HLA-C on peripheral blood mononuclear cells (PBMCs) in 23 allogeneic bone marrow transplantation (allo-BMT) patients to analyse the role of NKRs in alloresponse concerning graft-versus-host disease (GVHD). CD158a expression was low and there was little change in the expression after allo-BMT. Also, there was no difference in the proportion of CD158a+/CD3- after allo-BMT. In contrast, the proportion of CD158b+/CD3- cells, mainly NK cells, increased in the early stage (< 2 months) after allo-BMT and then gradually decreased (3.3 +/- 2.6% before BMT vs. 15.4 +/- 8. 6% in the early stage after BMT, 8.5 +/- 4.9% during the period 3-6 months after BMT and 7.0 +/- 3.0% > 6 months after BMT; P < 0.05). However, CD158b expression on CD3+ T cells increased 3 months after allo-BMT (1.1 +/- 1.1% before BMT vs. 5.1 +/- 7.7% during the period 3-6 months after BMT and 3.0 +/- 2.4% > 6 months after BMT, P < 0. 05). The highest percentages of CD158 expression in patients without chronic GVHD (cGVHD) and those with cGVHD were compared. The percentage of CD158b+/CD3+ cells and also that of CD158b+/CD8+ cells were significantly increased in patients with cGVHD compared with those in patients without cGVHD (2.6 +/- 2.0% vs. 8.0 +/- 11.2% and 2.3 +/- 1.5% vs. 8.3 +/- 11.7% respectively; P < 0.05). The exact clinical relevance of these CD158b-expressing cells is not clear. However, there is an interesting possibility that CD158b-expressing cells play some role in the regulation of GVHD after allo-BMT.

Bone Marrow Transplantation↗
PubMed2000

Nasu-Hakola disease: a review of its leukoencephalopathic and membranolipodystrophic features.

The clinicopathological features of Nasu-Hakola disease are described by reviewing previously reported cases and adding consideration to newly disclosed evidence. This disease is an autosomal recessive disorder characterized by membranocystic lipodystrophy in the skeletal system and sclerosing leukoencephalopathy in the nervous system. The leukoencephalopathic alterations are demyelinization of the cerebral white matter, associated with conspicuous fibrillary gliosis and preservation of the subcortical arcuate fibers. Sudanophilic granules are focally scattered in the perivascular space or widely infiltrated in the affected white matter, and some neuronal loss with deposits of calcospherites is encountered in the basal ganglia and also in the thalamus. Spheroid formation with an increased number of neurofilaments in the neuronal axon is considered a possible pathogenesis, and a primary vascular mechanism is also suggested. Interestingly, most of the reported cases of Nasu-Hakola disease are from Japan and Finland which suggests heredofamilial background as a cause.

Adipose Tissue↗
PubMed2000

Development and application of the 'Sleep Ukiha' automated sleep analysis system.

We attempted to develop an automated sleep analysis system that uses a personal computer as an aid to the entire sleep research process. Analysis is based on electroencephalogram, chin muscle electromyogram and electrooculography, while other physiological phenomena can be handled arbitrarily. Major characteristics of the system include: (i) simultaneous gathering of physiological phenomena from up to three patients; (ii) high-speed waveform analysis; (iii) user-friendly operating environment through the use of a graphical user interface; and (iv) versatile utilization of analytical data in research.

Humans↗
PubMed2000

Gq protein alpha subunits Galphaq and Galpha11 are localized at postsynaptic extra-junctional membrane of cerebellar Purkinje cells and hippocampal pyramidal cells.

Following cell surface receptor activation, the alpha subunit of the Gq subclass of GTP-binding proteins activates the phosphoinositide signalling pathway. Here we examined the expression and localization of Gq protein alpha subunits in the adult mouse brain by in situ hybridization and immunohistochemistry. Of the four members of the Gq protein alpha subunits, Galphaq and Galpha11 were transcribed predominantly in the brain. The highest transcriptional level of Galphaq was observed in cerebellar Purkinje cells (PCs) and hippocampal pyramidal cells, while that of Galpha11 was noted in hippocampal pyramidal cells. Antibody against the C-terminal peptide common to Galphaq and Galpha11 strongly labelled the cerebellar molecular layer and hippocampal neuropil layers. In these regions, immunogold preferentially labelled the cytoplasmic face of postsynaptic cell membrane of PCs and pyramidal cells. Immunoparticles were distributed along the extra-junctional cell membrane of spines, dendrites and somata, but were almost excluded from the junctional membrane. By double immunofluorescence, Galphaq/Galpha11 was extensively colocalized with metabotropic glutamate receptor mGluR1alpha in dendritic spines of PCs and with mGluR5 in those of hippocampal pyramidal cells. Together with concentrated localization of mGluR1alpha and mGluR5 in a peri-junctional annulus on PC and pyramidal cell synapses (Baude et al. 1993, Neuron, 11, 771-787; Luján et al. 1996, Eur. J. Neurosci., 8, 1488-1500), the present molecular-anatomical findings suggest that peri-junctional stimulation of the group I metabotropic glutamate receptors is mediated by Galphaq and/or Galpha11, leading to the activation of the intracellular effector, phospholipase Cbeta.

Amino Acid Sequence↗
PubMed2000

Surgery or gamma -knife for the treatment of arteriovenous malformations?

Decision making for either surgery or gamma-knife for the treatment of arteriovenous malformations (AVMs) cannot be uniform. The skill of the neurosurgeon in operating on AVMs is now being compared with that of the gamma-knife. The decision varies from case to case and is to be taken by the neurosurgeon. This report presents three cases in which such decision making was not easy. Case 1 was a non-ruptured cingulate AVM of 2.5 cm diameter in the cingulate cortex. The operative field was anticipated to be very narrow between the parietal bridging veins. Case 2 was a tiny ruptured AVM in the speech-motor area which was buried underneath the cortex. Case 3 was a large ruptured thalamo-stiriate-capsular AVM with feeders from the anterior and posterior choroidal arteries. All cases were operated without serious morbidity. A combination of pre-operative intravascular surgery (cases 1 and 3) or postoperative gamma-knife (case 3) was adopted. In conclusion, there is no unitary rule to decide on surgery or gamma-knife for the treatment of AVMs. It depends on what good or harm the responsible surgeon or the gamma-knife does.

Adult↗
PubMed2000

Glutathione as an essential factor for chaperon-mediated activation of lactonizing lipase (LipL) from Pseudomonas sp. 109.

Pseudomonas sp. 109 produces a unique lipase (LipL) which efficiently catalyzes intramolecular transesterification of omega-hydroxyesters to form macrocyclic lactones. The production of the enzymatically active LipL requires a specific molecular chaperon (LimL protein) together with a low-M(r) lipase-activation-factor (LAF) of unknown structure. From 50 g of Pseudomonas cells, 2.15 mg of LAF was purified as a sulfobenzofurazanyl derivative after methanol extraction, derivatization, and C(18) reverse-phase HPLC. One-dimensional and two-dimensional 600 MHz (1)H-NMR and fast atom bombardment mass spectrometry (FAB-MS) revealed that LAF is glutathione. Because several SH compounds (L-cysteine and mercaptoethanol) were similarly effective to native LAF in the activation of LipL, and because only LipL contains two cysteinyl residues forming an intramolecular disulfide bond, it is concluded that the reduction of and reformation of the intramolecular disulfide bond of LipL is essential to liberate free and fully active LipL.

Bacterial Proteins↗
PubMed2000

Evolution to acute myeloblastic leukemia from chronic neutrophilic leukemia with dysplastic features in granulocytic lineage.

We experienced the case of an 82-year-old man with chronic neutrophilic leukemia (CNL) with dysplastic features in the granulocytic lineage which subsequently progressed to acute myeloblastic leukemia (AML) with myelofibrosis. The patient had hepatosplenomegaly, but there was no evident cause of neutrophilic leukocytosis. The cytogenetic study showed that he had a normal karyotype. Concentrations of the serum granulocyte colony-stimulating factor (G-CSF) were not detectable. Two years after the diagnosis of CNL, blastic transformation to AML occurred with myelofibrosis and significant morphological abnormalities in neutrophils. The blasts were positive for myeloperoxidase, CD33, CD34, and HLA-DR, and the presence of dysplasia within the granulocytic lineage suggested that he had an abnormality at the level of the granulocyte-committed progenitors. Heterogeneous origins of CNL might lead to various clinicopathological features in each case.

Aged↗
PubMed2000

[Radiation dose measurement of the patient in interventional radiology using a transmission ionization chamber].

We propose a method to estimate patient radiation dose in radiologically guided interventional procedures using a transmission ionization chamber. A typical transarterial embolization (TAE) procedure for hepatocellular carcinoma was simulated, including 30 minutes of fluoroscopy and five series of DSA, each with appropriate collimation. The dose-area product was divided by the area and compared with values from a standard dosimeter placed in the center of the radiation entrance, to obtain a conversion factor. In this way, the entrance skin dose can be estimated immediately after the procedure by simply multiplying the value by the conversion factor, if the procedure roughly conforms to the simulated model. The average entrance skin dose of 33 patients who recently underwent TAE for HCC was found to be 0.66 (0.19-1.75) Gy. This technique can be applied to other areas of IVR and may help to reduce patient exposure to radiation.

Carcinoma, Hepatocellular↗
PubMed2000

Proliferation of CD4+ lymphocytes in a patient with chronic graft-versus-host disease after allogeneic bone marrow transplantation.

Expansion of donor-derived lymphocytes after allogeneic stem cell transplantation is a serious and sometimes fatal complication. Lymphoproliferative disorders are reportedly caused mainly by reactivation of Epstein-Barr virus (EBV) and non-EBV-associated secondary lymphoma or leukemia. In this paper, we report massive proliferation of CD4+ lymphocytes in peripheral blood of a patient with chronic graft-versus-host disease (GVHD) following allogeneic bone marrow transplantation (alloBMT) from an HLA-identical sibling donor. The abnormal lymphocytes showed CD3low, CD4+, CD8-, CD2+, CD5+, CD7+, CD25-, CD19-, CD20-, CD21-, CD16-, CD56low, T-cell receptor (TCR)-alpha/beta- and TCR-gamma/delta- phenotypes, and no rearrangement of either TCR-C beta 1 or IG(H)JH was detected from the lymphocytes by Southern blot analysis. EBV was not found in the nuclei of lymphocytes by an immunofluorescence antibody. The lymphoproliferation was resistant against immunosuppressive drugs, administered for the treatment of chronic GVHD, and it effectively inhibited aggravation of the chronic GVHD. Although antithymocyte globulin and cytosine arabinoside were administered later, the patient died of respiratory failure with bilateral pleural effusion and interstitial pneumonia. Because we found no evidence of monoclonality of the abnormal lymphocytes, we could not conclude that this patient had suffered from malignant lymphoproliferation. To our knowledge, this is the first case report of proliferation of CD4+ lymphocytes in a patient with chronic GVHD following alloBMT. In this paper, we discuss the possible pathophysiology of the patient.

Adult↗
PubMed2000

[Obstructive sleep apnea syndrome in a patient with superior vena cava syndrome caused by lung cancer].

A 48-year-old man was treated with chemotherapy and irradiation therapy for superior vena cava syndrome (SVCS) caused by adenocarcinoma of the lung, and his symptoms subsided temporarily. However, the same symptoms recurred, and severe snoring during sleep and daytime hypersomnolence developed. Obstructive sleep apnea syndrome (OSAS) was diagnosed by respiratory inductive plethysmography. After chemotherapy, the symptoms of edema of the face and arms, snoring, and daytime somnolence tendency were alleviated, and the patient's apnea hypopnea index decreased remarkably. In addition, lateral cephalograms disclosed improved patency of the upper respiratory tract and dilation of the soft palate. These findings suggested a relationship between SVCS and OSAS. OSAS may cause a deterioration of circulatory dynamics and the quality of life when it develops secondary to SVCS. Therefore, it is necessary to determine whether OSAS is present and accordingly provide suitable treatment in patients with SVCS.

Adenocarcinoma↗
PubMed2000

[Renal cell carcinoma in a patient with malignant lymphoma: a case report].

A 65-year-old woman was admitted for the treatment of malignant lymphoma. Computed tomography revealed a right renal tumor. After 3 cycles of CHOP (cyclophosphamide, adriamycin, vincristine, prednisone) chemotherapy, we performed right radical nephrectomy. The histopathological diagnosis was renal cell carcinoma. After nephrectomy she was treated with 3 cycles of CHOP chemotherapy and radiation therapy. She received no adjuvant therapy for renal cell carcinoma and had no recurrence after 8 months from the nephrectomy.

Aged↗
PubMed1999

Release of cytochrome c from mitochondria to cytosol in gerbil hippocampal CA1 neurons after transient forebrain ischemia.

We examined cytosolic cytochrome c in gerbil hippocampal CA1 and CA3 regions after induction of 5-min ischemia by immunoblotting. In the CA1 region, cytochrome c was detected in the cytosolic fraction from 1 to 6 h after ischemia by Western blotting, while it was not detected in the CA3 region. Following intraventricular administration of cyclosporin A (CsA), detectable cytosolic cytochrome c was dramatically decreased, and about 80% of CA1 neurons survived after ischemia. The present studies demonstrate that cytochrome c is translocated from mitochondria to the cytosol in the early stage of delayed neuronal cell death, and suggest the involvement of the mitochondrial permeability transition.

Animals↗