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R Koike

Publications and source records attributed to R Koike.

At least 37 records · Page 2Linked to original sources
PubMed1998

Cloning and characterization of the rat MAdCAM-1 cDNA and gene.

A cDNA clone for rat MAdCAM-1 homologue was isolated from mesenteric lymph nodes by RT-PCR using primers prepared from the exon sequences of the gene isolated from a genomic library of the WKAH rat, using mouse cDNA as a probe. A 1279 bp cDNA fragment contained an open reading frame (ORF) for a protein of 394 amino acids. Homology of nucleotide sequences between the mouse and rat MAdCAM-1 ORF was 85.1% with an amino acid identity of 80.5%. The rat MAdCAM-1 had two immunoglobulin-like domains, a mucinlike domain and the third immunoglobulin-like domain with a homology to alpha 3 domain of the rat MHC class I molecule. Northern blot analysis demonstrated transcripts in Peyer's patches and mesenteric lymph nodes but not in spleen. Organization of the gene in the rat was similar to that in the mouse, consisting of 5 exons located at about a 4 kbp genomic region.

Amino Acid Sequence↗
PubMed1998

[A refractory case of relapsing polychondritis].

We report here a case of relapsing polychondritis (RPC), who responded to salazosulfapyridine (SASP) after 1.5 years of active disease. A 15-year-old girl having chondritis of bilateral auricles, nose and respiratory tract, ocular inflammation, cochlear and vestibular dysfunction and seronegative polyarthritis was diagnosed as RPC, and oral corticosteroid was initially effective. She was admitted to our hospital with obstructive tract chondritis and was refractory to any of the treatment such as intravenous (i.v.) pulse steroid therapy, i.v. pulse cyclophosphamide (CPA), oral intermittent methotrexate (MTX) and high dose i.v. gamma globulin. Although she was partly responsive to oral cyclosporine A (CsA), but clinical symptoms did not completely subside. SASP, initiated in combination with oral corticostreroid and CsA, however, was successful not only to show steroid sparing effect but also to induce complete remission. SASP might be useful to refractory case of RPC.

Adolescent↗
PubMed1998

[Difference between transcortical sensory aphasia following the left frontal lesion and transcortical sensory aphasia following the left posterior lesion].

We assessed the difference between transcortical sensory aphasia (TCSA) following the left frontal lesions (F-TCSA) and TCSA following the left posterior lesions (P-TCSA). All the patients were right-handed and the 7 patients had the lesions in the only frontal lobe and the 10 patients had the lesions only in the left temporo-parieto-occipital regions. We administered pointing tasks, using 90 line drawings representing single nouns. We presented 6 line drawings a pointing board, and we used two kinds of pointing boards: one showed the line drawings each belonging to different categories (random categorized pointing task), the other showed the line drawings each belonging to only either two different categories (two categorized pointing task) and we presented 15 pointing boards each alternatively. The result was that regarding the patients of P-TCSA showed different number of correct answers between the random categorized pointing task and the two categorized pointing task with statistical significance. Regarding the patients of F-TCSA showed no difference between them. The results indicated that disturbance of P-TCSA on the pointing task was the disturbance of semantic process per se. And the disturbance of F-TCSA on the pointing task was that of not only semantic process but also the whole process including comprehending the presented words, searching the line drawings, comparing the line drawings with the presented word and final selection, which demanded persistent multiple memory process consistent with working memory.

Aphasia, Wernicke↗
PubMed1997

Analysis of expression of lymphocyte homing-related adhesion molecules in ALY mice deficient in lymph nodes and Peyer's patches.

The aly, alymphoplasia, is an autosomal recessive mutation in mice of an unknown etiology, which induces total aplasia of lymph nodes and Peyer's patches. We hypothesized that the lack of lymphoid tissue may be due to abnormalities of lymphocyte traffic into these tissues. Therefore, we analyzed the expression of various adhesion molecules associated with lymphocyte homing. Among the adhesion molecules examined, all were normally expressed except the mucosal addressin MAdCAM-1. In aly/aly mice MAdCAM-1 was absent in the spleen at mRNA and protein levels, but was normally expressed in the intestinal venules. The FISH analysis and linkage analysis using microsatellite markers demonstrated that the MAdCAM-1 gene is located on chromosome 10, indicating that MAdCAM-1 is not encoded by the aly gene, which is located on chromosome 11. Our results indicate that the aberrant expression of MAdCAM-1 is not the direct cause of aly mutation but rather a secondary defect.

Animals↗
PubMed1997

Rapid and sensitive determination of amprolium in chicken plasma by high-performance liquid chromatography with post-column reaction.

A rapid, sensitive and reproducible reversed-phase HPLC assay was developed for the determination of amprolium (APL) in chicken plasma. Protein in plasma sample was precipitated with 0.33 M perchloric acid and supernatant solution was injected into the HPLC system. Following the chromatographic separation of APL and the beclotiamine (I.S.) on a C18 column, the derivatives of APL and I.S. were formed by post-column reaction and detected by fluorescence detection (excitation at 400 nm, emission at 460 nm). The method showed excellent precision, accuracy and speed with a detection limit of 2 ng/ml. The intra- and inter-assay variance of this method were less than 11.2%. This method has been successfully applied to plasma determinations after oral administration of APL to chicken.

Amprolium↗
PubMed1997

Adult onset globoid cell leukodystrophy (Krabbe disease): analysis of galactosylceramidase cDNA from four Japanese patients.

We examined galactosylceramidase (GALC) cDNA in four Japanese patients with adult onset globoid cell leukodystrophy (Krabbe disease; AO-GLD) by polymerase chain reaction/single-strand conformation polymorphism (PCR-SSCP) analysis, subsequent sequence determination, and restriction enzyme digestion of PCR products, initial symptoms were the onset of slowly progressive spastic paraplegia from the middle of the second decade, and all patients had diminished GALC activity in their leukocytes. We identified three missense mutations (I66M, G270D, L618S) and one exon-6 skipping (535-573del). Two of the patients had only the I66M mutant mRNA, and one only the G27OD mutant mRNA. The fourth patient carried a compound heterozygous mutation of 535-573del and L618S. To determine the enzymatic activities produced by these mutations, we constructed mutated GALC cDNAs and expressed them in COS-1 cells. Three mutations, viz., G270D, L618S, and exon-6 skipping (535-573del), produced diminished GALC activity as expected. The I66M mutation in the wild-type GALC cDNA(I289) had normal activity, but when this mutation and the V289 polymorphism were introduced into the same allele, it had decreased activity. Thus, the combination of a unique mutation and polymorphism causes conformational change in the GALC enzyme, resulting in low enzymatic activity. AO-GLD mutations, including those found here, are located in the N-terminus (I66M, G270D, 535-573del) or C-terminus (L618S) of the GALC enzyme, whereas the reported mutations in the infantile form (IF-GLD) are in the central domain. This difference in mutation sites may affect the clinical features of GLD.

Adult↗
PubMed1997

[A refractory case of adult-onset Still's disease].

We report here a case of adult-onset Still's disease (AOSD), who finally responded to a combination of cyclophosphamide (CPA) and gold sodium thiomalate (GST) after two years of active disease. A 23-year-old man having continuous high fever with skin rash, polyarthralgia and increased serum ferritin, was diagnosed as AOSD, and oral corticosteroid was initially effective. His symptoms recurred one year later without clinical improvement to increased dosage of steroid. He was admitted to our hospital with pericarditis and pleural effusion but did not respond to either intravenous (i.v.) pulse steroid therapy, methotrexate (MTX) or high dose i.v. gamma-globulin. He was partly responsive to monthly i.v. injection of CPA, but clinical symptoms did not completely subside and hyperferritinemia persisted. GST, initiated in combination with CPA, however, was successful to induce complete remission. MTX has recently been reported to be efficacious to steroid-resistant AOSD, but CPA and gold compounds might be useful to refractory case of AOSD.

Adult↗
PubMed1997

Localization of a gene for an autosomal recessive form of juvenile Parkinsonism to chromosome 6q25.2-27.

An autosomal recessive form of juvenile Parkinsonism (AR-JP) (MIM 600116) is a levodopa-responsive Parkinsonism whose pathological finding is a highly selective degeneration of dopaminergic neurons in the zona compacta of the substantia nigra. By linkage analysis of diallelic polymorphism of the Mn-superoxide dismutase gene (SOD2), we found a family with AR-JP showing perfect segregation of the disease with the SOD2 locus. By extending the linkage analysis to 13 families with AR-JP, we discovered strong evidence for the localization of the AR-JP gene at chromosome 6q25.2-27, including the SOD2 locus, with the maximal cumulative pairwise LOD scores of 7.26 and 7.71 at D6S305 (theta = .03) and D6S253 (theta = .02), respectively. Observation of obligate recombination events, as well as multipoint linkage analysis, placed the AR-JP gene in a 17-cM interval between D6S437 and D6S264. Delineation of the AR-JP gene will be an important step toward our understanding of the molecular mechanism underlying selective degeneration of the nigral neurons.

Adolescent↗
PubMed1996

Ceramide induces apoptosis via CPP32 activation.

Although both ceramide and interleukin-1beta converting enzyme (ICE) family proteases are key molecules during apoptosis, their relationship remains to be elucidated. We report here that cell-permeable ceramide induced cleavage and activation of CPP32, a Ced-3/ICE-like protease, but not ICE. Ceramide-induced apoptosis of Jurkat cells was blocked by the CPP32-specific tetrapeptide inhibitor DEVD-CHO, but not by the ICE inhibitor YVAD-CHO. Furthermore, variant Jurkat cells with defective CPP32 activation were resistant to both anti-Fas- and ceramide-induced apoptosis. These results indicate that CPP32 activation is required for ceramide-induced apoptosis, and suggest sphingomyelin-ceramide pathway functions upstream of CPP32.

Apoptosis↗
PubMed1996

The splenic marginal zone is absent in alymphoplastic aly mutant mice.

aly is a unique spontaneous autosomal recessive mutation in mice that causes a deficiency in the systemic lymph nodes (LN) and Peyer's patches (PP). aly also induces abnormal histological findings in the spleen and a deficiency in humoral and cell-mediated immune functions, although lymphocytes of the aly/aly mouse show virtually normal immune responses in vitro. We studied the structure of the spleen of aly mice in detail by immunohistochemistry and electron microscopy. We found that the spleen of the aly/aly mouse was deficient in the expression of specific antigens for marginal metallophils (MM), marginal zone macrophages (MZM) and fibroblastic reticular cells (FRC), which are components of the marginal zone (MZ) of the spleen. Morphological analysis indicated that the aly/aly spleen is deficient in the structure of MZ, which may, in part, account for the severe immunodeficiency in the aly/aly mouse. We then performed reciprocal bone marrow transplantation experiments (BMT) between normal and aly mice and found a clear correlation between the formation of LN and the development of the splenic MZ in these mice; i.e. successful development of LN was invariably associated with the appearance of the MZ structure, whereas the failure of LN development was always associated with the absence of the development of MZ. These BMT results suggest that a common factor may regulate the generation of both LN and MZ of the spleen.

Animals↗
PubMed1996

Use of ELISA for in vitro potency test of rabies vaccines for animal use.

The use of ELISA for the potency test of inactivated rabies vaccines for animal use was evaluated. Sandwich ELISA was developed, using monoclonal antibodies which enabled to recognize the glycoprotein (G-protein) of rabies virus and showed a protective effect in mice. Soluble G-protein which displays an ELISA activity but a low immunogenicity was removed by gel filtration before ELISA was carried out. The ELISA titres of the first fraction of vaccines separated by gel filtration were correlated with the neutralizing antibody titres of vaccinated guinea-pigs. Our results suggest that the ELISA titres of the first fraction of vaccines separated by gel filtration reflected the protective G-protein contents for the in vitro potency test of rabies vaccines compared with the current in vivo test.

Animals↗
PubMed1996

[Two cases of lupus nephritis having a high titer of anti-(histone-DNA) complex antibody without IgG anti-dsDNA antibody].

IgG antibody specific to double-stranded DNA (dsDNA) has been recognized as a predictive indicator of the renal involvement in systemic lupus erythematosus. However, we recently experienced two cases of overt lupus nephritis without IgG anti-dsDNA antibody. In both cases, high titers of antibody to the histone dimer (H2A-H2B)-dsDNA complex were detected. They responded well to the corticosteroid therapy, with a cytotoxic agent in one case, and the titers of anti-(histone-DNA) antibody was decreased along with the improvement of proteinuria. Based on the recent reports suggesting a pathogenic role of this antibody in lupus nephritis, we suggest that measurement of the anti-(histone-DNA) antibody is necessary in lupus nephritis patients, especially when IgG anti-dsDNA antibody is not detectable.

Adult↗
PubMed1995

Radiation myelopathy: a clinicopathological study with special reference to correlation between MRI findings and neuropathology.

We describe magnetic resonance imaging (MRI) and neuropathological findings in a patient with chronic progressive radiation myelopathy (CPRM). An 81-year-old man with esophageal cancer underwent radiotherapy. Four years later he developed a progressive neurological deficit below the irradiated level of the spinal cord. Neurological examination revealed spastic paraplegia. MRI findings showed an area of high signal intensity on T2-weighted images of the thoracic spinal cord. On the basis of clinical and MRI findings, we diagnosed his condition as CPRM. MRI performed thirteen months after onset of neurological signs revealed mild atrophy of the spinal cord detected on T1-weighted images and an area of high signal intensity within the spinal cord detected on T2-weighted images. Neuropathological examination revealed findings consistent with radiation myelopathy. We speculate that the area of high signal intensity within the spinal cord detected on T2-weighted images might be a result of proliferation of small vessels, which was discovered upon autopsy.

Aged↗
PubMed1994

Development of intestinal intraepithelial T lymphocytes is independent of Peyer's patches and lymph nodes in aly mutant mice.

We have previously reported a new spontaneous recessive mutation that induces a generalized lack of lymph nodes (LNs) and Peyer's patches (PPs) accompanied by immunodeficiency in mice (gene symbol, aly). In this study, we have analyzed gut-associated lymphatic tissues of the mutant aly/aly mice and have compared the intestinal intraepithelial T lymphocytes (IEL) in aly/aly and normal aly/+ littermate mice. Immunohistochemical studies revealed that colonization of IEL and lamina propria T cells takes place in the absence of PPs and IgA-producing B cells in the lamina propria. Absolute numbers of Thy-1- IEL-alpha beta and -gamma delta are not altered in aly/aly mutant mice, whereas absolute numbers of Thy-1+ IEL-alpha beta and -gamma delta in aly/aly mice are about half of those in aly/+ mice. In IEL-alpha beta from aly/aly mice, the major CD8 alpha alpha+ and CD8 alpha beta+ subsets are maintained, whereas CD4+ and CD4+, CD8+ subsets are reduced. Although the population size of major CD8 alpha alpha+ and CD4-, CD8- IEL-gamma delta subsets is slightly reduced, the use of TCR-gamma- and -delta-chain variable gene segments by IEL-gamma delta remains almost the same in aly/aly mice. The constitutive cytolytic activity of IEL-alpha beta and -gamma delta is attenuated sharply in the aly/aly condition. This activity is, however, augmented significantly after in vitro stimulation with anti-CD3 mAb. These results indicate that most of the IEL subpopulations develop independently of passage through PPs and mesenteric LNs and that the aly mutation interrupts cytotoxic IEL development during relatively late differentiation steps that convert cytotoxic precursors to the constitutively cytolytic state.

Animals↗