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Biomedical subjects

H Kaneko

Publications and source records attributed to H Kaneko.

At least 253 records · Page 14Linked to original sources
PubMed1997

Role of curdlan sulfate in the binding of HIV-1 gp120 to CD4 molecules and the production of gp120-mediated TNF-alpha.

To clarify the mechanism by which curdlan sulfate (CRDS) inhibits human immunodeficiency virus (HIV)-1 infection, we examined its influence on the binding of gp120 to CD4 molecules on T cells and macrophages, as well as on the production of TNF-alpha by gp120-stimulated macrophages (which promotes HIV-1 replication). CRDS treatment of cells not only inhibited the binding of HIV-1 gp120 to CD4+ cells, but also inhibited TNF-alpha production induced by gp120. Inhibition of HIV-1 infection by CRDS may be related to these two actions.

Anti-HIV Agents↗
PubMed1997

Human immunodeficiency virus type 2 envelope glycoprotein binds to CD8 as well as to CD4 molecules on human T cells.

We report here that human immunodeficiency virus type 2 (HIV-2) envelope glycoprotein (gp105), but not HIV-1 gp120, can bind to CD8 molecules as well as to CD4 molecules on human T cells. This phenomenon may lead to differences in the life cycles of HIV-1 and HIV-2, and it may be related to the differences in disease manifestations of HIV-1 and HIV-2 infection, including longer survival of HIV-2-infected patients.

CD4 Antigens↗
PubMed1997

Hemangioma of the bladder with extravesical extension.

Bladder hemangioma is a rare benign tumor occurring in any age group. We report the case of a 76-year-old woman having a bladder hemangioma. On cystoscopic examination no typical features of the bladder hemangioma were found. Biopsy of the lesion revealed a cavernous hemangioma. A partial cystectomy was performed for the control of macroscopic hematuria.

Aged↗
PubMed1997

Ovarian response and FSH profile in cows following injection of various doses of inhibin antiserum.

Dose effect of inhibin antiserum on ovarian response and hormonal profiles were investigated. On day 12 of the estrous cycle (day 0 = estrus), 14 of 19 cows were given a single i.v. injection of 25 ml (n = 4), 37.5 ml (n = 5) or 50 ml (n = 5) antiserum against inhibin produced in a castrated male goat. The other 5 animals were given 50 ml castrated male goat serum (control serum). The animals in each group received a single i.m. injection of 0.5 mg prostaglandin F2 alpha analogue (PG) 48 hr following the serum injection. The population of follicles and ovulation rate (estimated by the number of corpora lutea) were examined by ultrasonography. Administration of inhibin antiserum consistently resulted in a significant (p < 0.01) increase in plasma concentrations of follicle-stimulating hormone (FSH) in inhibin-neutralized groups, although the increased FSH levels were sustained longer in 50-ml group than in the 25- and 37.5- ml groups. Levels in the circulating inhibin antibody titer were positively correlated with dosage of inhibin antiserum. A large number of antral follicles (> or = 4 mm in diameter) developed similarly after hypersecretion of FSH in all neutralized groups, coupled with a rise in plasma estradiol levels, while the number of large follicles (> or = 10 mm in diameter) on estrus showed a dose-dependent increase. Multiple ovulation (2 to 4) was recorded in all animals after injection of 50 ml inhibin antiserum, however all cows in the 25-ml group experienced only one ovulation and injection of 37.5 ml resulted in a variable number of ovulations (1 to 5). These results demonstrated that administration of inhibin antiserum on day 12, followed by injection of PG, was able to induce hypersecretion of FSH and subsequently multiple ovulations. The number of large follicles on estrus day and ovulations were affected by dosage of inhibin antiserum and were correlated with persistence of increased FSH levels or circulating antibody levels.

Animals↗
PubMed1997

Two Japanese siblings with Bloom syndrome gene mutation and B-cell lymphoma.

Bloom syndrome (BS) is a rare autosomal recessive genetic disorder characterized by lupus-like erythematous telangiectasia of the face, sun sensitivity, infertility and stunted growth. Upper respiratory tract and gastrointestinal infections are commonly associated with the decreased immunoglobulin levels found in BS patients. Chromosomal abnormalities are hallmarks of the disorder, and high frequencies of sister chromatid exchanges and quadriradial configurations in lymphocytes and fibroblasts are virtually diagnostic. Recently, the causative gene for BS (BLM) has been identified. We encountered and defined a family with a nonsense mutation in BLM. The brother and sister were homozygous for the mutation and both developed B-cell malignant lymphoma in their twenties. These findings indicate the importance of prenatal diagnosis and the detection of BS carriers based on molecular genetic analysis.

Adenosine Triphosphatases↗
PubMed1997

[Parkinsonism in a patient receiving interferon alpha therapy for chronic hepatitis C].

We report a case of Parkinsonism due to interferon alpha (IFN alpha) therapy for chronic hepatitis C. A 51-year-old female received IFN alpha (Sumipheron@6 x 10(6) IU), three times a week by intramuscular injection. Six months after the initiation of IFN alpha therapy, she noticed tremor of bilateral fingers, and was admitted to our hospital. Neurological examination revealed muscle rigidity, bilateral finger tremor, mild bradykinesia. Tremor was more extreme at posture rather than at rest. She was diagnosed as Parkinsonism, and carbidopa-levodopa therapy was effective. Attention must be paid to Parkinsonism, when IFN alpha is administered.

Chronic Disease↗
PubMed1997

[Systemic lupus erythematosus (SLE) and retrovirus].

Retrovirus have repeatedly been suggested as a possible trigger mechanism for animal and human autoimmune disease. Recent reports indicate that not only exogenous, but also endogenous, retrovirus could play an important role to induce autoimmunity. Here we described the relationship between retrovirus and systemic lupus erythematosus.

Animals↗
PubMed1997

[Manipulation of costimulatory pathways in autoimmune disease].

The past year has seen significant advances in our understanding of the role of costimulatory pathways in antigen-specific T cell activation and maintenance of self-tolerance. It has been suggested that the absence of costimulators on normal tissue cells could serve to induce self-tolerance and that inappropriate expression of costimulators on antigen-presenting cells (APC) could activate self-reactive T cells, resulting in autoimmunity. CD28 on T cells and CD80 and CD86 on APC are key molecules in the maintenance and breakdown of anergy. CTLA-4Ig fusion protein, that binds to both CD80 and CD86 with high affinity and thereby prevents interaction of CD80/CD86 with CD28/CTLA-4, prevents or ameliorates several autoimmune disease in experimental animal models, supporting an importance of this pathway in the development of autoimmune diseases. However, the studies using specific monoclonal antibodies against CD80 and CD86 have shown different outcomes in individual autoimmune models. This suggests that the actual regulatory mechanisms of this pathway in autoimmunity is much more complex, because of the existence of two receptors (CD28 and CTLA-4) and two ligands (CD80 and CD86) and the opposite function of CD28 and CTLA-4 in T cell activation. Further investigation on physiological function of this pathway in vivo may help for developing rational therapeutic approaches manipulating this pathway.

Abatacept↗
PubMed1997

Genetic aberrations in the development and subsequent progression of myelodysplastic syndrome.

We performed longitudinal analyses of chromosomes and studied the configuration of NRAS, TP53, NF1, and cFMS genes in 70 patients with myelodysplastic syndrome(MDS). The NRAS mutations were detected in 6 patients(9%) at codons 12 or 13. The TP53 mutations were found in 10 patients(14%) in exons 4 through 8. Longitudinal studies revealed that the NRAS mutation was a late-appearing event, while the TP53 mutations were detectable at the presentation of MDS. No patients had both NRAS and TP53 mutations, simultaneously. NF1 and cFMS genes showed any mutational event among these 70 patients. Patients with a TP53 mutation had a significantly shorter survival time than those with an NRAS mutation or those without NRAS or TP53 mutation. However, patients who showed an NRAS mutation had a shorter survival time once the mutation emerged, similar to that of patients with a TP53 mutation.

Adolescent↗
PubMed1996

Microsatellite instability in B-cell lymphoma originating from Bloom syndrome.

Bloom syndrome (BS) is a rare autosomal recessive genetic disorder characterized by lupus-like erythematous telangiectasias of the face, sun sensitivity, stunted growth infertility and immunodeficiency. In addition, BS patients are highly predisposed to cancers. Although recently the causative gene of BS (BLM) was identified as a DNA helicase homologue, the function of BLM in DNA replication has not been elucidated. In this study, p53 mutation and microsatellite instability in B-cell lymphomas originating from 2 sibling BS patients were investigated. In the originally developed tumor of both patients, no p53 mutation was detected. In one patient, however, after treatment by ionizing radiation the B-cell lymphoma recurred, showing a 9-bp deletion in exon 7. In lymphoma cells and an EB-virus-transformed cell line from BS lymphocytes of this patient, microsatellite instability was also detected from the reduced length of microsatellite DNA markers, although in the other patient microsatellite instability was not detected. Thus, 2 B-cell lymphomas, despite having the same BLM mutation, showed different phenotypes in terms of p53 mutation and microsatellite instability.

Adult↗
PubMed1996

The effect of a 5HT2 receptor antagonist sarpogrelate (MCI-9042) treatment on platelet function in Buerger's disease.

The effect of a new, specific 5-HT2 receptor antagonist sarpogrelate (MCI-9042) treatment on platelet function and serotonin levels in both plasma and whole blood in Buerger's disease, was assessed in a pilot study. We investigated 10 patients suffering from Buerger's disease. Sarpogrelate in a dose of 3 x 100 mg a day was given p.o. for a period of 8 weeks. It was well tolerated and no major side effects were noted. It was judged to be effective in some patients as assessed by its effect on both subjective complaints and objective evaluation of ankle pressure index (API). Sarpogrelate induced a significant decrease in plasma serotonin (5-HT) concentration starting after the 4th week which lasted through to the 8th week of the study, whereas plasma tryptophan concentration increased significantly after 2 and 4 weeks. There were no changes in plasma 5-HIAA concentration. On the other hand whole blood 5-HT concentration increased significantly after 2 weeks, and there was also a tendency to increase in whole blood tryptophan concentration (p = 0.052). Platelet aggregation induced by ADP and collagen did not show any statistically significant changes. Surprisingly, platelet aggregation induced by serotonin increased significantly after 2 weeks and even more so after 4 weeks of treatment, and then it returned to baseline values after 8 weeks. There was no effect on platelet count, APTT, TT and fibrinogen concentration.

Administration, Oral↗
PubMed1996

Novel neural adhesion molecules in the Contactin/F3 subgroup of the immunoglobulin superfamily: isolation and characterization of cDNAs from rat brain.

We cloned two kinds of cDNAs encoding novel Contactin/F3-subgroup adhesion molecules, which we termed NB-2 and NB-3. Nucleotide sequence analyses have shown that NB-2 and NB-3 are comprised of 1099 and 1028 amino acid residues, respectively. There was 51% similarity in the amino acid sequence of NB-2 and NB-3. NB-2 shared 46, 43, 55 and 55% identities with Contactin/F3, Tag-1, Big-1 and Big-2, respectively, at the amino acid sequence level. Likewise, the amino acid sequence of NB-3 exhibited 42, 44, 58 and 60% identities with Contactin/F3, Tag-1, Big-1 and Big-2, respectively. Expression of NB-2 mRNA was restricted to cerebrum, cerebellum and was hardly detectable, if any, in spinal cord. On the other hand, high expression of NB-3 mRNA was observed in spinal cord, as well as in cerebrum and cerebellum. In the other tissues, no expression of NB-2 and NB-3 mRNAs was detected.

Animals↗
PubMed1996

Controlling substrate preference and transglycosylation activity of neopullulanase by manipulating steric constraint and hydrophobicity in active center.

The substrate specificity and the transglycosylation activity of neopullulanase was altered by site-directed mutagenesis on the basis of information from a three-dimensional structure predicted by computer-aided molecular modeling. According to the predicted three-dimensional structure of the enzyme-substrate complex, it was most likely that Ile-358 affected the substrate preference of the enzyme. Replacing Ile-358 with Trp, which has a bulky side chain, reduced the acceptability of alpha-(1-->6)-branched oligo- and polysaccharides as substrates. The characteristics of the I358W-mutated enzyme were quite different from those of wild-type neopullulanase and rather similar to those of typical starch-saccharifying alpha-amylase. In contrast, replacing Ile-358 with Val, which has a smaller side chain, increased the preference for alpha-(1-->6)-branched oligosaccharides and pullulan as substrates. The transglycosylation activity of neopullulanase appeared to be controlled by manipulating the hydrophobicity around the attacking water molecule, which is most likely used to cleave the glucosidic linkage in the hydrolysis reaction. We predicted three residues, Tyr-377, Met-375, and Ser-422, which were located on the entrance path of the water molecule might be involved. The transglycosylation activity of neopullulanase was increased by replacing one of the three residues with more hydrophobic amino acid residues; Y377F, M375L, and S422V. In contrast, the transglycosylation activity of the enzyme was decreased by replacing Tyr-377 with hydrophilic amino acid residues, Asp or Ser.

Amino Acid Sequence↗
PubMed1996

Inhibition of amyloid beta protein aggregation and neurotoxicity by rifampicin. Its possible function as a hydroxyl radical scavenger.

Aggregation of physiologically produced soluble amyloid beta protein (Abeta) to insoluble, neurotoxic fibrils is a crucial step in the pathogenesis of Alzheimer's disease. Aggregation studies with synthetic Abeta1-40 peptide by the thioflavin T fluorescence assay and electron microscopy and cytotoxicity assays using rat pheochromocytoma PC12 cells showed that an antibiotic, rifampicin, and its derivatives, which possess a naphthohydroquinone or naphthoquinone structure, inhibited Abeta1-40 aggregation and neurotoxicity in a concentration-dependent manner. Hydroquinone, p-benzoquinone, and 1,4dihydroxynaphthalene, which represent partial structures of the aromatic chromophore of rifampicin derivatives, also inhibited A beta1 40 aggregation and neurotoxicity at comparable molar concentrations to rifampicin. Electron spin resonance spectrometric analysis revealed that the inhibitory activities of those agents correlated with their radical-scavenging ability on hydroxyl free radical, which was shown to be generated in cell-free incubation of Abeta1-40 peptide. These results suggest that at least one mechanism of rifampicin-mediated inhibition of A beta aggregation and neurotoxicity involves scavenging of free radicals and that rifampicin and/or appropriate hydroxyl radical scavengers may have therapeutic potential for Alzheimer's disease.

Alzheimer Disease↗