[Correlation between serum anti CagA antibody and gastric disease].
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Antibodies, Bacterial↗
Biomedical subjects
Y Kitamura
Publications and source records attributed to Y Kitamura.
[Treatment outcome of 288 cases of renal cell carcinoma].
The clinical outcome was analyzed on 288 patients with renal cell carcinoma who were admitted to the Niigata Cancer Center Hospital during the 33 years from 1961 to 1993; 254 patients had had nephrectomy and 244 of them had undergone curable operations. The survival rate was calculated by the Kaplan-Meier method. The 3-, 5- and 10-year survival rates by all causes of death in all 288 patients were 64.8, 55.9 and 36.4%, respectively. According to the stage based on the general rules for clinical and pathological studies on renal cell carcinoma (The 2nd Edition), the 5-year survival rate was 89.5, 78.7, 51.1 and 13.7% for stages I (n = 31), II (n = 128), III (n = 38) and IV (n = 83), respectively. The 5-year survival rate for the patients (n = 88) from 1961 to 1985 was 40.9%, while the rate for the patients (n = 200) from 1986 to 1993 was 64.3%. This improvement of survival rate for the patients after 1986 was brought by the increase of the stage I or II cases and by the improvement of the survival in the stage III cases after 1986. The 5-year disease-specific survival rate for the patients over 50 years old was 55.5%, while the rate for the patients under 50 years old was 83.6%. Female, low pT, low grade and small tumor size were proven to be favourable prognostic factors in renal cell carcinoma.
Adult↗
Pain-related brain responses following CO2 laser stimulation: magnetoencephalographic studies.
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Adult↗
Chronic forced swim stress of rats increases frontal cortical 5-HT2 receptors and the wet-dog shakes they mediate, but not frontal cortical beta-adrenoceptors.
We studied the effects of chronic forced swim stress on 5-HT2 receptors and beta-adrenoceptors in the rat frontal cortex. The number of 5-HT2 receptors was increased immediately after the last chronic stress, but not after an acute stress. In vivo, the number of wet-dog shakes induced by a 5-HT2 receptor agonist, (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI), was increased 24 h after the last chronic stress. However, the concentrations of 5-HT and 5-hydroxyindole acetic acid (5-HIAA), measured by high pressure liquid chromatography (HPLC), were not altered by this stress. Binding sites for [3H]CGP-12177, i.e., beta-adrenoceptor sites, were unchanged after both the acute and the chronic stress. These results suggest that, in the rat, the chronic forced swim stress increases the number of frontal cortical 5-HT2 receptors and the number of wet-dog shakes mediated by these receptors, while the number of frontal cortical beta-adrenoceptors is not increased by this treatment.
Amphetamines↗
Pyruvate kinase deficiency of mice associated with nonspherocytic hemolytic anemia and cure of the anemia by marrow transplantation without host irradiation.
Mutant mice with splenomegaly and nonspherocytic hemolytic anemia were found in an inbred colony of the CBA/N (hereafter CBA) strain maintained in the Japan SLC Haruno farm (Shuchi-gun, Shizuoka, Japan). The activity of pyruvate kinase (PK) in red blood cells (RBCs) of the anemic mutants decreased to 16.2% of normal (+/+) CBA mice. Because the mutant CBA mice showed a remarkable reticulocytosis (41.6%) and because the PK activity of reticulocytes is much higher than that of mature RBCs, the PK activity in mature RBCs of the mutant CBA mice was calculated to be 2.8% that of mature RBCs of CBA-(+/+) mice. Because RBC type PK is encoded by the Pk-1 locus of the mouse (chromosome 3), we designated the mutant locus as Pk-1slc. The anemia and PK deficiency of CBA-Pk-1slc/Pk-1slc mice were cured by bone marrow transplantation (BMT) from CBA-(+/+) mice. Prior irradiation was not necessary for the curative BMT. On the other hand, the BMT from CBA-Pk-1slc/Pk-1slc mice to nonirradiated CBA-(+/+) mice did not result in the decrease of RBCs and the reduction of PK activity. The present results indicate that CBA-Pk-1slc/Pk-1slc mice are a potentially useful animal model for studying pathophysiology of PK deficiency and for developing new therapeutic methods to correct PK deficiency.
Anemia, Hemolytic, Congenital Nonspherocytic↗
Neuroprotective effects of NBQX on hypoxia-induced neuronal damage in rat hippocampus.
Models of cerebral ischaemia were used for analysis of mechanism of neuronal cell death and/or damage. Ischaemia is caused dominantly by severe hypoxia and hypoglycaemia: in the present study, we examined the influence of severe in vivo hypoxia (5% O2/95% N2 for 30 min at 22 degrees C). After hypoxia, neuronal damage was observed in the CA3 and dentate gyrus (DG) after 3 and 21 days of survival, but not in the CA1.2,3-Dihydroxy-6-nitro-7-sulphamoyl-benzo(F)quinoxaline (NBQX), an antagonist for AMPA/kainate receptors, showed neuroprotective effects in the CA3 and DG. These results suggest that hypoxia may induce neuronal damage in the CA3 and DG through activation of AMPA/kainate receptors.
Analysis of Variance↗
Antisense oligonucleotide inhibits the expression of procollagen type III gene in mouse fibroblasts.
The effects of transfection of phosphorothioate antisense oligonucleotides (ASOs) into BALB/c 3T3 mouse fibroblasts on procollagen type III production were examined. Immunohistochemistry and Western blots showed that the expression of procollagen type III decreased. Semi-quantitative reverse transcription polymerase chain reaction revealed that the expression of procollagen type III mRNA was inhibited. ASOs were effective for inhibiting procollagen type III production at the gene level, although the effect was transient.
3T3 Cells↗
Primary structure of murine red blood cell-type pyruvate kinase (PK) and molecular characterization of PK deficiency identified in the CBA strain.
To clarify the molecular abnormality of pyruvate kinase (PK) deficiency identified in the mutant mice of CBA-Pk-1slc/Pk-1slc, we cloned murine red blood cell-type PK (R-PK) cDNA of those animals. The cDNA sequence spans 1827 bp, including an open reading frame that can encode 574 amino acids. Homology in the coding sequences between murine and human R-PK was 86.1% at nucleotide and 91.5% at amino acid levels. A homozygous missense mutation at nucleotide 1013 GGT-->GAT was identified in the cDNA sequence of the mutant, causing a single amino acid substitution at no. 338Gly-->Asp of the murine R-PK. Six amino acid residues, 335Val-336Ala-337Arg-338Gly-339Asp-340L eu, were encoded in exon 8 of both human and rat L (liver-type)/R-PK genes and were evolutionarily conserved in PK from bacteria through humans. 337Arg was reported to be important for substrate binding, suggesting that the amino acid change would impair substrate affinity of the PK subunit. A homozygous missense mutation at the catalytic domain has been identified in a human PK variant, PK Hong Kong (941ATT-->ACT, 314 Ile-->Thr). Although both 1013A and 941C gave rise to an amino acid change adjacent to the active site and may interfere with substrate binding to the subunit, the degree of anemia was much more severe in the human case. The erythroid-progenitor cell number increased in the spleen of Pk-1slc/Pk-1slc mice to a level approximately 66 times higher than that in normal CBA mice, suggesting that compensatory extramedullary erythropoiesis in the spleen of the mutant mice, but not in the human variant, might account for the observed difference in the phenotype.
Amino Acid Sequence↗
High incidence of ultraviolet-B-or chemical-carcinogen-induced skin tumours in mice lacking the xeroderma pigmentosum group A gene.
Xeroderma pigmentosum (XP) is an autosomal recessive disorder characterized by a high frequency of skin cancer on sun-exposed areas, and neurological complications. XP has a defect in the early step(s) of nucleotide-excision repair (NER) and consists of eight different genetic complementation groups (groups A-G and a variant). We established XPA (group-A XP) gene-deficient mice by gene targeting of mouse embryonic stem (ES) cells. The XPA-deficient mice showed neither obvious physical abnormalities nor pathological alterations, but were defective in NER and highly susceptible to ultraviolet-B- or 9,10-dimethyl-1,2-benz[a]anthracene-induced skin carcinogenesis. These findings provide in vivo evidence that the XPA protein protects mice from carcinogenesis initiated by ultraviolet or chemical carcinogen. The XPA-deficient mice may provide a good in vivo model to study the high incidence of skin carcinogenesis in group A XP patients.
9,10-Dimethyl-1,2-benzanthracene↗
Somatosensory evoked magnetic fields after mechanical stimulation of the scalp in humans.
Somatosensory evoked magnetic fields after mechanical stimulation by air-pressure-induced tapping which was applied to the forehead and occiput were examined in normal human subjects. The equivalent current dipole (ECD) of the initial magnetic field, 1M, was identified in the primary somatosensory cortex (SI) in the hemisphere contralateral to the stimulation. The ECD of the subsequent magnetic fields, 2M, was identified in bilateral second sensory cortices (SII). The ECD position of 1M in SI generated after the scalp stimulation was closely inferior to the hand area of the SI, which was consistent with the well-known somatotopic organization, 'homunculus'.
Adult↗
Pain-related magnetic fields following painful CO2 laser stimulation in man.
The initial somatosensory evoked magnetic fields following painful heat stimulation by CO2 laser beam applied to the upper and lower limb were investigated in normal subjects. The main deflections, 'Pain MA' and 'Pain ML' following the arm and leg stimulation, respectively, were identified in the bilateral second sensory cortices (SII). The onset latencies of Pain MA and Pain ML were approximately 150 and 200 ms, respectively. No consistent equivalent current dipole was found in other areas including the primary sensory cortex in each hemisphere. Therefore, we consider that neurons in the bilateral SII are initially activated following painful heat stimulation.
Adult↗
Inhibition of constitutive nitric oxide synthase in the brain by pentamidine, a calmodulin antagonist.
Nitric oxide (NO) which is produced by activation of Ca2+/calmodulin-dependent NO synthase is known to induce neuronal damage. We examined the effects of 3'-azido-2',3'-dideoxythymidine (AZT, a reverse transcriptase inhibitor), pentamidine (a therapeutic drug for Pneumocystis carinii pneumonia) and calmodulin antagonists such as trifluoperazine and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) on NO synthase activation. Although AZT had no effect on the activity of constitutive neuronal NO synthase, pentamidine inhibited the activation of neuronal NO synthase as did trifluoperazine and W-7. The inhibition by pentamidine was prevented by the addition of purified calmodulin. In addition, pentamidine inhibited calmodulin-dependent activation of neuronal NO synthase purified from rat cerebellum. From these results, it is suggested that pentamidine inhibits the neuronal NO synthase activation by probably acting as a calmodulin antagonist.
Amino Acid Oxidoreductases↗
Characterization of c-kit-positive neurons in the dorsal root ganglion of mouse.
Previously, we showed that c-kit receptor tyrosine kinase is expressed by a subpopulation of dorsal root ganglion (DRG) neurons, and that the ligand for the c-kit receptor, stem cell factor (SCF), induces the neurite outgrowth and supports the survival of these neurons in culture [16]. However, it is unknown which class of DRG neurons express c-kit receptor and which factor regulates differentiation and survival of c-kit-positive neurons. In the present study, we attempted to characterize c-kit positive neurons in the mouse DRG. The c-kit-positive neurons were small or medium in size, and 44% of these neurons contained substance P. Central fibers of the c-kit-positive neurons terminated in laminae I and II of the gray matter of the spinal cord. These results suggest that c-kit-positive neurons in the DRG belong to a functional subpopulation. The c-kit receptor protein was presented on the membrane of processes and growth cones in neurons. When DRG cells of embryonic day 15.5 or 17.5 were cultured, the survival of c-kit-positive neurons was supported by SCF, nerve growth factor (NGF) or leukemia inhibitory factor. SCF and NGF synergistically supported the survival of c-kit-positive neurons at submaximal concentrations. c-kit-positive DRG neurons from neonatal mice survived without addition of any factor in culture, suggesting that the requirement for trophic support in c-kit-positive neurons changes during development.
Age Factors↗
Infection with Nippostrongylus brasiliensis induces invasion of mast cell precursors from peripheral blood to small intestine.
Precursors of mast cells were defined as cells that formed mast-cell colonies in methylcellulose culture (CFU-mast). Mononuclear cells (MNC) were obtained from the bone marrow, peripheral blood, and small intestine of Ws/Ws rats with a small deletion at the tyrosine kinase domain of c-kit and of control normal (+/+) rats. In the culture containing concanavalin A-stimulated spleen cell conditioned medium (ConA-SCM) alone, the numbers of mast-cell colonies produced by Ws/Ws MNC were comparable with those of +/+ MNC. In the culture containing both ConA-SCM and stem cell factor (a ligand of c-kit), however, the numbers of mast-cell colonies produced by +/+ blood MNC were 107 times as great as that of Ws/Ws blood MNC. Using this culture condition, we investigated changes in concentration of CFU-mast in the marrow, blood, and intestine of +/+ rats after infection with Nippostrongylus brasiliensis (NB), which induced marked mast-cell accumulation in the small intestine. The concentration of CFU-mast in blood dropped to 21% of preinfection levels 1 week after the NB infection. In contrast, a sevenfold increase of CFU-mast occurred in the small intestine. The proportion of CFU-mast in S phase of the cell cycle remained at low levels in the marrow and blood after NB infection, but it increased significantly in the small intestine. The present result suggests that NB infection induces the invasion of CFU-mast into the intestine from blood and their subsequent proliferation in the tissue site.
Animals↗
Constitutively activating mutations of c-kit receptor tyrosine kinase confer factor-independent growth and tumorigenicity of factor-dependent hematopoietic cell lines.
The c-kit receptor tyrosine kinase (KIT) is activated upon ligand binding, thereby leading to a variety of signaling events that play a fundamental role in hematopoiesis. In addition to ligand-dependent activation, we have previously shown that KIT is constitutively activated in a ligand-independent manner by two point mutations, Val-559-->Gly (G559) mutation in the juxtamembrane domain and Asp-814-->Val (V814) mutation in the phosphotransferase domain. To investigate the biochemical consequence and biologic significance of these mutations, retroviral vectors encoding KITG559 or KITV814 were introduced into murine pro-B-type Ba/F3 cells and myeloid FDC-P1 cells, both of which require interleukin-3 (IL-3) for their growth and survival. In the cells, KITG559 or KITV814 were found to be constitutively phophorylated on tyrosine in the absence of stem cell factor (SCF) that is a ligand for KIT. Chemical cross-linking analysis showed that a substantial fraction of the phosphorylated KITG559 underwent dimerization even in the absence of SCF, whereas the phosphorylated KITV814 did not, suggesting the distinct mechanisms underlying constitutive activation of KIT by G559 and V814 mutations. Furthermore, the cells expressing either KITG559 or KITV814 were found to show a factor-independent growth, whereas the cells expressing wild-type KIT (KITWT) proliferated in response to SCF as well as IL-3. Moreover, subcutaneous injection of Ba/F3 cells expressing KITG559 or KITV814 into nude mice resulted in production of large tumors at all sites of the injection within 2 weeks, and all nude mice quickly succumbed to leukemia and died. These results suggest that, although the mechanisms underlying constitutive activation of KITG559 or KITV814 may be different, both of the activating mutations have a function to induce a factor-independent and tumorigenic phenotype. Also, the data of this study raise the possibility that the constitutively activating mutations of c-kit may play a causal role in development of hematologic malignancies.
Amino Acid Sequence↗
Possible involvement of protein kinase C and low molecular weight GTP-binding proteins in thrombin-induced histamine secretion in human platelets.
Thrombin and 12-O-tetradecanoylphorbol 13-acetate (TPA) caused histamine secretion from human platelets. To clarify the intracellular signalling mechanism of thrombin-induced histamine secretion, the effects of pertussis toxin (PTX) and botulinus toxin (BTX) on thrombin- and TPA-induced histamine secretion were examined in human platelets. The secretion by thrombin was sensitive to BTX, but not PTX. The secretion by TPA was also inhibited by BTX. These results suggest that protein kinase C and low molecular weight G-proteins sensitive to BTX are involved in histamine secretion.
Arachidonic Acid↗
bcl-2 deficiency in mice leads to pleiotropic abnormalities: accelerated lymphoid cell death in thymus and spleen, polycystic kidney, hair hypopigmentation, and distorted small intestine.
Transgenic mice homozygously lacking in the bcl-2 gene were generated using homologous recombination in embryonal stem cells. The complete absence of Bcl-2 alpha and -beta proteins did not interfere with normal embryonic development. Abnormalities became evident after birth, although the severity varied among homozygous null mice, bcl-2-/- mice displayed pleiotropic abnormalities similar to those in the previously described bcl-2-/- mice, including growth retardation, smaller ears, short lives, polycystic kidney, atrophic thymus and spleen with accelerated apoptotic cell death of lymphocytes, and hair hypopigmentation in the second hair follicle cycle. Our bcl-2-/- mice also revealed novel defects in the small intestine, characterized by retarded development, accelerated exfoliation of epithelial cells, and very few mitotic progenitor cells.
Abnormalities, Multiple↗
Clinicopathological study of clear-cell tumors of the thyroid: an evaluation of 22 cases.
Twenty-two cases of partial or wholly composed clear-cell thyroid tumors were reviewed to differentiate between a primary nodule and metastatic clear-cell renal carcinoma in the thyroid. Pathological reevaluation of HE-stained specimens, immunohistochemical observation using anti-thyroglobulin (TG) antibody, and periodic acid-Schiff (PAS) staining were performed. The pathological characteristics in metastases from the kidney have a greater tendency to demonstrate a strikingly clear cytoplasm with small nuclei, rich vascularization, and a trabecular arrangement of tumor cells than do primary thyroid cases. The immunohistochemical TG staining in conjunction with PAS staining for the recognition of follicular colloid could provide much more reliable information of primary cases compared to that using TG staining alone. Clinically, in primary cases, the female:male ratio is substantially higher while the mean age is lower than in metastatic cases reflecting differentiated thyroid carcinoma. In conclusion, immunohistochemical staining for TG with PAS staining for the recognition of follicular colloid proved to be the most sensitive method for identifying primary clear cell thyroid tumors. In addition, a careful assessment of past and/or present kidney disorders to rule out metastatic renal cell carcinoma is advisable. Age, gender, and physiological findings are also informative when differentiating between them.
Adenocarcinoma, Clear Cell↗