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Biomedical subjects

A Ando

Publications and source records attributed to A Ando.

At least 145 records · Page 8Linked to original sources
PubMed1995

Crystallization and preliminary X-ray crystallographic analysis of chitosanase from Bacillus circulans MH-K1.

Chitosanase, an enzyme which hydrolyzes chitosan, isolated from Bacillus circulans MH-K1, was crystallized by a vapor-diffusion procedure at 293 K using ammonium sulfate as a precipitant. Rod-shaped colorless crystals, which grew to 0.05 x 0.15 x 1.2 mm within a week, belong to the orthorhombic system and the space group P222(1) or P2(1)2(1)2 with unit-cell dimensions of a = 43.3, b = 57.7, and c = 128.0 A. The asymmetric unit is thought to contain one chitosanase molecule (29 024 Da). The crystals diffract X-rays to at least 2.3 A resolution and are suitable for high-resolution X-ray structure analysis.

Journal Article↗
PubMed1995

Demonstration of axon collateral projections from the substantia nigra pars reticulata to the superior colliculus and the parvicellular reticular formation in the rat.

It was revealed in the rat that single neurons in the substantia nigra pars reticulata (SNr) innervated both the superior colliculus (SC) and the parvicellular reticular formation (RFp) in the pons and medulla oblongata by way of axon collaterals. After injecting Fluoro-gold into the lateral part of the SC and Fluoro-ruby into the RFp on the same side, some SNr neurons were double-labeled with both tracers. They were localized in the dorsolateral part of the caudal half of the SNr ipsilateral to the injection sites.

Animals↗
PubMed1995

A boundary of long-range G + C% mosaic domains in the human MHC locus: pseudoautosomal boundary-like sequence exists near the boundary.

The human genome is composed of long-range G+C% (GC%) mosaic structures related to chromosome bands. We found the human MHC locus to be an example of megabase-level GC% mosaic structures and predicted a possible boundary of the megabase-level domains within an undercharacterized 450-kb region harboring the junction of MHC classes II and III. Chromosome walking of the 450-kb region and base-compositional analysis precisely located the boundary of the mosaic domains, disclosing a sharp GC% transition. Near the transition point there was a 20-kb dense Alu cluster, a 30-kb dense LINE-1 cluster, and a sequence highly homologous with the pseudoautosomal boundary of the short arms of human sex chromosomes (PAB1X and PAB1Y); PAB1X and PAB1Y are the interface between sex-specific and pseudoautosomal regions. Many PAB1XY-like sequences (PABLs) were detected by hybridization against genomic DNA, and the new sequences defined the complete form of PABLs to be about 650 nt.

Base Composition↗
PubMed1995

Physical mapping of the retinoid X receptor B gene in mouse and human.

Retinoid X receptors (RXRs) are zinc finger-containing nuclear transcription factors. They belong to the nuclear receptor superfamily that contains retinoid receptors, vitamin D receptors, thyroid hormone receptors, and steroid hormone receptors as well as the so-called orphan receptors. We previously mapped all three RXR genes on mouse chromosomes, using a panel of Mus spretus-Mus musculus interspecific backcross mice: Namely, the RXRA-gene (Rxra) on Chr 2 near the centromere, the RXRB gene (Rxrb) on Chr 17 in the H2 region, and the RXRG gene (Rxrg) on distal Chr 1. Using cosmid clones that cover the major histocompatibility complex (MHC) region, we determined the precise physical map positions of the gene encoding mouse and human RXRB, respectively. The mouse gene (Rxrb) maps between H2-Ke4 and H2-Ke5: namely, immediately telomeric to H2-Ke4 which encodes a histidine-rich transmembrane protein, and 12 kilobases centromeric to H2-Ke5 which is expressed in lymphoid tissues. Rxrb and H2-Ke4 are transcribed into opposite directions from a CpG-rich promoter of about 250 base pairs. This gene organization is well conserved also in the human genome at the HLA-DP subregion of Chr 6p, underscoring the strong conservation of the gene organization in the MHC region between the two mammals.

Animals↗
PubMed1995

Improved lung function by urokinase infusion in canine lung transplantation using non-heart-beating donors.

We evaluated the effect of urokinase on pulmonary microthrombi formation of the donor lung using a canine cadaver left lung allotransplantation model. Donor animals were sacrificed with an intravenous injection of potassium chloride without heparinization and were divided into three groups. In group 1 (n = 6), cadavers were left at room temperature for 1 hour, and lung retrieval was then performed after flushing the lung block with low potassium-dextran-glucose solution. Donor lungs were stored for 3 hours at 8 degrees C. In group 2 (n = 6), donor lungs were treated as in group 1 except that the cadavers were left at room temperature for 2 hours instead of 1 hour before lung retrieval. In group 3 (n = 6), donor lungs were treated as in group 2 except that high-dose urokinase (120,000 IU) was injected into the main pulmonary artery after flushing with low-potassium-dextrose-glucose solution. In all groups after left lung transplantation, the right pulmonary artery was ligated, and recipient animals were followed up for 6 hours after reperfusion. The fibrin degradation product level in the donor lung tissue was also measured. All recipient animals in group 1 survived the 6-hour observation period with excellent gas exchange and stable hemodynamics. Group 3 had significantly better gas exchange than group 2 and similar cardiopulmonary function as group 1. The fibrin degradation product level in the donor lungs before transplantation was significantly higher in group 3 than in group 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Nuclear localization of the truncated hepatitis C virus core protein with its hydrophobic C terminus deleted.

The core protein of hepatitis C virus (HCV) is considered to be cleaved from the N terminus of the large precursor polyprotein by cellular signalase. The HCV cDNA encoding the core protein was expressed (i) in monkey COS cells by a plasmid expression vector driven by the SR alpha promoter, and (ii) in insect cells by a recombinant baculovirus. The expressed product had an M(r) of 22,000 and was located in the cytoplasm. When the C-terminal hydrophobic domains were deleted, however, the truncated core proteins were translocated into the nucleus. The truncated core proteins were located in the nucleus even when they were expressed as a fusion protein with E. coli beta-galactosidase, which is essentially localized in the cytoplasm. Plasmids containing HCV cDNAs with a deletion in one of the regions encoding clusters of basic amino acids were expressed in COS cells and the localization of the core protein was examined. The residues PRRGPR were suggested to play an important role in nuclear localization. HCV is an RNA virus and its life cycle was originally considered to be confined to the cytoplasm; the present study, however, suggests that the HCV core protein can translocate into the nucleus under certain circumstances.

Amino Acid Sequence↗
PubMed1995

Establishment of a cell line constitutively expressing E2 glycoprotein of hepatitis C virus and humoral response of hepatitis C patients to the expressed protein.

A Chinese hamster ovary cell line was established which abundantly expresses the second envelope protein (E2) of hepatitis C virus under the control of an exogenous promoter. The expressed E2 protein was found to be a glycoprotein of 58 kDa by immunoprecipitation with sera from patients that had chronic hepatitis C. Using this cell line as antigen in immunofluorescence tests, as high as 93% of patients with non-A non-B hepatitis had antibodies against E2 protein. In Western blots using SDS-denatured E2 protein, however, the detectability of the antibody was drastically reduced to 30%. Immunoprecipitation assays and ELISA, using both native and denatured E2 protein, revealed that antibodies to E2 protein were present in most of the chronic hepatitis C patients and that they reacted only to the native forms.

Animals↗
PubMed1995

Correlation between the exercise-induced increase in left ventricular filling pressure and the extent of ischemic or infarcted myocardium.

We investigated the correlation between left ventricular filling pressure and the extent of ischemic or infarcted myocardium in 39 patients with coronary artery disease: 25 with angina pectoris (group A) and 14 with old myocardial infarction but without overt transient myocardial ischemia (group B). Hemodynamic parameters were measured at rest and during exercise. The extent and severity scores of ischemia or infarct were calculated using thallium-201 (201Tl) myocardial single-photon emission computed tomography. In group A, the extent and severity scores of ischemia were strongly correlated with pulmonary artery wedge pressure at peak exercise (r = 0.71, p < 0.001, r = 0.62, p < 0.01, respectively). In group B, the extent and severity scores of the infarct were significantly correlated with left ventricular ejection fraction (r = -0.81, p < 0.001, r = -0.77, p < 0.01, respectively), but were not correlated with pulmonary artery wedge pressure. Since no relationship was found between the extent of infarct and left ventricular filling pressure, dynamic exercise appears to elicit a different compensatory mechanisms in nonischemic myocardium for exercise-induced transient ischemia and in noninfarcted myocardium for old infarction. The compensatory mechanism in patients with old myocardial infarction may be affected by ventricular remodeling.

Adult↗
PubMed1995

Angiotensin II stimulates interleukin-6 release from cultured mouse mesangial cells.

Interleukin-6 (IL-6) is a multifunctional cytokine exerting a wide variety of biologic responses, including cell proliferation. Recently, IL-6 has been known to play a role in the pathogenesis of mesangial proliferative glomerulonephritis. IL-6 is now recognized as an autocrine growth factor for glomerular mesangial cells, and various inflammatory mediators have been shown to promote IL-6 release from mesangial cells. However, little is known about the noninflammatory stimuli of IL-6 release from mesangial cells. In this study, it was hypothesized that angiotensin II (AngII) is one of the noninflammatory mediators of IL-6 release in mesangial cells, and the effects of AngII on IL-6 release and mRNA expression in cultured mouse mesangial cells (CMMC) were investigated. It was demonstrated that AngII (10(-7) M or higher) caused IL-6 release and mRNA accumulation in CMMC. IL-6 release was detected at 4 h and reached a plateau at 8 h after the addition of AngII, whereas IL-6 mRNA expression peaked at 4 h. The effects of AngII on IL-6 release and gene expression were completely blocked by the AngII receptor type 1 (AT1 receptor) antagonist CV-11974. AngII and IL-6 were both shown to stimulate DNA synthesis in CMMC, and the blockade of IL-6 signaling with anti-IL-6 receptor antibody abolished the enhanced DNA synthesis induced by AngII. These results raise a possibility that the growth-promoting effect of AngII on mesangial cells is at least partially mediated by IL-6 released from mesangial cells.

Angiotensin II↗
PubMed1995

Effects of glutamate dehydrogenase, choline oxidase, and glucose-6-phosphatase on 67Ga accumulation in lysosome.

AIM: To clarify the effects of the activities of hepatic enzymes in liver, hepatoma, and malignant tumor on 67Ga accumulation in lysosome. METHODS: 67Ga-citrate solution was prepared from carrier-free 67Ga-citrate solution 0.08 mol.L-1 and sodium citrate solution 0.08 mol.L-1, and was injected iv 0.4 ml to the rats. Subcellular fractions of the liver were measured for radioactivity of 67Ga by a well-type scintillation counter (Aloka JDC-701). Glutamate dehydrogenase, choline oxidase, and G-6-P activities were calculated as described by Shimizu H, Ikuta S, and Baginski E, respectivily. RESULTS: 67Ga radioactivity in normal liver lysosome (55%) was significantly higher than those in hepatoma AH 109A (32%) and Yoshida sarcoma (18%). Glutamate dehydrogenase activities were 1830 +/- s 320 U.L-1 in normal liver while 23 +/- s 6 U.L-1 in hepatoma AH 109A, and 7 +/- s 2 U.L-1 in Yoshida sarcoma. Choline oxidase activities were 46 +/- s 10 U.L-1 for normal, 25.0 +/- s 0.4 U.L-1 for hepatoma AH 109A, and 2.0 +/- s 0.4 U.L-1 for Yoshida sarcoma. G-6-P activities were 2550 +/- s 180 U.L-1 in normal, 84 +/- s 14 U.L-1 in hepatoma AH 109A, and 78 +/- s 13 U.L-1 in Yoshida sarcoma. CONCLUSION: Lysosome of normal rat liver in which hepatic enzymes work actively played a major role in the tissue concentration of 67Ga, but the role diminishes with the neoplastic transformation into hepatoma. The lysosome of Yoshida sarcoma does not play any role in 67Ga accumulation because it does not possess any features of liver.

Alcohol Oxidoreductases↗
PubMed1995

[Clinical analysis of lung cancer in patients with chondromatous hamartoma].

Between 1978 and 1993, 776 patients with lung cancer and 18 patients with chondromatous hamartoma were operated on in the department of Surgery II in Okayama University Hospital. 3 patients had both lung cancers and chondromatous hamartomas. They were all men. Two patients were 65 years old and the other was 82 years old. They all pointed out them by a medical examination of chest X-ray. 2 patients had lung cancers and chondromatous hamartomas in the same lobe, the other had them in other lobe of the same side. Lung cancer and chondromatous hamartoma localized in near area. It was difficult to discriminate chondromatous hamartoma between pulmonary metastasis of lung cancer before an operation.

Adenocarcinoma↗
PubMed1995

[Osmolality].

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Diabetes Insipidus↗
PubMed1994

Three genes in the human MHC class III region near the junction with the class II: gene for receptor of advanced glycosylation end products, PBX2 homeobox gene and a notch homolog, human counterpart of mouse mammary tumor gene int-3.

Cosmid walking of about 250 kb from MHC class III gene CYP21 to class II was conducted. The gene for receptor of advanced glycosylation end products of proteins (RAGE, a member of immunoglobulin superfamily molecules), the PBX2 homeobox gene designated HOX12, and the human counterpart of the mouse mammary tumor gene int-3 were found. The contiguous RAGE and HOX12 genes were completely sequenced, and the human int-3 counterpart was partially sequenced and assigned to a Notch homolog. This human Notch homolog, designated NOTCH3, showed both the intracellular portion present in the mouse int-3 sequence and the extracellular portion absent in the int-3. It thus corresponds to the intact form of a Notch-type transmembrane protein. About 20 kb of dense Alu clustering was found just centromeric to the NOTCH3.

Amino Acid Sequence↗
PubMed1994

Descending projections from the superior colliculus to the reticular formation around the motor trigeminal nucleus and the parvicellular reticular formation of the medulla oblongata in the rat.

We observed by the anterograde and retrograde tracing techniques in the rat that the lateral part of the superior colliculus (SC), where the nigrotectal fibers from the dorsolateral part of the substantia nigra pars reticulata (SNr) terminated, sent projection fibers to the reticular region around the motor trigeminal nucleus (RFmt) and parvicellular reticular formation (RFp) of the medulla oblongata, where many premotor neurons for the orofacial motor nuclei were known to be distributed. The SC neurons sending their axons to the RFmt and RFp were mainly located in the stratum griseum intermedium, and additionally in the stratum griseum profundum. Our results suggest that neuronal signals conveyed through the nigro-tecto-bulbar pathway to the RFmt and RFp may exert control influences upon oral behavior.

Animals↗
PubMed1994

1-Phosphatidylinositol 3-kinase activity is required for insulin-stimulated glucose transport but not for RAS activation in CHO cells.

Insulin stimulation drives the formation of a complex between tyrosine-phosphorylated insulin receptor substrate 1 (IRS-1) and 1-phosphatidylinositol 3-kinase (PI 3-kinase; ATP:1-phosphatidyl-1D-myo-inositol 3-phosphotransferase, EC 2.7.1.137), a heterodimer consisting of regulatory 85-kDa (p85) and catalytic 110-kDa (p110) subunits. This interaction takes place via the phosphorylated YMXM motifs of IRS-1 and the Src homology region 2 (SH2) domains of p85. In this study, the stable overexpression in a Chinese hamster ovary (CHO) cell line of a mutant p85 alpha (delta p85) protein, which lacks a binding site for p110, disrupted the complex formation between IRS-1 and the catalytic subunit of PI 3-kinase in intact cells during insulin stimulation. Activation of insulin receptor kinase and the tyrosine phosphorylation of IRS-1 remained unaffected. In this cell line, both insulin-stimulated accumulation of phosphatidylinositol 3,4,5-trisphosphate and the insulin-stimulated glucose uptake due to the translocation of GLUT1 glucose transporters were markedly impaired, whereas neither phorbol 12-myristate 13-acetate-stimulated glucose uptake nor the insulin-stimulated activation of RAS was impaired. These results suggest that PI 3-kinase is required for glucose transport in insulin signaling in CHO cells.

Animals↗
PubMed1994

A complex of GRB2-dynamin binds to tyrosine-phosphorylated insulin receptor substrate-1 after insulin treatment.

Insulin drives the formation of a complex between tyrosine-phosphorylated IRS-1 and SH2-containing proteins. The SH2-containing protein Grb2 also possesses adjacent SH3 domains, which bind the Ras guanine nucleotide exchange factor Sos. In this report, we examined the involvement of another SH3 binding protein, dynamin, in insulin signal transduction. SH3 domains of Grb2 as GST fusion proteins bound dynamin from lysates of CHO cells expressing wild-type insulin receptor (IR) (CHO-IR cells) in a cell-free system (in vitro). Immunoprecipitation studies using specific antibodies against Grb2 revealed that Grb2 was co-immunoprecipitated with dynamin from unstimulated CHO-IR cells. After insulin treatment of CHO-IR cells, anti-dynamin antibodies co-immunoprecipitated the IR beta-subunit and IRS-1, as tyrosine-phosphorylated proteins and PI 3-kinase activity. However, purified rat brain dynamin did not bind directly to either the IR, IRS-1 or the p85 subunit of PI 3-kinase in vitro. Together, these results suggest that in CHO-IR cells, insulin stimulates the binding of dynamin to tyrosine-phosphorylated IRS-1 via Grb2 and that IRS-1 also associates with PI 3-kinase in response to insulin. This complex formation was reconstituted in vitro using recombinant baculovirus-expressed IRS-1, GST-Grb2 fusion proteins and dynamin peptides containing proline-rich sequences. Furthermore, dynamin GTPase activity was found to be stimulated when an IRS-1-derived phosphopeptide, containing the Grb2 binding site, was added to the dynamin-Grb2 complex in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptor Proteins, Signal Transducing↗