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Biomedical subjects

H Sato

Publications and source records attributed to H Sato.

At least 271 records · Page 15Linked to original sources
PubMed2001

A surgical intervention using percutaneous cardiopulmonary support for contralateral pneumothorax following pneumonectomy.

We here, describe a 63-year-old man presenting with a contralateral pneumothorax following pneumonectomy. After setting up a percutaneous cardiopulmonary support (PCPS) system in advance in preparation for hypoxemia during the operation, resection of bullae was performed. His oxygen saturation and hemodynamic status were stable intraoperatively and we achieved a successful and safe operation swiftly. He had no complications and was discharged on the 10th postoperative day.

Carcinoma, Squamous Cell↗
PubMed2001

[Cord blood transplantation with two mismatched HLA loci in a child with acute lymphoblastic leukemia in second remission: follow-up of minimal residual disease using a clone-specific probe].

A 9-year-old girl with acute lymphoblastic leukemia in second remission underwent cord blood transplantation (CBT) from an HLA-mismatched (2 loci by serotype, 3 loci by genotype) unrelated donor. The infused nucleated cell count was 1.95 x 10(7)/kg. FK506 and mini-MTX were used to prevent graft-versus-host disease (GVHD), but grade II acute GVHD developed on the skin (stage III). The GVHD subsided after administration of corticosteroid, but marked hyperglycemia developed, which required transient insulin therapy for its control. Minimal residual disease (MRD) was assessed using a clone-specific probe for the JH region. MRD was positive before CBT, but became negative one month after CBT. Now, at 14 months after CBT, the patient is in a disease-free state without detectable MRD. These observations suggest that CBT with two mismatched HLA loci can be performed safely, and that sequential analysis of MRD is useful for evaluation of the disease status after CBT.

Blood Donors↗
PubMed2001

Renin containing cells are present predominantly in scarred areas but not in dysplastic regions in multicystic dysplastic kidney.

PURPOSE: Hypertension is an important complication of multicystic dysplastic kidney and it has been suggested that it is induced by renin. Little information is available on renin production in this disease. To assess renin production we examined the distribution of renin containing cells in multicystic dysplastic kidneys using immunohistochemical methods. MATERIALS AND METHODS: Immunohistochemical examination of renin was performed in 29 multicystic dysplastic kidneys from 14 boys and 15 girls 1 month to 10 years old using rabbit anti-human renin antibodies. In all cases normal renal function was confirmed by the serum creatinine level and no proteinuria on urinalysis. Two patients had the complication of hypertension before removal of the multicystic dysplastic kidney but plasma renin activity was normal. RESULTS: Immunostaining of renin was observed in 26 of 29 multicystic dysplastic kidneys (90%). Histologically multicystic dysplastic kidney involved scarred and dysplastic areas. Renin positive cells were observed predominantly in the scarred areas, mainly in the juxtaglomerular apparatus of mature glomeruli, interlobular arteries and some mature tubules. Immunopositive renin was sparsely noted in the juxtaglomerular apparatus or Bowman's capsules of occasional immature glomeruli in dysplastic areas. CONCLUSIONS: Our observations suggest that multicystic dysplastic kidney may have the ability to produce renin. Renin producing cells in the juxtaglomerular apparatus of mature glomeruli and interlobular arteries in the scarred areas may be the predominant source of renin production in this organ.

Female↗
PubMed2001

[Transient myelodysplasia associated with human parvovirus B19 infection in a child without underlying disease].

Human parvovirus B19 (HPV-B19) infection is known to frequently induce aplastic crisis in patients with hemolytic anemia, but rarely causes hematological disorders in healthy subjects. We report a 5-year-old boy who showed transient myelodysplasia associated with HPV-B19 infection. He was admitted with severe nasal bleeding, and laboratory data showed marked thrombocytopenia (1,000/microliter), anemia (Hb: 8.4 g/dl), and mild leukopenia (3,000/microliter). A bone marrow smear revealed myelodysplastic changes in three cell lineages, but no giant proerythroblasts or megakaryocytes. The pancytopenia and myelodysplastic changes were resolved spontaneously within a week without any medication other than transfusion of red blood cells and platelets. Serological examination revealed an elevation of IgG antibody against HPV-B19 on days 15 and 120 and its subsequent decrease thereafter, although HPV-B19-specific DNA was not detected in the serum at onset. The clinical course and laboratory data suggest an etiologic role of HPV-B19 infection in the occurrence of transient myelodysplasia.

Child, Preschool↗
PubMed2001

Effects of nifedipine retard on heart rate and autonomic balance in patients with ischemic heart disease.

The aim of this study was to explore the effects of nifedipine retard on heart rate and autonomic balance in patients with ischemic heart disease. Fourteen patients with ischemic heart disease (12 men and two women; mean age 64 years) were administered nifedipine retard at a daily dose of 20-40 mg. Changes in heart rate and autonomic balance were studied using Holter monitoring before and after 12 weeks of nifedipine therapy Heart rate was unchanged during sleep but was higher during the day after nifedipine retard administration. The high frequency power spectrum of heart rate variability (indicating parasympathetic activity) was lower during the day after nifedipine retard therapy but was unchanged during sleep. The low frequency power to high frequency power ratio, indicating sympathetic activity was unchanged during the day and during sleep. Nifedipine retard increased the heart rate of patients with ischemic heart disease only during the day and reduced parasympathetic activity.

Aged↗
PubMed2001

Monoclonal antibodies reactive with dendritic cells of Mongolian gerbils.

Mongolian gerbils (Meriones unguiculatus) serve as an valuable model animal for several infectious diseases of medical and veterinary importance. Reagents available for characterization of the immune response of Mongolian gerbils are strictly limited. We describe three novel murine monoclonal antibodies (mAbs) to dendritic cells of Mongolian gerbils. These include HUSM-M.g.11 of IgG2b isotype, HUSM-M.g. 20 of IgG2a isotype, and HUSM-M.g.30 of IgG1 isotype. All of these mAbs had an identical profile of immunohistochemical reactions with various tissues taken from immune-naive Mongolian gerbils, and were intensively expressed on dendritic cells, including epidermal Langerhans cells, B-cell follicles, and the thymic reticulum. Positive reactions of the epidermis and intestinal mucosa with these mAbs were induced by cutaneous or intestinal infections with parasites. Competitive enzyme-linked immunosorbent assay and immunoblot analysis (western blotting) indicated that all of these mAbs recognize an identical peptide epitope on a molecule with approximate molecular mass of 29 kDa. These data suggest that the mAbs recognize major histocompatibility complex class-II molecules of gerbils. Use of described mAbs would facilitate characterization of immune responses as well as investigations on host responses to infections of medical and veterinary importance, using the gerbil model.

Animals↗
PubMed2000

An essential cytoplasmic domain for the Golgi localization of coiled-coil proteins with a COOH-terminal membrane anchor.

Giantin is a resident Golgi protein that has an extremely long cytoplasmic domain (about 370 kDa) and is anchored to the Golgi membrane by the COOH-terminal membrane-anchoring domain (CMD) with no luminal extension. We examined the essential domain of giantin required for Golgi localization by mutational analysis. The Golgi localization of giantin was not affected by the deletion of its CMD or by substitution with the CMD of syntaxin-2, a plasma membrane protein. The giantin CMD fused to the cytoplasmic domain of syntaxin-2 could not retain the chimera in the Golgi apparatus. Sequential deletion analysis showed that the COOH-terminal sequence (positions 3059--3161) adjacent to the CMD was the essential domain required for the Golgi localization of giantin. We also examined two other Golgi-resident proteins, golgin-84 and syntaxin-5, with a similar membrane topology as giantin. It was confirmed that the cytoplasmic domain of about 100 residues adjacent to the CMD was required for their Golgi localization. Taken together, these results suggest that the COOH-terminally anchored Golgi proteins with long cytoplasmic extensions have the Golgi localization signal(s) in the cytoplasmic sequence adjacent to the CMD. This is in contrast to previous observations that a transmembrane domain is required for Golgi localization by other Golgi proteins transported from the endoplasmic reticulum.

Animals↗
PubMed2000

Thrombin inhibition by HCII in the presence of elastase-cleaved HCII and thrombin-HCII complex.

The rate of thrombin inhibition by heparin cofactor II (HCII) is facilitated by heparin or dermatan sulfate in vitro. The distributions of these glycosaminoglycans (GAGs) in vivo are not the same; heparin-like substance is rich on the surface of endothelial cells and dermatan sulfate is relatively dominant in the extravascular region. When inflammation takes place, at least two other possible existent forms of HCII, the complexed form with thrombin and the cleaved form by leukocyte elastase, are assumed to be present at relatively high concentrations in a local circumstance. We examined the interactions of HCII with the two forms of HCII on thrombin inhibition in the presence of the GAGs. By HCII in complex with thrombin or cleaved by leukocyte elastase, the affinity of HCII moiety for heparin increases and that for dermatan sulfate decreases. The two forms possibly occur at relatively high concentrations in a local pathological situation, although the heparin cofactor activity for thrombin inhibition by HCII decreases and dermatan sulfate determines the cofactor activity. These results indicate efficient thrombin inhibitory activity of HCII in the extravascular region.

Heparin Cofactor II↗
PubMed2000

Genetic alterations in DNA diploid, aneuploid and multiploid colorectal carcinomas identified by the crypt isolation technique.

Loss of heterozygosity (LOH) and microsatellite instability (MSI) commonly occur in colorectal carcinomas. However, the role of these genetic alterations in determining DNA ploidy status of tumors (diploid, aneuploid and multiploid) remains unclear. In the present study, we attempted to clarify the relationship between genetic alterations and DNA ploidy status. Crypt isolation coupled with DNA cytometric sorting and polymerase chain reaction assay (17 microsatellite markers) were used to study allelic losses and MSI in 59 colorectal carcinomas (diploid, 15; aneuploid, 10 and multiploid, 34). Of the 15 diploid carcinomas, 6 exhibited MSI in which allelic losses were rarely found. The other 9 diploid tumors mostly exhibited allelic losses, but none displayed MSI status. Whereas allelic losses frequently occurred in the aneuploid carcinomas and the aneuploid populations of multiploid carcinomas, they were rarely detected in the diploid populations of multiploid carcinomas. MSI status was not observed in aneuploid carcinomas nor in either population of multiploid carcinomas. Although multiploid carcinomas genetically resemble aneuploid carcinomas in the expression of the severe LOH phenotype, the genetic alterations seen in the diploid populations of multiploid carcinomas may differ from those of diploid carcinomas. Furthermore, all diploid, aneuploid and both the diploid and aneuploid fractions of the multiploid tumors that were non-MSI exhibited a high rate of LOH, suggesting that LOH is independent of the tumor's ploidy status.

Adenocarcinoma↗
PubMed2000

Atomic Force Microscopy Study of Ultrafine Particles Prepared in Reverse Micelles.

The imaging of ultrafine Au, Pd, CdS, and ZnS particles prepared in reverse micelles has been studied by atomic force microscopy (AFM). Mica substrates, derivatized with a monolayer of amine or thiol-terminated silanes, were used to immobilize the particles. The substrates were exposed to reverse micellar solutions containing the particles and were then immersed in appropriate solvent media to remove surfactants. This resulted in a partial coating of the surfaces by the particles. The particle size was estimated as the height of protrusion, shown on the AFM images. The size values for the Pd and CdS particles, thus obtained, were found to be almost identical to those obtained by transmission electron microscopy (TEM), whereas those for the Au and ZnS particles were larger than those obtained by TEM. Scanning electron microscopy showed that the Au particles tended to aggregate on the surfaces, while Pd particles were isolated from one another. Copyright 2000 Academic Press.

Journal Article↗
PubMed2000

Microtubule depolymerization normalizes in vivo myocardial contractile function in dogs with pressure-overload left ventricular hypertrophy.

BACKGROUND: Because initially compensatory myocardial hypertrophy in response to pressure overloading may eventually decompensate to myocardial failure, mechanisms responsible for this transition have long been sought. One such mechanism established in vitro is densification of the cellular microtubule network, which imposes a viscous load that inhibits cardiocyte contraction. METHODS AND RESULTS: In the present study, we extended this in vitro finding to the in vivo level and tested the hypothesis that this cytoskeletal abnormality is important in the in vivo contractile dysfunction that occurs in experimental aortic stenosis in the adult dog. In 8 dogs in which gradual stenosis of the ascending aorta had caused severe left ventricular (LV) pressure overloading (gradient, 152+/-16 mm Hg) with contractile dysfunction, LV function was measured at baseline and 1 hour after the intravenous administration of colchicine. Cardiocytes obtained by biopsy before and after in vivo colchicine administration were examined in tandem. Microtubule depolymerization restored LV contractile function both in vivo and in vitro. CONCLUSIONS: These and additional corroborative data show that increased cardiocyte microtubule network density is an important mechanism for the ventricular contractile dysfunction that develops in large mammals with adult-onset pressure-overload-induced cardiac hypertrophy.

Animals↗
PubMed2000

Physiological and anatomical organization of multiwhisker response interactions in the barrel cortex of rats.

To understand the physiological properties and anatomical organization of the spatiotemporal interaction of the responses to multiwhisker stimulation in neurons of the rat barrel cortex, single-unit recordings of 114 neurons were performed across all layers (layer II/III, n = 39; IV, n = 33; V/VI, n = 42) of the posteromedial barrel subfield of the primary somatosensory cortex of anesthetized rats. Two neighboring principal and adjacent whiskers (PW and AW, respectively) in the same row were deflected rostrally or caudally at varying interstimulus intervals (ISIs). In 37% of the neurons, the response to the combined stimulus was significantly larger than the sum of the responses to stimulation of the individual whiskers. In instances in which response facilitation was observed, selectivity was noted for the combination (75%) of the PW with a particular AW or for a particular direction (60%) of whisker deflection. The direction bias of the responses to multiwhisker stimulation was well correlated with that of the sum of the responses to single whisker stimulation (r = 0.83; p < 0.001). The pattern and magnitude of the response interaction in the neurons of the superficial layers were closely related to the location of the recorded cell in the barrel columns. Multiwhisker stimulation at short ISIs (</=3 msec) evoked prominent response facilitation in cells located close to the border between two columns (p < 0.05, one-way ANOVA), where two excitatory inputs were expected to arrive at the same time. Our results suggest that the spatiotemporal patterns of multiwhisker stimulation, such as whisker combination, direction of deflection, and timing, are expressed as different magnitudes of response interaction, which depends on the proximity of cells to home and adjacent barrel columns.

Animals↗
PubMed2000

Low-capacity cation-exchange chromatography of ultraviolet-absorbing urinary basic metabolites using a reversed-phase column coated with hexadecylsulfonate.

A low-capacity cation-exchange HPLC method for the determination of UV-absorbing organic cations such as amino acids, histidine dipeptides, and creatinine was developed. A commercially available reversed-phase column was dynamically coated with hexadecylsulfonate, and was successfully used for the cation-exchange separation with ethylenediammonium eluting ion at pH 2.5. The coated column was enough stable for the specific use with a completely aqueous mobile phase at low and constant pH; and the day-to-day reproducibility for retention time was 0.9-1.7% of RSD (relative standard deviation). The linear relation between concentrations and detector responses (area) by using a photodiode-array UV detection at 210 nm ranged from 0.2 to 1000 microM (sample size 50 microl) for 1-methylhistidine, 3-methylhistidine, histidine, creatinine, anserine, carnosine, and homocarnosine, and from 0.5 to 2000 microM for creatine, tyrosine, and phenylalanine, with less than 5% of RSD. The UV spectrum (190-300 nm) obtained during chromatography was very indicative for each analyte. Overall recoveries were 97-104%. The developed HPLC method in conjunction with preliminary fractionation technique could be applied to the analysis of urine of patient with metabolic disorder such as phenylketonuria.

Cation Exchange Resins↗
PubMed2000

Annexin V inhibits the 12-O-tetradecanoylphorbol-13-acetate-induced activation of Ras/extracellular signal-regulated kinase (ERK) signaling pathway upstream of Shc in MCF-7 cells.

Annexin V is a Ca2+-dependent phospholipid binding protein. Although it has been shown to inhibit protein kinase C (PKC) in cell-free systems, its role in the intact cell is unclear. A stable MCF-7 human breast cancer cell overexpression system was established to investigate the function of annexin V. In these cells, 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced phosphorylation and kinase activity of ERK1/2 were suppressed. Morphological changes induced by TPA were reduced by annexin V overexpression as well as by the pan-PKC inhibitor, bisindolylmaleimide I, and by the mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MEK) inhibitor, PD98059. TPA-induced MEK1/2 and Raf-1 phosphorylation were reduced in these cells. The TPA-enhanced active Ras, and its association with Raf-1, were reduced. TPA treatment of MCF-7 cells caused an increased association of Shc with Grb2. However, this increased association was prevented in the annexin V-overexpressors. p21WAF/CIP1 is responsible for inhibition of cell cycle progression in MCF-7 cells. TPA induced the expression of p21WAF/CIP1 to a greater extent in MCF-7 parent and control plasmid cells than in annexin V overexpressors. PD98059 inhibited this increase, suggesting that TPA upregulation of p21WAF/CIP1 occurs via the MEK pathway, and that annexin V overexpression blunts it. This work shows that annexin V overexpression suppresses the TPA-induced Ras/ERK signaling by inhibiting at/or upstream of Shc, possibly through the inhibition of PKCs. Oncogene (2000).

Annexin A5↗
PubMed2000

Transcription factor Nrf2 coordinately regulates a group of oxidative stress-inducible genes in macrophages.

Electrophiles and reactive oxygen species have been implicated in the pathogenesis of many diseases. Transcription factor Nrf2 was recently identified as a general regulator of one defense mechanism against such havoc. Nrf2 regulates the inducible expression of a group of detoxication enzymes, such as glutathione S-transferase and NAD(P)H:quinone oxidoreductase, via antioxidant response elements. Using peritoneal macrophages from Nrf2-deficient mice, we show here that Nrf2 also controls the expression of a group of electrophile- and oxidative stress-inducible proteins and activities, which includes heme oxygenase-1, A170, peroxiredoxin MSP23, and cystine membrane transport (system x(c)(-)) activity. The response to electrophilic and reactive oxygen species-producing agents was profoundly impaired in Nrf2-deficient cells. The lack of induction of system x(c)(-) activity resulted in the minimum level of intracellular glutathione, and Nrf2-deficient cells were more sensitive to toxic electrophiles. Several stress agents induced the DNA binding activity of Nrf2 in the nucleus without increasing its mRNA level. Thus Nrf2 regulates a wide-ranging metabolic response to oxidative stress.

Adaptor Proteins, Signal Transducing↗