[Regulation of cyclin D-dependent kinases and molecular mechanisms of G1 progression].
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Animals↗
Biomedical subjects
J Kato
Publications and source records attributed to J Kato.
[Truncal valvoplasty for post-operative truncal valve regurgitation of truncus arteriosus: a case report].
The surgical treatment for truncal valve regurgitation is still controversial in patients with truncus arteriosus. A two-year-old girl with complaints of low weight gain and tachypnea was referred for treatment of truncal valve regurgitation. She had undergone an emergency pulmonary artery banding for severe congestive heart failure due to truncus arteriosus-type I at six months of age. This anomaly had been corrected by Barbero-Marcial method at seven months of age. But the truncal valve regurgitation started appearing at sixteen months of age with the progression of the stenosis of the pulmonary artery orifice and the right ventricular outflow tract regurgitation. Echo cardiography and cineangiography revealed the truncal valve to be bicuspid, and the regurgitation severe, especially through the prolapsed left sided cusp. The truncal valve was repaired by commissural suspension method, and the right ventricular outflow tract reconstructed with patch angioplasty of the pulmonary artery orifice and Carpentier-Edwards pericardial Bioprosthesis (19 mm). The post-operative course was uneventful. One year after, truncal valve regurgitation is small by color Doppler study. We conclude that valvoplasty is to be considered as the first choice of treatment for truncal valve regurgitation.
Child, Preschool↗
More on p53 antigen loss in stored paraffin slides.
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Breast Neoplasms↗
Efficacy of TNF-alpha gene-transduced tumor cells in treatment of established in vivo tumor.
The therapeutic effect of TNF gene-transduced mouse fibrosarcoma cells (Meth-A: C5) on pre-inoculated parental cells (Meth-A: M0) was studied. Subcutaneous (s.c.) transplantation of M0 cells into one flank of syngeneic BALB/c mice was followed by s.c. injection of irradiated MO or C5 into the opposite flank 1 week later. The initial M0 tumor (T-MO) completely regressed in C5-vaccinated mice, whereas in M0-vaccinated mice continuous growth of T-M0 was observed. When a similar experiment was carried out in SCID mice, no regression of T-MO was observed, suggesting that the tumor regression in BALB/c mice was not due to direct anti-tumor activity of TNF secreted from C5, but to systemic immunity. Regression of the rechallenged M0 tumor was observed in mice which had shown T-MO regression by C5 vaccination, but rechallenged Colon 26 cells (syngeneic to BALB/c mice) continued to grow, indicating a specific immunity to Meth-A cells). The systemic immunity evoked in C5-vaccinated mice was directly demonstrated by enhanced killer activities of LAK and CTL with a proliferation of T-cell population in their splenocytes. Abrogation of the therapeutic effect of C5 vaccination with anti-Thy 1 and anti-Lyt 2 also demonstrates the involvement of cellular immunity in tumor regression.
Animals↗
Human proadrenomedullin N-terminal 20 peptide in pheochromocytoma and normal adrenal medulla.
Proadrenomedullin N-terminal 20 peptide (PAMP) is a novel hypotensive peptide found in adrenomedullin precursor. Using a radioimmunoassay for human PAMP, we purified immunoreactive PAMP (ir-PAMP) from human pheochromocytoma and determined its complete amino acid sequence. The major component of PAMP-like immunoreactivity was found to be PAMP [1-20] NH2 with an amino acid sequence identical to that of the deduced amino acid sequence by cDNA analysis. Both ir-PAMP and ir-adrenomedullin were found to be abundant in normal adrenal medulla as well as pheochromocytoma tissue arising from adrenal medulla, and there was a significantly (p < 0.05) positive correlation between ir-adrenomedullin and ir-PAMP concentrations in these tissues. However, the PAMP/adrenomedullin ratio in pheochromocytoma tissues (0.197 +/- 0.013) was significantly (p < 0.005) lower than that in adrenal medullae (0.384 +/- 0.041). The present data indicate that PAMP is biosynthesized from adrenomedullin precursor, but the biosynthesis or metabolism of PAMP in pheochromocytoma may be different from that of normal adrenal medulla.
Adrenal Gland Neoplasms↗
Receptors for adrenomedullin in human vascular endothelial cells.
Accumulation of the intracellular cyclic AMP (cAMP) was measured in cultured endothelial cells of the human umbilical vein following the incubation with adrenomedullin, a newly discovered hypotensive peptide, to determine the presence of specific receptors for adrenomedullin. Adrenomedullin increased the intracellular cAMP in a dose-dependent fashion in the endothelial cells, and the EC50 value was as low as 10(-9) M. Calcitonin gene-related peptide (CGRP) that has a homology to adrenomedullin in its amino-acid sequence also increased the intracellular cAMP with an EC50 value greater than 10(-7) M. The effect of CGRP was attenuated in the presence of CGRP-(8-37), a CGRP receptor antagonist. However, CGRP-(8-37) had no effect on the cAMP accumulation by adrenomedullin. These findings indicate that the cultured endothelial cells of human umbilical vein possess specific adrenomedullin receptors coupled with the adenylate cyclase activity that may have little affinity with CGRP.
Adrenomedullin↗
Autoantibody against a 78 kDa membrane protein of HepG2 cell in the sera of patients with alcoholic liver diseases.
Sera from 14 normal control subjects, 30 patients with alcoholic liver diseases (fatty liver, n = 8; hepatitis, n = 13; liver cirrhosis, n = 9), 7 controls with chronic hepatitis B, and 8 controls with chronic hepatitis C were masured for their concentrations of antibodies against HepG2 membrane protein by a binding assay utilizing 125I-labeled protein A. When the cut-off level was set as the mean value plus 2 SD of normal control subjects, the incidence of positivity was 75%, 69.2%, and 77.8% in patients with alcoholic fatty liver, alcoholic hepatitis, and alcoholic cirrhosis, respectively. Both the mean serum antibody values and the positive incidence were significantly higher in patients with alcoholic liver diseases than in either the normal controls or in the control patients with chronic hepatitis. Sodium dodecylsulfate polyacrylamide gel electrophoresis of 125I-labeled HepG2 membrane protein precipitated with IgG from patients with alcoholic liver diseases revealed an immunoreactive band at a molecular weight of 78,000 daltons (gp78). The antibody activity remained after immunoabsorption by human liver-specific lipoprotein (LSP) but decreased when HepG2 cells were pre-treated with trypsin or neuraminidase. Consequently, gp78 appears to be a glycoprotein distinct from LSP, and is specifically recognized by IgG from patients with alcoholic liver diseases. This assay may provide a new system to measure autoantibody to hepatocytes in alcoholic liver diseases.
Autoantibodies↗
Appearance of dynorphin in the spinal trigeminal nucleus complex following experimental tooth movement in the rat.
Changes in the expression of dynorphin were investigated immunohistochemically. Cells showing dynorphin immunoreactivity first appeared 2 days and disappeared 15 days after the unilateral insertion of separating elastics between the upper molars. These immunopositive cells were localized in the superficial layers in the medial third of the subnucleus caudalis on the ipsilateral side, except at 1 and 15 days. On the contralateral side, a few immunoreactive cells only were observed in the subnucleus caudalis of the 3- to 8-day groups. No immunoreactivity was observed in the subnucleus interpolaris, subnucleus oralis spinal trigeminal nucleus complex (STNC), principal trigeminal nucleus and mesencephalic trigeminal nucleus of the experimental rats and all the trigeminal nuclei of control animals. The findings indicate that experimental tooth movement induced the expression of dynorphin in the superficial layers of the subnucleus caudalis STNC. The subnucleus caudalis may play an important part in modulation of the discomfort and pain evoked by tooth movement.
Animals↗
Purification and characterization of cytoplasmic dynein of rabbit liver.
Cytoplasmic dynein is a microtubule-dependent motor protein, which plays a role in intracellular transport. However, there have been few studies regarding the role of cytoplasmic dynein in the liver. Purification of cytoplasmic dynein from rabbit liver took advantage of the affinity of microtubule-dependent motor proteins for microtubules. Purified dynein contained heavy chain (450 kDa), intermediate chain (75 kDa), light chains (45-58 kDa) and dynactin (150 kDa). The subunit composition was consistent with previously reported data on brain cytoplasmic dynein. Microtubules prepared from bovine brain were driven by purified cytoplasmic dynein from rabbit liver, and movements of microtubules were visualized by video-enhanced differential interference contrast microscopy. The mean velocity of the motile microtubules was 1.09 +/- 0.13 microns/s. Our study provides evidence of rapid intracellular transport in hepatocytes controlled by cytoplasmic dynein.
Animals↗
The immuno-stimulant OK-432 enhances liver regeneration after 70% hepatectomy.
The effect of reticuloendothelial system activation on hepatic regeneration after 70% hepatectomy was investigated. OK-432, a killed streptococcal preparation which increases reticuloendothelial system function, was administered to rats prior to 70% hepatectomy. Hepatic incorporation of 3H-thymidine 24 h after 70% hepatectomy was enhanced by OK-432 pretreatment. DNA synthesis was greater in pretreated than in control rats and correlated highly with reticuloendothelial system phagocytic activity prior to surgery. Methyl palmitate, which decreases reticuloendothelial system function, was administered to rats prior to 70% hepatectemy. Hepatic incorporation of 3H-thymidine 24 h after 70% hepatoctomy was significantly depressed by methylpalmitate-pretreatment. These data suggest that reticuloendothelial system plays a role in liver regeneration and that hepatocyte proliferation might be enhanced by protection from surgical stress and endotoxins with reticuloendothelial system stimulation by OK-432.
Adjuvants, Immunologic↗
Analysis of the expression and the first exon of aromatase mRNA in monkey brain.
To elucidate the mechanism of the region-specific expression of the aromatase in the primate brain, we investigated the distribution and level of the total aromatase mRNA and the aromatase mRNA with the exon 1-f, which was reported to be the brain-specific exon 1 of the human aromatase gene, in male Japanese monkeys. Total RNAs extracted from the hypothalamus-preoptic area (HPOA), amygdala (AMY), cerebellum, hippocampus, brainstem, five regions of cerebral cortex and four peripheral tissues: liver, kidney, adipose tissue and testis were subjected to a semi-quantitative reverse transcription-polymerase chain reaction-Southern blotting (RT-PCR-SB) assay. The levels of the total aromatase mRNA was high in the HPOA, AMY and testis with a low level of message in the other regions. These results roughly paralleled the distribution of aromatase activity of the monkey brain previously reported. The level of the aromatase mRNA with the exon 1-f was high in the HPOA and AMY, and low in the other regions of the brain and the testis with an undetectable level of the messenger in the other peripheral tissues. Furthermore, the ratio of the aromatase mRNA with the exon 1-f to the total aromatase mRNA was different among various regions of the monkey brain, for example, the ratio in the AMY was distinctly higher than that in the HPOA. These results indicated that the level of the aromatase mRNA mainly regulated the level of aromatase protein and aromatase activity in a region-specific manner, and that the exon 1-f was used in most of the monkey brain regions. Moreover, the ratio of the aromatase mRNA with the exon 1-f to the total aromatase mRNA varied in the brain regions. It was implied that the aromatase mRNA using the other first exons was also expressed in the brain and was involved in the region-specific expression of the brain aromatase.
Amino Acid Sequence↗
Identification of a transforming growth factor beta-1 activator derived from a human gastric cancer cell line.
It has been shown that some types of tumour cells produce activated transforming growth factor beta-1 (TGF-beta 1). However, the mechanism for the activation of TGF-beta 1 derived from tumour cells has not been fully elucidated. The present study was undertaken to characterise an activator of latent TGF-beta 1 secreted from a human gastric cancer cell line, KATO-III. Western blot analyses using antibodies for TGF-beta 1, latency associated peptide (LAP) and latent TGF-beta 1-binding protein (LTBP) revealed that, in the cell lysate of KATO-III, TGF-beta 1 protein was expressed as a small latent complex of TGF-beta 1 and LAP. This was also confirmed by a gel chromatographic analysis of the cell lysate obtained from KATO-III. A 2.5 kb transcript of TGF-beta 1 mRNA was detected in KATO-III cells by Northern blot analysis. A gel chromatographic analysis of the conditioned medium from KATO-III cells revealed, in addition to the active form of TGF-beta 1, a factor which activated latent TGF-beta 1 from NRK-49F cells at fractions near a molecular size of 65,000. This factor was inactivated by heat (100 degrees C), acidification, trypsin and serine protease inhibitors. TGF-beta 1 activity in KATO-III cell lysate was not detected in the untreated state, but potent TGF-beta 1 activity was detected after acid treatment. These results suggest that KATO-III releases not only a latent TGF-beta 1 complex but also a type of serine protease, different from plasmin, plasminogen activator, cathepsin D, endoglycosidase F or sialidase, which activates the latent TGF-beta 1 complex as effectively as acid treatment.
Blotting, Northern↗
CMV viraemia demonstrated in the serum of a patient with cytomegalovirus pneumonia.
We attempted to demonstrate the expression of cytomegalovirus (CMV) particles in the serum of an acute lymphocytic leukaemia patient with CMV pneumonia. The serum sample was applied to an affinity column coupled with human monoclonal antibody C23 which recognizes the envelope glycoproteins of CMV virus and neutralizes the viral activity. The DNA obtained from each fraction was amplified by double polymerase chain reaction (PCR) and analysed by gel electrophoresis. Bands were clearly observed in the eluted fraction. These results strongly suggest that CMV particles exist in the sera of patients with CMV pneumonia.
Base Sequence↗
Clinical trial of daily low-dose oral etoposide for patients with residual or recurrent cancer of the ovary or uterus.
OBJECTIVE: To determine the efficacy of long-term therapy of oral etoposide in patients with residual or recurrent gynecological malignancies. METHODS: Twenty-five Japanese patients with resistant or recurrent carcinoma of the uterus or ovary were treated with oral etoposide at a dose of 25 mg/day/body for 21 consecutive days, and cycles were repeated every 4 weeks. The residual or recurrent lesion could be objectively evaluated in all patients by measuring it directly. RESULTS: The response rate after 6 cycles of therapy was 40% for the group of all patients, and 42.8%, 28.6% and 50% for those with ovarian carcinoma, cervical carcinoma, and endometrial carcinoma, respectively. Side effects of etoposide treatment included gastrointestinal discomfort in 14 patients and leukopenia of grade 3 or higher in 2 patients. However, these side effects were mild, and all patients could continue treatment. CONCLUSION: These findings indicate that long-term, low-dose oral etoposide was effective for and well-tolerated by patients with refractory or recurrent carcinoma of the ovary or uterus.
Administration, Oral↗
[A case report of toxic shock-like syndrome due to group A streptococcal infection in an alcoholic].
A 47-year-old male with a history of alcohol abuse had a sore throat on June 8, 1994. On June 13, he had swelling and pain on his right fore-arm. He had tense swelling, redness and pain on the right lower abdomen, left upper arm and left lower leg with high fever and noticed erythema and blisters on his back of the right hand on June 18, which gradually expanding to the entire fore-arm. He was admitted to the local hospital on July 2, where he was operated with excision of the skin and drainage for an abdominal subcutaneous abscess and was given three antibiotics and an intravenous immunoglobulin preparation. Although he showed transient hypotension and moderate liver dysfunction, his condition improved day by day under such treatment. He was transferred to our hospital on July 7 because of the unknown etiology. Aspirate from the abscess contained gram-positive cocci in chains, and group A streptococci were isolated. Panipenem/betamipron was used for an antibiotic during roughly two weeks and excision of the skin and drainage for abscess was performed twice. His skin lesions were continued to improve, normalizing peripheral white blood cell counts, serum levels of CRP and the liver function. On July 24, the antibiotic was changed to intravenous ampicillin and administered for 16 days and amoxicillin was given orally after that, and he was discharged on August 16. An isolate of the infecting Streptococcus pyogenes produced pyrogenic exotoxin A, B and the serotype was T-3 type.
Alcoholism↗
Molecular cloning and characterization of a chemotactic transducer gene in Pseudomonas aeruginosa.
A Pseudomonas aeruginosa mutant, defective in taxis toward L-serine but responsive to peptone, was selected by the swarm plate method after N-methyl-N'-nitrosoguanidine mutagenesis. The mutant, designated PCT1, was fully motile but failed to show chemotactic responses to glycine, L-serine, L-threonine, and L-valine. PCT1 also showed weaker responses to some other commonly occurring L-amino acids than did the wild-type strain PAO1. A chemotactic transducer gene, denoted pctA (Pseudomonas chemotactic transducer A), was cloned by phenotypic complementation of PCT1. Nucleotide sequence analysis showed that the pctA gene encodes a putative polypeptide of 629 amino acids with a calculated mass of 68,042. A hydropathy plot of the predicted polypeptide suggested that PctA may be an integral membrane protein with two potential membrane-spanning regions. The C-terminal domain of PctA showed high homology with the enteric methyl-accepting chemotaxis proteins (MCPs). The most significant amino acid sequence similarity was found in the region of MCPs referred to as the highly conserved domain. The pctA gene was inactivated by insertion of a kanamycin resistance gene cassette into the wild-type gene, resulting in the same observed deficiency in taxis toward L-amino acids as PCT1. In vivo methyl labeling experiments with L-[methyl-3H]methionine showed that this knockout mutant lacked an MCP with a molecular weight of approximately 68,000.
Amino Acid Sequence↗
Isolation and characterization of chemotaxis mutants and genes of Pseudomonas aeruginosa.
Two chemotaxis-defective mutants of Pseudomonas aeruginosa, designated PC1 and PC2, were selected by the swarm plate method after N-methyl-N'-nitro-N-nitrosoguanidine mutagenesis. These mutants were fully motile but incapable of swarming, suggesting that they had a defect in the intracellular signalling pathway. Computer-assisted capillary assays confirmed that they failed to show behavioral responses to chemical stimuli, including peptone, methyl thiocyanate, and phosphate. Two chemotaxis genes were cloned by phenotypic complementation of PC1 and PC2. From nucleotide sequence analysis, one gene was found to encode a putative polypeptide that was homologous to the enteric CheZ protein, while the other gene was cheY, which had been previously reported (M. N. Starnbach and S. Lory, Mol. Microbiol. 6:459-469, 1992). Deletion and complementation analysis showed that PC1 was a cheY mutant, whereas PC2 had a double mutation in the cheY and cheZ genes. A chromosomal cheZ mutant, constructed by inserting a kanamycin resistance gene cassette into the wild-type gene, changed its swimming direction much more frequently than did wild-type strain PAO1. In contrast, cheY mutants were found to rarely reverse their swimming directions.
Amino Acid Sequence↗
Loss of E-cadherin-dependent cell-cell adhesion due to mutation of the beta-catenin gene in a human cancer cell line, HSC-39.
Detachment of cell-cell adhesion is indispensable for the first step of invasion and metastasis of cancer. This mechanism is frequently associated with the impairment of either E-cadherin expression or function. However, mechanisms of such abnormalities have not been fully elucidated. In this study, we demonstrated that the function of E-cadherin was completely abolished in the human gastric cancer cell line HSC-39, despite the high expression of E-cadherin, because of mutations in one of the E-cadherin-associated cytoplasmic proteins, beta-catenin. Although immunofluorescence staining of HSC-39 cells by using an anti-E-cadherin antibody (HECD-1) revealed the strong and uniform expression of E-cadherin on the cell surface, cell compaction and cell aggregation were not observed in this cell. Western blotting (immunoblotting) using HECD-1 exhibited a 120-kDa band which is equivalent to normal E-cadherin. Northern (RNA) blotting demonstrated a 4.7-kb band, the same as mature E-cadherin mRNA. Immunoprecipitation of metabolically labeled proteins with HECD-1 revealed three bands corresponding to E-cadherin, alpha-catenin, and gamma-catenin and a 79-kDa band which was apparently smaller than that of normal beta-catenin, indicating truncated beta-catenin. The 79-kDa band was immunologically identified as beta-catenin by using immunoblotting with anti-beta-catenin antibodies. Examination of beta-catenin mRNA by the reverse transcriptase-PCR method revealed a transcript which was shorter than that of normal beta-catenin. The sequencing of PCR product for beta-catenin confirmed deletion in 321 bases from nucleotides +82 to +402. Southern blotting of beta-catenin DNA disclosed mutation at the genomic level. Expression vectors of Beta-catenin were introduced into HSC-39 cells by transfection. In the obtained transfectants, E-cadherin-dependent cell-cell adhesiveness was recovered, as revealed by cell compaction, cell aggregation, and immunoflourescence staining. From these results, it was concluded that in HSC-39 cells, impaired cell-cell adhesion is due to mutations in beta-catenin which results in the dysfunction of E-cadherin.
Antibodies, Monoclonal↗