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Biomedical subjects

T Ando

Publications and source records attributed to T Ando.

At least 289 records · Page 16Linked to original sources
PubMed1996

[Experience with surgery for synchronous double cancer of rectum and lung detected after long-term follow-up for pneumoconiosis].

A 60-year-old man has been followed up for pneumoconiosis for 7 years. He was admitted to our hospital because of melena. He was undergone a colonofiberscopy and was diagnosed as rectal cancer. We performed anterior resection of the rectum (Stage I). About 5 months after the first operation, abnormal shadows of the both lungs were growing in size. Bronchoscopic examination revealed adenocarcinoma, we performed left upper lobectomy (Stage I) and this case was judged a synchronous double cancer.

Adenocarcinoma↗
PubMed1995

Clinicopathologic spectrum of resected extraductal mass-forming intrahepatic cholangiocarcinoma.

BACKGROUND: The mode of tumor growth of intrahepatic cholangiocarcinoma (CC) varies considerably from patient to patient. This study describes the clinicopathologic variety of the extraductal mass-forming type of CC. METHODS: Patients with CC characterized by an extraductal mass (n = 26) who underwent hepatectomy from 1976 through 1992 were clinicopathologically classified into three types: Type I (n = 7), no biliary stricture; Type II (n = 13), biliary stricture without jaundice; and Type III (n = 6), biliary stricture with jaundice. RESULTS: Type I included three patients with microductular-trabecular arrangement and behavior reminiscent of hepatocellular carcinoma (high association with chronic liver disease, mild positivity for alpha-fetoprotein [AFP], no lymph node metastasis, but frequent intrahepatic metastasis), in contrast to the other typical cholangiocarcinoma. Hepatolithiasis was associated only with Type II CC: The serum positivity for AFP and carcinoembryonic antigen was much higher in Type I CC, whereas positivity of CA 19-9 was highest in Type III. Involvement of the portal vein, hepatic artery, or hepatic duct was most frequent in Type III CC, which necessitated resection of the extrahepatic bile duct and hepatectomy. CONCLUSION: The clinicopathologic behavior of intrahepatic CC differs considerably according to the presence or absence of stricture of the biliary tree. Thus, CC without biliary stricture behaves more like hepatocellular carcinoma, whereas CC with biliary stricture is more like hilar or extrahepatic bile duct carcinoma.

Adult↗
PubMed1995

Synthesis of sialyl Lewis X ganglioside analogues containing modified L-fucose residues.

Sialyl Le(x) ganglioside analogues containing 2-epi-, 2,3-di-epi-, 4-epi-, and 2-O-methyl-L-fucose in place of the L-fucose residue have been synthesized. Glycosylation of 2-(trimethylsilyl)ethyl O-(2-acetamido-4,6-O-benzylidene-2-deoxy-beta-D-glucopyranosyl)-(1-->3)- 2,4,6- tri-O-benzyl-beta-D-galactopyranoside with the methyl 1-thioglycoside derivatives of the respective fucose analogues, using dimethyl(methylthio)sulfonium triflate (DMTST) as a promoter, gave the corresponding protected 2-(trimethylsilyl)ethyl deoxy-alpha-L-hexopyranosyl-(1-->3)-O-(2- acetamido-2-deoxy-beta-D-glucopyranosyl)-(1-->3)-beta-D-galactopyrano sid es. These were transformed by reductive ring-opening of their benzylidene acetal groups into the glycosyl acceptors. Dimethyl (methylthio)sulfonium triflate-promoted glycosylation of these compounds with methyl O-(methyl 5-acetamido-4,7,8,9-tetra-O-acetyl-3,5-dideoxy-D-glycero-alpha-D-galacto -2- nonulopyranosylonate)-(2-->3)-2,4,6-tri-O-benzoyl-1-thio-beta-D- galactopyranoside afforded the desired pentasaccharides, which were converted via reductive removal of their benzyl groups, O-acetylation, selective removal of the 2-(trimethylsilyl)ethyl group, and reaction with trichloroacetonitrile, into the corresponding alpha-tri-chloroacetimidates. Glycosylation of (2S,3R,4E)-2-azido-3-O-benzoyl-4-octadecene-1,3-diol these in the presence of boron trifluoride etherate afforded the expected beta-glycosides, which were transformed in good yields, via selective reduction of the azido group, coupling with octadecanoic acid, O-deacylation, and deesterification, into the target gangliosides. The 2-(trimethylsilyl)ethyl glycosides of sialyl Le(x) oligosaccharides containing modified fucose were also prepared from the intermediates of the ganglioside synthesis.

Carbohydrate Sequence↗
PubMed1995

Assignment of the 49-kDa (PRIM1) and 58-kDa (PRIM2A and PRIM2B) subunit genes of the human DNA primase to chromosome bands 1q44 and 6p11.1-p12.

DNA primase is an essential replication protein that catalyzes the synthesis of oligoribonucleotide primers. DNA primase, consisting of two subunits (p49 and p58), plays a key role in both the initiation of DNA replication and the synthesis of Okazaki fragments for lagging strand synthesis. We mapped the locations of human chromosomes of the genes coding for both subunits [p49 (PRIM1) and p58 (PRIM2)] by PCR amplification using DNAs of a panel of somatic hybrids, to chromosomes 1 and 6, respectively. The PRIM1 gene was mapped to 1q44, and two PRIM2 loci (PRIM2A and PRIM2B) were detected at 6p11.1-p12 by fluorescence in situ hybridization using several genomic DNA probes.

Animals↗
PubMed1995

A novel non-xanthine adenosine A1 receptor antagonist.

FK453, (+)-(R)-[(E)-3-(2-phenylpyrazolo[1,5-alpha]pyridin-3-yl) acryloyl]-2-piperidine ethanol, was examined for adenosine receptor antagonistic activity using isolated guinea-pig atria and aorta and for affinity for adenosine receptors in the rat cerebral cortex and striatum in comparison with FR113452 (S enantiomer of FK453), PD116948 (1,3-dipropyl-8-cyclopentylxanthine), theophylline (1,3-dimethylxanthine) and CGS15943 ([1,2,4]triazolo[1,5-c]quinazolone). FK453 showed potent inhibition of the negative inotropic activity elicited by 10 microM adenosine with an IC50 of 560 pM in guinea-pig atria. However, FK453 was less potent in inhibiting the relaxation induced by 3.2 microM adenosine and had an IC50 of 1.18 microM in guinea-pig aorta. The IC50 values for FR113452, PD116948, theophylline and CGS15943 were 1.18 microM, 1.31 nM, 20.2 microM and 74.2 nM in atria and > 100 microM, 656 nM, 239 microM, 127 nM in aorta respectively. In the binding study, FK453 antagonized [3H]N6-cyclohexyladenosine binding to the rat cortical adenosine A1 receptor with an IC50 of 17.2 nM. The IC50 values for FR113452, PD116948, theophylline and CGS15943 were 10.1 microM, 4.7 nM, 67.7 microM and 241 nM respectively. FK453 inhibited [3H]5'-N-ethylcarboxamideadenosine binding to rat striatum adenosine A2 receptor with an IC50 of 11.3 microM. FK453 had no adenosine A1 receptor agonistic activity, since it had no negative inotropic activity up to 100 microM in isolated guinea-pig atria. These results demonstrate that FK453 is a novel non-xanthine adenosine receptor antagonist and is potent and selective for the adenosine A1 receptor subtype.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1995

An outbreak of Norwalk virus gastroenteritis associated with eating raw oysters. Implications for maintaining safe oyster beds.

OBJECTIVE: To determine the characteristics and the cause of an outbreak of gastroenteritis associated with eating raw oysters. DESIGN: Survey of groups of persons reporting illness to the health department after eating oysters; survey of convenience sample of oyster harvesters; and tracing of implicated oysters. SETTING: General community. MAIN OUTCOME MEASURES: Relative risk for illness after oyster consumption, source bed of contaminated oysters, presence of antibodies to Norwalk virus in serum, presence of a Norwalk virus in stool by direct electron microscopy and reverse transcription-polymerase chain reaction (RT-PCR), and DNA sequences of RT-PCR products. RESULTS: Seventy (83%) of 84 persons who ate raw oysters became ill vs three (7%) of 43 people who did not eat raw oysters (relative risk, 11.9; 95% confidence interval, 4.0 to 34.2). Eleven (79%) of 14 serum pairs had at least a fourfold increase in antibody to Norwalk virus. All 12 stool samples tested were positive by electron microscopy and/or RT-PCR for Norwalk virus. The RT-PCR products from all seven stool samples tested had identical DNA sequences. Implicated oysters were harvested November 9 through 13, 1993, from a remote oyster bed. Crews from 22 (85%) of 26 oyster harvesting boats working in this area reported routine overboard disposal of sewage. One harvester with a high level of antibodies to Norwalk virus reported having gastroenteritis November 7 through 10 and overboard disposal of feces into the oyster bed. CONCLUSIONS: This outbreak was caused by contamination of oysters in the oyster bed, probably by stool from one or more ill harvesters. Education of oyster harvesters and enforcement of regulations governing waste disposal by oyster harvesting boats might prevent similar outbreaks.

Adolescent↗
PubMed1995

Epidemiologic applications of novel molecular methods to detect and differentiate small round structured viruses (Norwalk-like viruses).

The molecular epidemiology of a large, multistate outbreak of oyster-associated gastroenteritis [Kohn et al. (1995): Journal of the American Medical Association 273:466-471. Dowell et al. (1995): Journal of Infectious Diseases 171:1497-1503.] was examined using new methods to detect small round structured viruses (SRSVs) by reverse transcription-polymerase chain reaction (RT-PCR) and to characterize strains by Southern hybridization and nucleotide sequencing of 81-bp of a PCR product amplified from the RNA polymerase gene. Of 37 stool specimens examined from patients in eight clusters of the multistate outbreak, 32 (86%) gave RT-PCR products specific for SRSVs of P1-A phylogenetic group. Nineteen PCR products from the eight clusters were confirmed to have the identical sequence, indicating that this large outbreak was attributed to a single strain of SRSV. In one of the eight clusters, five (63%) of eight patients had a mixed infection with a second SRSV strain that belonged to P2-B phylogenetic group. Of 12 specimens from patients in five other outbreaks and one sporadic case which occurred at the same time as the multistate outbreak, 10 (83%) gave products specific for SRSVs representing four phylogenetic groups (P1-A, P1-B, P2-A, and P2-B). The sequences of the P1-A products from two outbreaks and that of the P2-B product from another outbreak were identical to the P1-A sequence from the eight clusters and the P2-B sequence from the one cluster of the multistate outbreak, respectively. These results demonstrate the first application of these methods to enhance our understanding of the molecular epidemiology of SRSVs and provide answers of public health interest that could not have been obtained using classical epidemiologic methods alone.

Animals↗
PubMed1995

Mechanism for species-specific induction of Leydig cell tumors in rats by lansoprazole.

Lansoprazole is a substituted benzimidazole which inhibits gastric acid secretion by inhibiting the hydrogen-potassium ATPase (proton pump) in the parietal cell. The finding of Leydig cell hyperplasia and Leydig cell tumors in 2-year oral studies in Sprague-Dawley rats but not in CD-1 mice prompted investigative studies to determine the mechanism for the Leydig cell changes. hCG challenge studies in Sprague-Dawley rats revealed decreased testosterone responsiveness in rats treated orally for 1 or 2 weeks with lansoprazole. After 4 weeks of daily oral treatment increases in serum LH and decreases in serum testosterone were detected within a few hours after dosing. In a study where 9-month-old male F344 rats were given testosterone supplementation via Silastic implants and then treated with lansoprazole for 6 months, a high incidence of Leydig cell tumors was seen in lansoprazole-treated, unsupplemented rats, whereas no Leydig cell tumors were seen in testosterone supplemented rats. This implied that reduction of the normal feedback inhibition at the level of the hypothalamus and/or pituitary due to reduced testosterone levels, thus giving rise to elevated levels of LH, was involved in the induction of Leydig cell tumors by lansoprazole. In vitro studies with Leydig cells from rats using various stimulators and precursors of testosterone biosynthesis demonstrated that the most sensitive site for inhibition of testosterone synthesis by lansoprazole is the transport of cholesterol to the cholesterol side chain cleavage enzyme. The IC50s for inhibition of LH or hCG-stimulated testosterone synthesis in Leydig cells from rats, mice, and monkeys were 11-12, 8, and 24.7 micrograms/ml, respectively. In vitro studies with metabolites of lansoprazole revealed that three metabolites were more potent inhibitors of testosterone synthesis than the parent drug, two of them being at least 10 times more potent. These metabolites are present in rats at substantial levels but are undetectable in humans. The lack of induction of Leydig cell tumors in mice, lower sensitivity of primate Leydig cells, and the absence of testosterone synthesis-inhibiting metabolites in man suggest that Leydig cell tumors found in rats represent a species-specific sensitivity and does not imply a risk for clinical use in man.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1995

Characterization of the hog cholera virus 5' terminus.

Hog cholera virus (HoCV) 5' terminus of the ALD and GPE(-) strains were analyzed by using rapid amplification of cDNA end method (5'RACE). An additional nine nucleotides were found at the 5' termini of genomic RNA in the ALD and GPE(-) strains of HoCV. These nine nucleotides were also conserved in BVDV and were suggested to form a hairpin structure at the 5' terminus by computer-assisted analysis. It seems possible that the secondary structure and/or the 5' terminus sequence has a significant role in the HoCV virus genome.

Animals↗
PubMed1995

Phenotypic and functional characterization of T-cell lines generated from colonoscopic biopsy specimens in patients with ulcerative colitis.

Intestinal T-cell lines were generated from lamina propria mononuclear cells isolated from colonoscopic biopsies in ulcerative colitis patients and controls. In both ulcerative colitis and controls, expanded cells were constituted largely by T-cell receptor alpha beta+, CD4+, CD45RA- (helper), and CD8+, CD11b- (cytotoxic) phenotypes. T-cell receptor V beta gene usage was not significantly changed after cell expansion and no difference was observed between ulcerative colitis and controls. Ulcerative colitis cells, especially those derived from the patients with long-standing disease, showed significantly higher levels of cytotoxicity against the target cells, including those of colonic epithelial origin, and enhanced production of tumor necrosis factor-alpha and interferon-gamma after short incubation with anti-CD3 antibody. Generation of T-cell lines from colonoscopic biopsy specimens may be useful for detailed functional characterization of locally infiltrating T cells in ulcerative colitis patients.

Adolescent↗
PubMed1995

Elevation of interleukin-6 in inflammatory bowel disease is macrophage- and epithelial cell-dependent.

Local interleukin-6 (IL-6) activity was studied using colonic mucosal tissues in inflammatory bowel disease (IBD) and inflammatory control patients. Active IBD specimens exhibited significantly higher IL-6 activity than control specimens in both cultures of isolated lamina propria mononuclear cells (LPMC) and mucosal tissues with an increased number of IL-6-producing cells. However, the activity in inactive IBD or inflammatory controls did not differ from controls. Northern blot analysis demonstrated IL-6 messenger RNA in LPMC and colonic epithelial cells isolated from active IBD specimens but not in control cells. Furthermore, immunofluorescent microscopic study of active IBD specimens showed more conspicuous staining of IL-6 in infiltrating LPMC (mostly CD68+ cells) and colonic epithelial cells. These results suggest that elevation of local IL-6 activity may be a characteristic feature of active IBD and both macrophages and colonic epithelial cells are the major cell types responsible for this phenomenon.

Adenocarcinoma↗
PubMed1995

Sea urchin egg tropomyosin isoforms with muscle-type and nonmuscle-type antigenicities.

Egg tropomyosins were prepared from four sea urchin species, Stronglyocentrotus intermedius, Anthocidaris crassispina, Hemicentrotus pulcherrimus and Pseudocentrotus depressus, and their molecular heterogeneity was investigated by electrophoresis and immunoblotting. The molecular heterogeneity of egg tropomyosins was species-specific, and two to four kinds of tropomyosin isoforms were detected, the apparent molecular weights of which were 29,000-32,000. The egg tropomyosin isoforms could be classified into two groups with muscle- and nonmuscle-type antigenicities in each species. No obvious difference in their cytological localization was observed immunocytochemically in S. intermedius and H. pulcherrimus.

Actins↗
PubMed1995

Localization of transforming growth factor-beta and latent transforming growth factor-beta binding protein in rat kidney.

TGF-beta plays an important role in maintaining the renal histological structure, and glomerular and tubular function. TGF-beta is usually secreted in a biologically inactive or latent form with high molecular weight by normal cells. The latent form of TGF-beta is composed of three distinct components: (a) mature TGF-beta (b) TGF-beta latency associated peptide (LAP) (c) latent TGF-beta binding protein (LTBP). LTBP plays a central role in the assembly, secretion and activation of TGF-beta 1. Most cells secrete a large latent TGF-beta with LTBP, while the other cells secrete a small latent TGF-beta without LTBP. However, the precise localization of TGF-beta and LTBP in the kidney is still not known. In the present study, we used the reverse transcription in combination with polymerase chain reaction (RT-PCR) to investigate the precise localization of TGF-beta 1 and LTBP in the microdissected glomeruli, renal tubules and arterioles. Our findings showed that TGF-beta 1 mRNA was detected in all nephron segments, glomeruli, and arterioles. On the other hand, LTBP mRNA was present in the glomeruli and arterioles, while it was absent in every segment of the renal tubules. Moreover, the immunohistochemical study of LTBP showed that the LTBP protein was localized on the glomeruli and arterioles but not on the renal tubules at the same localization as LTBP mRNA. These results indicate that the tubular epithelial cells secrete the small latent TGF-beta 1, while glomerular cells secrete the large latent TGF-beta 1, suggesting that they both have different structures and thus potentially different biological functions.

Animals↗