[Heptocellular carcinoma (HCC) fed from cystic artery--report of a case and review of the literature].
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Aged↗
Biomedical subjects
M Onda
Publications and source records attributed to M Onda.
[Evaluation of peritoneal lavage smears and intraperitoneal administration of anti-neoplastic agents in stage III and IV gastric cancer].
Examinations of peritoneal lavage smears (cy) in gastric cancer surgical stages III and IV are very important for determining the disease stage. We have been carrying out these examinations for 8 years. One hundred sixty patients with gastric cancer were examined. The incidence of cy positivity was higher in T4 than in T3, and higher in P1,2,3 than in P0. We performed intraperitoneal administration of CDDP in 10 patients with gastric cancer using a reservoir (Infuse-A-Port) implanted in the abdominal wall once a week. No difference in survival was observed between patients who received chemotherapy via i.p. and those who received it i.v.
Adenocarcinoma↗
Expression and chromosomal localization of the human alpha 4/IGBP1 gene, the structure of which is closely related to the yeast TAP42 protein of the rapamycin-sensitive signal transduction pathway.
To study the function of the B cell signal transduction molecule alpha 4 (IGBP1), we isolated a human alpha 4 (IGBP1) gene that has sequence similarity to the yeast protein (TAP42) involved in the rapamycin-sensitive signal transduction pathway. The human alpha 4 has sequence identities with murine alpha 4 of 83.4% nucleotide and 82.9% amino acid sequence, and a stretch of consensus motifs in the carboxyl terminal is conserved among the related genes of human, mouse, yeast, and rice. The gene is expressed as a 1.4-kb mRNA in the spleen, lymph node, thymus, appendix, peripheral blood leukocytes, bone marrow, fetal liver, heart, brain, placenta, skeletal muscle, kidney, and pancreas. The anti-human alpha 4 antibody detected a 45-kDa protein in human lymphoid cell lines. Moreover, human alpha 4 (IGBP1) gene is located at q13.1-q13.3 on chromosome X.
Adaptor Proteins, Signal Transducing↗
Isolation of a candidate gene, CAB1, for cholesterol transport to mitochondria from the c-ERBB-2 amplicon by a modified cDNA selection method.
An improved cDNA selection method was established to isolate expressed genes efficiently from an amplified chromosome region in human cancer. Biotinylated yeast artificial chromosome DNA containing c-ERBB-2 was hybridized in solution with PCR-amplifiable cDNAs of an esophageal cancer cell line bearing the c-ERBB-2 amplification. After capturing the hybrids on avidin-coated magnetic beads, the cDNAs were amplified by PCR. Four new genes (A39, C51, CAB1, and GRB-7) coamplified with c-ERBB-2 were isolated from the enriched cDNA library. CAB1, GRB-7, and c-ERBB-2 were overexpressed in gastric and esophageal cancer cells in correspondence with the amplification. The deduced amino acid sequence of the CAB1 gene had significant homology to the recently discovered steroidogenic acute regulatory protein, StAR, which plays an essential role in cholesterol transport to mitochondria. It was established that multiple overexpressed genes are frequently present in a single amplicon.
Amino Acid Sequence↗
Refolding process of ovalbumin from urea-denatured state. Evidence for the involvement of nonproductive side chain interactions in an early intermediate.
Ovalbumin contains one cystine disulfide (Cys73-Cys120) and four cysteine sulfhydryls (Cys11, Cys30, Cys367, and Cys382) in a single polypeptide chain of 385 amino acid residues. The refolding mechanism of ovalbumin was investigated under disulfide-bonded and disulfide-reduced conditions using the denatured protein state, DA, as the starting protein sample. For the preparation of DA, the disulfide-intact and disulfide-reduced forms of ovalbumin were denatured by protein incubation in 9 M urea at pH 2.2. When DA was placed in a refolding buffer, pH 8.2, an intermediate state IN was produced in either the disulfide-bonded or the disulfide-reduced condition; IN showed about 60% of the native CD ellipticity at 222 nm and the intrinsic tryptophan fluorescence with the native spectrum peak but with decreased intensity. The formation of IN as detected by far UV CD ellipticity was quite rapid and finished within a mixing dead time of 20 ms. When DA was diluted with an acidic buffer, pH 2.2, a partially folded equilibrium intermediate IA with the structural characteristics equivalent to those of IN was formed. After the formations of IN and IA, the regains in CD ellipticity and tryptophan fluorescence at pH 8.2 followed biphasic kinetics in the disulfide-bonded condition but monophasic kinetics in the disulfide-reduced condition. As unexpected findings, the native disulfide in DA and IA underwent nonproductive disulfide rearrangements in the disulfide-bonded condition at an early refolding stage and then was recovered during the subsequent refolding. The integrity of overall refolding was confirmed by the observation that the proteins refolded for 20 h in the disulfide-bonded and disulfide-reduced conditions showed, on differential scanning calorimetry analyses, almost exactly the same denaturation temperatures as their native protein counterparts. These results were consistent with a refolding process for ovalbumin which includes nonproductive side chain-side chain interactions in the early intermediate IN, which requires subsequent reorganization for the correct refolding.
Animals↗
Hepatic lobar differences in progression of chronic liver disease: correlation of asialoglycoprotein scintigraphy and hepatic functional reserve.
We studied the hepatic functional reserve in the lobes of the liver in 28 patients with chronic liver disease and 13 controls using single photon emission computed tomography (SPECT) imaging with a radiolabeled asialoglycoprotein analog, Technetium-99m-diethylenetriaminepentaacetic acid-galactosyl-human serum albumin (Tc-99m GSA). Counts of Tc-99m GSA radioactivity in the liver on SPECT images significantly correlated (P < .0001) with the serum albumin level (r = .612), log (serum cholinesterase activity) (r = .618), serum bilirubin level (r = .628), prothrombin time (r = .715), hepaplastin test (r = .637), and indocyanine green retention rate at 15 minutes (r = .771), making it possible to estimate the distribution of functional reserve in the liver based on counts. Using the intact hepatocyte theory, we estimated the number of viable hepatocytes based on the counts. With progression of hepatic functional degeneration, counts per unit hepatic volume decreased (rho = .779, P < .0001), and left lobe to right lobe ratio of this parameter increased (rho = .491, P = .0019) significantly. These findings suggest that the reduction of hepatic functional reserve per unit hepatic volume and numerical density of the hepatocytes, and the proliferation of fibrosis in patients with chronic liver disease is slower in the left lobe than in the right. We discuss a possible biological basis for these apparent lobar differences and for hepatic morphological changes seen in cirrhosis.
Adult↗
Endoscopic dexamethasone injection following balloon dilatation of anastomotic stricture after esophagogastrostomy.
BACKGROUND: Anastomotic stricture is common after esophagogastrostomy. Recent advances in nonsurgical treatment include the silicon bougie and balloon dilatation. However, simple dilatation alone with a silicon bougie or endoscopic balloon dilator was repeated a mean of 4.7+/-5.4 times to control anastomotic stricture because of its temporary effect. METHODS: For 11 patients, endoscopic injection of dexamethasone (8 mg) around the anastomosis was done immediately after balloon dilatation (40 psi for 5 minutes). RESULTS: This method significantly reduced the number of the dilatations to 1.1+/-0.3 (P < 0.05). Ten of the 11 patients did not need any further treatment. There were no side effects or complications of dexamethasone injection. CONCLUSION: A combination of endoscopic balloon dilatation and dexamethasone injection provided an easy and safe method for preventing the recurrence of anastomotic stricture.
Anastomosis, Surgical↗
Helicobacter pylori infection and genetic polymorphisms for cancer-related genes in gastric carcinogenesis.
The development of gastric cancer is a multistep process that is multi-factorial. An association with the Helicobacter pylori infections, gastric atrophy and gastric cancer has received recent attention. The objective of this study was to elucidate the risk factors for gastric cancer by using molecular epidemiological techniques for genetic susceptibility, gastric atrophy and serum markers including H pylori infection. We used an age- and gender-matched case-control study, where patients with benign gastric lesions were the controls. Low serum pepsinogen I levels (cut-off < 50 ng/mL) and low pepsinogen I/pepsinogen II ratios (cut-off < 3.0) were significantly associated with the risk of gastric cancer (odds ratio [OR] = 3.53: 95% confidence interval [CI] = 2.46-5.09 and OR = 4.73: 3.26-6.88, respectively). However, seropositivity of serum immunoglobulin G (IgG) antibody against H pylori (OR = 1.09: 0.74-1.61) was not associated with gastric cancer, even when analyzed by age greater than or less then 50 years. Specific genotypes of the cytochrome p450 2E1 (CYP2E1) RsaI polymorphism and glutathione-S-transferase (GST) M1 gene deletion were determined but were not associated with gastric cancer; however, a Lmyc genetic polymorphism was associated with gastric cancer (OR = 1.55: 1.03-2.34). Therefore, in this Japanese study, atrophic mucosal change, indicated by serum pepsinogen levels, is a possible risk factor for gastric cancer.
Helicobacter Infections↗
Progression of articular destruction and the production of tumour necrosis factor-alpha in antigen-induced arthritis in rabbits.
We examined the progression of articular destruction and the production of tumour necrosis factor-alpha (TNF-alpha) in antigen-induced arthritis (AIA) in rabbits, i.e. flare-ups of inflammation induced by repeated intra-articular injections (single, twice and three times) of antigen. A marked progression of articular destruction and an infiltration of inflammatory cells in the synovium were observed with the increase in the number of antigen injections. An immunohistochemical analysis of the synovial lesions following three injections of antigen revealed that the lymphoid follicles consisted mainly of CD4+ T cells and IgG/IgM+ B cells. There were marked infiltrations of IgG+ plasma cells around the lymphoid follicles. In contrast, the production of TNF-alpha in the synovial fluid and the erythrocyte sedimentation rate (ESR), which is a marker of systemic inflammatory activity in rheumatoid arthritis, peaked at 6 h 24 h, respectively, following the last injection of antigen. These values were also greater following the repeated injections of antigen compared with the single injection. The TNF-alpha was produced markedly in the joints at the onset of the flare-ups of arthritis following the repeated injections of antigen, and the elevation of the ESR and an acceleration of the inflammatory response in the synovium were observed with a concomitant progression of severe articular destruction, suggesting that the marked production of TNF-alpha at the time of flare-ups may be involved in the exacerbation of AIA in rabbits.
Animals↗
Refolding of urea-denatured ovalbumin that comprises non-native disulfide isomers.
Ovalbumin, which contains one cystine disulfide (Cys73-Cys120) and four cysteine sulfhydryls (Cys11, Cys30, Cys367, and Cys382) in the native state, undergoes intrachain sulfhydryl-disulfide exchanges at high concentrations of urea, generating many non-native disulfide isomers [E. Tatsumi, N. Takahashi, and M. Hirose (1994) J. Biol. Chem. 269, 28062-28067]. The refolding of ovalbumin from the urea-denatured state was investigated. When the denatured protein was diluted 20-fold with a refolding buffer (pH 8.2), an initial burst intermediate I(N) was produced within the 20 ms instrumental dead time; I(N) showed about 60% of the native CD ellipticity at 222 nm. The intrinsic tryptophan fluorescence of I(N) showed the same peak (338 nm), but with decreased intensity (57%), as compared to the native protein. After the rapid formation of I(N), most of the ovalbumin molecules correctly refolded into the native state with slow biphasic kinetics, as evaluated by far-UV CD, tryptophan fluorescence, and trypsin-resistance analyses. Furthermore, a peptide-mapping analysis revealed that sulfhydryl/disulfide exchange reactions occurred during the refolding, thereby increasing the formation of the native disulfide. The integrity of overall refolding was confirmed by a differential scanning calorimetry analysis. These data were consistent with the view that most, if not all, of the mispaired disulfide isomers in the urea-denatured ovalbumin can correctly refold into the native state via intrachain disulfide rearrangements.
Calorimetry, Differential Scanning↗
Role of Helicobacter pylori infection in perforation of peptic ulcer: an age- and gender-matched case-control study.
Evidence showed a marked decrease in recurrence rate of peptic ulcer after eradication of Helicobacter pylori infection. However, whether H. pylori infection is etiologically related to perforation of peptic ulcer remains to be clarified. We therefore conducted an age- and gender-matched case-control study between perforated and nonsurgical peptic ulcers in H. pylori infection and examined differences in the cytotoxin genes cagA and vacA. Serum H. pylori IgG antibody (ELISA) was positive in 20/21 (95%) of perforated vs. 37/40 (93%) of nonsurgical duodenal ulcers and in 5/5 (100%) of perforated vs. 24/28 (86%) of nonsurgical gastric ulcer patients. Positivity of H. pylori DNA in gastric juice, which was amplified by PCR and identified by Southern blot hybridization, was 17/23 (74%) of perforated vs. 32/45 (71%) in the nonsurgical duodenal ulcer group. Positivity of the cytotoxin genes cagA and vacA in H. pylori DNA-positive gastric juice was as follows: perforated vs. nonsurgical duodenal ulcer, cagA 11/ 13 (85%) vs. 24/27 (89%); vacA1: 9/13 (69%) vs. 22/27 (82%); vacA2 8/13 (62%) vs. 21/27 (78%). There were no significant differences between the perforated and nonsurgical peptic ulcer groups for these H. pylori serum and gene markers. It is assumed that H. pylori infection is not etiologically related to perforation of peptic ulcer.
Antigens, Bacterial↗
Cytotoxin genes of Helicobacter pylori in chronic gastritis, gastroduodenal ulcer and gastric cancer: an age and gender matched case-control study.
Helicobacter pylori (H. pylori) infection is involved in many gastrointestinal diseases, such as chronic gastritis (CAG), peptic ulcer and gastric cancer (GCA). Both host factors and H. pylori strain differences may contribute to differences in the diseases. Thus, we conducted an age and gender matched case-control study of 35 patients each with CAG, gastric ulcer (GUL), duodenal ulcer (DUL) and gastric cancer (GCA) to examine the role of strain differences of the H. pylori cytotoxin genes cagA and vacA in these diseases. We employed polymerase chain reaction to examine the gastric juice for H. pylori DNA. The test was positive for 26 (74.3%) CAG, 29 (82.9%) GUL, 28 (80.0%) DUL and 27 (77.1%) GCA patients, showing no statistically significant difference among the diseases (P = 0.84). cagA and vacA genes (picked up by using a vacA1 + vacA2 primer pair which detected non-variable regions of the vacA gene) were detected by PCR in the H. pylori DNA-positive cases as follows: CAG, 92.3% and 76.9%; GUL, 100% and 86.2%; DUL, 89.3% and 89.3%; GCA, 92.6% and 85.2%, respectively. No statistically significant differences were found in the frequencies of these cytotoxin genes in H. pylori-positive cases among the various gastric diseases (P = 0.39 for cagA and P = 0.64 for vacA).
Adult↗
[Predisposition of subclones of pancreatic carcinoma cells, AsPC-1, to changes in functional and histopathological features of xenograft tumors with response to extracellular matrix].
We cloned two characteristics subclones from a human pancreatic carcinoma cell line, AsPC-1, according to their distinctive cell shapes; one an epithelial morphology and designated as "Beto-1" and the other a fibroblastic morphology and designated as "Fib-1". Fib-1 grew faster than Beto-1, but the growth rate of the cells on plastics was as high as that of the cells on the extracellular matrix extracts, matrigel. The pancreatic tumor-marker proteins, alpha-amylase, insulin, CEA, POA, PP, and AFP, but not CA 19-9, were positive in both subclones. Type IV collagen, fibronectin, and laminin, were all positive in both subclones; furthermore, the integrin adhesion receptor molecules, alpha 2 beta 1-subunit, alpha 5-subunit, and alpha 6-subunit, were also positive. The intercellular adhesion molecules, E-cadherin and ICAM-1, were detected in Beto-1 and Fib-1, respectively. Although both subclonal cells attached to type IV collagen, fibronectin, and laminin in a concentration-dependent manner. Beto-1 adhered most strongly to type IV collagen and Fib-1 attached most strongly to fibronectin. Beto-1 showed morphological differentiation on matrigel and in the tumor xenografts. Further, there was more fibroblast infiltration and type IV collagen production in Beto-1 tumor tissues, and more lymphocyte and neutrophil infiltration in tumors of Fib-1 which expressed ICAM-1 proteins. This study indicated that the histological diversity observed in the pancreatic carcinoma was evolved from the composition of the tumor cells which express the specific adhesion receptors.
Animals↗
[Helicobacter pylori clones in the stomach].
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Clone Cells↗
[The role of hepatic sinusoidal cells in homing of lymphocytes. Preferential hepatic trapping of PNA(+) lymphocyte and its modulation during liver regeneration].
It was demonstrated that the reaction of some cell species to peanut agglutinin (PNA) involved the maturity of the cells. We investigated the selective adhesion of circulating hemopoietic cells and lymphoid cells to hepatic sinusoidal cells. We experimented with thymocyte (TYC) models that could be easily isolated into PNA positive [PNA(+)] and PNA negative [PNA(-)] subsets, and transfused these subsets, labeled with 51Cr into the isogenic mice, then measured the radioactivity in the kidney, lung, spleen, liver, Peyer's patch (P.P.), and thymus, after 48 hrs. The radioactivity (% total dose recovered) in the liver and spleen represented the degree of cellular distribution and indicated that a significantly higher dose had accumulated in the liver and spleen than in other organs. Additionally, TYC-PNA(+), recognized to be immature cells, demonstrated high aggregation in the liver, while TYC-PNA(-), recognized to be mature cells, demonstrated high aggregation in the spleen. Similar results were observed in our subsequent experiment using wheat germ agglutinin (WGA), other indicator of maturity, and spleen cells (SPC). Next, we transfused TYC-PNA(+) to mice at various intervals after 70% hepatectomy. The degree of aggregation (radioactivity/weight) in the liver was reduced 1 day after hepatectomy, and that in the spleen increased proportionately. Whereas the aggregation degree of TYC-PNA(-) in the same experiment did not change significantly. We postulated that hepatic sinusoidal cells recognize and, sequentially, trap specific carbohydrates on lymphoid cells by a lectin, PNA or WGA, like receptor. Reviewing our previous report, adhesion to Kupffer cells induced SPC activation and proliferation, this recognition and trapping mechanism seems to play an important role of intrahepatic hematolymphoid system.
Animals↗
[The significance of blood group-related antigen A in a pancreatic cell line (PGHAM-1) in hamsters. With special reference to cell proliferation].
The relationship between blood group-related antigen A and cell proliferation was studied in a pancreatic carcinoma cell line (PGHAM-1) induced by N-nitrosobis (2-oxopropyl) amine (BOP) in hamsters. In vitro, the cell proliferation of PGHAM-1 was inhibited in a culture medium with an added monoclonal antibody (MoAb) against blood group-related antigen A depending on its concentration. In in vivo experiments, immunohistochemical double staining was performed using MoAb against blood group-related antigen A and bromodeoxyuridine (BrdU) in pancreatic carcinomas by intrapancreatic transplantation of PGHAM-1. Antigen A was expressed in the cell membrane and cytoplasm of PGHAM-1 cells. The BrdU labeling index (LI) in lesions with strong expression of MoAb A (> or = 50%) was 27.4 +/- 5.00, whereas the BrdU LI in lesions with weak expression of MoAb A (< or = 10%) was 11.9 +/- 2.10. The mean LIs in strongly expressed lesions of MoAb A were higher than those in weakly expressed lesions of MoAb A (p < 0.01). These results indicated that antigen A might be associated with cell proliferation in pancreatic carcinomas induced in hamsters.
ABO Blood-Group System↗
p53 mutations in MeIQ-induced mouse forestomach tumors.
A method was established for detecting mutations in the mouse p53 gene by cDNA-PCR-SSCP, using four cell lines which were derived from forestomach tumors induced in CDF, mice by 2-amino-3,4-dimethylimidazo [4,5-f]quinoline (MeIQ). All the cell lines were demonstrated to have mutations in exons 4, 5, 7 and 10, respectively, and the method was confirmed to be efficient and reliable. It was therefore used to analyse the role of p53 gene mutations in forestomach carcinogenesis induced by MeIQ, by examining four original tumors, one papilloma, two primary carcinomas and one lymph node metastasis. The papilloma (F 14) and the carcinoma (F 12) had mutations, but the lymph node metastasis of F 12 mouse (F 12 LN) did not. These results thus indicate that p53 mutations may occur relatively early but do not confer any predisposition for lymph node metastasis.
Animals↗