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Biomedical subjects

M Onda

Publications and source records attributed to M Onda.

At least 163 records · Page 9Linked to original sources
PubMed1996

[Neoadjuvant intra-arterial infusion chemotherapy in over stage III and inflammatory carcinoma of the breast].

From 1991 to 1996, 11 eligible patients (median age 50.4 years, range 33-71 years) with over Stage III and inflammatory breast carcinoma have been treated with neoadjuvant intra-arterial infusion chemotherapy. There were three Stage III a, one III b, three IV and four inflammatory carcinoma. Patients were treated with Epirubicin (10) and Doxorubicin (1), with a total amount of 120-190 mg. Three cases were combined with endocrine therapy (MPA 1,200 mg). In terms of morphological efficacy, 10 of 11 achieved PR, and three of those with endocrine therapy had over Grade 2 in histological efficacy. Carcinoma cells were especially deceased in one inflammatory carcinoma with MPA. Three of 11 died of liver metastasis, the others are still alive (median 24.5 months, range 7-51 months). Combined endocrine therapy should be considered applicable for the treatment strategy of the breast carcinoma.

Adult↗
PubMed1996

[Interventional radiology for portal hypertension. PTO.TIO].

Percutaneous transhepatic obliteration (PTO) and transileocolic vein obliteration (TIO) are techniques of interventional radiology for embolization of collaterals due to portal hypertension 1) We can obtain good results from the precise selection of these techniques in accordance with the patient's hemodynamics and general condition. 2) Endoscopic injection sclerotherapy (EIS) combined with PTO or TIO for esophageal varices proves to be superior in reliability and durability to EIS alone, and the time before retreatment is much longer when this combination therapy is used. 3) In the intractable EIS only cases, a distinct improvement in results and prognosis appears in using PTO or TIO and also in adding more EIS thereafter. 4) After treatment with EIS and PTO or TIO for cardiac varices, we obtain better results in the disappearance rate as well as in the recurrence rate compared with EIS alone. 5) Gastric varices disappear and hepatic encephalopathy due to porto-systemic shunt is improved after PTO or TIO or using these with balloon occluded retrograde transvenous obliteration (BRTO). Thus PTO and TIO would be analogous to surgical devascularization or ligation. Therefore it is concluded that the best results would be obtained with PTO or TIO with other nonsurgical treatments.

Aged↗
PubMed1996

[Expression of trefoil group antigen pS2 in human gastric cancer].

Expression of trefoil group antigen pS2 was examined immunohistochemically in resected stomachs from 121 patients with gastric cancer. Gastric cancer was classified as either undifferentiated or differentiated by histology, and was also divided into gastric type or non-gastric type by mucin-histochemistry. Immunoreactive pS2 was present in 20% of early cancers and 30% of advanced cancers (NS), and in 25% of undifferentiated and 15% of differentiated early cancers (NS), whereas the antigen was present in 38% of undifferentiated and 15% of differentiated advanced cancers (p = 0.04). Positivity for pS2 was found more often in gastric type early cancer (p = 0.04) as well as advanced cancer (p = 0.0002), and was also more frequent in cancers showing scirrhous (p = 0.04) and infiltrative growth (p = 0.03). Cancer positive for pS2 was characterized by mucin-histochemistry and microscopy as gastric type with scirrhous growth and diffuse infiltration, and thus the expression of pS2 in gastric cancer appears to be related to the growth of cancer with these characteristics.

Adenocarcinoma, Scirrhous↗
PubMed1995

Detailed physical mapping of the genes encoding glycophorins A, B and E, as revealed by P1 plasmids containing human genomic DNA.

Human glycophorins A, B and E (GPA, GPB and GPE) are members of the glycophorin gene family encompassing a 330-kb genomic segment located on chromosome 4, band q31 [Onda et al., J. Biol. Chem., 269 (1994) 13013-13020]. This gene family was apparently generated by two successive duplications of an ancestral gene. One of the progenitor genes, resulting from the first duplication, directly evolved into the GPA gene. The other progenitor gene acquired a unique 3'-region sequence and was then duplicated to yield GPB and GPE. In order to obtain a more detailed understanding of how these different members of the gene family evolved, we isolated several P1 plasmid clones encoding GPA, GPB or GPE. The precise locations of exon 1 and the exon encoding the transmembrane (TM) domain in GPA, GPB and GPE were then determined by hybridization with specific probes after restricted DNA fragments were separated by pulsed-field gel electrophoresis. The results obtained showed that the distances between exon 1 and exon 2 are almost equal for GPA and GPB, whereas this distance is larger in GPE. In contrast, the distance between exon 2 and the exon encoding the TM domain was shown to be the same among GPA, GPB and GPE. These results suggest that the gene divergence, i.e., insertions or deletions, took place after two successive duplications and supports the hypothesis that GPE acquired a portion of the GPA sequence surrounding exon 2 by gene conversion.

Biological Evolution↗
PubMed1995

Clinical significance of epidermal growth factor (EGF), EGF receptor, and c-erbB-2 in human gastric cancer.

The EGF stimulation system for growth regulation is implicated in normal and neoplastic cell proliferation. The role of EGF, the EGF receptor, and c-erbB-2 in human gastric cancer is reviewed on the basis of several reports, which have been mainly oriented toward their clinical significance. EGF has been shown immunohistochemically to be present in 26% of gastric cancers (n = 395). The presence of EGF in gastric cancer is correlated with the degree of gastric wall invasion and lymph node metastasis. The 5-year survival of patients with EGF-positive tumors is worse than that of patients with EGF-negative tumors. The presence of EGF in human gastric cancer may therefore represent a higher malignant potential. Fifteen percent of gastric cancers (n = 352) were also shown to be positive for both EGF and the EGF receptor immunohistochemically, and the simultaneous occurrence of EGF and the EGF receptor suggests that these tumors grow in an autocrine fashion. Tumors exhibiting EGF and the EGF receptor simultaneously show a greater degree of local invasion and lymph node metastasis. Increased expression of EGF receptor protein in gastric cancer appears to be related to biologic aggressiveness, although gene amplification has occurred only to a small extent. Twelve percent of gastric cancers (n = 486) were found to be positive for c-erbB-2. This type of tumor has a frequent metastasis, and patients with c-erbB-2-positive cancer have a poorer prognosis than those with c-erbB-2-negative tumors. Selective blockade of the EGF receptor and c-erbB-2 from their ligands with monoclonal antibodies (MoAbs) inhibits the growth of human gastric cancer xenografts. These MoAbs may therefore be effective antitumor agents against gastric cancer showing overexpression of EGF receptors or c-erbB-2.

Epidermal Growth Factor↗
PubMed1995

Mucosal IgA antibody against Helicobacter pylori in chronic gastritis and intestinal metaplasia detected by the Tes-Tape method in resection specimens after gastrectomy for gastric cancer.

BACKGROUND: Subjects with atrophic body gastritis have a high prevalence of Helicobacter pylori seropositivity and a low prevalence of H. pylori infection. Disappearance of the organism appears to correlate with the development of intestinal metaplasia. To investigate this point, intestinal metaplasia was biochemically subclassified into complete and incomplete types by the Tes-Tape method, and tissue IgA and IgG antibodies against H. pylori were measured by enzyme-linked immunosorbent assay (ELISA). METHODS: Twenty-five stomachs resected for gastric cancer were examined using the Tes-Tape method. Serum H. pylori IgA and IgG antibodies and tissue IgA and IgG antibodies against H. pylori and tissue secretory IgA (sc-IgA) were examined in areas of intestinal metaplasia, nonmetaplastic gastric mucosa, and gastric carcinoma by ELISA: RESULTS: Tissue H. pylori IgA antibody was positive in 6 of 19 (32%) specimens taken from complete and 2 of 7 (29%) incomplete types of intestinal metaplasia and was positive in 6 of 14 (43%) nonmetaplastic gastric mucosa from the antrum and 14 of 23 (61%) from the body. Duodenal mucosa and cancer tissue were positive for tissue IgA antibody in 1 of 6 (17%) and 0 of 17 (0%), respectively. Tissue H. pylori IgG antibody was negative in all the tissues examined. sc-IgA in the areas of intestinal metaplasia was 120 +/- 65 (mean +/- standard error; ng/mg wet weight) and in the nonmetaplastic gastric mucosa was 113 +/- 72, showing no difference. Positivity and negativity of serum IgA and IgG antibodies against H. pylori coincided with presence or absence of tissue IgA antibody in nonmetaplastic gastric mucosa in 15 of 19 (79%) and 16 of 19 (84%) patients examined, respectively. CONCLUSION: Positivity rates of tissue IgA antibody against H. pylori were lower in the mucosa of intestinal metaplasia than in nonmetaplastic gastric mucosa and were negative in carcinoma. No significant difference in levels of sc-IgA between intestinal metaplasia and non-metaplastic gastric mucosa was found.

Antibodies, Bacterial↗
PubMed1995

Frequent and characteristic K-ras activation in aberrant crypt foci of colon. Is there preference among K-ras mutants for malignant progression?

BACKGROUND: To investigate very early lesion of colorectal cancer, K-ras activation and nuclear p53 accumulation were studied in aberrant crypt focus (ACF). METHODS: ACF were microscopically identified in grossly normal mucosa of patients with colorectal cancer who underwent surgery. Each ACF was microdissected from the surgical specimen and divided into two pieces, one for histologic and immunohistochemical examinations and the other for K-ras activation. K-ras mutations in codons 12 and 13 were sequenced after being screened by polymerase chain reaction amplification followed by restriction fragment length polymorphism analysis. Intranuclear accumulation of p53 protein was immunostained with the avidin-biotin complex method. RESULTS: ACF was predominantly distributed in the sigmoid colon and rectum, and its incidence was increased with age. Unexpectedly, ACF was very rare in colons of three patients with hereditary nonpolyposis colorectal carcinoma. K-ras mutations were detected in 58% (33 of 57) of ACF cases and in 44% (11 of 25) of adenocarcinoma cases. Although GTT mutation in codon 12 was predominantly observed in adenocarcinoma (10 of 11), GAT mutation (12 of 33) was as frequent as GTT mutation (11 of 33) in ACF together with mutation at codon 13 (7 of 33). No accumulation of p53 protein was found in any ACF. CONCLUSION: ACF were not diagnosed as neoplasms histologically, but they were considered to be neoplastic lesions, and K-ras activation is one of the key events to form ACF. The G-T substitution in K-ras codon 12 may undergo malignant growth easily compared with G-A substitution in colorectal carcinogenesis.

Adenocarcinoma↗
PubMed1995

Increases in pulmonary artery pressure and cardiac output due to the inhibition of nitric oxide synthesis during operative stress.

Pulmonary artery pressure (PAP), cardiac output (CO), and urinary nitrate, a stable endproduct of nitric oxide (NO), were measured pre- and postoperatively in eight patients who underwent esophagectomy for squamous cell carcinoma of the thoracic esophagus. A significant elevation of PAP and CO on the day of operation (POD 0) was accompanied by a low concentration of urinary nitrate. A reduction in PAP and CO, and an increase in nitrate to the preoperative levels, were found on PODs 2 and 3, respectively, but urinary nitrate decreased again after POD 3. Consequently, the changes in PAP and CO were closely correlated with the nitrate concentration. These results suggest that operative stress inhibited NO synthesis with a transitory induction of endogenous NO synthesis postoperatively.

Aged↗
PubMed1995

Detection of Helicobacter pylori DNA in gastric juice by the polymerase chain reaction: comparison with findings in bacterial culture and the detection of tissue IgA and serum IgG antibodies against Helicobacter pylori.

The detection of Helicobacter pylori in gastric juice by the polymerase chain reaction (PCR) was undertaken in 124 patients with peptic ulcer or chronic gastritis. PCR products were evaluated by agarose gel electrophoresis and Southern hybridization of H. pylori-specific DNA sequences. Positive and negative results of the PCR analysis in 72 examinations were compared with those from bacterial culture, and with the detection of tissue IgA antibody against H. pylori by enzyme-linked immunosorbent assay ELISA; Serion, Wuerzburg, Germany, and detection of serum IgG antibody against H. pylori by ELISA; Radim Pomezia, Italy. Thirty-four PCR-positive samples evaluated by electrophoresis and hybridization coincided with positive samples in 56% of bacterial cultures, 59% of tissue IgA antibody identifications, and 94% of serum IgG antibody evaluations; 26 PCR-negative samples coincided with negative samples in 96% of bacterial cultures, 81% of tissue IgA antibody evaluations, and 38% of serum IgG assessments. We compared the detection achieved with the H. pylori PCR assay in gastric juice with that in biopsies taken from the antrum and upper corpus in 90 examinations, and found them to be both positive in 34 (38%) and 36 (40%) of specimens, both negative in 37 (41%) and 30 (33%) specimens, gastric juice-positive but biopsy-negative in 10 (11%) and 12 (13%) specimens, and vice versa in 9 (10%) and 12 (13%) specimens, when detected by electrophoresis and hybridization, respectively, showing equivalent detection rates. In relation to the type of disease, the positive PCR assay results with gastric juice, evaluated by electrophoresis and hybridization, respectively, were: gastric ulcer 34/53 (64%) and 39/53 (74%), duodenal ulcer 23/38 (61%) and 25/38 (66%), and chronic gastritis 20/33 (61%) and 23/33 (70%), showing no significant difference in positive rates between peptic ulcer and chronic gastritis. Of the samples of 16 patients with H. pylori-positive gastric juice by the PCR assay, 7 were negative by PCR assay analyzed by electrophoresis and hybridization after the completion of treatment H. pylori. However, after treatment, 3 were negative on electrophoresis but still had positive results with hybridization, indicating that a minimal number of bacilli may have still remained. Detection of H. pylori in gastric juice has potential advantages for examining H. pylori infection in the entire stomach and for follow up after treatment for the eradication of H. pylori.

Antibodies, Bacterial↗
PubMed1995

Frequent and characteristic K-ras activation and absence of p53 protein accumulation in aberrant crypt foci of the colon.

BACKGROUND/AIMS: The relationship of aberrant crypt foci (ACF) to colorectal carcinogenesis is still controversial. Histological examination and analyses of K-ras mutations and p53 gene expression were performed to characterize ACF. METHODS: ACF were identified microscopically in grossly normal colorectal mucosa. The ACF were separated into two pieces, one for histological and immunohistochemical examinations and the other for molecular analysis. K-ras mutations in codons 12 and 13 were analyzed by polymerase chain reaction amplification, followed by restriction fragment length polymorphism and sequencing analyses. Intranuclear p53 protein was immunostained by the avidin-biotin complex method. RESULTS: Histologically, elongation and apical branching of the crypts in ACF were striking. K-ras mutations were detected in 58% of ACF (33 of 57; 46% [26 of 57] in codon 12, and 12% [7 of 57] in codon 13) and in 44% of adenocarcinomas (11 of 25; all in codon 12). In ACF, GAT mutations (12 of 26) were as frequent as GTT mutations (11 of 26) in codon 12, although GTT mutations in codon 12 were predominant in adenocarcinomas (10 of 11). No accumulation of p53 protein was detected in any ACF, although it was detected in 52% (13 of 25) of the colorectal carcinomas. CONCLUSIONS: ACF do not seem histologically to be neoplasms, although genetically they are monoclonal lesions. K-ras mutation is critical in the formation of ACF, but p53 alteration could play a causal role in tumor progression.

Adult↗
PubMed1995

p53 mutations and overexpressions in Japanese breast cancer.

Mutations in the p53 gene were analysed in 50 cases with breast cancer by PCR-SSCP and direct DNA sequencing. Mutations were found in 10 of 50 cases (20%) including a case with Tis, and loss of the normal allele was found in five of these cases. Eight of the 10 mutations occurred within highly conserved domains, but no mutational hot spots were found. GC to AT transitions were the most frequent mutations (six of 10 cases), while mutations at CpG dinucleotides were found in three cases (30%). AT to TA transversions were the second most frequent mutation (20%). The level of expression of p53 protein was assessed by Western blot analysis in 62 cases. Overexpression of p53 protein was detected in 21 of 62 cases (34%) including a case with Tis. There was a strong correlation between missense mutations in the p53 gene and overexpression of p53 protein. Overexpression of p53 protein was closely associated with increasing tumour size and ER-negative status among the various factors investigated, suggesting that p53 overexpression may reflect the lack of differentiation in breast cancer.

Base Sequence↗
PubMed1995

Cytochrome P4502E1 (CYP2E1) genetic polymorphism in a case-control study of gastric cancer and liver disease.

Cytochrome P4502E1 (CYP2E1) activates carcinogenic N-nitrosamines, benzene, urethane and other low molecular weight compounds. This enzyme is also inducible by ethanol, and metabolizes alcohol. A restriction fragment length polymorphism (RFLP) using the Rsa I restriction enzyme has been identified in the CYP2E1 transcription regulatory region; recent studies suggest that this polymorphism may affect gene expression. We investigated the frequency of the Rsa I RFLP in a Japanese population in relation to gastric cancer and liver disease susceptibility. The frequency of this polymorphism was determined in 150 gastric cancer, 16 hepatocellular cancer, 48 liver cirrhosis and 203 benign gastric disease (controls) patients. This preliminary study shows no association of the specific genotype with gastric cancer in all subjects (odds ratio = 1.04, 95% CI = 0.74-3.08 for the heterozygote and 0.57, 95% CI = 0.22-1.50 for the homozygous rare allele, respectively). To further confirm this lack of association, an age and gender matched case-control study should be performed. Separately, there was no association of the Rsa I RFLP with hepatocellular carcinoma (p = 0.911), but there was a suggested difference between the non-viral associated liver cirrhosis patients and control patients. Thus, this polymorphism may be related to ethanol metabolism and consequential liver diseases in a Japanese population.

Base Sequence↗
PubMed1995

[Effect of coenzyme Q10 on endotoxin induced hepatocyte injury modulation of endotoxin-activated polymorphonuclear neutrophils].

The effect of coenzyme Q10 (CoQ10) on hepatocyte injury during endotoxin (ET) shock in rats was studied with special reference to the role of polymorphonuclear neutrophils (PMN). ET shock was induced by intravenous administration of 5 mg/kg ET, and CoQ10 was given at 20 mg/kg once or 3 times orally or intravenously. We examined plasma glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and glutamate dehydrogenase (GLDH) levels, superoxide production by PMN, the phagocytic activity of PMN, the cytotoxicity of PMN to liver cells, and histological changes in the liver. The CoQ10-treated rats showed lower levels of GOT, GPT, and GLDH than rats treated with ET only. When compared to the group given ET only superoxide production by PMN induced by 2-methyl-6-phenyl-3,7-dihydroimidazol [1,2-alpha]pyrazin-3-one (MCLA) was significantly inhibited in the group given CoQ10 intravenously and 3 times orally, but there was no significant difference in the group given CoQ10 once orally. However, the level of superoxide production by PMN stimulated by phorbol myristate acetate (PMA) was lower in all CoQ10-treated rats than in those given ET only. There was no difference in either peripheral PMN counts or PMN phagocytes between the CoQ10-treated group and the group given ET only. Histologically, the hepatocyte injury in all groups that received CoQ10 was milder than that in the ET-only group. No hepatocyte cytotoxicity by PMN was observed in any group that received CoQ10. These results suggest that both intravenous and oral administration of CoQ10 can modulate the endotoxin-activated PMN, and is useful for preventing hepatocyte injury during ET shock.

Animals↗