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Biomedical subjects

T Fujimori

Publications and source records attributed to T Fujimori.

At least 73 records · Page 4Linked to original sources
PubMed1999

Apoptosis, coronary arterial remodeling, and myocardial infarction after nitric oxide inhibition in SHR.

This study was designed to investigate the relationship between apoptosis (programmed cell death) and coronary arterial remodeling in spontaneously hypertensive rats (SHR) following prolonged nitric oxide synthesis inhibition. In addition, we evaluated whether the development of coronary arterial smooth muscular cell apoptosis was related to hemodynamics or to vascular hypertrophy. Three groups of 20-week-old male SHR were investigated: controls, and two groups that received two doses of N(G)-nitro-L arginine (L-NAME, 50 mg/L and 80 mg/L) each for 3 weeks. Mean arterial pressure and total peripheral resistance index increased whereas cardiac index diminished with L-NAME. Pathohistological study demonstrated increased pericardiac fibrosis and coronary arterial injury score in the L-NAME group in a dose-dependent manner. The high dose of L-NAME (Group 3) produced myocardial infarction in 78% of the rats. The wall:lumen ratio of epicardial coronary arteries was greater in L-NAME treated SHR (0.23+/-0.02 versus 0.16+/-0.02; P<0.05) and was associated with markedly increased apoptosis (15.3+/-6 versus 1. 9+/-1; P<0.05) without smooth muscle cell proliferation (PCNA positive cells). Apoptosis occurred predominantly in hypertrophic coronary arterial smooth muscular cells; myocardial infarction and ventricular fibrosis were exacerbated by impaired hemodynamics induced by L-NAME. These data suggest that coronary endothelial dysfunction and myocardial ischemic disease induced by L-NAME were responsible for apoptosis of coronary arterial smooth muscle cells, myocardial fibrosis, and infarction, all pathological findings that are consistent with what may be found in clinical hypertensive heart disease.

Animals↗
PubMed1999

[Effect of Helicobacter pylori eradication from patients with gastritis evaluated by the pathological grading and cell proliferation related factors].

We used Image Analysis Processor to clarify the relation ship between cell proliferation, apoptosis and inflammation before and after eradication in H. pylori gastritis. Fifty-two patients with H. pylori gastritis were diagnosed using the Rapid Urease Test under endoscopical and histological examination. The grading of gastritis was determined by the Updated Sydney System. While the effects of Ki-67 on epithelial cell proliferation were examined by immunohistochemistry using Image Analysis Processor, and apoptosis in epithelial cells was counted after staining by in situ TDT. H. pylori density, the number of neutrophils, mononuclear cell, and number of lymphoid follicles had significantly decreased after eradication. Ki-67 labeling index significantly decreased from 11.74 percent to 0.98 percent after eradication (p < 0.0001). The apoptotic index had also decreased after eradication, but with a lack of significant difference (p < 0.06). These data suggest that H. pylori gastritis was remarkably ameliorated by eradication, have led to being capable of improving epithelial cell damage, and activity of proliferative cells and apoptotic cells were becoming normalization.

Apoptosis↗
PubMed1999

Semi-quantitative procedure for telomeric repeat amplification protocol (TRAP) assay in colorectal carcinomas.

Telomerase activity is intensively studied as a prognostic marker in malignancies, and generally detected by telomeric repeat amplification protocol (TRAP) assay. Recently, Ohyashiki et al. demonstrated a semi-quantitative procedure for TRAP assay, which is more useful than the qualitative one to analyze the correlation between telomerase activity and clinicopathological features in carcinomas. Therefore, we used semi-quantitative TRAP assay to analyze the correlation between telomerase activity and clinicopathological factors in colorectal carcinomas. Twenty-nine cases of advanced colorectal carcinoma, obtained by surgery, were studied. A telomerase detection kit, TRAP-eze, was used for the PCR based TRAP assay, and a DNA sequencer for a semi-quantitative analysis was used for a analysis. Telomerase activity was positively detected in all samples, and its mean value was 2.076+/-1.634 units (range; 0.536-8.932 units). Based on Dukes' classification, the activity tended to be higher in Dukes' A (2.722 units; P = 0.0525) and C (2.430 units) than in Dukes' B (1.552 units). The activity was higher in the right colon than at other locations. (right vs. left, rectum = 3.167 vs. 1.216 units; P<0.05, 1.604 units; P<0.01). The activity was higher in poorly differentiated adenocarcinoma than in well differentiated adenocarcinoma (3.743 vs. 1.491 units; P<0.05). Semi-quantitative TRAP assay is useful to analyze the correlation between telomerase activity and clinicopathological factors in colorectal carcinomas.

Aged↗
PubMed1998

[The study of genetic changes in colorectal cancer accompanied with ulcerative colitis].

The usefulness of gene information was studied when used in conjunction with a morphological diagnosis of either dysplasia or carcinoma that later develops into ulcerative colitis (UC). The cases investigated consisted of those operated on for UC with carcinoma complications and those operated on for UC over 7 years previously without carcinoma complications. Ras and DCC were examined for the presence of any point mutations in codon 12 and polymorphism in codon 201 using the PCR-RFLP method, while p53 was also studied immunohistologically. A mutation in ras was found in 25% of the UC-IV cases and also in 17% of the UC-III cases, while no mutation at all was found in the UC-I and UC-II cases. p53 showed a high rate of positivity in the UC-IV and UC-III cases with carcinoma complications, while it was negative in all cases in the control group cases. Gly in DCC codon 201 was also found in many cases including the control group. This study demonstrated that a gene aberration can thus influence the pathophysiology and cancerization of UC and therefore the p53 findings were thus considered to be useful in the morphological diagnosis of dysplasia and carcinoma.

Adult↗
PubMed1997

Mouse LIM-kinase 2 gene: cDNA cloning, genomic organization, and tissue-specific expression of two alternatively initiated transcripts.

LIM-kinase 1 and LIM-kinase 2 (LIMK1 and LIMK2) are members of a novel protein kinase subfamily containing LIM motifs at the N-terminus. There are two isoforms of Limk2 transcripts coding proteins with distinct N-terminal structures: LIMK2a, containing two LIM motifs, and LIMK2b, with one and one-half LIM motifs. Here we report the cDNA and genomic structures of mouse LIMK2. The deduced 638-aminoacid sequence of mouse LIMK2a shows 98% identity with that of rat LIMK2a. The mouse Limk2a gene consists of at least 16 exons and spans more than 50 kb. Exon/intron boundaries of the mouse Limk2a gene are exactly conserved with those of the mouse Limk1 gene. An additional exon encoding the Limk2b-specific 5'-terminal sequence was found to be located between exons 2 and 3, suggesting that Limk2a and 2b mRNAs are transcribed from a single Limk2 gene by an alternative usage of exons near the 5' end of the gene. Limk2a and Limk2b transcripts were expressed at different ratios in a variety of mouse tissues.

Alternative Splicing↗
PubMed1997

Evidence that absence of Wnt-3a signaling promotes neuralization instead of paraxial mesoderm development in the mouse.

Wnt-3a mutant embryos show defects caudal to the forelimb level; somites are absent, the notochord is disrupted, and the central nervous system has a pronounced dysmorphology. Previous studies revealed that the primary defects of the mutant embryos are likely to be in the process of paraxial mesoderm formation. In this study, we analyzed the phenotype of Wnt-3a mutant embryos at early somite stages (8.0 days post coitum), when somite formation is initiated. In Wnt-3a mutants, cells which have ingressed through the primitive streak do not migrate laterally but remain under the streak and form an ectopic tubular structure. Several neural-specific molecular markers, but no paraxial mesoderm markers, are expressed in this structure, suggesting that the ectopic tube is an additional neural tube. In normal embryos, Wnt-3a is expressed in the primitive ectoderm, including the cells which are fated to give rise to the paraxial mesoderm and neurectoderm, but expression is absent in migrating mesoderm cells. These results suggest that Wnt-3a signaling may play a role in regulating paraxial mesodermal fates, at the expense of neurectodermal fates, within the primitive ectoderm of the gastrulating mouse embryo.

Animals↗
PubMed1997

Codon 201Arg/Gly polymorphism of DCC (deleted in colorectal carcinoma) gene in flat- and polypoid-type colorectal tumors.

Recent studies have identified the distinct existence of flat-type colorectal tumors. The low incidence of ras gene mutations in these tumors suggests that their genetic pathways of tumor progression may be different from those of the polypoid type. To elucidate further genetic alterations in flat-type colorectal tumors, codon 201Arg/Gly polymorphism in the DCC (deleted in colorectal carcinoma) gene was analyzed in normal tissue (normal colonic mucosa or peripheral lymphocytes) and in tumor tissue from 191 patients with colorectal tumors (36 patients with flat-type colorectal tumors, 81 patients with polypoid-type colorectal tumors, and 74 patients with advanced carcinomas). For normal controls, 30 samples obtained from patients who had neither colorectal tumors (confirmed by total colonoscopy) nor a family history of colorectal carcinoma were analyzed. DCC gene codon 201Arg/Gly polymorphism was investigated by polymerase chain reaction-based restriction fragment length polymorphism analysis, fluorescence-based dideoxy sequencing, or both. For the flat type, the frequency of codon 201Gly of the DCC gene was 64% and 54% in the normal tissue of patients with adenoma with high-grade dysplasia and submucosal carcinoma, respectively. It was 49%, 52%, and 49% in the normal tissue of patients with polypoid-type adenoma with high-grade dysplasia, submucosal carcinoma, and advanced carcinoma, respectively. In the normal tissue, codon 201Gly of the DCC gene was more frequently observed in patients with flat-type adenoma with low-grade dysplasia (67%) than in those with polypoid-type adenoma with low-grade dysplasia (18%) or in normal controls (17%, P < 0.05, chi2 test). Codon 201Arg/Gly polymorphism in tumor tissues did not differ from that in the corresponding normal tissues, except for 10 cases of carcinoma with loss of heterozygosity (LOH). In carcinomas with LOH, preferential loss of the codon 201Arg allele was noted (9/10 cases). These results suggest that codon 201Gly of the DCC gene is not only associated with flat-type colorectal tumors, but that it may serve as a useful genetic marker for identifying groups at higher risk for colorectal cancer.

Carcinoma↗
PubMed1997

Combination chemotherapy for malignant paraganglioma.

Treatment with a combination chemotherapeutic regimen consisting of cyclophosphamide, vincristine, and dacarbazine for malignant paraganglioma with hepatic metastasis is reported. A 51-year-old male presented with tumors in the retroperitoneal space and liver. The patient was diagnosed as having paraganglioma based on elevated levels of serum neuron-specific enolase, urinary catecholamine and vanillylmandelic acid, and on histological findings of the liver specimen. The patient was treated with this combination chemotherapy in repeated 21-day cycles. Temporary improvement in laboratory findings and a 20% reduction in the size of the hepatic masses were observed without severe adverse effects.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1997

Helicobacter pylori infection in early gastric adenocarcinoma: relationship between histologic subtypes and ulcer-formation.

Early stage of gastric cancers were divided into two subtypes; differentiated and undifferentiated adenocarcinomas, histologically. We examined the involvement of Helicobacter pylori (Hp) infection in the development and progression of cancer, and presence or absence of peptic ulcer (UL+/UL-). From the results, these findings obtained as follows; 1) Hp positive rate of UL+ group was significantly higher than that of UL-group. 2) Neither of gross features nor depth of the tumor did not correlate with Hp positive rates. 3) Hp positive rate of undifferentiated type carcinoma was significantly higher than that of differentiated type, contrarily to our expectation. These findings suggested that Hp infection might relate with ulcer formation in the cancerous lesion. The hypothesis which is "gastritis-intestinal metaplasia-differentiated type carcinoma sequence" was not supported by present study. Hence, Hp infection was suggested as an important factor of the gastric cancer development and progression, not only in differentiated type but also in undifferentiated type.

Adenocarcinoma↗
PubMed1996

Effects of growth factors and gut hormones on proliferation of primary cultured gastric mucous cells of guinea pig.

Almost completely homogenous gastric mucous epithelial cells of guinea pigs were grown to confluence in the presence of 10% fetal calf serum (FCS). FCS, epidermal growth factor (EGF), and insulin significantly increased 5-bromo-2'-deoxyuridine (BrdU) uptake by the cells and EGF together with insulin increased the cells' [3H] thymidine uptake. Basic fibroblast growth factor (bFGF) enhanced EGF-induced DNA synthesis by the cells, but vasoactive intestinal peptide (VIP), secretin, prostaglandin E2 (PGE2), and dibutyryl cyclic AMP (dbcAMP) neither induced DNA synthesis nor enhanced the effect of EGF on DNA synthesis by the cells. Gastrin, cholecystokinin-octapeptide (CCK8), and carbamylcholine chloride (CCh) also did not enhance the effect of EGF on DNA synthesis. 125I-EGF, 125I-bFGF, and 125I-gastrin binding to the gastric mucous cells revealed the presence of high-affinity receptors for EGF and bFGF, but not for gastrin. Northern blot analysis showed the expression of EGF receptor mRNA, but not gastrin receptor mRNA. These results suggest that EGF, insulin, and bFGF may cooperatively regulate gastric mucous cell growth, but that gastrin and other gastrointestinal hormones do not have a direct stimulatory effect on mucous cell growth in the guinea pig.

Animals↗