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Shin-ichi Nakamura

Publications and source records attributed to Shin-ichi Nakamura.

At least 19 recordsLinked to original sources
PubMed2006

A putative acyl-CoA-binding protein is a major phloem sap protein in rice (Oryza sativa L.).

The N-terminal amino-acid sequence of a major rice phloem-sap protein, named RPP10, was determined. RPP10 is encoded by a single gene in the rice genome. Its complete amino-acid sequence, predicted from the corresponding rice full-length cDNA, showed high similarity to plant acyl-CoA-binding proteins (ACBPs). Western blot analysis using anti-ACBP antiserum revealed that putative ACBP is abundant in the phloem sap of rice plants, and is also present in sieve-tube exudates of winter squash (Cucurbita maxima), oilseed rape (Brassica napus), and coconut palm (Cocos nucifera). These findings give rise to the idea that ACBP may involve lipid metabolism and regulation in the phloem.

Acyl Coenzyme A↗
PubMed2006

Clinicopathological significance of loss of heterozygosity in intestinal- and solid-type gastric carcinomas: a comprehensive study using the crypt isolation technique.

The clinicopathological significance of loss of heterozygosity (LOH) in gastric carcinoma remains poorly understood. We and other researchers have previously demonstrated that LOH is fairly common in intestinal- and solid-type gastric carcinomas, but rare in diffuse-type tumors. In this study, we investigated the relationship between clinicopathological variables and LOH status in intestinal- and solid-type gastric carcinomas. The crypt isolation technique was utilized to analyze LOH at 1p36, 3p14, 4p15, 5q21-22, 8p11-12, 9p21, 13q22, 17p13.1 18q21 and 22q13.31 in 113 intestinal- and solid-type gastric carcinomas using a polymerase chain reaction assay. Immunostaining with D2-40 and Elastica van Gieson staining were used to detect lymphatic invasion and vessel invasion, respectively. High LOH rates (49-71%) were observed in all chromosomal regions tested. 1p36 loss was significantly associated with advanced tumors and lymph node metastasis. 8p11-12 loss was significantly associated with lymph node metastasis, lymphatic invasion, and vessel invasion. 17p13.1 (TP53) loss was significantly associated with vessel invasion. 22q13.31 loss was significantly associated with advanced tumors, lymph node metastasis, lymphatic invasion, vessel invasion and late TNM stage. No significant associations were observed between LOH at other chromosomal regions and aggressive behaviors. In addition, significantly higher LOH rates at 1p36, 9p21, 18q21 and 22q13.31 were observed in cardiac tumors compared with noncardiac tumors. These results suggest that in intestinal- and solid-type gastric carcinomas, LOH on 3p14, 4p15, 5q21-22, 9p21, 13q22 and 18q21 is associated with carcinogenesis, while LOH on 1p36, 8p11-12, 17p31.1 and 22q13.31 is associated with tumor progression.

Adult↗
PubMed2006

Analysis of molecular alterations in left- and right-sided colorectal carcinomas reveals distinct pathways of carcinogenesis: proposal for new molecular profile of colorectal carcinomas.

To clarify distinct genetic profiles of colorectal cancers based on tumor location (left- and right-sided), we evaluated the status of loss of heterozygosity (LOH), CpG islands methylation phenotype (CIMP), microsatellite instability (MSI), and mutations of p53, Ki-ras, and APC genes in 119 colorectal cancers. Statuses of LOH (at 5q, 8p, 17p, 18q, and 22q), MSI, and CIMP (MINT1, MINT2, MINT31, MLH-1, MGMT, p14, p16, and RASSF1A) were determined using microsatellite polymerase chain reaction and methylation-specific polymerase chain reaction coupled with a crypt isolation method, respectively. In addition, mutations of p53, Ki-ras, and APC genes were also examined. LOH, MSI, and CIMP status allowed us to classify samples into two groups: low or negative and high or positive. Whereas the frequency of p53 mutations in the LOH-high status was significantly higher in left-sided cancers than in right-sided cancers, CIMP-high in the LOH-high status and MSI-positive status were more frequently found in right-sided cancers compared with left-sided cancers. Finally, location-specific methylated loci were seen in colorectal cancers: type I (dominant in right-sided cancer) and type II (common in both segments of cancer). Our data confirm that distinct molecular pathways to colorectal cancer dominate in the left and right sides of the bowel.

Aged↗
PubMed2005

Mapping of the methylation pattern of the MUC2 promoter in pancreatic cancer cell lines, using bisulfite genomic sequencing.

Expression of the MUC2 gene is controlled by the methylation of CpG sites in the promoter region, but the detailed methylation status of this region has yet to be reported. We have mapped the complete methylation status of the MUC2 promoter from position -1989 to position +288 upstream, a region that contains 59 CpG sites, using bisulfite genomic sequencing in two pancreatic cancer cell lines (PANC1, BxPC3) and in isolated normal colon crypts as a control. The MUC2 promoter in PANC1, a cell line that does not express MUC2, was highly methylated (average 87%, complete methylation at 28 of the 59 CpG sites), while the promoter region in the MUC2-expressing BxPC3 cell line (average 43%, complete methylation at 2 of 59 CpG sites) and in MUC2-expressing normal colon crypts (average 33%, no CpG site was completely methylated) were only partially methylated (P<0.0001). 5-Aza-2'-deoxycytidine treatment of PANC1 cells reduced the methylation level (average 36%) and induced MUC2 mRNA expression. However, mRNA expression of AP2, SP1 and CDX2 was not affected by this treatment. Our data provide the first detailed methylation map of the MUC2 promoter region for the first time, using the conversion-specific bisulfite genomic sequencing. Previously unproven methylation sites were detected, and some AP2 and SP1 binding sites showed different methylation levels among PANC1, BxPC3 and colonic crypt cells. Our mapping data provide an essential basis for further studies of methylation-regulated MUC2 inactivation.

Azacitidine↗
PubMed2005

Ruptured vertebral artery dissecting aneurysm followed by spontaneous acute occlusion and early recanalization: case report.

A 47-year-old man presented with a ruptured vertebral artery dissecting aneurysm manifesting as subarachnoid hemorrhage followed by acute occlusion and early recanalization of the affected artery. Cerebral angiography 2 hours after the onset of the symptom showed pearl-and-string sign in the right vertebral artery. Serial angiography showed that the affected artery was occluded at 12 hours but was recanalized on the 4th day. The dissecting aneurysm was resected with side-to-side anastomosis between the bilateral posterior inferior cerebellar arteries. Postoperative cerebral angiography demonstrated disappearance of the lesion and patency of the right posterior inferior cerebellar artery via the anastomosis. Histological examination of the lesion showed hematoma between the media and adventitia, disrupting the internal elastica and intima. Acute occlusion and early recanalization of the affected artery may occur in ruptured vertebral artery dissecting aneurysms. Serial neurological and neuroradiological examinations are essential to decide the timing and method of treatment.

Acute Disease↗
PubMed2005

[Assessment of dihydropyrimidine dehydrogenase and thymidylate synthase expression in gastric carcinoma and colonic carcinoma].

We measured DPD activity and TS content in cancer and normal mucosa obtained from 23 patients with colorectal carcinoma and 7 patients with gastric carcinoma. DPD activity in colorectal carcinoma cases was significantly decreased in cancer tissues compared to those in adjacent normal mucosa (p<0.001), while TS content was significantly increased in cancer tissues (p<0.01). No significant correlation was found between cancer and adjacent normal mucosa in DPD activity and TS content of gastric carcinoma cases. Immunohistochemically, DPD and TS overexpression were found in 11 out of 23 patients (47.8%) and 3 out of 23 patients (13%) in colorectal carcinoma cases, respectively. In gastric carcinoma cases, DPD and TS overexpression were found in 3 out of 7 patients (42.9%) and 3 out of 7 patients (42.9%), respectively. No significant correlation was found between quantitative measurement and immunohistochemical overexpression in colorectal and gastric carcinoma cases. DPD and TS protein were partially overexpressed in some cases. Heterogeneity of the tumor is thought to be one of the reasons for the discrepancy between quantitative measurement and immunohistochemical overexpression.

Aged↗
PubMed2004

Pigmented pleomorphic adenoma, a novel melanin-pigmented benign salivary gland tumor.

This paper reports a pleomorphic adenoma with grossly visible pigmentation resulting in the macroscopic appearance of melanotic lesion in a 33-year-old Japanese male. In addition to the characteristic histopathological features of a benign pleomorphic adenoma, variously formed and -sized cells, many of which were considered to be melanocytes, containing melanin pigment in their cytoplasm, were distributed in the epithelial component. In addition, melanin pigment was deposited in tumor cells of duct structures. Furthermore, condensed secretory substances with marked pigmentation were frequently seen in the tubular lumina. Perusal of the English language literature revealed only two cases of parenchymal pigmentation of salivary gland tumors: both were mucoepidermoid carcinoma. The possible histogenesis of melanocytes in the salivary gland lesions is discussed, though no firm conclusion could be drawn.

Adenoma, Pleomorphic↗
PubMed2004

Three independent genetic profiles based on mucin expression in early differentiated-type gastric cancers--a new concept of genetic carcinogenesis of early differentiated-type adenocarcinomas.

Recent molecular studies have shown that the genetic profiles of differentiated-type adenocarcinomas of the stomach are associated with distinct cellular mucin phenotypes (gastric- intestinal- and mixed-phenotypes). Therefore, we examined whether these cellular mucin phenotypes reflect specific molecular genetic alterations, and whether the phenotypes can be used to help categorize the intramucosal neoplasias of gastric tumors. We subclassified tumors into four cellular phenotypes using immunohistochemical mucin analysis. In all, 62 early gastric carcinomas (gastric-phenotype, 13; intestinal-phenotype, 17; mixed-phenotype, 31; unclassified-phenotype, 1) were examined using a combination of polymerase chain reaction microsatellite assays and immunohistochemical analysis in order to detect chromosomal allelic losses of multiple cancer-related chromosomal loci (1p, 3p. 4p, 5q, 8p, 9p, 13p, 17p, 18q and 22q), microsatellite instability (MSI), and overexpression of the p53 protein. In addition, we analyzed the relationship between MSI status and hMLH1 promoter hypermethylation, which is thought to be a cause of high MSI status. For gastric phenotype cancers, the frequency of 3p allelic loss was higher than that of other microsatellite markers, whereas 5q allelic loss was frequently found in intestinal phenotype cancers. The genetic profile of mixed phenotype cancers is comprised of two distinct genetic types: LOH and MSI types. In the former, 5q, 3p and 18q allelic losses are seen frequently in intramucosal carcinomas. On the other hand, 17p, 1p and 9p allelic losses are associated with the development of submucosal carcinomas. MSI was observed only in mixed phenotype cancers (six of 31 mixed phenotype cancers). Overexpression of the p53 protein is common in differentiated-type gastric cancers. In addition, the MSI status of the tumor cells was correlated with the extent of hypermethylation of the hMLH1 promoter. We suggest that the cellular mucin phenotypes of the differentiated-type adenocarcinomas result from distinct genetic alterations.

Adaptor Proteins, Signal Transducing↗
PubMed2004

[Reporting system in surgical pathology].

The questionnaire survey on quality assurance in pathology departments and certified hospitals was performed by Japanese Society of Pathology in 2001 and it showed that most institutions do not have guidelines for the reporting system. In this paper, how to write histopathology reports is described. The reports are composed of 1) clinical data, 2) pathology data, 3) macroscopic findings, 4) microscopic findings, 5) diagnoses, and 6) comments. Neither of the components should be made light of. We also describe the results of questionnaire survey on histopathology reports we performed.

Cytodiagnosis↗
PubMed2003

Polymorphism in glutamate-cysteine ligase modifier subunit gene is associated with impairment of nitric oxide-mediated coronary vasomotor function.

BACKGROUND: The minor -588T allele of polymorphism -588C/T of a modifier subunit gene in glutamate-cysteine ligase (GCLM), a rate-limiting enzyme for glutathione (GSH) synthesis, was associated with lower plasma GSH levels and was a risk factor for myocardial infarction. METHODS AND RESULTS: We examined effects of the -588C/T polymorphism on coronary arterial diameter and blood flow responses to intracoronary infusion of acetylcholine in 157 consecutive subjects who had normal coronary angiograms. In multivariate linear regression analysis with covariates including traditional risk factors, the minor -588T allele had an independent association with impaired dilation or enhanced constriction of epicardial coronary arteries in response to acetylcholine, and it was independently associated with blunted increase in coronary flow response to acetylcholine. In a subgroup of 59 consecutive subjects, constrictor responses of epicardial coronary diameter to intracoronary infusion of NG-monomethyl-l-arginine, reflecting the presence of coronary nitric oxide (NO) bioactivity, had an inverse and independent association with the -588T allele in multivariate analysis. CONCLUSIONS: The -588T polymorphism of the GCLM gene causes a decrease in endothelial NO bioactivity, leading to impairment of endothelium-dependent vasomotor function in large and resistance coronary arteries. The GCL-GSH-NO axis may play a role in the defense system against coronary artery disease.

5' Flanking Region↗
PubMed2003

Association of polymorphism in glutamate-cysteine ligase catalytic subunit gene with coronary vasomotor dysfunction and myocardial infarction.

OBJECTIVES: The purpose of this study was to test the hypothesis that polymorphisms in the promoter region of the glutamate-cysteine ligase catalytic subunit (GCLC) gene may be associated with coronary endothelial vasomotor dysfunction and myocardial infarction (MI). BACKGROUND: Glutamate-cysteine ligase is a rate-limiting enzyme for synthesis of glutathione (GSH) that plays a crucial role in the intracellular antioxidant defense systems. Oxidants transcriptionally upregulate the GCLC gene for GSH synthesis, providing a protective mechanism against oxidant-induced endothelial dysfunction or activation, which plays a pathogenetic role in cardiovascular diseases. METHODS: The association of the possible polymorphisms with coronary arterial diameter responses to acetylcholine was determined in 62 male subjects. The frequency of polymorphisms was compared between 255 male patients with MI and 179 male control subjects. RESULTS: We found a polymorphism (-129C/T) in which the T allele showed lower promoter activity (50% to 60% of the activity of the C allele) in response to H(2)O(2) in human endothelial cells. Endothelium-dependent dilation of coronary arteries was impaired in subjects with the -129T allele (n = 31), as compared with the age-matched subjects without the -129T allele (n = 31). The T allele was highly frequent in patients with MI as compared with control subjects, and it was a significant risk factor for MI, independent of traditional coronary risk factors (odds ratio [OR] 1.81, 95% confidence interval [CI] 1.08 to 3.03; p = 0.03). CONCLUSIONS: The -129T polymorphism of the GCLC gene may suppress the GCLC gene induction response to an oxidant, and it is implicated in coronary endothelial vasomotor dysfunction and MI.

Adult↗
PubMed2003

Analysis of genetic alterations, classified according to their DNA ploidy pattern, in the progression of colorectal adenomas and early colorectal carcinomas.

DNA aneuploidy is a biological marker of the oncogenic potential of colorectal adenomas. The accumulation of genetic alterations of cancer-related genes is also essential for colorectal carcinogenesis. However, it is unclear whether there is any relationship between these genetic alterations and the DNA ploidy of colon tumour cells in the progression of colorectal adenomas and early colorectal carcinomas. Here we have studied the DNA ploidy state and genetic alterations occurring in colorectal tumours using the crypt isolation technique. Crypts isolated from a total of 106 colorectal tumors (adenoma, 93; early carcinoma, 13) were examined using a combination of flow cytometric analysis of DNA content, polymerase chain reaction-microsatellite assay, and single-strand conformation polymorphism assay for evidence of chromosomal allelic imbalance (AI; 17p; 5q; 18q) or p53 gene mutation. In addition, we examined microsatellite instability (MSI) with BAT 26 primer sets. DNA multiploidy was infrequently detected in colorectal adenomas (15.1%), in contrast to early carcinomas (46.2%). There was a significant difference in the incidence of AI of chromosome 18q between diploid adenomas and aneuploid populations of multiploid adenomas (18.1% vs 57.1%, p = 0.0043). Mutation of p53 was also found more frequently in aneuploid populations of early multiploid colorectal carcinomas than in early diploid colorectal carcinomas (66.7% vs 0%, p = 0.021). MSI was found in only 2 of 93 adenomas, with no MSI detected in early colorectal cancers. The two MSI-positive adenomas were diploid. We subdivided multiploid adenomas into two groups: those with a low or a high DNA index (DI). The incidence of genetic alterations of high-DI adenomas did not differ from those of low-DI adenomas. Allelic imbalance involving loci on chromosome 18q and mutations of p53 seems to be associated with the progression of diploidy to multiploidy in colorectal tumours. On the other hand, MSI may be associated with the development of some diploid tumours. In addition, the incidence of genetic alterations in the colorectal adenomas that we examined appears to be independent of the tumour's DNA index.

Adenoma↗
PubMed2003

Sialolith of the submandibular gland with bone formation.

An unusual case of sialolith with bone formation, occurring in the submandibular gland of a 33-year-old woman, is reported. In addition to the irregularly laminated structure of sialolith, sparsely scattered foci of bone tissue were found. Some of them were mature, lamellar bone with lacunae containing osteocytes, endosteum and a bone marrow-like element. Others were immature bone associated with or without multinucleated giant cells. Foci of bone tissue were in contact with caliculi or fibrous tissue, and no epithelial component was seen around them. These observations suggest that bone formation in the present case may be in the nature of pathological ossification, and that in the earlier stage, the bone that is deposited is woven and is replaced through successive remodeling cycles by lamellar bone. This is the first case of sialolith with bone formation, although sialolithiasis is a common disease of the salivary glands.

Adult↗
PubMed2003

Adenoma, adenocarcinoma and mixed carcinoid-adenocarcinoma arising in a small lesion of the colon.

A unique tumor measuring 8 x 8 x 5 mm and composed of adenoma, adenocarcinoma and mixed carcinoid-adenocarcinoma arising in the ascending colon is reported. The mixed carcinoid-adenocarcinoma, in which adenocarcinomatous and carcinoid components intermingled, originated in the mucosa, penetrated the muscularis mucosa and extended into the submucosa. Immunohistochemically, carcinoid cells were positive for neuroendocrine markers and adenocarcinoma cells were intracytoplasmicly positive for carcinoembryonic antigen. Ultrastructurally, membrane-bound electron dense granules varying in shape, size and electron density were detected in the cytoplasm of carcinoid cells. No mutations of p53 and k-ras genes were detected in adenomatous, adenocarcinomatous or mixed carcinoid-adenocarcinoma components. The morphological appearances of the present case strongly suggests the histogenesis of this tumor in an adenoma-adenocarcinoma-carcinoid tumor sequence.

Adenocarcinoma↗
PubMed2003

Latent form of multiple dermoid cysts in the jaw bone.

Dermoid cysts of the jaw are exceedingly rare, and only six such cases have been documented. The present paper reports a case with multiple microcysts showing histological characteristics of dermoid cyst in the surgically resected mandibular bone. These cysts were located near the inferior border of the mandibular bone, and histologically composed of an inner thin layer of squamous epithelium with marked hyperorthokeratinization and an outer layer of fibrous tissue containing numerous mature sebaceous glands. In addition, a hair follicle-like epithelial sphere was seen in part. The present microcysts suggest that it arises de novo, and one possible cause of jaw cysts could be sequestration of the stomadeal ectoderm that may have been trapped deep in the surface and embedded in the developing mandibular bone during embryogenesis. It may not be possible that such cysts developed from the odontogenic epithelial remnant undergoing dermoid metaplasia.

Adult↗
PubMed2003

Analysis of Ki-ras and p53 gene mutations in laterally spreading tumors of the colorectum.

A laterally spreading tumor (LST) is considered to be a specific subtype of superficial colorectal tumors, in view of its characteristic clinicopathological features. We attempted to compare genetic alterations found in LST (>10 mm) with those found in IIa-type adenomas (10 mm or less (small superficial elevated lesion)) and conventional polypoid adenomas (>10 mm). In addition, multiple sampling by microdissection was performed for 14 LST to examine genetic heterogeneity in the Ki-ras and p53 gene mutation patterns. Polymerase chain reaction, single-strand conformation polymorphism and direct sequencing were used to analyze Ki-ras and p53 gene mutations in 73 sporadic colorectal adenomas: 28 LST; 22 IIa-type adenomas; and 23 polypoid adenomas. Ki-ras gene mutations were found more frequently in LST (6/28 tumors) and polypoid adenomas (6/23 tumors) than in IIa-type adenomas (2/22 tumors), although this difference was not statistically significant. The frequency of p53 gene mutations in the 28 LST was 25% (7/28), which was significantly higher than that found in IIa-type adenomas (P < 0.05). However, although p53 gene mutations were found more frequently in LST than in polypoid adenomas, this difference was not statistically significant. Seven LST exhibited a combination of wild-type and mutant-type tumor cells having the p53 gene mutation pattern, whereas a pattern of different Ki-ras gene mutations was found in two of three LST that exhibited Ki-ras gene mutation heterogeneity. We suggest that the LST exhibited a characteristic pattern in terms of the Ki-ras as well as the p53 gene mutation pattern, thereby supporting the hypothesis that LST is a specific subtype of colorectal tumors.

Adenoma, Villous↗