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Biomedical subjects

R Satodate

Publications and source records attributed to R Satodate.

At least 55 records · Page 3Linked to original sources
PubMed1995

Ceroid pigment deposition in circulating blood monocytes and T lymphocytes in Hermansky-Pudlak syndrome: an ultrastructural study.

An electron microscopic study of peripheral leukocytes obtained from a 39 year old woman with Hermansky-Pudlak syndrome was performed. Ceroid pigment granules were found within the lysosomes in 3.5% of monocytes and 5.4% of lymphocytes. Infrequently, pigment granules were also found in the parallel tubular arrays of lymphocytes. The lymphocytes containing ceroid pigment granules were confirmed to be T cells by immunoelectron microscopy. It was speculated that intralysosomal accumulation of ceroid pigment granules in Hermansky-Pudlak syndrome may be due to lysosomal dysfunction.

Adult↗
PubMed1995

Structural characteristic of splenic sinuses in idiopathic portal hypertension.

Splenic sinuses in idiopathic portal hypertension (IPH; 8 patients), liver cirrhosis (LC; 14 patients) and in regenerating autotransplanted spleens from 25 rats were compared with each other by scanning electron microscopy (SEM) and immunohistochemistry using antibodies against proliferating cell nuclear antigen (PCNA). Spleens obtained from six patients with gastric carcinoma and from five untreated adult rats were examined as controls. SEM of the sinuses showed that in IPH endothelial cells became irregular in shape, and the interendothelial slits of sinuses were irregularly enlarged. Sinus endothelial processes traversing the sinusal lumen were also found. The same changes were observed in the proliferating sinuses during regeneration of splenic tissue after autotransplantation in rats, but disappeared when the regeneration was completed. Irregular endothelial cells were few in LC. PCNA-positive sinus endothelial cells were increased in number in IPH as compared with those in LC; the mean number of PCNA-positive ones per cm2 was 45.4 in IPH and 8.2 in LC. It was suggested that, from SEM observation of sinus endothelial cells and counting PCNA-positive sinus endothelial cells, the sinuses of the spleen in IPH consist of proliferating endothelial cells or are in the state of increased proliferation. In conclusion, splenomegaly in IPH was presumed to be caused by proliferation of sinus endothelial cells, and by the increased splenic blood flow in the irregularly widened interendothelial slits of the sinuses.

Adult↗
PubMed1994

Aberrations of tumor-suppressor genes (p53, apc, mcc and Rb) in esophageal squamous-cell carcinoma.

Loss of heterozygosity at 4 tumor-suppressor gene loci (p53, apc, mcc and Rb) was investigated using polymerase chain reactions, in 49 esophageal squamous-cell carcinoma specimens from patients who had undergone curative resection. Mutations in the p53 gene within exons 5 to 8 were also examined. LOH was detected in 9 (43%) of 21 p53 genes, 16 (55%) of 29 apc genes, 10 (48%) of 21 mcc genes, and 13 (52%) of 25 Rb genes for which heterozygosity could be determined. Mutations in the p53 gene were detected in 18 (36%) of 49 cases and were significantly more frequent in stage-III tumors and in tumors exhibiting DNA aneuploidy. In 5 cases where heterozygosity could be determined for all the loci, all had 2 or more aberrations. Additionally, a heterozygous deletion of p53 gene was associated with a mutation of the remaining allele in 8 (89%) of 9 cases. Short-term relapse within 3 to 12 months occurred significantly more frequently in patients having tumors with both p53 aberrations (p < 0.05). Thus, aberration of tumor-suppressor genes was a frequent occurrence in esophageal squamous-cell carcinoma and inactivation of the p53 gene may contribute to the progression of this tumor.

Aged↗
PubMed1994

Mutations of the APC gene occur during early stages of gastric adenoma development.

Mutations of the adenomatous polyposis coli (APC) gene have recently been shown to play an important role in colorectal tumorigenesis. We investigated mutations of the APC gene in 30 gastric adenomas obtained endoscopically. Mutations of the APC gene were examined by polymerase chain reaction-single-strand conformation polymorphism analysis followed by sequencing of the polymerase chain reaction products. Mutations were detected in 20% (6 of 30) of gastric adenomas. In addition, deletion of the remaining allele that subsequently led to complete inactivation of the APC gene was confirmed in one-half (3 of 6) of the tumors with APC gene mutations. Sequencing analysis confirmed that the mutations resulted in truncation of the gene products or in an amino acid change. The incidences of mutations of the APC gene remained constant regardless of the size or degree of histological atypia. Our observations suggest that mutations of the APC gene, similarly to those in colorectal tumorigenesis, occur during the early stages of gastric adenoma development.

Adenoma↗
PubMed1994

Lack of mutations of the adenomatous polyposis coli gene in oesophageal and gastric carcinomas.

The adenomatous polyposis coli (APC) gene is the target of the loss of chromosome 5q heterozygosity observed frequently in gastrointestinal tract carcinomas and is inactivated in these carcinomas. We screened 94 gastrointestinal tract carcinomas for APC mutations, by polymerase chain reaction single-strand conformation polymorphism (SSCP) analysis. Mutations were detected in 8 of 21 (38%) colorectal carcinomas in the mutation cluster region of the APC gene whereas no mutation was detected in any of 49 oesophageal and 24 gastric carcinomas, even though SSCP analysis was extended to include the 5' half of the APC gene exon 15. Direct DNA sequencing revealed that six of eight (75%) mutations in colorectal carcinomas resulted in truncated gene products. These findings confirm the significance of APC gene mutations in colorectal, but not oesophageal or gastric carcinomas. Some other tumour suppressor genes near the APC gene may be the target of the frequent allelic loss of chromosome 5q in oesophageal and gastric carcinomas.

Base Sequence↗
PubMed1994

Enteroviral RNA in dilated cardiomyopathy.

The exact cause of dilated cardiomyopathy (DCM) remains uncertain. However, a possibility of transition from coxsackievirus-infected myocarditis to DCM has been suspected. We investigated the role of enteroviral infection in the pathogenesis of DCM. The nested reverse transcriptase polymerase chain reaction (nRT-PCR) was used to detect enteroviral RNA in 45 endomyocardial biopsy tissues obtained from 35 patients with DCM and 10 patients (controls) with other non-infectious cardiac diseases. Enteroviral RNA was detected in 17 (49%) of the 35 patients with DCM. The progression to cardiac failure was rapid, usually within 12 months, and myocardial fibrosis and myocytic hypertrophy were marked in patients that were enteroviral RNA positive. Enteroviral RNA was not detected in any controls.

Base Sequence↗
PubMed1994

Improved detection of loss of heterozygosity at retinoblastoma gene locus in human breast carcinoma.

Loss of heterozygosity (LOH) at the retinoblastoma (Rb) gene locus was investigated in 33 breast carcinomas by polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) analysis after tumor cell enrichment by cell sorting. The efficacy of cell sorting was evaluated by comparing the results of PCR-SSCP with and without cell sorting. Ten of 17 (59%) informative cases showed LOH at this locus by cell sorting combined with PCR-SSCP, although LOH was detectable in six (35%) cases without cell sorting. Flow cytometry and histologic examination revealed that this underestimation may occur when the tumor cell population is less than 50% in the specimens analyzed. It is concluded that LOH of the Rb gene occurs more frequently in human breast carcinoma than previously thought, and thus may contribute significantly to the development and/or progression of this tumor.

Adenocarcinoma↗
PubMed1994

Ultrasonographic findings of epididymal sarcoidosis.

We report a rare case of systemic sarcoidosis involving the epididymis. An irregularly shaped heterogeneous lesion was identified with ultrasonography in the left caput epididymidis. Microscopically, a number of noncaseating epithelioid cell granulomas were found in the epididymal tissue.

Adult↗
PubMed1994

Analysis of genetic alterations in renal cell carcinoma using the polymerase chain reaction.

Very frequent loss of heterozygosity (LOH) on chromosome 3p has been found in human renal cell carcinoma (RCC). In the present study, we examined LOH at the retinoblastoma (RB), mutated in colorectal cancer (MCC) and adenomatous polyposis coli (APC) tumour suppressor genes loci, and mutations of the H-, K-, and N-ras oncogenes. We performed these studies using the polymerase chain reaction (PCR) method followed by restriction fragment length polymorphism (RFLP) and single-strand conformation polymorphism (SSCP) analyses. LOH was detected in 2 of 11 (18.2%), and 2 of 14 (14.3%) informative cases at the MCC and APC loci, respectively, and in none of 15 informative cases at the RB locus in 25 RCCs. LOH at the MCC was accompanied by LOH at the APC locus in two RCCs. No mutation was detected in H-, K-, and N-ras genes in 39 RCCs. Thus, alterations of the known tumour suppressor genes and the ras oncogenes were infrequent events in RCC. The results suggest that the genetic pathway in the genesis of RCC differs considerably from that of other common human carcinomas.

Adult↗
PubMed1993

Adenomyoepithelioma (myoepithelioma) of the breast in a male.

Adenomyoepithelioma (myoepithelioma) of the breast in a 47-year-old man is reported. The tumor consisted of a prominent proliferation of spindle cells surrounding mammary ducts. Immunohistochemical and electron microscopic observations confirmed the myoepithelial origin of these spindle cells. This is the first report of an adenomyoepithelioma of the breast that developed in a male.

Breast Neoplasms↗
PubMed1993

Primary gastric carcinoma cells frequently lose heterozygosity at the APC and MCC genetic loci.

Loss of heterozygosity (LOH) at APC and MCC gene loci (both mapped to 5q21) was investigated in 24 surgical specimens of primary gastric carcinomas using the polymerase chain reaction after tumor cell enrichment by cell sorting based on differences in DNA content. LOH at APC and/or MCC was detected in 87% (13/15) of the cases; at the APC in 86% (12/14) and at the MCC locus in 100% (7/7). LOH at the APC locus was always accompanied by LOH at the MCC locus. LOH at the APC and/or MCC was found in both differentiated and undifferentiated types in both early and advanced stages of gastric carcinoma. Thus, LOH at APC and/or MCC is considered to be one of the most prevalent genetic alterations in human gastric carcinoma and occurs at an early stage of the carcinogenesis.

Base Sequence↗
PubMed1993

Quantitative assessment of a change of hemosiderin deposition with age in splenic compartments of rats.

Hemosiderin deposition was quantitatively estimated in paraffin sections stained using Perls' iron reaction in the spleens of untreated male rats aged from 0 to 28 months. Hemosiderin was deposited in the periarteriolar lymphocyte sheath (PALS), lymph follicles, and marginal zone, as well as in the red pulp which was the main compartment of hemosiderin deposition. Special attention was paid to the PALS and marginal zone. Marked hemosiderin deposition was evident from 4 months, although only few hemosiderin-laden macrophages appeared in the first 3 months. Hemosiderin deposition peaked at 12 months in the red pulp and at 20 months in the white pulp and marginal zone. The deposition in the white pulp and marginal zone was about 1/9 to 1/4 of that in the red pulp. A few hemosiderin-laden macrophages were found in the lymph follicles after 2 months. In the periarterial region of the splenic hilus, deposition of hemosiderin granules was observed even at 1 month when there was little hemosiderin deposition elsewhere. Since no arteries open there, the presence of hemosiderin-laden macrophages in the PALS and lymph follicles suggested movement of some macrophages from the red pulp and/or the marginal zone. In addition, hemosiderin deposition in the PALS increased with age after it decreased in the other compartments.

Aging↗
PubMed1993

Quantitative measurement of hemosiderin deposition in tissue sections of the liver by image analysis.

Hemosiderin has been quantitated in tissue sections by image analysis employing Perls' Berlin blue reaction. A linear correlation was observed between the mean optical density of the tissue section measured with a commercial image analyzer and the iron concentration measured with an atomic absorption spectrophotometer. The correlation coefficient of .945 (P < .001) indicated that a linear correlation existed between these measurements. Thus, the hemosiderin volume in tissue sections can be measured quantitatively by image analysis.

Hemosiderin↗
PubMed1992

Prognostic assessment of superficial squamous cell carcinoma of the esophagus using karyometric analysis and nucleolar organizer regions.

To investigate prognostic values for squamous cell carcinoma, we measured nuclear area (NA), nuclear shape factor (NSF), DNA content and mean number of nucleolar organizer regions (NOR), using formalin-fixed, paraffin-embedded tissue sections from 39 patients with superficial squamous cell carcinoma of the esophagus. NA and DNA content were significantly higher in patients with lymph node metastasis than in those without metastasis. NA and the NOR number were also significantly higher in patients with recurrence than in those surviving for more than 3 years without recurrence. To determine the optimal combination of these parameters for prognostic assessment, we used a stepwise discriminant analysis to obtain two linear discriminant functions. One (f = 0.331 x NA + 6.64 x NSF + 9.85) gave an accuracy of 87.2% in predicting lymph node metastasis, and the other (f = -0.071 x NA - 2.34 x NOR + 13.0) yielded an overall accuracy of 88.9% in classifying patients into two groups with a better and worse prognosis. These results suggest that karyometric analysis and determination of the NOR number are useful for the prediction of disease outcome in patients with superficial squamous cell carcinoma of the esophagus.

Aged↗
PubMed1992

Infrequent mutation of p53 gene in human renal cell carcinoma detected by polymerase chain reaction single-strand conformation polymorphism analysis.

Mutation of the p53 gene, which plays an important role in the genesis of diverse human cancers, was investigated in 23 surgical specimens of human renal cell carcinoma using the polymerase chain reaction single-strand conformation polymorphism method of analysis. Only one of the 23 tumors (4.3%) carried a mutated p53 gene, which was present in exons 7-8. Direct DNA sequencing confirmed a point mutation at codon 276 (GCC to CCC) resulting in a substitution of alanine for proline. No specific clinicopathological characteristics were observed in the case with the p53 gene mutation in human renal cell carcinoma. These observations suggest that mutation of the p53 gene is rare and thus does not contribute significantly to the genesis of this tumor.

Amino Acid Sequence↗
PubMed1992

p53 gene mutations in esophageal cancer detected by polymerase chain reaction single-strand conformation polymorphism analysis.

Mutations of the p53 gene play an important role in the development of common human malignancies. We investigated mutations of this gene in 26 surgical specimens of esophageal cancer using the polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) analysis. The results were correlated with histological findings, DNA ploidy and the short-term relapse of the disease. PCR-SSCP analysis detected mutations of the p53 gene in 10 tumors (38%), eight in exons 5-6 and two in exons 7-8. A higher incidence of lymph node metastasis, poorly differentiated tumor, DNA aneuploidy and short-term relapse of the disease was observed in cases with p53 gene mutations, although the findings were not statistically significant.

Base Sequence↗
PubMed1992

Sensitive detection of p53 gene mutations in esophageal endoscopic biopsy specimens by cell sorting combined with polymerase chain reaction single-strand conformation polymorphism analysis.

For the rapid and sensitive detection of p53 gene mutations in esophageal endoscopic biopsy specimens, we combined cell sorting with the polymerase chain reaction and single-strand conformation polymorphism (PCR-SSCP) analysis. Mutations in exons 5-8 of the p53 gene were investigated by PCR-SSCP analysis using 10(3) sorted nuclei obtained from each endoscopic biopsy specimen of 16 patients with esophageal cancer. DNAs extracted from their respective surgical specimens were investigated by a conventional method of PCR-SSCP analysis. Mutations in the biopsy specimens were detected in 6 of the 12 aneuploid tumors but in none of the 4 diploid tumors. After tumor cell enrichment by cell sorting, one mutation in exon 8 became apparent, which could not be detected from the surgical specimen by a conventional method of PCR-SSCP analysis. This method should improve the sensitivity of detecting p53 gene mutations, and provides additional information concerning the DNA ploidy pattern in the tumors.

Aged↗