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Biomedical subjects

H Saisho

Publications and source records attributed to H Saisho.

At least 91 records · Page 5Linked to original sources
PubMed1998

The two different states of hepatitis B virus DNA in asymptomatic carriers: HBe-antigen-positive versus anti-HBe-positive asymptomatic carriers.

During the course of hepatitis B virus (HBV) infection, there exists a long period of normal liver function tests with different states of HBeAg/Ab. As the state of HBV in asymptomatic carriers was not well characterized, we quantitatively and qualitatively examined HBV in both HBeAg-positive and anti-HBe-positive asymptomatic carriers. Sera from 10 HBeAg-positive and 27 anti-HBe-positive asymptomatic carriers were analyzed. The amount of HBV DNA was determined by dot-blot hybridization and polymerase chain reaction. The mutations in precore and core regions, spanning 636 nucleotides, of hepatitis B virus were examined by directly sequencing the amplified HBV DNA. HBV DNA was detected in all 10 HBeAg-positive cases, whereas it was found in only 7 of 27 (26%) anti-HBe-positive cases by the nested PCR method. The mean amount of HBV DNA in HBeAg-positive cases was 10(9.1 +/- 0.7) copies/ml, while that in anti-HBe-positive cases was 10(1.0 +/- 1.5) copies/ml. There were no missense mutations in the entire precore and core genes of HBV DNA taken from HBeAg-positive asymptomatic carriers. In contrast, many mutations (mean 9.0 +/- 3.3, range 6-14) were detected in the core gene of seven anti-HBe-positive asymptomatic carriers including two cases with increments of the mutations. Analysis of the precore region revealed three wild-type and four mutant-type (including one coexisting with wild-type) cases. These data suggest that HBV exists in quite different ways in "asymptomatic" carriers; in the HBeAg-positive phase HBV probably coexists with the host and remains as the wild type, whereas in the anti-HBe-positive phase a drastically reduced amount of HBV with many mutations remains, probably as a consequence of the long-lasting interaction with the host. Nevertheless, such small amount of virus could cause fulminant hepatic failure. It is important to make further clinical and virological investigations in order to understand the state of asymptomatic carrier.

Adult↗
PubMed1998

Expression of p53 and p21WAF1/CIP1 proteins in gastric and esophageal cancers: comparison with mutations of the p53 gene.

The p53 gene has been shown to be commonly mutated in various human cancers, and mutant p53 can act as a dominant oncogene. The intact p53 protein is also known to induce the cyclin-dependent kinase inhibitor p21WAF1/CIP1 and is implicated in cell cycle arrest. We investigated p53 gene alterations in gastric adenocarcinoma and esophageal squamous cell carcinoma to elucidate the association of the nuclear accumulation of the p53 protein and/or p21WAF1/CIP1 protein. Abnormalities of the tumor suppressor gene p53 protein and the expression of p21WAF1/CIP1 protein were analyzed by immunohistochemical techniques in 32 cases of gastric adenocarcinoma and 15 cases of esophageal squamous cell carcinoma. Twenty cases of gastric cancer and five cases of esophageal cancer were also analyzed for p53 gene mutation by polymerase chain reaction and direct nucleotide sequencing. Overexpression of p53 protein was found in 13/32 (41%) of gastric cancers and 5/15 (33%) of esophageal cancers. We found immunodetectable p53 in 10/14 cases with mutations and in none of 11 cases without mutations in gastric and esophageal cancers. Hence, immunohistochemical and genetic analyses gave concordant results in 84% of 25 cases, revealing a good correlation between immunostaining of p53 and missense mutation of the p53 gene. p53 immunostaining was not observed in cases with frameshift or splicing mutation. The expression of p21WAF1/CIP1 protein was found in 9/32 (29%) of gastric cancers and 4/15 (27%) of esophageal cancers and in 2/14 (14%) cases with alteration of the p53 gene and in 5/11 (45%) without. These results suggest that abnormalities of p53 may be closely associated with the pathogenesis of gastric adenocarcinoma and esophageal squamous cell carcinoma and that the immunoreactivity of p53 protein is a general indicator of the tumors with altered p53 function. The expression of p21WAF1/CIP1 protein was suppressed in the neoplastic tissues with and without p53 gene alteration.

Adenocarcinoma↗
PubMed1998

Etiologic considerations of fulminant non-A, non-B viral hepatitis in Japan: analyses by nucleic acid amplification method.

The etiology of fulminant non-A, non-B hepatitis has remained unclear, even after the identification of hepatitis C and E viruses. To study the possible involvement of hepatitis B, C, D, and E virus infections, viral genomes were amplified by a sensitive polymerase chain reaction method in sera and liver tissues obtained from 20 patients serologically diagnosed with non-A, non-B fulminant hepatitis (n = 14), acute hepatitis severe type (n = 2), and ordinary acute hepatitis (n = 4). Hepatitis C or E virus RNA could not be detected in sera obtained at admission from these patients. Hepatitis B virus DNA was detected in sera from 3 patients with fulminant hepatitis and in liver from 9 patients with fulminant hepatitis or acute hepatitis severe type. These results suggest that HCV might not be involved in fulminant non-A, non-B hepatitis, and HBV might be related to some of the serologic "non-A, non-B" viral hepatitis cases in Japan.

Adult↗
PubMed1998

Immunohistochemical study of transforming growth factor-beta 1, matrix metalloproteinase-2,9, tissue inhibitors of metalloproteinase-1,2, and basement membrane components at pancreatic ducts in chronic pancreatitis.

Little is known about the pathogenesis of fibrosis in chronic pancreatitis. To reach a better understanding of this problem, we investigated the immunolocalizations of type IV collagen (Col-IV) and laminin around pancreatic ducts, and those of matrix metalloproteinase-2,9 (MMP-2,9), tissue inhibitors of metalloproteinase-1,2), and transforming growth factor-beta 1 (TGF beta 1) at the ductal epithelia in chronic pancreatitis. This study included 20 surgical specimens of fibrotic pancreas from patients with chronic pancreatitis and five normal samples from autopsy cases. Immunostaining was performed by the streptavidin-biotin method after antigen retrieval. We evaluated the staining patterns and the percentage of positive cells of each antigen. In chronic pancreatitis, the immunostainings of Col-IV and laminin along the basement membrane (BM) of pancreatic ducts were disrupted in 11 (55%) of 20 and eight (40%) of 20, respectively, whereas no disruption was detected in normal pancreas. Positive immunostainings for MMP-2, MMP-9, TIMP-1, and TIMF-2 in ductal epithelia were 15 (75%) of 20, five (25%) of 20, four (20%) of 20, and 10 (50%) of 20, respectively, whereas no immunostaining was seen in normal pancreas. The staining intensity of MMP-2 in ductal epithelia was associated with the staining intensity of Col-IV around the pancreatic ducts. Also, the staining intensity of MMP-2 was progressively increased in proportion to the staining intensity of TGF beta 1. These findings suggest that TGF beta 1 induced in pancreatic duct cells also induced MMP-2 in an autocrine or paracrine manner, and that this MMP-2 decomposed Col-IV of the BM of pancreatic ducts in chronic pancreatitis.

Adult↗
PubMed1998

An image analyzing system using an artificial neural network for evaluating the parenchymal echo pattern of cirrhotic liver and chronic hepatitis.

To objectively evaluate the parenchymal echo pattern of cirrhotic liver and chronic hepatitis, we applied an image analyzing system (IAS) using a neural network. Autopsy specimens in a water tank (n = 13) were used to examine the relationship between the diameter of the regenerative nodule and the coarse score (CS) calculated by IAS. CS was significantly correlated with the diameter of the regenerative nodule (p < 0.0001, r = 0.966). CS is considered to be useful for evaluating the coarseness of the parenchymal echo pattern.

Hepatitis, Chronic↗
PubMed1998

Expression of cellular adhesion regulatory molecule in hepatocellular carcinoma.

Cellular adhesion regulatory molecule (CMAR) enhances the adhesiveness of cells to collagen and laminin and is considered to be a candidate anti-oncogene. The purpose of the present study was to investigate the relationship between the expression of CMAR and clinical features of hepatocellular carcinoma (HCC). Small amounts of liver tissue were obtained from HCC and non-cancerous portions of the liver in 29 patients and from normal liver in seven patients with metastatic liver tumour by biopsy under ultrasound guidance. RNA was extracted with acid guanidinium thiocyanate-phenol-chloroform. Expression of CMAR was assessed by quantitative PCR using beta-actin as an internal standard. A 4 b.p. insertion polymorphism at nucleotide 241 of the CMAR coding region was then investigated using extracted RNA to assess the relationship between the expression of variant mRNA of CMAR and HCC carcinogenesis. The relative expression of CMAR was significantly reduced in HCC compared with non-cancerous and normal livers and had a relationship with certain clinical background factors. The reduced expression of CMAR was thought to be closely associated with the progression of HCC. However, the 4 b.p. insertion polymorphism pattern of CMAR was the same between HCC and non-cancerous liver in all cases in which it was found. These results suggest that progression of HCC may be predicted based on the relative expression of CMAR.

ATPases Associated with Diverse Cellular Activitie↗
PubMed1998

BAZF, a novel Bcl6 homolog, functions as a transcriptional repressor.

The BCL6 gene, which has been identified from the chromosomal translocation breakpoint in B-cell lymphomas, functions as a sequence-specific transcriptional repressor. We cloned a novel Bcl6-homologous gene, BAZF (encoding Bcl6-associated zinc finger protein). The predicted amino acid sequence of BAZF indicated that the BTB/POZ domain and the five repeats of the Krüppel-like zinc finger motif are located in the NH2-terminal region and the COOH-terminal region, respectively. BAZF associated with Bcl6 at the BTB/POZ domain and localized in the nucleus. Since zinc finger motifs of BAZF were 94% identical to those of Bcl6 at the amino acid level, BAZF bound specifically to the DNA-binding sequence of Bcl6 and functioned as a transcriptional repressor. The repressor activity was associated with both the BTB/POZ domain and the middle portion of BAZF. The 17-amino-acid sequence in the middle portion was completely conserved between BAZF and Bcl6, and the conserved region was critical for the repressor activity. Expression of BAZF mRNA, like that of Bcl6 mRNA, was induced in activated lymphocytes as an immediate-early gene. Therefore, the biochemical character of BAZF is similar to that of Bcl6 although the tissue expression pattern of BAZF differs from that of Bcl6. This is apparently the first report of a gene family whose members encode zinc finger proteins with the BTB/POZ domain.

Amino Acid Sequence↗
PubMed1998

[Diagnosis and treatment for recurrent hepatocellular carcinoma].

In order to investigate the mechanism of recurrence of hepatocellular carcinoma (HCC), 322 patients with HCCs (size: < or = 3 cm) treated by percutaneous ethanol injection (PEI), transcatheter arterial embolization (TAE) or radiation therapy were evaluated. Cumulative recurrent rates of new lesions after the initial therapy were 25% (1-year), 57% (2-year) and 71% (3-year). In 116 patients whose tumors were multiple at the time of initial therapy, the recurrent rates were higher compared with 206 patients with a single tumor. In 228 of all patients, new lesions were observed in the noncancerous liver after initial therapy. We observed a single new lesion in 67% of the 134 patients, whose HCC was single at the time of initial therapy. In the remaining 33% of these patients, multiple new lesions were observed. As for the recurrence site, we found new lesions at a different segment of the liver from the initial HCC in 52% of these 134 patients. In the patients with multiple recurrent HCCs, the survival rates were lower in comparison with the patients whose recurrent HCC was single. In the patients whose new lesions were found within 1 year after the initial therapy, the survival rates were also lower compared with the patients whose new lesions were not detected during 1 year. In conclusion, the mechanism of multicentric occurrence may be closely correlated with the intrahepatic recurrence of HCC in consideration of the high incidence of recurrent rates of HCCs and their recurrent pattern.

Antineoplastic Agents↗
PubMed1998

[Repeated arterial infusion of zinostatin stimalamer using port for advanced hepatocellular carcinoma].

Four patients with advanced hepatocellular carcinoma were treated by repeated arterial infusion of zinostatin stimalamer (SMANCS). Every 4 weeks, 4 mg of SMANCS and 4 ml of Lipiodol were administered via the proper hepatic artery using an implantable arterial port. Three patients with advanced liver cirrhosis (Child B or C) could no longer be treated after 2 or 3 courses of SMANCS infusion because of hepatic failure. In the remaining patient also with compensated liver cirrhosis (Child A), a partial response was observed after 5 courses of chemo-infusion, but we discontinued infusion of SMANCS because of hepatic failure. To assess the usefulness of SMANCS for repeated arterial chemo-infusion by the port, we evaluated 103 patients with advanced HCC treated by Lipiodol emulsion mixed with 70 mg of epirubicin (EPI) using a port. An average course was 11 arterial infusions, and the overall response rate was 40%. One-year survival rates were 62% in Child A, 59% in Child B, and 53% in Child C. Compared with Child A and B patients, both elevation of serum total bilirubin levels and decrease of serum albumin levels were observed after 9 months in Child C patients. In conclusion, SMANCS may have more severe hepatic toxicity in comparison with Lipiodol emulsion mixed with EPI.

Aged↗
PubMed1998

[Enhanced color flow findings in small hepatocellular carcinoma].

Features of enhanced color flow images of small hepatocellular carcinoma (HCC) were studied to elucidate their usefulness in evaluating tumor hemodynamics. Enhanced color Doppler using the contrast agent "SH/TA508" was performed on 16 patients, 13 with HCC, 1 with regenerative nodule, and 2 with hemangiomas, in whom the size of the tumor were smaller than 30 mm. Enhanced color flow appearance was compared with angiographic findings. Significant improvement in the detection of color flow signals was obtained in small HCC using SH/TA508, from 33% in pre-contrast to 92% in post-contrast (p < 0.005). Three patterns of enhanced color flow images, which were related to the angiographic findings, were observed. Enhanced color flow imaging promises to be a useful method for evaluating tumor vascularity noninvasively, and to contribute to the elucidation of the hemodynamics in liver tumor.

Carcinoma, Hepatocellular↗
PubMed1998

Natural course of small hepatocellular carcinoma with underlying cirrhosis. A study of 30 patients.

To anticipate the prognosis and choose therapy for patients with relatively early-stage HCCs, we elucidate the natural course of such patients. Thirty cirrhotic patients with small hepatocellular carcinoma (HCC) < 3 cm in size and not receiving anti-cancer treatment were followed by sonography for periods of 6-48 mots. The growth speed varied considerably from case to case, with an average of 6.5+/-5.7 months of doubling time (DT). Growth speed of small HCC is significantly related to histological differentiation of tumors: a slow-growing HCC tends to be well-differentiated and a rapid-growing HCC moderately- or poorly-differentiated. Furthermore, there was a tendency to grow without changing from nodular type in slow-growing HCCs and to multiple nodular or massive types in intermediate- and rapid-growing HCCs. The survival rates of these untreated HCC patients showed a 1-yr survival of 90.7%, a 2-yr survival of 55.0%, and a 3-yr survival of 12.8%. Factors significantly influencing survival of these patients were serum total bilirubin level and DT. This study will provide invaluable data for diagnosing and treating for small HCCs.

Aged↗
PubMed1997

Characterization of a specific region in the hepatitis B virus enhancer I for the efficient expression of X gene in the hepatic cell.

Hepatitis B virus (HBV) enhancer I has been shown to consist of several cis-acting sequences for the HBV gene expression efficiently in certain types of cells. Transcriptional regulation of HBV X gene mediated by enhancer I might be one of the mechanisms by which HBV obtains hepatotropism. By mutagenesis analysis of enhancer I function in the enhancer I/X gene promoter complex, we characterized a specific transcriptional regulatory region (designated as a LSR element, nt 989-1030) of enhancer I for the X gene promoter by means of the transient transfection technique using hepatic and nonhepatic cells. Based on the analysis of protein factors interacting with the LSR element, liver-enriched transcriptional factors, HNF3 and HNF4 or retinoid X receptor alpha (RXR alpha), are probably implicated in the activity of enhancer I for the efficient expression of X gene through their interaction with the LSR element in the hepatic cell. Furthermore, the isolated LSR element was demonstrated to function alone as a specific cis-acting element and to be able to activate transcription from the X gene promoter efficiently in the hepatic cell in an orientation-independent manner.

Base Sequence↗
PubMed1997

Detection of GBV-C RNA in patients with non-A-E fulminant hepatitis by reverse-transcription polymerase chain reaction.

GBV-C might be a causative agent of fulminant hepatitis of unknown etiology. Fulminant hepatitis is an indication for liver transplantation. However, in Japan, because of the legal difficulties associated with cadaveric donation, patients with fulminant hepatitis are still treated by plasmapheresis and multiple transfusions of fresh frozen plasma. So, the possibility that GBV-C might be transmitted by transfusions after the onset of fulminant hepatitis is real. Therefore, we have examined the possible role of GBV-C in non-A-E fulminant hepatitis. Nine patients with non-A-E fulminant hepatitis and one with non-A-E late onset hepatic failure were examined. Sera were obtained from the patients at admission before any blood or blood products were given, and again after transfusions. GBV-C RNA was detected by nested reverse transcription polymerase chain reaction with primers based on the reported sequence. GBV-C RNA was negative in all 10 pretransfusion patients with non-A-E fulminant hepatitis or late onset hepatic failure. Then, fresh frozen plasma was transfused to these patients, and four of them became seropositive. GBV-C is unlikely to be a major etiologic agent for non-A-E fulminant hepatitis in Japan.

Adult↗
PubMed1997

Expression of basic fibroblast growth factor (FGF-2)-associated with tumour proliferation in human pancreatic carcinoma.

Basic fibroblast growth factor (FGF-2) is one of the mitogens that facilitate epithelial proliferation and angiogenesis. We analysed the expression of FGF-2 and type I fibroblast growth factor receptor (FGFR1) in 20 selected cases of human pancreatic carcinoma (PC) in connection with proliferation of tumour cells and intratumour endothelial cells (ECs), using immunohistochemistry and in situ hybridization (ISH). By FGF-2 immunostaining, tumour cells were strongly positive in 10 cases (50%). By FGFR1 immunostaining, stromal fibroblasts and ECs occasionally showed positive staining. Tumour cells in 12 cases (60%) were strongly positive. Expression of FGF-2 mRNA, as examined by ISH, was detected in 12 cases (60%) of PC, and its distribution pattern was similar to that of FGF-2 immunostaining. We divided these cases into two groups according to the result of FGF-2 immunostaining, and examined the Ki67 labelling indices of tumour cells and ECs between these two groups. These two proliferative indices were significantly higher in FGF-2-positive than in FGF-2-negative cases (P<0.05, P<0.05, respectively). These findings suggest that the expression of FGF-2 in PC is strongly associated with the proliferation of tumour cells and ECs and its increased expression may give tumour a growth advantage.

Carcinoma, Adenosquamous↗
PubMed1997

Ultrastructure of cholesterol gallstones as observed by electron microscopy after freeze-fracturing.

The ultrastructure of cholesterol gallstones (mixed type) was studied in detail for the first time under the transmission electron microscope after freeze-fracturing. Gallstones consisted essentially of cholesterol crystals, some impurities, and fluid. In accord with the theoretical 3.4 nm bilayered structure of cholesterol crystals, 3-4 nm periodicity of crystal layering was observed. However, gallstone cholesterol crystals were not perfect and often showed structural defects. Between crystals, complete edge-to-surface, edge-to-edge and surface-to-surface adhesions, and overall block-like aggregations were found. These may represent the structural basis for the stability of cholesterol crystal aggregation. The easy breakdown of cholesterol gallstones by extracorporeal shock wave lithotripsy is discussed in relation to their ultrastructure.

Aged↗
PubMed1997

GB virus-C RNA in Japanese patients with hepatocellular carcinoma and cirrhosis.

BACKGROUND/AIMS: The involvement of non-B, non-C virus in the incidence of hepatocellular carcinoma (HCC) is not yet known. We have therefore examined the occurrence of GBV-C RNA in such patients. METHODS: One hundred and eleven patients diagnosed as having HCC and 67 patients with cirrhosis without HCC were examined for the prevalence of GBV-C RNA by nested reverse transcription polymerase chain reaction with primers located at the helicase region. Sera were obtained and kept at -20 degrees C until analysis. RESULTS: GBV-C RNA was positive in 11/111 (9.9%) cases with HCC, in 10/74 (13.5%) anti-HCV positive cases, in 1/25 (4%) HBsAg positive cases, and in 0/8 (0%) anti-HCV and HBsAg negative cases. GBV-C RNA was also positive in 7/67 (10.4%) cases with cirrhosis, in only 1/18 (5.6%) anti-HCV and HBsAg negative cases, in 4/33 (12.1%) anti-HCV positive, and in 2/14 (14.3%) HBsAg positive cases. The clinical background of patients with anti-HCV positive HCC who were also positive for GBV-C RNA did not differ from the background of those negative for GBV-C RNA. CONCLUSIONS: GBV-C is unlikely to be a major etiologic agent of non-B, non-C chronic liver diseases and HCC in Japan.

Adult↗
PubMed1997

Telomerase activity and telomere length in hepatocellular carcinoma and chronic liver disease.

BACKGROUND & AIMS: The maintenance of the telomere to a certain length is considered to be vital for cellular immortality. Recently, the presence of telomerase, an enzyme that elongates telomere length, was reported in various malignancies. The aim of this study was to characterize telomerase activity and telomere length in hepatocellular carcinoma and chronic liver diseases to facilitate better understanding and more accurate diagnosis of hepatocellular carcinoma. METHODS: In tumorous and nontumorous tissues from 26 hepatocellular carcinomas and from 20 liver tissues without overt hepatocellular carcinoma, telomerase activity was examined by telomeric repeat amplification protocol and telomere length was detected by Southern blot hybridization method. RESULTS: Telomerase activity was detected in 22 of 26 (85%) hepatocellular carcinoma specimens. In contrast, it was weakly detected in 4 of 46 (9%) nonneoplastic tissues. Telomere length in hepatocellular carcinoma was shorter than that of corresponding nontumorous tissue in 44% and longer in 17%. CONCLUSIONS: The presence of telomerase activity was confirmed in a majority of cases with hepatocellular carcinoma, and alteration of telomere length from nonneoplastic tissue was observed in approximately two thirds of hepatocellular carcinomas. Therefore, these markers might be good indicators for the diagnosis of hepatocellular carcinoma.

Adult↗