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Masayuki Shiraishi

Publications and source records attributed to Masayuki Shiraishi.

10 recordsLinked to original sources
PubMed2006

Expression of anti-apoptotic protein, Bcl-2, in liver regeneration after a partial hepatectomy.

BACKGROUND: Although Bcl-2 is well known to have anti-apoptotic activities in vitro and in vivo, the role of Bcl-2 relating to liver regeneration remains controversial. The aim of this study was to document the effect of Bcl-2 expression on liver regeneration in rats undergoing a partial hepatectomy. MATERIAL AND METHODS: Adult male Wistar rats (n = 4/group) at 72 h before undergoing a 70% partial hepatectomy (PH) were administered 1 x 10(9) plaque-forming units of adenovirus vector encoding either human Bcl-2 (group 1) or LacZ (group 2) intravenously and were sacrificed at 0, 12 h, and at 1, 2, 3, 7, 14, and 21 days postoperatively. In group 3, normal saline was injected instead of adenovirus vector. Liver regeneration was monitored by measuring the restituted liver mass and proliferating cell nuclear antigen (PCNA) immunostaining. The incidence of apoptosis in the liver was analyzed by the immunohistochemical detection of single-stranded DNA at 14 and 21 days postoperatively. RESULTS: The restituted liver mass showed significantly higher values in group 1 (26.1 +/- 7.2%) than in group 2 (14.7 +/- 6.8%) and 3 (13.6 +/- 5.0%) at 1 day after PH (P < 0.05). The PCNA labeling index was significantly higher in group 1 (47.2 +/- 9.9%) than in groups 2 (19.0 +/- 7.8%) and 3 (19.2 +/- 15.2%) at 1 day after a partial hepatectomy (P < 0.05). The hepatocyte growth factor (HGF) mRNA expression was significantly lower in group 1 than in group 2 at 12 h after PH (P < 0.05). The number of single-stranded DNA-positive cells decreased significantly more in group 1 (5.67 +/- 1.53 positive cells/10 fields per tissue) than those in group 2 (18.33 +/- 7.57 positive cells/10 fields per tissue) at 14 days after PH. CONCLUSIONS: These results thus indicated that an overexpression of anti-apoptotic protein Bcl-2 does not necessarily have an anti-apoptotic effect on liver regeneration but appears to have a pro-proliferative effect in the early phase of liver regeneration.

Adenoviridae↗
PubMed2004

No regional spread of vancomycin-resistant enterococci with vanA or vanB in Kitakyushu, Japan.

Outbreaks of vancomycin-resistant enterococci (VRE) infection occur sporadically in Japan, and their frequency has been gradually increasing. We experienced a nosocomial outbreak of VRE in two hospitals in the city of Kitakyushu, and the spread of VRE strains was suspected in this area. To examine the prevalence rate of infection and colonization of VRE in Kitakyushu, we screened a total of 24 297 clinical samples from patients in hospitals and clinics in Kitakyushu from October through December 2002 for VRE. The isolates screened as positive for VRE accounted for 2.3% (566/24 297) of the tested clinical samples. Polymerase chain reaction (PCR) analyses for vanA, vanB, vanC1, and vanC2/3 were performed to confirm the screening test results. Neither vanA nor vanB genes were detected in any isolates. The 265 vanC1-positive isolates were Enterococcus gallinarum, and the 150 vanC2/3-positive isolates were E. casseliflavus. Other Enterococcus species were negative in this PCR-detection test. In this study, the PCR procedure was considered reliable and successful because although neither vanA nor vanB was detected, vanC1 and vanC2/3 were completely detectable. Therefore, we concluded that the regional spread of VRE with vanA and vanB had not occurred in Kitakyushu in 2002. In the near future, the prevalence of VRE with vanA or vanB is likely to increase in Japan, as it has in other countries. We should continue to find and prevent nosocomial outbreaks of infection and colonization by VRE.

Anti-Bacterial Agents↗
PubMed2004

Liver abscess.

Explore the source record for details and available documents.

Abdominal Pain↗
PubMed2003

Up-regulation of hepatocyte growth factor caused by an over-expression of transforming growth factor beta, in the rat model of fulminant hepatic failure.

BACKGROUND: The role of transforming growth factor beta (TGF-beta), a potent regulator of cellular growth, was investigated in the rat model of fulminant hepatic failure (FHF). MATERIALS AND METHODS: The rat FHF model was created by a combination of a 68% partial hepatectomy (PH) and 7% of necrosis (each n = 25 in Groups 1, 2 and 3). Adenovirus mediated gene transfer of mature human TGF-beta1 gene was performed by the systemic injection of AxCAhTGFb1 (1 x 10(9) pfu) in Group 1, 3 days before FHF. In control Groups 2 and 3, recombinant lacZ adenovirus (AxCAlacZ, Group 2) and normal saline (1 ml, Group 3) were used, instead of AxCAhTGFb1. RESULTS: An excessive expression of TGF-beta1 in Group 1 resulted in an inhibition of hepatocyte proliferation (24-48 h after FHF) and gaining of liver weight (24-48 h), increased expression of HGF in liver tissue (24 h), and decreased expression of TGF-alpha (24 h), compared to those in control Groups 2 and 3. Serum IL-6 levels were also elevated by a TGF-beta1 over-expression at 24 hrs after FHF in Group 1. CONCLUSIONS: The forced expression of TGF-beta1 in the FHF liver yields both a secondary increase of HGF production and a suppression of liver regeneration, which might explain the mechanism of increased serum HGF observed in a clinical FHF. TGF-beta1 is thus thought to have an important role in inhibiting liver regeneration after FHF.

Adenoviridae↗
PubMed2002

Adenovirus-mediated gene transfer of triple human complement regulating proteins (DAF, MCP and CD59) in the xenogeneic porcine-to-human transplantation model. Part I: in vitro assays using porcine aortic endothelial cells.

We assessed whether the adenovirus-mediated gene transfer of triple human complement regulating proteins (hCRPs) to the porcine aortic endothelium (PAE), could possibly exert a synergistic effect to inhibit human complement activation. Adenovirus vectors, encoding E.Coli beta-galactosidase (AxCALacZ), human membrane cofactor protein (MCP) (AxCAMCP), decay-accelerating factor (DAF) (AxCADAF), and CD59 (AxCACD59) were produced by the COS-TPC method. AxCALacZ was transfected to porcine aortic endothelium cells (PAECs) under various multiplicities of infection (MOI) to determine the efficiency of adenovirus-mediated gene transfer by 5-bromo-4-chloro-3-indolyl beta- D-galactopyranoside (X-gal) staining. The mRNA expressions of transfected CRPs were examined by reverse transcriptase-polymerase chain reaction (RT-PCR). Cellular damage to the PAEC was assessed by an MTT assay. PAEC was most efficiently transfected with the LacZ gene at 10(3) MOI/60-min incubation time (89.1%). In all samples transfected with the CRP gene, the corresponding mRNAs were detected in the RT-PCR. In the MTT assay, PAECs co-cultured with 20% human serum, showed the highest cellular viability after gene transfer of triple CRPs (117.7%), when compared with those of marker LacZ, single or double CRPs. The adenovirus-mediated multiple gene transfer of CRPs may thus be an efficient method for suppressing complement activation in the porcine-to-human model of hyperacute rejection.

Adenoviridae↗
PubMed2002

Adenovirus-mediated gene transfer of triple human complement regulating proteins (DAF, MCP and CD59) in the xenogeneic porcine-to-human transplantation model. Part II: xenogeneic perfusion of the porcine liver in vivo.

In this study, the adenovirus-mediated gene transfer of triple human complement regulating proteins was investigated in xenogeneic pig liver perfusion. The porcine liver was perfused in situ at 4 degrees C under a pump-driven veno-venous shunt of the portal vein and inferior vena cava, with 5 to 15x10(11) plaque-forming units (pfu) of adenovirus vector (group 1: AxCALacZ; 2: AxCACD59; 3: AxCACD59 + AxCADAF; 4: AxCACD59 + AxCADAF + AxCAMCP) for 1 h (for each, n=3). The livers were harvested 24 h after gene transfer and then were reperfused ex-vivo with fresh human blood for 2 h. In immunohistochemical staining, each complement regulating protein (CRP) showed a distribution similar to that of the LacZ expression. The C3 levels in the perfusate were also maintained at higher levels in group 4 from 60 to 120 min after reperfusion (C3: 85% to 95% of the initial level) than in groups 1 to 3 (C3: 80% to 90% of the initial level) from 60 to 120 min after reperfusion. The complement deposition on the porcine liver [C3, membrane attack component (MAC)] decreased significantly more in group 4 than in groups 1 to 3. In conclusion, the adenovirus-mediated multiple gene transfer of human CRPs (hCRPs) was found to effectively suppress the complement activation in xenogeneic pig liver perfusion.

Adenoviridae↗
PubMed2002

Adenovirus mediated gene transfer of antiapoptotic protein in hepatic ischemia-reperfusion injury: the paradoxical effect of Bcl-2 expression in the reperfused liver.

BACKGROUND: Although Bcl-2 is well known to have antiapoptotic activities in vitro and in vivo, the role of Bcl-2 remains controversial. In the present study, we evaluated whether the adenovirus mediated gene transfer of hBcl-2 could exert an antiapoptotic effect in a rat model of hepatic ischemia-reperfusion (I/R) injury. MATERIALS AND METHODS: Each 6 x 10(9) plaque forming unit adenovirus vector encoding LacZ (AxCAilacZ) or hBcl-2 (AxCAhbcl2) was intravenously administered 48 h before I/R injury, in groups 1 and 2, respectively. In group 3, 1 ml of normal saline was injected instead of the virus vectors. Hepatic I/R injury was induced by the temporal occlusion of all hepatic influent vessels for 30 min under a portosystemic shunt. The animals were sacrificed at 6 h, 1, 3, and 14 days after reperfusion (each n = 12 in groups 1 and 2, and n = 8 in group 3). The expressions of hBcl-2 and Bax were evaluated at both the mRNA level by reverse transcription polymerase chain reaction and the protein level by immunohistochemistry. To assess the hepatocyte and sinusoidal endothelial cell damage after I/R injury, the serum asparate aminotransferase (AST), alanine aminotransferase, and hyaluronic acid were all evaluated. The number of apoptotic cells was evaluated by terminal deoxynucleotidyl transferase-mediated dUTP biotin nick end-labeling (TUNEL). RESULTS: To evaluate the antiapoptotic activities of the hBcl-2 sequence encoded into AxCAhbcl2, rat hepatocarcinoma cells were transfected with AxCAhbcl2 (10(3) moi) or AxCAilacZ (10(3) moi) and then challenged with TGF-beta1 protein (5 ng/ml) to induce apoptosis. Apoptotic cells were counted by TUNEL staining in about 2500 cells, and it was found that adenovirus mediated gene transfer of hBcl-2 significantly protected rat hepatocarcinoma cells from TGF-beta1 induced apoptosis (14.2 +/- 1.2%) in comparison to those of LacZ (21.9 +/- 1.4%). In the reperfused liver in vivo, the mRNA expression of hBcl-2 was detected only in the hBcl-2 transfected group 2. In group 2, a strong degree of Bcl-2 immunoreactivity was recognized as early as 6 h after reperfusion, while it was not recognized in groups 1 and 3 at 6 h after reperfusion. The AST levels were significantly higher in group 2 (AST: 356 +/- 100.1 IU/L) than those in group 1 (AST: 102.7 +/- 15 IU/L) at 1 day after reperfusion (P < 0.05). The number of TUNEL positive cells was significantly higher in group 2 than in groups 1 and 3 at 1 day after reperfusion. CONCLUSIONS: These results indicated that an overexpression of antiapoptotic protein Bcl-2 paradoxically exerted a proapoptotic effect in the reperfused liver. The in vivo role of Bcl-2 should thus be carefully evaluated, depending on the levels of expression and the target organ.

Adenoviridae↗
PubMed1999

Microsatellite instability in patients with gastric remnant cancer.

BACKGROUND: About 2% of patients who undergo partial distal gastrectomy for gastroduodenal diseases develop gastric remnant cancer 10 to 30 years after the gastrectomy. It is important in clinical practice to determine a molecular marker to identify patients susceptible to gastric remnant cancer.METHODS: We investigated nine gastric remnant cancers (from nine individuals who had gastrectomies for primary gastric cancer or gastroduodenal ulcer) for microsatellite instability (MSI) at six loci, using the polymerase chain reaction (PCR). A control group of ten patients with sporadic gastric cancers in the upper third of the stomach was also similarly analyzed.RESULTS: MSI was demonstrated in eight of nine cancers from the individuals who had had primary gastric cancer or gastroduodenal ulcer (88.9%) compared with two of ten cancers from the individuals with sporadic gastric cancer in the upper third of the stomach (20%).CONCLUSION: These results suggest that one or more MSI is associated with remnant gastric cancer after gastrectomy.

Journal Article↗
PubMed1998

Barrett's adenocarcinoma associated with acquired eventration of the diaphragm.

We report a rare case of Barrett's adenocarcinoma asso-ciated with acquired eventration of the diaphragm in a 71-year-old woman. She initially developed dysphagia and epigastric discomfort in May, 1997. On July 9, she was referred to our Department of Surgery at the Ryukyus University Hospital for thorough examination and treatment. Esophageal adenocarcinoma and eventration of the diaphragm were revealed by exhaustive examinations, including chest X-ray, computed tomography, and magnetic resonance imaging, and proximal gastrectomy with reconstruction of jejunal interposition was performed, on August 8. Histologically, the tumor revealed that the adenocarcinoma arose from short-segment Barrett's esophagus (SSBE). It thus appears that eventration of the diaphragm may induce SSBE and Barrett's adenocarcinoma. We therefore recommend that periodic examinations of the esophagus and stomach be performed in patients with eventration of the diaphragm. Barrett's adenocarcinoma associated with acquired eventration of the diaphragm is reported. Patients with eventration of the diaphragm should undergo periodic examinations of the esophagus and stomach.

Journal Article↗