bluuebunny/crossref_metadata_2025_split huggingface dataset:
Transcytotic vesicle fusion with canalicular membranes is modulated by phospholipid species: Implications for biliary lipid secretion
Authors: HIRANO NAOMICHI , TAZUMA SUSUMU , KAJIYAMA GORO 
Published: March 2008

ABSTRACTPhospholipid species modulate bile metastability and the subselection of such species for biliary secretion occurs at the canalicular membrane. In this study, the role of phospholipid head groups and hydrophobic indices in transcytotic vesicle fusion with the canalicular membrane inner leaflet was investigated using rat canalicular membrane vesicles (CMV) and liposomes. The CMV were purified from Sprague‐Dawley rat liver, and small unilamellar vesicles (SUV) of phosphatidylserine (PS), phosphatidylcholine (PC) and mixtures of PS/PC (1:1, 2:1 and 4:1) were labelled with 8 mol% of octadecyl rhodamine B chloride (R18). The PC species used in this study were egg yolk PC (EYPC), soybean PC (SBPC), dipalmitoyl PC (DPPC) and dilinoleoyl PC (DLPC). Fusion of SUV with CMV was initiated by the addition of a millimolar concentration of Ca2+ and the degree of fusion was estimated by the increase of R18 fluorescence. Ca2+‐dependent fusion of SUV consisting of PS, and PS/PC (4:1) with CMV was observed (PS > PS/PC; 4:1), whereas no detectable fusion was evident between CMV and SUV of PC alone or PS/PC (1:1 or 2:1). The rank order of fusibility between CMV and SUV of PS/PC (4:1) containing various PC species was PS/DLPC > PS/SBPC > PS/EYPC > PS/DPPC. The hydrophobic index of PC as determined by high performance liquid chromatography (HPLC) was related closely to liposome fusibility (r=‐0.88). These results suggest that transcytotic vesicie fusion with the canalicular membrane inner leaflet is regulated by the phospholipid hydrophobicity of the vesicles.
Molecular biology of hepatitis B virus e antigen
Authors: OU JING‐HSIUNG 
Published: March 2008

ABSTRACTHepatitis B virus (HBV) e antigen (HBeAg) was discovered in 1972 as one of the serological markers of HBV infection. Although 25 years have passed since its initial discovery, the function of this antigen in the life cycle of HBV has remained elusive. Mutations in the HBV genome that prevent the expression of HBeAg do not abolish the replication of HBV, indicating that this antigen is not essential for HBV replication. In contrast, the conservation of the HBeAg gene in the genomes of related animal viruses, including the distantly related duck HBV, argues for an important function of this antigen. The purpose of the present article is to review the molecular biology of HBeAg and to examine its possible functions in the life cycle of HBV.
Histopathology and pathobiology of hepatotropic virus‐induced liver injury
Authors: HUANG SN , CHEN TC , TSAI SL , LIAW YF 
Published: March 2008

ABSTRACTThe present report concerns current knowledge regarding immunopathogenesis that can be applied in the interpretation of histopathological changes in acute and chronic viral hepatitis. The histopathological features of viral hepatitis have not been changed and light microscopic examination remains essential for making a diagnosis and classification of chronic hepatitis and for the provision of objective parameters on grading and staging. However, new understanding and knowledge of viral pathogenesis, host immune responses, the biological behaviour of the causative viral agents and, in particular, viral interference in multiple hepatotropic viral infections must be taken into consideration in the interpretation of histopathological and immunopathological findings of liver tissues. This report also presents some histopathological analyses on multiple hepatotropic viral infections. It can be concluded that the diagnostic histological criteria for acute hepatitis remain applicable in such settings. However, the cause of acute flare up in chronic hepatitis could not be determined without clinical, virological and serological information. Routine histopathology cannot distinguish a new infection from an acute exacerbation due to a high level of viral replication or mutant virus. A repertoire of immunocyto‐chemical stainings for viral antigens is helpful, but caution must be exercised in suggesting a specific viral aetiology due to the fact that suppression of pre‐existing viral antigens can be pronounced when the new or concurrent infection is hepatitis C virus related.
Evoked potentials in liver diseases
Authors: CHU NAI‐SHIN , YANG SIEN‐SING , LIAW YUN‐FAN 
Published: March 2008

ABSTRACTEvoked potentials are objective and quantitative methods capable of evaluating functions of both peripheral and central nervous systems (PNS and CNS). During the past 8 years, we have been using somatosensory, brainstem auditory, and pattern‐reversal visual evoked potentials (SEP, BAEP, VEP) to study hepatic encephalopathy (HE) as well as functional status of the PNS and CNS in various liver diseases including viral hepatitis B, alcoholic liver disease and Wilson's disease (WD). In HE irrespective of its etiologies, there is a sequential prolongation and eventual disappearance of cortical components of the median nerve evoked SEP while there is no change in BAEP, suggesting that HE is primarily due to a disturbance in cerebral cortical function and that median SEP may be used for early detection of HE and for monitoring its clinical course. In addition, absence of the N20‐P25 component, or presence of only the N20 component of the wave complex in fulminant hepatic failure is associated with high mortality, whereas presence of late cortical components in HE is usually associated with reversibility of clinical course. Central conduction time (CCT) of the BAEP is prolonged in patients with WD, alcoholic liver disease and liver cirrhosis due to hepatitis B. Furthermore, BAEP abnormality is most severe in WD, followed by alcoholic liver disease, and finally hepatitis B. Peripheral nerve conduction as determined by the N9 latency of SEP is slowed in alcoholic liver disease and liver cirrhosis of chronic hepatitis B, but normal in WD. Our studies, therefore, suggest that evoked potentials may be useful in the evaluation of both CNS and PNS functions in various liver diseases and also in the diagnosis and monitoring of HE.
Nucleic acid‐based antiviral and gene therapy of chronic hepatitis B infection
Authors: WANDS JR , GEISSLER M , PUTLITZ JZU , BLUM H , VON WEIZSÄCKER F , MOHR L , YOON SK , MELEGARI M , SCAGLIONI PP 
Published: March 2008

ABSTRACTPersistent hepatitis B virus (HBV) infection often leads to the development of chronic hepatitis, cirrhosis and hepatocellular carcinoma. There is a need to develop new antiviral approaches for the treatment of this disease. We have explored various nucleic acid‐based strategies designed to inhibit HBV replication including: the use of antisense RNA and DNA constructs, DNA‐based immunization techniques to stimulate broad‐based cellular immune responses with particular emphasis on the generation of cytotoxic lymphocyte (CTL) activity to viral structural proteins, hammerhead ribozymes to cleave HBV pregenomic RNA in vitro and dominant negative HBV core mutant proteins as inhibitors of nucleocapsid formation within cells. In order to optimize these antiviral effects, various novel expression vectors have been developed to deliver such DNA constructs to cells. For example, adenoviral vectors carrying genes that encode for dominant negative proteins have been employed to transfect hepatocytes in vitro and in vivo. In addition, plasmid vectors have been produced to promote expression of HBV structural genes following injection into muscle cells as a means to stimulate the host's cellular and humoral immune response in the context of histocompatibility antigen (HLA) class I and II antigen presentation. These experimental approaches may have important implications for the generation of efficient antiviral effects during chronic HBV infection.
Relationship between local immune response to Helicobacter pylori and the diversity of disease: Investigation of H. pylori‐specific IgA in gastric juice
Authors: WATANABE TAKEHITO , GOTO HIDEMI , ARISAWA TOMIYASU , HASE SATOSHI , NIWA YASUMASA , HAYAKAWA TETSUO , ASAI JUNPEI 
Published: March 2008

ABSTRACTIn order to evaluate the relationship between local immune response to Helicobacter pylori and the diversity of disease, 77 asymptomatic subjects who underwent a health examination were studied. Helicobacter pylori‐specific IgG in serum and H. pylori‐specific IgA in gastric juice were measured by ELISA, and the measured IgA titre was classified into two grades, low or high. Histological classification of gastritis was performed according to the Sydney system. Cytokines in gastric juice were also measured, and the cytotoxin‐associated gene A (cagA) status of H. pylori was tested by PCR. Of the 65 subjects who were positive for H. pylori‐specific IgG in serum, 38 (58.5%) were classified as H. pylori‐specific IgA low titre in gastric juice and 27 (41.5%) had high titres. In the IgG‐positive, IgA‐low group, the rate of peptic ulcers (especially duodenal ulcers) in endoscopic findings was higher (P < 0.05); the score of activity and the density of H. pylori were higher (P < 0.001 and P < 0.05, respectively); the score of metaplasia was lower (P < 0.05); and the level of interleukin‐1β was lower (P < 0.05) than in the IgG‐positive, IgA‐high group. The positive rate of the cagA gene was 84.4% and there was no significant difference between the two groups. There were differences in endoscopic and histological findings between the IgG‐positive, IgA‐low and the IgG‐positive, IgA‐high groups. It is suggested that persons infected with H. pylori can be divided into two different states of disease according to local immune response.
Report of the 1997 Asia Pacific Consensus Conference on the management of Helicobacter pylori infection
Authors: LAM SK , TALLEY NJ 
Published: March 2008

ABSTRACTWhile European and United States guidelines for the management of Helicobacter pylori infection have been developed, there are no guidelines for the Asian Pacific. International experts and recognised local authorities met in Singapore in 1997 to develop appropriate guidelines, taking into account the high background prevalence of infection, high incidence rates of gastric cancer and resource limitations. Recommendations were made based on randomised controlled trials or where this was not possible, they were based on the current best available evidence or on good clinical practice. A number of acceptable diagnostic tests for infection are available throughout the region. The non‐endoscopic methods of choice are the urea breath test or a locally validated antibody test. If endoscopy was to be performed, a biopsy urease test was recommended as the test of first choice, with histology recommended only if this was negative. Post treatment testing was not recommended for all patients; a urea breath test was considered the test of choice if available. All gastric and duodenal ulcer patients who are infected with H. pylori should be treated for H. pylori whether the ulcer is active or in remission. Patients requiring long term non‐steroidal anti‐inflammatory drug therapy who have a current or recent history of dyspepsia, patients with early gastric cancer or low grade gastric mucosa associated lymphoid tissue lymphoma, and patients with a family history of gastric cancer should be treated. However, it was concluded that there wasn't sufficient evidence that cure of H. pylori infection reduces the risk or prevents the development of gastric adenocarcinoma. Many patients with dyspepsia in the region will request or require early upper endoscopy because of an inherent fear of gastric cancer. However, where endoscopy is not available or is too costly, alternative acceptable approaches were recommended in high risk cancer regions. While evidence is inconclusive to support treatment of H. pylori infection in non‐ulcer dyspepsia, it was agreed that treatment be offered to patients with documented infection on a case‐by‐case basis. Treatment regimens need to attain an eradication rate of 90% or greater by per protocol analysis and 80% or greater by intention‐to‐treat analysis. A number of 7‐day regimens were recommended based on available evidence. These regimens were considered likely to maximize the chances of successful eradication with one course of treatment, thereby reducing the risk of acquired antibiotic resistance and leading to long term cost savings.
Histological changes of concurrent hepatitis C virus infection in asymptomatic hepatitis B virus patients
Authors: LAU GEORGE KK , WU PUI CHEE , LO CHI KIN , LAU VICKY , LAM SHIU KUM 
Published: March 2008

ABSTRACTIn chimpanzees and in vitro cell culture studies, hepatitis C infection has been shown to suppress hepatitis B virus expression. In addition, hepatitis C infection can cause much more severe liver disease in patients chronically infected with hepatitis B virus. The aims of the present study were to determine the prevalence of hepatitis C infection in asymptomatic chronic hepatitis B Hong Kong Chinese patients and the histological changes and hepatic expression of hepatitis B virus and hepatitis C virus. Five hundred and seventy‐one Hong Kong Chinese asymptomatic chronic hepatitis B patients were studied. Only four (0.7%) were hepatitis C virus antibody positive; they were also all positive for hepatitis C viral RNA in serum by reverse transcription‐polymerase chain reaction (RT‐PCR). Portal lymphoid aggregates and bile duct damage was noted in the liver sections of three of the four patients. Hepatic expression of hepatitis B surface antigen was detected in three patients; none had detectable hepatitis B core antigen. By branched DNA assay, serum hepatitis B DNA could not be detected in any of the four patients, but three had hepatitis C RNA. By in situ RT‐PCR, hepatitis C RNA was detected in the cytoplasm of three of the four patients. These findings suggest that hepatitis C coinfection in asymptomatic chronic hepatitis B patients is uncommon in Hong Kong Chinese and active hepatitis B viral replication is absent in these patients.
A protease inhibitor attenuates gastric erosions and microcirculatory disturbance in the early period after thermal injury in rats
Authors: YOSHIDA MASASHI , WAKABAYASHI GO , ISHIKAWA HIDEKI , OTANI YOSHIHIDE , SHIMAZU MOTOHIDE , KUBOTA TETSURO , KUMAI KOICHIRO , KUROSE IWAO , MIURA SOICHIRO , ISHII HIROMASA , KITAJIMA MASAKI 
Published: March 2008

ABSTRACTThe effects of camostat mesilate, a synthetic serine protease inhibitor on gastric microcirculation and active oxygen species generated by leucocytes from the gastric and jugular veins in the early period after thermal injury were assessed. Male Wistar rats were anaesthetized and a 30% full skin‐thickness dorsal burn was inflicted. Camostat mesilate (100 mg/kg) was dissolved in distilled water and administered orally to rats 40 min before thermal injury (the camostat group). The control animals (the vehicle group) were administered distilled water orally. Rolling leucocytes as well as Monastral blue B deposits in venules were observed using in vivo microscopy. Active oxygen species were measured by chemiluminescence. Camostat mesilate decreased the total length of gastric erosion, venular deposits of Monastral blue B, and rolling of leucocytes in venules, and relatively increased luminol‐dependent chemiluminescence activity generated by zymosan‐stimulated leucocytes 15 min after thermal injury. These results suggest that serine proteases are involved in the formation of gastric erosions and gastric microcirculatory disturbance in the early period after thermal injury.
CASE REPORT: Intrahepatic portal‐hepatic venous shunts associated with a huge pelvic leiomyoma
Authors: AIBA NOBUYASU , MORIOKA JUNICHIRO , MIYAZONO TAKAYOSHI , OKITA HIDEAKI , YATA YUTAKA , OKADA KAZUHIKO , NAMBU SHUJI , WATANABE AKIHARU , SHIMIZU MASASHI , FUJIMURA MASAKI , IZUMI RIKUICHI 
Published: March 2008

ABSTRACTWe present a case of portal‐systemic encephalopathy due to intrahepatic multiple portalhepatic venous shunts. A 71‐year‐old woman was admitted to our hospital because of recurrent episodes of disturbed consciousness. She showed no clinical signs of portal hypertension. Liver function was normal, except for an indocyanine green retention rate of 34% at 15 min and blood ammonia level of 282 μg/dL. Portal venography revealed dilatation of the portal vein and multiple portal‐hepatic venous shunts, and a liver biopsy specimen revealed almost normal liver. Further clinical examination revealed a huge pelvic tumour. At laparotomy, two dilated veins were seen to arise from the pelvic tumour with blood flow into the mesentery. The tumour was resected successfully and a histological diagnosis of leiomyoma was made. The blood ammonia concentration decreased to the normal range postoperatively. A follow‐up portal venogram demonstrated decreased portal vein dilatation and minor portalhepatic venous shunts, considered to be congenital in origin. It is concluded that liepatic encephalopathy was produced in this patient due to an excess portal blood flow from the huge pelvic leiomyoma via the mesentery, with portosystemic shunting through pre‐existent (probably congenital) intrahepatic anastomoses.
Use of fructose 1,6‐diphosphate aldolase to detect tumour necrosis after transcatheter arterial embolization of hepatocellular carcinoma
Authors: KHAN KHALEQUE NEWAZ , NAKATA KEISUKE , KUSUMOTO YUKIO , NAKAO KAZUHIKO , KATO YUJI , NAGATAKI SHIGENOBU 
Published: March 2008

ABSTRACTTranscatheter arterial embolization (TAE) is a popular and well‐established devascularization treatment modality for hepatocellular carcinoma (HCC). The persistent retention of lipiodol on follow‐up computed tomography (CT) scan and time‐dependent decrease in size of the lipiodol‐stained area of tumour after TAE does not reveal the biological death of tumour cells. Moreover, it is difficult to clinically evaluate the effective necrosis of tumour cells by TAE in cases of HCC that do not produce α‐fetoprotein (AFP). We therefore studied the release of a relatively tumour‐specific protein by the necrotic hepatoma cells to evaluate the effectiveness of TAE. Transcatheter arterial embolization was performed in 17 patients with the imaging diagnosis of HCC; either superselective (n= 6) or non‐superselective (n= 11) techniques were used. We measured serum levels of relatively tumour‐specific fructose 1,6‐diphosphate (FDP) aldolase and non‐tumour‐specific fructose 1‐phosphate (F1P) aldolase by substrate‐specific enzymatic methods. Enzyme activities were performed before and after TAE. The time‐dependent decrease in size of the lipiodol‐stained areas was studied on follow‐up CT scans after TAE. Pre‐ and post‐treatment serum AFP levels were determined by radio‐immunoassay. The six cases of superselective TAE underwent marked tumour regression by CT compared with the 11 cases of non‐superselective TAE. Fructase 1,6‐diphosphate aldolase output correlated well with post‐necrotic tumour regression after TAE (r= 0.87, P= 0.001). The elevation of serum FDP aldolase was also significantly associated with a decrease in serum AFP (r= 0.72, P < 0.01). In contrast, serum F1P aldolase output was inversely correlated with either tumour regression or serum AFP concentrations after TAE. The serum levels of the tumour‐specific enzyme FDP aidolase correlated significantly with effective tumour necrosis and consequent tumour regression after TAE. We suggest that measurement of FDP aldolase activity in serum after TAE can be used clinically to detect the degree of tumour necrosis by TAE.
Relationships between serum aminotransferase levels, liver histologies and virological status in patients with chronic hepatitis C in Taiwan
Authors: LUO JIING‐CHYUAN , HWANG SHINN‐JANG , LAI CHIUNG‐RU , LU CHING‐LIANG , LI CHUNG‐PIN , TSAY SHYH‐HAW , WU JAW‐CHING , CHANG FULL‐YOUNG , LEE SHOU‐DONG 
Published: March 2008

ABSTRACTIn patients with chronic hepatitis C, the relationships between serum alanine aminotransferase (ALT) levels, histological liver injury and serum hepatitis C virus (HCV) RNA titres remain controversial. To evaluate these relationships, 93 Chinese patients with histological diagnosis of chronic hepatitis C were enrolled for this study. Serum ALT levels, HCV‐RNA titres and HCV genotypes were examined. The histology was evaluated according to a modified histological activity score based on the degree of periportal necro‐inflammation, intralobular necro‐inflammation, portal inflammation, total necro‐inflammation and fibrosis. The mean serum ALT level was significantly higher in patients with severe intralobular necro‐inflammation activity than in patients with mild or no activity (P= 0.013). However, scores of intralobular activity were only weakly correlated with serum ALT levels (r= 0.27) and could not be used to adequately predict ALT values. Serum ALT levels showed no significant correlation with the scores of portal inflammation, periportal necro‐inflammation, total necro‐inflammation and fibrosis. Also, there was no significant difference in the mean serum ALT level among different serum HCV‐RNA levels and HCV genotypes. Serum HCV‐RNA titres and genotypes showed no significant correlation with liver histology and serum HCV‐RNA titres were only weakly correlated with the total necro‐inflammatory score (r= 0.27). In conclusion, although serum ALT levels were higher in patients with more severe intralobular necro‐inflammatory activity, the correlation was not strong enough to adequately predict ALT values. Serum HCV‐RNA titres and genotypes also showed no significant correlation with serum ALT levels and liver histologies.
Induction of CINC (interleukin‐8) production in rat liver by non‐parenchymal cells
Authors: OHKUBO KEIJI , MASUMOTO TOSHIKAZU , HORIIKE NORIO , ONJI MORIKAZU 
Published: March 2008

AbstractThe production of interleukin‐8 (CINC: cytokine‐induced neutrophil chemo‐attractant) from different cell populations in the rat liver was studied and cells related to the initiation of CINC production in lipopolysaccharide (LPS)‐injected endotoxaemic rats were characterized. Sinusoidal endothelial cells (16.4 ± 10.6 ng/mL) produced significantly higher amounts of CINC in 24 h primary cultures compared with hepatocytes (0.9 ± 0.9 ng/mL; P < 0.05) and Kupffer cells (6.5 ± 5.1 ng/mL; P < 0.05). Lipopolysaccharide, tumour necrosis factor‐α (TNF‐α), and interleukin‐1α (IL‐1α) stimulated different liver cell populations to produce CINC; LPS mainly stimulated Kupffer cells, TNF‐α stimulated hepatocytes and IL‐1α stimulated all three types of cells. Intraperitoneal injection of LPS (4 mg/kg) caused CINC accumulation in non‐parenchymal cells of the rat liver within 1 h of injection, as shown by immunohistochemical staining. In contrast, CINC‐positive hepatocytes were not seen until 3 h after injection of LPS. Ethanol was not a direct inducer of CINC production by rat hepatocytes in vitro. These findings strongly suggest that non‐parenchymal liver cells, including sinusoidal endothelial cells, are the main source of CINC. Our data also suggest that during endotoxaemia, CINC production is initiated by non‐parenchymal cells and this is followed by production from hepatocytes.