bluuebunny/crossref_metadata_2025_split huggingface dataset:
Preventive therapy of first gastrointestinal bleeding in patients with cirrhosis: Results of a controlled trial comparing propranolol, endoscopic sclerotherapy and placebo
Authors: Andreani Toni , Poupon Reneé E. , Balkau Beverley J. , Trinchet Jean-Claude , Grange Jean-Didier , Peigney Nicolas , Beaugrand Michel , Poupon Raoul 
Published: March 2007

Propranolol and endoscopic sclerosis of esophageal varices are the two approaches currently used in prophylaxis of the first gastrointestinal hemorrhage in the cirrhotic patient. One hundred twenty-six cirrhotic patients with esophageal varices and no histories of bleeding were included in the trial regardless of the gravity of the cirrhosis or the size of the esophageal varices. Patients with hepatocarcinomas or other cancers, clearly impossible follow-up, previous treatment for portal hypertension or contraindication to β-blockers were excluded. After randomization, 43 patients received propranolol twice daily at a dose reducing the heart rate by 25%; 42 patients were treated with intravariceal and extravariceal injections of Polidocanol; 41 control patients received vitamin K orally as placebo. The patients were seen at 3-mo intervals for 2 yr. On entry to the trial the three groups were comparable in terms of clinical and biological parameters, including size of esophageal varices (grade I = 51, grade II = 54, grade III = 17), Child-Pugh classification (A = 29, B = 61, C = 32) and the origin of cirrhosis (alcoholic in 79% of cases).
Twenty-four patients bled (two bled in the propranolol group, nine bled in the endoscopic sclerosis of esophageal varices group and 13 bled in the placebo group). Actuarial estimates (Kaplan-Meier) of the time of onset of first bleeding showed that the differences were significant between propranolol and placebo (p < 0.004) and between propranolol and sclerotherapy (p < 0.03) but not between sclerotherapy and placebo. The multivariate Cox model indicated that the size of esophageal varices and the Child-Pugh class were prognostic factors for the onset of GI bleeding; the treatment effect remained after adjusting for these factors. No significant difference in survival was observed among the three treatment groups. The multivariate Cox model indicated that female gender and Child-Pugh class were factors predictive of survival and that treatment played no part in predicting survival. In conclusion, our study suggests that propranolol is effective in preventing the first gastrointestinal bleeding in the cirrhotic patient but does not improve the survival rate. (HEPATOLOGY 1990;12:1413-1419).
Regulation of insulin-like growth factor II Gene expression by hepatitis B virus in hepatocellular carcinoma
Authors: d'arville CAROLYN N. , Nouri-Aria Kayhan T. , Johnson Philip , Williams Roger 
Published: March 2007

In this study we investigated the regulation of insulin-like growth factor II gene expression to explain a role for this growth factor in concert with hepatitis B virus involvement in the development of hepatocellular carcinoma from cirrhosis.
Sections of normal liver and tumor and non-tumorbearing liver disease tissue were hybridized in situ with [35S]-labeled insulin-like growth factor II oligonucleotide probe. Parallel sections were tested for presence of insulin-like growth factor II polypeptide using immunohistochemistry. To investigate a possible role for hepatitis B virus in insulin-like growth factor II gene expression in hepatocellular carcinoma, results were analyzed against patient seropositivity for hepatitis B virus.
Levels of insulin-like growth factor II transcripts in normal liver (n = 4) sections and in those from nontumor-bearing individuals (n = 10) were so low that specific signal was not detectable above homogeneous tissue background. In contrast, 4 of 8 (50%) of the sections of hepatocellular carcinoma arising from cirrhosis or noncirrhotic chronic liver disease with hepatitis B virus involvement showed increased expression of insulin-like growth factor II messenger RNA transcripts. Up-regulation was observed in cell foci in the hepatocellular regions of the surrounding cirrhotic lobular cells and the fibrous septa. Numerous cell foci were observed in patchy distribution in the tumor areas. The level of insulin-like growth factor II messenger RNA transcripts in sections of hepatocellular carcinoma arising from cirrhotic and noncirrhotic tissues obtained from patients seronegative for hepatitis B virus was similar to that of normal liver. Immunohistochemical study demonstrated that similar cells in the cirrhotic liver lobules containing insulin-like growth factor II messenger RNA transcripts also contained immunoreactive polypeptide. In contrast, we saw no positive staining for insulin-like growth factor II in tumor cells.
These results imply a role for insulin-like growth factor II in the pathogenesis of cirrhotic/noncirrhotic chronic liver disease to hepatocellular carcinoma where there is evidence of hepatitis B virus involvement. Alterations in posttranscriptional events for insulin-like growth factor II in tumor cells may contribute to the maintenance or progression of the malignant phenotype. (Hepatology 1991;13:310-315).
Hepatitis B virus integration in hepatitis B virus-related hepatocellular carcinoma in childhood
Authors: Chang Mei-Hwei , Chen Pei-Jer , Chen Jen-Yang , Lai Ming-Yang , Hsu Hey-Chi , Lian Der-Cheng , Liu Yueh-Giao , Chen Ding-Shinn 
Published: March 2007

In Taiwan, hepatocellular carcinoma is one of the major malignancies in children between 5 and 14 yr of age. We studied the status of hepatitis B virus DNA in the hepatocellular carcinoma and nontumorous liver tissues of eight children with positive serum HBsAg and maternal HBsAg.
The hepatocellular carcinoma tissues from five of the eight children showed integration of hepatitis B virus DNA into host cellular DNA sequences. A pattern of single-site integration in four children and a multiple-site integration pattern in one child were demonstrated. In the remaining three children, hepatitis B virus DNA could not be demonstrated in the tumor tissues. Using subgenomic fragments of the hepatitis B virus genome as probes, we found that the X gene fragment and the surface antigen gene fragment were the most conserved sequences. The single-site integration of hepatitis B virus DNA in childhood hepatocellular carcinoma may have hit the critical region, resulting in insertional mutagenesis and early development of hepatocellular carcinoma. With a short incubation period and less exposure to environmental carcinogens during early life, childhood hepatocellular carcinoma may provide a good model to study the carcinogenic potential of hepatitis B virus. (Hepatology 1991;13:316-320).
Lichen planus and the liver
Authors: Gumucio Jorge J. , Powell Frank C. , Rogers Roy S. , Dickson Rolland E. 
Published: March 2007

Objective-
To assess the association of lichen planus with liver complaints and with known etiological factors of liver diseases.

Design-
A multicentre case-control study. Interviews were conducted by trained medical investigators on the basis of a structured questionnaire. At the interview patients and controls were asked for consent to blood samples being taken to determine transaminase activities and the presence of hepatitis B virus surface antigen.

Setting-
Outpatient departments of 27 Italian general and teaching hospitals that were collaborating in the Gruppo Italiano Studi Epidemiologici in Dermatologia (GISED).

Subjects-
Incident cases and controls were eligible. A total of 577 patients with lichen planus and 1031 controls with dermatological diseases other than lichen planus were interviewed. Less than 1% of the people contacted refused to participate. Patients and controls were matched for sex and age in 5 year intervals.

Results-
The risk of lichen planus was higher in patients with a history of liver diseases requiring hospital admission or specialist consultation (relative risk = 1.6; 95% confidence interval = 1.2 to 2.2), those who had had liver biopsy (5.5; 1.9 to 15.6) and those with a history of viral hepatitis (1.9; 1.1 to 3.1). High activities of liver enzymes and positive results of tests for hepatitis B virus surface antigen were also associated with lichen planus. The association with alcohol consumption was not clearly confirmed by a dose-risk relationship.

Conclusion-
This study adds quantitative epidemiological evidence to the clinical observation that liver disease is a risk factor for lichen planus although not a specific marker of it.
Characterization of liver-associated natural killer cells in patients with liver tumors
Authors: Winnock Maria , Lafon Marie-Edith , Boulard Annick , Ferrer Anne-Marie , Saric Jean , Dubuisson Liliane , Bioulac-Sage Paulette , Balabaud Charles 
Published: March 2007

The existence of a marginal lymphocyte population in rat liver sinusoids has already been demonstrated using the sinusoidal lavage method. We used the same technique to study the lymphocyte population in human liver obtained ex vivo after partial hepatectomy for benign or malignant tumors and compared it with peripheral and portal blood lymphocyte populations. Percentages of lymphocyte surface phenotypes were evaluated by flow cytometry.
The lymphocyte population obtained from human liver is mainly made up of CD56+ (35%) cells. This percentage is three times greater than that found in peripheral and portal blood. Two-color flow cytometry analysis showed that within the CD56+ liver cell population, at least three distinct subsets could be found: (a) CD3+/CD56+/CD16−; (b) CD3−/CD56+/CD16−; and (c) CD3−/CD56+/CD16+. Although these subsets were also present in peripheral and portal blood, the percentage distribution was completely different because most CD56+ cells in peripheral and portal blood belonged to the CD3−/CD56+/CD16+ subset.
These results show the existence of a heterogeneous natural killer cell population in human livers with tumors. The functional significance of this heterogeneity still needs to be explained. (Hepatology 1991;13:676-682.)
Adenine arabinoside monophosphate and acyclovir monophosphate coupled to lactosaminated albumin reduce woodchuck hepatitis virus viremia at doses lower than do the unconjugated drugs
Authors: Ponzetto Antonio , Fiume Luigi , Forzani Barbara , Song Shi Yun , Busi Corrado , Mattioli Alessandro , Spinelli Cosima , Marinelli Maria , Smedile Antonina , Chiaberge Elisabetta , Bonino Ferruccio , Gervasi Gian Battista , Rapicetta Mariella , Verme Giorgio 
Published: March 2007

The woodchuck was selected to study the efficacy of liver-targeted antiviral drugs on hepadnavirus replication. Nineteen woodchucks chronically infected with woodchuck hepatitis virus were treated with adenine arabinoside monophosphate or acyclovir monophosphate, either free or conjugated with the liver-targeting molecule lactosaminated human serum albumin.
Circulating woodchuck hepatitis virus DNA levels remained unchanged in untreated animals and in those receiving the carrier lactosaminated human serum albumin alone; in contrast, they were consistently lower after 5 days of treatment with the antiviral drugs. Free and conjugated adenine arabinoside monophosphate were active at doses of 10 and 0.75 mg/kg, respectively, and free and coupled ACVMP were active at doses of 20 and 2.6 mg/kg, respectively.
These results indicate that the dosages of adenine arabinoside monophosphate and acyclovir monophosphate required to inhibit hepadnavirus growth can be sharply reduced by coupling the drugs to lactosaminated human serum albumin. (HEPATOLOGY 1991;14:16-24.)
Specificities of serum α-fetoprotein in HBsAg+ and HBsAg− patients in the diagnosis of hepatocellular carcinoma
Authors: Lee Hyosuk , Chung Young Hwa , Kim Chung Yong 
Published: March 2007

Serum α-fetoprotein level is often elevated in patients with chronic liver disease and patients with hepatocellular carcinoma. One of the most difficult problems frequently encountered in practice is differentiating hepatocellular carcinoma from chronic liver disease. This study investigated the specificity and predictive value positive of serum α-fetoprotein at various levels in the diagnosis of hepatocellular carcinoma, using 54 patients with histologically proven hepatocellular carcinoma and 200 patients with chronic liver disease (40 patients with chronic active hepatitis and 160 patients with cirrhosis) as nontumor controls. Among 254 patients, 170 (66.9%) were HBsAg+. A wide range of overlap (from 0 to 6,400 ng/ml) in the distribution of serum α-fetoprotein levels between hepatocellular carcinoma and chronic liver disease patients was observed mainly among HBsAg+ patients. In contrast, the overlapping range of serum α-fetoprotein levels between HBsAg− patients with hepatocellular carcinoma and chronic liver disease was remarkably narrow (from 0 to 200 ng/ml). Therefore the specificity and predictive value positive of α-fetoprotein at a given level were significantly lower in HBsAg+ than in HBsAg− patients, especially when α-fetoprotein was between 25 and 200 ng/ml. The specificities of α-fetoprotein at 200 ng/ml and 400 ng/ml in HBsAg+ patients were 79.8% and 91.5%, respectively, whereas these specificities were both 100% in HBsAg+ patients. The predictive values positive at 200 ng/ml and 400 ng/ml in HBsAg+ patients were 53.6% and 72.5%, respectively, in contrast to 100% at both levels in HBsAg− patients. The serum α-fetoprotein level, which showed a predictive value positive of 95% in HBsAg+ hepatocellular carcinoma patients, was 3,200 ng/ml, whereas that in HBsAg− hepatocellular carcinoma patients, was 200 ng/ml.
We conclude that serum HBsAg status should be considered when serum α-fetoprotein is measured as an independent test to diagnose hepatocellular carcinoma, and suggest that regular serum α-fetoprotein determination may be more useful in HBsAg− patients with chronic liver disease for the early diagnosis of hepatocellular carcinoma than in HBsAg+ patients. (HEPATOLOGY 1991;14:68-72.)
ATP-dependent canalicular transport of cysteinyl leukotrienes
Authors: Ballatori Ned 
Published: March 2007

The liver is the major organ which eliminates leukotriene C4 (LTC4) and other cysteinyl leukotrienes from the blood circulation into bile. Transport of LTC4 was studied using inside-out vesicles enriched in canalicular and sinusoidal membranes from rat liver. The incubation of canalicular membrane vesicles with [
3
H]LTC4 in the presence of ATP resulted in an uptake of LTC4 into vesicles. The initial rate of ATP-stimulated LTC4 uptake was about 40-fold higher in canalicular than in sinusoidal membrane vesicles.
When liver plasma membrane vesicles were incubated in the absence of ATP, an apparent transient uptake of LTC4 was observed which was temperaturedependent and not affected by the osmolarity. This indicates that LTC4 was bound to proteins on the surface of plasma membrane vesicles. Two proteins with relative molecular weights of 17,000 and 25,000 were detected by direct photoaffinity labeling as major LTC4-binding proteins. One protein (M

r
25,000) was ascribed to subunit 1 (Ya) of glutathione S-transferase which was associated with the membrane.
LTD4, LTE4, N-acetyl-LTE4, and ω-carboxy-N-acetyl-LTE4 were also transported into liver plasma membrane vesicles in an ATP-dependent manner with initial rates relative to LTC4 (1.0) of 0.46, 0.11, 0.35, and 0.22, respectively. Mutual competition between the cysteinyl leukotrienes and S-(2,4-dinitrophenyl)-glutathione for uptake indicated that they are transported by a common carrier. Apparent K

m
values of the transport system for LTC4, LTD4, and N-acetyl-LTE4 were 0.25, 1.5, and 5.2 μM, respectively. The ATP-dependent transport of LTC4 into vesicles was not inhibited by doxorubicin, daunorubicin, or verapamil, or by the monoclonal antibody C219, suggesting that the transport system differs from P-glycoprotein.
Liver plasma membrane vesicles prepared from mutant rats deficient in the hepatobiliary excretion of cysteinyl leukotrienes lacked the ATP-dependent transport of cysteinyl leukotrienes and S-(2,4-dinitrophenyl)-glutathione. These results demonstrate that the ATP-dependent carrier system is responsible for the transport of cysteinyl leukotrienes and glutathione S-conjugates from the hepatocytes into bile.
Cystic fibrosis—correct chloride conductance can cure cells
Authors: van Dyke Rebecca W. 
Published: March 2007

We have used retrovirus-mediated gene transfer to demonstrate complementation of the cystic fibrosis (CF) defect in vitro. Amphotropic retroviruses were used to transduce a functional cystic fibrosis transmembrane conductance regulator (CFTR) cDNA into CFPAC-1, a pancreatic adenocarcinoma cell line derived from a patient with CF that stably expresses the chloride transport abnormalities characteristic of CF. CFPAC-1 cells were exposed to control virus (PLJ) and CFTR-expressing virus (PLJ-CFTR); viral-transduced clones were isolated and subjected to molecular and physiologic analysis. RNA analysis detected a viralderived CFTR transcript in all of the PLJ-CFTR clones that contained unrearranged proviral sequences. Agents that increase intracellular cAMP stimulated 125I efflux in PLJ-CFTR clones but not PLJ clones. Whole-cell patch-clamp performed on three responding clones showed that the anion efflux responses were due to cAMP stimulation of Cl conductance. Our findings indicate the expression of the normal CFTR gene confers cAMP-dependent Cl channel regulation on CF epithelial cells.
The cystic fibrosis transmembrane conductance regulator (CFTR) was expressed in cultured cystic fibrosis airway epithelial cells and Cl− channel activation assessed in single cells using a fluorescence microscopic assay and the patch-clamp technique. Expression of CFTR, but not of a mutant form of CFTR (ΔF508), corrected the Cl channel defect. Correction of the phenotypic defect demonstrates a causal relationship between mutations in the CFTR gene and defective Cl transport which is the hallmark of the disease.
Surface modification and characterization of chitosan or PLGA membrane with laminin by chemical and oxygen plasma treatment for neural regeneration
Authors: Huang Yi‐Cheng , Huang Chun‐Chieh , Huang Yi‐You , Chen Keh‐Shaw 
Published: March 2007

AbstractAttachment to and proliferation on the substrate are deemed important considerations when Schwann cells (SCs) are to be seeded in synthetic nerve grafts. Good attachment is a prerequisite for the SCs to survive. Fast proliferation will yield large numbers of SCs in a short time, which appears to be promising for stimulating peripheral nerve regeneration. However, surface properties are the dominating factor in influencing the interactions between cells and synthetic nerve grafts. The aim of this study was to investigate the surface effects of laminin modified PLGA and chitosan membranes after chemical method and plasma treatment. Laminin, the extracellular matrix protein, is a permissive protein for SCs adhesion used in neural regeneration. The surface properties of laminin modified membranes were assayed by BCA, FTIR and XPS analysis. Results showed that laminin was covalently bonded onto the surface of both PLGA and chitosan membranes either by chemical method or by oxygen plasma treatment. The cell affinity of the laminin modified membranes was verified by Schwann cells culturing. Our results also indicate that oxygen plasma is indeed a better method to incorporate laminin onto the surface of membrane. Laminin‐modified chitosan membrane significantly increases SCs attachment and affinity for directing peripheral nerve regeneration. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
Antibacterial and osteogenic properties of silver‐containing hydroxyapatite coatings produced using a sol gel process
Authors: Chen W. , Oh S. , Ong A.P. , Oh N. , Liu Y. , Courtney H.S. , Appleford M. , Ong J.L. 
Published: March 2007

AbstractSince bacterial infection is a rising complication following the wide use of implant, there is considerable attention on the effect of implant surface properties on bacterial adhesion. In this study, the effect of silver (Ag) doped hydroxyapatite (HA) coatings on initial antibacterial adhesion and osteoblast cell proliferation and differentiation was investigated. Using a sol‐gel process, HA coatings doped with 1 wt % AgNO3 (AgHA1.0) and 1.5 wt % Ag (AgHA1.5) were prepared. Coated surfaces were characterized using X‐ray diffraction (XRD) and contact angles measurements. The initial bacteria adhesion was evaluated using a RP12 strain of Staphylococcus epidermidis (ATCC 35984) and the Cowan I strain of Staphylococcus aureus, whereas osteoblast proliferation and differentiation were evaluated using human embryonic palatal mesenchyme cells (HEPM), an osteoblast precursor cell line. In this study, XRD analysis of all surfaces indicated peaks corresponding to HA. Contact angles for AgHA surfaces were observed to be significantly lower when compared to HA surfaces. In vitro initial bacterial adhesion study indicated a significantly reduced number of S. epidermidis and S. aureus on AgHA surfaces when compared to HA surface. The use of HEPM cells indicated no significant difference in double‐stranded DNA (dsDNA) production between all surfaces. Additionally, no differences in alkaline phosphatase specific activity were observed between HA and AgHA1.0 surfaces. Overall, it was concluded that AgHA1.0 has the similar biological activity as HA, with respect to bone cell proliferation and differentiation. In addition, the AgHA1.0 was also concluded to have the ability to minimize the initial bacteria adhesion. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007
Hemocompatibility evaluation of poly(diol citrate) in vitro for vascular tissue engineering
Authors: Motlagh Delara , Allen Josephine , Hoshi Ryan , Yang Jian , Lui Karen , Ameer Guillermo 
Published: March 2007

AbstractOne of the ongoing challenges in tissue engineering is the synthesis of a hemocompatible vascular graft. Specifically, the material used in the construct should have antithrombogenic properties and support the growth of vascular cells. Our laboratory has designed a novel biodegradable, elastomeric copolymer, poly(1,8‐octanediol citrate) (POC), with mechanical and degradation properties suitable for vascular tissue engineering. The hemocompatibility of POC in vitro and its ability to support the attachment and differentiation of human aortic endothelial cell (HAEC) was assessed. The thrombogenicity and inflammatory potential of POC were assessed relative to poly(l‐lactide‐co‐glycolide) and expanded poly(tetrafluoroethylene), as they have been used in FDA‐approved devices for blood contact. Specifically, platelet aggregation and activation, protein adsorption, plasma clotting, and hemolysis were investigated. To assess the inflammatory potential of POC, the release of IL‐1β and TNF‐α from THP‐1 cells was measured. The cell compatibility of POC was assessed by confirming HAEC differentiation and attachment under flow conditions. POC exhibited decreased platelet adhesion and clotting relative to control materials. Hemolysis was negligible and protein adsorption was comparable to reference materials. IL‐1β and TNF‐α release from THP‐1 cells was comparable among all materials tested, suggesting minimal inflammatory potential. POC supported HAEC differentiation and attachment without any premodification of the surface. The results described herein are encouraging and suggest that POC is hemocompatible and an adequate candidate biomaterial for in vivo vascular tissue engineering. © 2007 Wiley Periodicals, Inc. J Biomed Mater Res, 2007