bluuebunny/crossref_metadata_2025_split huggingface dataset:
Production of Interferon and of Plaque Enhancing Factor by Rinderpest‐Virus*
Authors: El‐Zein A. , Srour E. 
Published: August 2010

SummaryRinderpest virus required high multiplicity of infection and prolonged growth in cell cultures for optimal interferon production. More interferon was produced by “aged” than by “young” cultures. Early after infection, culture medium had a plaque‐enhancing effect on vesicular stomatitis virus but when the same materials were treated with heat instead of low pH the plaque‐enhancing activity was lost.ZusammenfassungProduktion von Interferon und Plaque‐vergrößernde Faktoren beim RinderpestvirusMit Rinderpestvirus ist eine starke Vermehrung der infektiösen Einheiten und eine verzögerte Anzucht in Zellkulturen nötig, um eine optimale Interferonproduktion zu induzieren.Es wurde von „älteren” Zellkulturen mehr Interferon synthetisiert als von „jün‐geren”.Kurz nach der Infektion bewirkte das Kulturmedium eine Vermehrung der Plaquebildung durch das Virus der Vesikulären Stomatitis (VSV), aber wenn dasselbe Material antsatt mit Hitze mit niederem pH behandelt wurde, ging diese Plaquevermehrende Aktivität verloren.RésuméProduction d'interféron et du vacteur d'augmentation de plaques chez le virus de la peste bovineUne forte multiplication des unités infectieuses et une production accélérée dans des cultures de cellules sont nécessaires avec le virus de la peste bovine pour induire une production optimale d'interféron. Les cultures cellulaires plus «vieilles» ont synthétisé davantage interféron que les plus «jeunes».Le milieu de culture a provoqué peu après l'infection une augmentation de la formation de plaques avec le virus de la stomatite vésiculeuse (VSV), mais si le même matériel avait été traité avec un pH plus bas à la place de la chaleur, cette activité d'augmentation des plaques se perdait.ResumenLa producción de interferón y del factor que aumenta los plaqués por el virus peste bovinaPara inducir la producción óptima de interferón con el virus peste bovina, se precisa de una multiplicación muy intensa de las unidades infecciosas y un prendimiento retardado en cultivos celulares.Los cultivos celulares «más viejos» sintetizaron más interferón que los «jóvenes».Poco después de la infección provocaba el medio de cultivo una multiplicación de la formación de plaqués por el virus de la estomatitis vesicular (VEV), pero cuando el mismo material era tratado con un pH bajo, en lugar de con calor, se perdía esta actividad multiplicadora de los plaqués.
Openings in the body of ‘capitalism’: Capital flows and diverse economic possibilities in Kiribati
Authors: Pretes Michael , Gibson Katherine 
Published: August 2010

AbstractMuch of the post‐development agenda is concerned with decoupling Eurocentric imaginings of development from development practices in ‘remote’ regions and exploring new forms of economy that can enhance local well‐being. In the South Pacific (and elsewhere), small peripheral economies have confronted globalisation in varying ways. Some places, such as the Micronesian island state of Kiribati, have engaged directly with the global economy by investing capital generated locally in international financial markets rather than in domestic industries. Kiribati's trust fund, the Revenue Equalisation Reserve Fund, maintains a balanced portfolio of international equity and fixed income assets that produces a financial return, helping to augment Kiribati's other national income sources. In this paper we explore the results of capital flowing from Kiribati to global financial markets, noting that this alternative development practice can enhance local well‐being.
PREDICTION‐FOCUSED MODEL SELECTION FOR AUTOREGRESSIVE MODELS
Authors: Claeskens Gerda , Croux Christophe , Van Kerckhoven Johan 
Published: August 2010

SummaryIn order to make predictions of future values of a time series, one needs to specify a forecasting model. A popular choice is an autoregressive time‐series model, for which the order of the model is chosen by an information criterion. We propose an extension of the focused information criterion (FIC) for model‐order selection, with emphasis on a high predictive accuracy (i.e. the mean squared forecast error is low). We obtain theoretical results and illustrate by means of a simulation study and some real data examples that the FIC is a valid alternative to the Akaike information criterion (AIC) and the Bayesian information criterion (BIC) for selection of a prediction model. We also illustrate the possibility of using the FIC for purposes other than forecasting, and explore its use in an extended model.
Genetic contribution of major histocompatibility complex class II region to type 1 autoimmune hepatitis susceptibility in Venezuela
Authors: Fortes María del Pilar , Machado Irma V. , Gil Gisselle , Fernández‐Mestre Mercedes , Dagher Lucy , León Roberto V. , Bianco Nicolás E. , Tassinari Paolo 
Published: August 2010

AbstractAims: Autoimmune hepatitis (AIH) is a progressive liver disease characterized by the presence of circulating autoantibodies, hypergammaglobulinaemia and a favourable response to immunosuppressive treatment. Although the pathogenesis of type 1 AIH is unknown, disease susceptibility is partially determined by genes linked to the class II region of the major histocompatibility complex. Type 1 AIH has been associated with DRB1*03, DRB1*04 and DRB3 alleles in European and North American Caucasians, with DRB1*0405 in Japanese, with DRB1*0404 in Mexican, and with DRB1*1301 in Argentinean populations.Methods: To analyse the molecular basis of these associations in Venezuela (mestizo population), we examined the frequency of human leucocyte antigens (HLA)‐A ‐B ‐C, HLA‐DQ and HLA‐DR genes by low‐ and high‐resolution oligonucleotide typing in a population of 41 type 1 AIH patients and 111 ethnic‐ and aged‐matched healthy subjects.Results: The frequencies of both DRB1*1301 (P<0.0001) and DRB1*0301 (P<0.005) were significantly higher in patients than in controls. In addition, patients showed a strong association with the DRB3 allele (P<0.01). In contrast, the DQB1*04 allele was significantly decreased in the patient group (P<0.01). The frequencies of haplotypes A*01‐B*08‐DQB1*02‐DRB1*03‐DRB3, DQB1*05‐DRB1*1301, DQB1*06‐DRB1*1301 and A*02‐DRB1*1301, B*45‐DRB3 were significantly increased in type 1 AIH patients compared with the controls (P<0.01).Conclusions: In conclusion, our data indicate that type 1 AIH predisposition in a Venezuelan mestizo population of different ethnic backgrounds is associated with DRB1*1301 and DRB1*0301 alleles. In addition, our findings suggest that protection against disease might be conferred by the DQB1*04 allele, with distinct ethnic differences from other populations.
A new hepatic encephalopathy model to monitor the change of neural amino acids and astrocytes with behaviour disorder
Authors: Isobe‐Harima Yumiko , Terai Shuji , Miura Izumi , Segawa Makoto , Murata Tomoaki , Itamoto Kazuhito , Taura Yasuho , Shinoda Koh , Sakaida Isao 
Published: August 2010

AbstractBackground/Aims: To elucidate the pathogenesis of hepatic encephalopathy (HE), we developed a new HE model with behaviour disorder.Methods: Male Wistar rats were divided into four treatment groups: a HE model: acetaminophen (APAP)+3‐methylcholanthrene (3‐MC) group (APAP+MC group); control group: acetaminophen group; 3‐methylcholanthrene group; and a no‐treatment group. We monitored the changes of neural amino acids in the synaptic cleft and astrocytes in the brain during behaviour disorder.Results: In the APAP+MC group, alanine amino transferase, blood ammonia and glucose increased from 3 h and total bilirubin increased at 6 h. Prothrombin time was prolonged from 3 h in the APAP+MC group. The APAP+MC group exhibited centrilobular necrosis in the liver after 8 h. In the APAP+MC group, rats jumped vertically and this vertical activity increased significantly from 4 to 7 h. During the behaviour disorder, we found that glutamate and aspartate increased in the synaptic cleft from 4 h after treatment with APAP+3‐MC, glutamate increased 23.9‐fold at 7 h and aspartate increased 16.1‐fold at 4 h, whereas glutamine did not change. At that time, we observed morphological changes of the astrocytes by immunostaining for the glial fibrillary acidic protein.Conclusions: Our new HE model demonstrated that increased excitatory neural amino acids and morphological change in astrocytes were involved in the behaviour disorder that occurs with HE.
Prevalence of hepatic iron overload and association with hepatocellular cancer in end‐stage liver disease: results from the National Hemochromatosis Transplant Registry
Authors: Ko Cynthia , Siddaiah Narendra , Berger Jose , Gish Robert , Brandhagen David , Sterling Richard K. , Cotler Scott J. , Fontana Robert J. , McCashland Timothy M. , Han Steven H. B. , Gordon Frederic D. , Schilsky Michael L. , Kowdley Kris V. 
Published: August 2010

AbstractBackground: It is unclear whether mild to moderate iron overload in liver diseases other than hereditary haemochromatosis (HH) contributes to hepatocellular carcinoma. This study examined the association between hepatic iron grade and hepatocellular carcinoma in patients with end‐stage liver disease of diverse aetiologies.Methods: The prevalence of hepatic iron overload and hepatocellular carcinoma was examined in 5224 patients undergoing liver transplantation. Explant pathology reports were reviewed for the underlying pathological diagnosis, presence of hepatocellular carcinoma and degree of iron staining. The distribution of categorical variables was studied using χ2 tests.Results: Both iron overload and hepatocellular carcinoma were the least common with biliary cirrhosis (1.8 and 2.8% respectively). Hepatocellular carcinoma was the most common in patients with hepatitis B (16.7%), followed by those with hepatitis C (15.1%) and HH (14.9%). In the overall cohort, any iron overload was significantly associated with hepatocellular carcinoma (P=0.001), even after adjustment for the underlying aetiology of liver disease. The association between hepatic iron content and hepatocellular carcinoma was the strongest in patients with biliary cirrhosis (P<0.001) and hepatitis C (P<0.001).Conclusions: Iron overload is associated with hepatocellular carcinoma in patients with end‐stage liver disease, suggesting a possible carcinogenic or cocarcinogenic role for iron in chronic liver disease.
Plasmatic vitamin C in nontreated hepatitis C patients is negatively associated with aspartate aminotransferase
Authors: Souza dos Santos Rosane M. , De Bem Andreza F. , Colpo Elisângela , Bertoncello Iara , Nogueira Cristina W. , Rocha João B. T. 
Published: August 2010

AbstractObjectives: To evaluate the possible relationship between aminotransferases levels and markers of oxidative stress in chronic hepatitis C patients.Design and methods: Patients without treatment for hepatitis were divided in to group I (15–39 U/L); group II (41–76 U/L) and group III (81–311 U/L) of activity alanine aminotransferase (ALT). Blood markers of oxidative stress [catalase (CAT), glutathione peroxidase (GPx), thiobarbituric acid‐reactive species (TBARS), nonprotein and protein thiol (NP‐SH and P‐SH) groups and vitamin C] were determined.Results: P‐SH and NP‐SH levels, TBARS, GPx and CAT were not different between groups. Vitamin C was significantly decreased in groups II (P=0.03) and III (P=0.001) when compared with group I and correlated negatively with aspartate aminotransferase (AST; r=−0.29, P=0.042).Conclusion: Vitamin C levels were negatively associated with AST, suggesting that vitamin C could be an additional indicator of hepatitis C severity.
Overexpression of NK2 promotes liver fibrosis in carbon tetrachloride‐induced chronic liver injury
Authors: Hagiwara Satoshi , Otsuka Toshiyuki , Yamazaki Yuichi , Kosone Takashi , Sohara Naondo , Ichikawa Takeshi , Sato Ken , Kakizaki Satoru , Takagi Hitoshi , Mori Masatomo 
Published: August 2010

AbstractBackground/Aims: Hepatocyte growth factor (HGF) inhibits liver fibrosis induced by carbon tetrachloride (CCl4) in animal models. NK2 is a natural splice variant of HGF, but its in vivo function remains to be elucidated. We investigated the in vivo effects of NK2 on CCl4‐induced liver fibrosis.Methods: NK2 transgenic mice and wild‐type (WT) mice were injected intraperitoneally with CCl4 twice a week. The extent of hepatic fibrosis was evaluated by Azan–Mallory staining. Expression levels of mRNAs of transforming growth factor‐β1 (TGF‐β1) and matrix metalloproteinase‐13 (MMP‐13) were examined by real‐time polymerase chain reaction. The protein levels of α‐smooth muscle actin (α‐SMA), c‐Met and its phosphorylation were determined by Western blot analysis.Results: Liver fibrosis was significantly more severe in NK2 transgenic mice than in WT mice. CCl4 administration increased the expression levels of TGF‐β1 mRNA and α‐SMA protein, and decreased the expression of MMP‐13 mRNA in livers of NK2 transgenic mice compared with those of WT mice. c‐Met protein expression in the liver was compatible with the degree of fibrosis. As for c‐Met activation, no difference was found between NK2 and WT livers.Conclusion: Overexpression of NK2 acts as an antagonist of HGF and promotes liver fibrosis in CCl4‐induced chronic liver injury.
Lack of cilia and differentiation defects in the liver of human foetuses with the Meckel syndrome
Authors: Clotman Frédéric , Libbrecht Louis , Killingsworth Murray C. , Loo Christine C. K. , Roskams Tania , Lemaigre Frédéric P. 
Published: August 2010

AbstractBackground/Aims: Meckel syndrome is an autosomal‐recessive disease characterized by a combination of renal cysts, anomalies of the central nervous system, polydactyly and ductal plate malformations (DPM), which are hepatic anomalies consisting of excessive and abnormal foetal biliary structures. Among the genomic loci associated with Meckel syndrome, mutations in four genes were recently identified. These genes code for proteins associated with primary cilia and are possibly involved in cell differentiation. The aim of the present work was to investigate the formation of the primary cilia and the differentiation of the hepatic cells in foetuses with Meckel syndrome.Methods: Sections of livers from human foetuses with Meckel syndrome were analysed by immunofluorescence, immunohistochemistry and electron microscopy.Results: The primary cilia of the biliary cells were absent in some Meckel foetuses, but were present in others. In addition, defects in hepatic differentiation were observed in Meckel livers, as evidenced by the presence of hybrid cells co‐expressing hepatocytic and biliary markers.Conclusions: Defects in cilia formation occur in some Meckel livers, and most cases show DPM associated with abnormal hepatic cell differentiation. Because differentiation precedes the formation of the cilia during liver development, we propose that defective differentiation may constitute the initial defect in the liver of Meckel syndrome foetuses.
New ablation procedure for a radiofrequency liver tissue coagulation system using an expandable needle
Authors: Hirakawa Miharu , Ikeda Kenji , Kawamura Yusuke , Kobayashi Masahiro , Hosaka Tetsuya , Yatsuji Hiromi , Sezaki Hitomi , Akuta Norio , Suzuki Fumitaka , Suzuki Yoshiyuki , Saitoh Satoshi , Arase Yasuji , Kumada Hiromitsu 
Published: August 2010

AbstractObjective: The stepwise hook extension technique for an expandable needle, which we reported previously, allowed roll‐off in short time with low power. The aim of this study was to investigate experimentally the efficacy of a modified extension procedure.Methods: Three pigs underwent 10 radiofrequency ablation (RFA) procedures using the 10‐hook electrode of LeVeen needle. The conventional technique was used in five RFA (group 1; the electrode was deployed in four steps to full extension), while the new technique was used in the other five RFA (group 2; the electrode was closed after the same three steps as group 1 and then fully extended).Results: The shape of the RFA‐induced zone was cone‐like or irregular in group 1 and oval‐like in group 2. The diameter vertical to the shaft was larger in group 2 (37, range 33–42 mm) than in group 1 (23, range 20–29 mm). The median ablation time was longer in group 2 (10 min 13 s) than in group 1 (3 min 56 s). Although the required energy was higher in group 2 than in group 1, that per volume was comparable between the groups (median 0.9 vs. 1.4 kJ/mm3).Conclusions: Our new procedure requires a longer session but produces larger necrosis of a uniform ellipsoid volume, making it potentially suitable for tumours more than 3 cm in diameter.
In vivo1H magnetic resonance spectroscopy‐derived metabolite variations between acute‐on‐chronic liver failure and acute liver failure
Authors: Verma Ashish , Saraswat Vivek Anand , Radha Krishna Y. , Nath Kavindra , Thomas M. Albert , Gupta Rakesh Kumar 
Published: August 2010

AbstractBackground and Aims: Acute‐on‐chronic liver failure (ACLF), acute liver failure (ALF) and chronic liver disease (CLD) are common forms of liver failure and present with similar clinical profiles. The aim of this study was to compare brain metabolite alterations in all the three groups of patients with controls, using in vivo proton magnetic resonance spectroscopy (MRS), and to look for any significant differences in metabolites that may help in differentiating between these three conditions.Methods: Nine patients with ACLF, 10 with ALF, 10 patients with CLD and 10 age‐matched controls were studied. The relative concentrations of N‐acetylaspartate (NAA), choline (Cho), glutamine/glutamate (Glx) and myoinositol (mI) with respect to creatine (Cr) were measured.Results: ACLF (3.07±0.72), ALF (4.39±1.25) and CLD (3.15±0.69) patients exhibited significantly increased Glx/Cr ratios compared with controls (2.14±0.42). The NAA/Cr ratio was significantly decreased in both ACLF (mean=0.84±0.28) and CLD (mean=0.97±0.21) patients as compared with that in controls (mean=1.24±0.20). No significant difference among ALF, ACLF and CLD patients was noted in the Cho/Cr ratios. ACLF patients showed significantly lower mI/Cr and Glx/Cr ratios compared with the ALF group.Conclusion: In vivo proton MRS‐derived cerebral metabolite alterations in hepatic encephalopathy owing to ALF are significantly different from the one owing to ACLF and CLD; these may be due to the differences in the pathogenesis of these two overlapping clinical conditions.
Large‐conductance calcium‐activated potassium channels modulate vascular tone in experimental cirrhosis
Authors: Rodríguez‐Vilarrupla Aina , Graupera Mariona , Matei Vasilica , Bataller Ramón , Abraldes Juan G. , Bosch Jaume , García‐Pagán Joan‐Carles 
Published: August 2010

AbstractBackground:Large‐conductance calcium‐activated potassium (BKCa) channels regulate vascular tone in different vascular systems. Moreover, activated hepatic stellate cells (HSC) contain BKCachannels. The aim of this study was to evaluate the role of BKCachannels in the regulation of vascular tone in control (CT) and carbon tetrachloride‐cirrhotic (CH) rat livers.Methods:Changes in intrahepatic vascular resistance were assessed by evaluating the portal perfusion pressure (PP) response to methoxamine (Mtx) in the presence of Iberiotoxin (Ibtx; a BKCachannel blocker), NS1619 (a BKCachannel opener), Ibtx plus the nitric oxide (NO) synthase inhibitor,NG‐nitro‐l‐arginine (l‐NNA) orl‐NNA alone. In addition, in CH livers, PP dose–response curves to the NO donor,S‐nitroso‐N‐acetyl‐d,l‐penicillamine (SNAP), were performed after pre‐incubation with Ibtx or its vehicle. BKCamRNA expression was assessed in liver homogenates, and BKCaprotein expression in HSC isolated from CT and CH livers.Results:In CH livers, Ibtx significantly increased baseline PP and exacerbated the PP response to Mtx. Conversely, NS1619 induced a mild nonsignificant decrease of baseline PP and attenuated the hyperresponse to Mtx. CH livers exhibited an upregulation of both mRNA and protein of the α‐subunit of BKCa.Conclusion:Large‐conductance calcium‐activated potassium channels are overexpressed in CH livers and might represent a compensatory mechanism modulating the increased hepatic vascular tone of cirrhosis.
Steatosis correlates with hepatic expression of death receptors and activation of nuclear factor‐κB in chronic hepatitis C
Authors: Hung Chao‐Hung , Lee Chuan‐Mo , Kuo Fang‐Ying , Jiang Shu‐Rong , Hu Tsung‐Hui , Chen Chien‐Hung , Wang Jing‐Houng , Lu Sheng‐Nan , Eng Hock‐Liew , Changchien Chi‐Sin 
Published: August 2010

AbstractBackground: Steatosis is recognized as a predictor of the severity as well as the progression of fibrosis in chronic hepatitis C. The mechanisms that cause increased hepatocellular injury associated with steatosis remain largely unknown.Methods: We studied the correlation of hepatic expression of death receptors: Fas and tumour necrosis factor‐α receptor 1 (TNF‐R1), and downstream caspase (caspase‐3) with hepatic steatosis by immunohistochemical study in chronic hepatitis C and determined the role of nuclear factor‐κB (NF‐κB).Results: Ninety patients (49 males and 41 females, mean age of 50.5 ± 10.4 years, genotype 1 or 2) with chronic hepatitis C virus infection were recruited. The factors associated with steatosis grade were body mass index (P=0.004) and fibrosis stage (P=0.034). Moderate/severe steatosis was an independent variable associated with advanced fibrosis stage by stepwise logistic regression analysis. The expression of immunoreactivity for Fas, TNF‐R1 and active caspases‐3 in liver tissues was significantly correlated with the steatosis grade (P<0.001, P<0.001 and P<0.001 respectively). The extent of active caspases‐3 correlated significantly with the expression of Fas (r=0.659, P<0.001) and TNF‐R1 (r=0.617, P<0.001). NF‐κB p65 expression correlated significantly with the extent of Fas (r=0.405, P<0.001), TNF‐R1 (r=0.448, P=0.002) and active caspase‐3 (r=0.313, P=0.003), and correlated with steatosis grade (P<0.001) but not with inflammatory and fibrosis scores.Conclusion: Our observations suggest a mechanism whereby steatosis contributes to the progression of liver injury in chronic hepatitis C through upregulation of death receptors and activation of NF‐κB.
Molecular bases of the fetal liver–placenta–maternal liver excretory pathway for cholephilic compounds
Authors: Marin Jose J. G. , Macias Rocio I. R. , Briz Oscar , Perez Maria J. , Blazquez Alba G. , Arrese Marco , Serrano Maria A. 
Published: August 2010

AbstractPotentially toxic endogenous compounds, such as bile acids (BAs) and biliary pigments, as well as many xenobiotics, such as drugs and food components, are biotransformed and eliminated by the hepatobiliary system with the collaboration of the kidney. However, the situation is very different during pregnancy because the fetal liver produces biliary compounds despite the fact that this organ, owing to its immaturity, is not able to eliminate them into bile. Moreover, the excretory ability of the fetal kidneys is also very limited. Thus, during the intra‐uterine life, the major route to eliminate fetal BAs and biliary pigments is their transfer to the mother across the placenta. The maternal liver and, to a lesser extent, the maternal kidney, are then in charge of their biotransformation and elimination into faeces and urine respectively. This review describes current knowledge of the machinery responsible for the detoxification and excretion of cholephilic compounds through the pathway formed by the fetal liver–placenta–maternal liver trio.