bluuebunny/crossref_metadata_2025_split huggingface dataset:
Features of compulsive checking behavior mediated by nucleus accumbens and orbital frontal cortex
Authors: Dvorkin Anna , Silva Charmaine , McMurran Thomas , Bisnaire Liane , Foster Jane , Szechtman Henry 
Published: August 2010

AbstractThe quinpirole sensitization model of obsessive‐compulsive disorder was used to investigate the functional role that brain regions implicated in a neuroanatomical circuit of obsessive‐compulsive disorder may play in compulsive checking behavior. Following repeated injections of saline or quinpirole (0.5 mg/kg, twice per week, ×8 injections) to induce compulsive checking, rats received N‐methyl‐d‐aspartate lesions of the nucleus accumbens core (NAc), orbital frontal cortex (OFC) and basolateral amygdala, or sham lesions. When retested at 17 days post‐surgery, the results showed effects of NAc and OFC but not basolateral amygdala lesion. NAc lesions affected measures indicative of the amount of checking behavior, whereas OFC lesions affected indices of staying away from checking. The pattern of results suggested that the functional roles of the NAc and OFC in checking behavior are to control the vigor of motor performance and focus on goal‐directed activity, respectively. Furthermore, similarities in behavior between quinpirole sham rats and saline NAc lesion rats suggested that quinpirole may drive the vigor of checking by inhibition of NAc neurons, and that the NAc may be a site for the negative feedback control of checking.
Anabolic–androgenic steroids and liver injury
Authors: Sánchez‐Osorio Magdalena , Duarte‐Rojo Andrés , Martínez‐Benítez Braulio , Torre Aldo , Uribe Misael 
Published: August 2010

AbstractAthletes and nonathletes have been using anabolic–androgenic steroids (AAS) for a long time, in an inadequate and unsurveilled manner, with the aim of improving sports performance or for cosmetic purposes. AAS consumption is becoming more widespread and involving younger people, and there is a trend for self‐administration of higher doses and for combining AAS with other potentially harmful drugs. Almost any subject abusing AAS will experience adverse effects. Therefore, adverse effects from these exposures, including liver toxicity, are expected to increase in the years to come. The present manuscript describes a representative case of intrahepatic cholestasis with the intention to discuss AAS‐related liver toxicity (including the potential therapeutic role of ursodeoxycholic acid) and to comment on several aspects of the clinical scenario the gastroenterologist should be aware of.
Basal core promoter T1762/A1764 and precore A1896 gene mutations in hepatitis B surface antigen‐positive hepatocellular carcinoma: a comparison with chronic carriers
Authors: Tong Myron J. , Blatt Lawrence M. , Kao Jia‐Horng , Cheng Jason Tzuying , Corey William G. 
Published: August 2010

AbstractBackground: Chronic hepatitis B virus (HBV) infection is associated with hepatocellular carcinoma (HCC), and specific viral factors have been identified that may increase the risk for HCC development. However, the differences in these viral factors in chronic carriers who seldom develop HCC compared with HCC patients have not been adequately evaluated.Methods: From 1989 to 2005, 101 hepatitis B surface antigen‐positive patients presented to our clinic with HCC. Baseline basal core promoter (BCP) T1762/A1764 mutants, precore (PC) A1896 mutants, HBV genotypes and HBV DNA in HCC patients were compared with 67 chronic carriers who had been followed for a mean of 112.1±77.7 standard deviation months.Results: At baseline, HCC patients had lower levels of serum albumin, but higher values of alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, bilirubin and α‐foetoprotein than those of chronic carriers (P<0.001 for all comparisons). The presence of genotype C, higher frequencies of PC A1896 mutants, BCP T1762/A1764 mutants and higher circulating levels of HBV DNA were more frequently detected in HCC patients than that in chronic carriers (P<0.001 for all observations). Logistic regression analysis revealed that BCP T1762/A1764 mutants [odds ratio (OR) 11.14, 95% confidence interval (CI) 3.05–40.72; P<0.001] and PC A1896 mutants (OR 3.75, 95% CI 1.14–12.34; P<0.05) were significantly associated with HCC development.Conclusion: Our results indicate that the presence of BCP and PC mutations significantly increases the risk for HCC in chronic hepatitis B patients. These mutations were less often detected in chronic carriers who seldom develop HCC.
Hepatocellular carcinoma appearance in patients with hepatitis C virus‐related chronic liver disease 90 and 70 months after sustained virological response to interferon and ribavirin
Authors: Vukotic Ranka , Gramenzi Annagiulia , Vitale Giovanni , Cursaro Carmela , Serra Carla , Biselli Maurizio , Scuteri Alessandra , Andreone Pietro , Bernardi Mauro 
Published: August 2010

AbstractWe report here two cases of hepatocellular carcinoma (HCC) 90 and 70 months, respectively, after successful treatment with interferon (IFN) and ribavirin for hepatitis C virus (HCV)‐related cirrhosis. A 50‐year‐old Caucasian man and a 66‐year‐old Caucasian woman with HCV‐related cirrhosis were treated with IFN and ribavirin and in both cases a sustained virological response (SVR) was obtained with persistent normalization of serum aminotransferases and continuous disappearance of serum HCV‐RNA. Both patients were subsequently followed up within an HCC surveillance programme based on biochemical and ultrasound (US) evaluation every 6 months and the appearance of HCC was detected 90 and 70 months, respectively, after discontinuation of therapy. We introduce these two cases to call attention to the importance of not underestimating the risk of HCC development even many years after complete HCV eradication, especially in the presence of established cirrhosis and concomitance of other risk factors for HCC.
Evolution of hepatitis C virus infection under host factor influence in an ethnically complex population
Authors: Cursino‐Santos Jeny R. , Donadi Eduardo A. , Martinelli Ana L. C. , Louzada Paulo , Martinez‐Rossi Nilce M. 
Published: August 2010

AbstractBackground: The ethnic influence makes it difficult to reach a consensual definition of host‐dependent genetic factors controlling the hepatitis C virus (HCV) disease course.Aims: To investigate, in an ethnically complex Brazilian population, whether human leucocyte antigen (HLA) molecules are associated with susceptibility to HCV infection, self‐limiting viral clearance and predisposition to chronic disease.Methods: One hundred and four HCV‐antibody‐positive patients (stratified into groups with spontaneous viral clearance and chronic HCV infection) and 166 healthy controls were submitted to HLA genotyping.Results: Two strong associations were observed between the susceptibility to HCV infection and DRB3 [odds ratio (OR), 4.03; 95% confidence interval (CI), 2.40–6.77; Pc=0.0000041] and DQB1*02 (OR, 1.72; 95% CI, 1.05–2.84; P=0.041), and between the spontaneous viral clearance and DRB1*01 (OR, 4.59; 95% CI, 1.70–12.41; P=0.003) and DQB1*03 (OR, 2.83; 95% CI, 1.14–7.02; P=0.029). No evidence was observed regarding the epidemiology or viral genotype influence on the disease course.Conclusion: We could confirm with a highly admixed population the association of viral clearance with two allele groups (DRB1*01 and DQB1*03) previously reported in homogeneous populations. The identification of DRB1*01 and DQB1*03 involved with self‐limiting hepatitis in different ethnic groups is a very important finding that will contribute to the current knowledge about HCV–host interaction and the development of therapeutic vaccines.
Liver transplantation and quality of life: relevance of a specific liver disease questionnaire
Authors: Gotardo Daniela R. M. , Strauss Edna , Teixeira Maria‐Cristina D. , Machado Marcel C. C. 
Published: August 2010

AbstractAim:A positive effect of liver transplantation on health‐related quality of life (HRQOL) has been well documented in previous studies using generic instruments. Our aim was to re‐evaluate different aspects of HRQOL before and after liver transplantation with a relatively new questionnaire the ‘liver disease quality of life’ (LDQOL).Methods:The LDQOL and the Short Form 36 (SF‐36) questionnaires were applied to ambulatory patients, either in the transplant list (n=65) or after 6 months to 5 years of liver transplant (n=61). The aetiology of cirrhosis, comorbidities, model for end‐stage liver disease (MELD) Child–Pugh scores and recurrence of liver disease after liver transplantation were analysed using the Mann–Whitney and Kruskall–Wallis tests.Results:In patients awaiting liver transplantation, MELD scores ≥15 and Child–Pugh class C showed statistically significant worse HRQOL, using both the SF‐36 and the LDQOL questionnaires. HRQOL in pretransplant patients was found to be significantly worse in those with cirrhosis owing to hepatitis C (n=30) when compared with other aetiologies (n=35) in 2/7 domains of the SF‐36 and in 7/12 domains of the LDQOL. Significant deterioration of HRQOL after recurrence of hepatitis C post‐transplant was detected with the LDQOL questionnaire although not demonstrated with the SF‐36. The statistically significant differences were in the LDQOL domains: symptoms of liver disease, concentration, memory and health distress.Conclusions:The LDQOL, a specific instrument for measuring HRQOL, has shown a greater accuracy in relation to liver symptoms and could demonstrate, with better reliability, impairments before and after liver transplantation.
High incidence of type 1 diabetes mellitus during or shortly after treatment with pegylated interferon α for chronic hepatitis C virus infection
Authors: Schreuder Tim C. M. A. , Gelderblom Huub C. , Weegink Christine J. , Hamann Dörte , Reesink Henk W. , DeVries J. Hans , Hoekstra Joost B. L. , Jansen Peter L. M. 
Published: August 2010

AbstractBackground: Development of diabetes mellitus (DM) during or shortly after treatment with interferon α (IFN‐α) in patients with chronic hepatitis C virus (HCV) infection has been reported sporadically. We prospectively screened for DM during and after IFN‐α therapy for chronic HCV infection.Methods: Blood glucose levels of patients with chronic HCV infection were routinely assessed at all outpatient visits during and after treatment with pegylated‐IFN‐α (Peg‐IFN‐α) and ribavirin (Riba).Results: Between December 2002 and October 2005, 189 non‐diabetic patients were treated with Peg‐IFN‐α/Riba, of whom five developed type 1 DM (2.6%), three type 2 DM (1.6%) and one an indeterminate type of DM. Classical symptoms of DM were present in three patients who developed DM shortly after cessation of Peg‐IFN‐α/Riba. In the other patients, symptoms of DM were either indistinguishable from side effects caused by Peg‐IFN‐α/Riba or absent.Conclusion: Our study showed a high incidence of type 1 DM during Peg‐IFN‐α/Riba therapy for chronic HCV infection. Symptoms of DM may be absent or mistaken for Peg‐IFN‐α/Riba‐associated side effects. To diagnose DM without delay, we propose routine assessment of blood glucose at all outpatient visits during and after Peg‐IFN‐α/Riba treatment in chronic HCV patients.
Prophylaxsis against recurrance of hepatitis B virus after liver transplantation: a retrospective analysis spanning 20 years
Authors: Yilmaz Nevin , Shiffman Mitchell L. , Todd Stravitz R. , Sterling Richard K. , Luketic Velimir A. , Sanyal Arun J. , Maluf Daniel , Coterell Adrian , Posner Marc P. , Fisher Robert A. 
Published: August 2010

AbstractLiver transplantation (LT) in patients with hepatitis B virus (HBV) infection is associated with a high rate of graft loss and poor survival, unless re‐infection can be prevented. Human hepatitis B immune globulin (HBIG) has long been utilized to prevent re‐infection. More recently, an anti‐viral agent has been utilized along with HBIG. However, the regimens utilized have varied considerably among LT programmes and the optimal regimen has never been defined. We conducted a retrospective analysis of 41 patients who underwent LT for HBV at our centre since 1985 and received either HBIG with or without an anti‐viral agent. The mean age of these patients was 46 years; 81% were male and 88% white. The mean and maximal follow‐up were 5.9 and 15 years respectively. Eight out of 15 E‐antigen‐positive patients who received HBIG alone developed recurrence after a mean of 17 months. In contrast, none of 10 E‐Ag‐negative patients who received HBIG alone and none of the 10 E‐antigen‐positive patients who received both HBIG and either lamivudine or adefovir developed recurrence. As long as the anti‐HB surface remained detectable, no absolute minimum serum level appeared to lead to recurrent HBV. We concluded that recurrence of HBV following LT can be prevented in E‐antigen‐positive patients with a combination of HBIG and an anti‐viral agent. In contrast, recurrence can be prevented in E‐antigen‐negative patients with HBIG alone. Maintaining a serum anti‐HB surface level above a minimum arbitrary titre of 200 pg/mL did not appear to be necessary for effective HBIG prophylaxis.
Effect of peroxisome proliferator‐activated receptors‐γ and co‐activator‐1α genetic polymorphisms on plasma adiponectin levels and susceptibility of non‐alcoholic fatty liver disease in Chinese people
Authors: Hui Yang , Yu‐Yuan Li , Yu‐Qiang Nie , Wei‐Hong Sha , Yan‐Lei Du , Xiao‐Bo Lai , Yong‐Jian Zhou 
Published: August 2010

AbstractBackground/Aims: Peroxisome proliferator‐activated receptors‐γ (PPAR‐γ) and its co‐activator‐1α (PGC‐1α) are involved in the regulation of lipid and glucose metabolisms. This study aimed to investigate the genetic polymorphisms of PPAR‐γ and PGC‐1α in Chinese people and their influence on plasma adiponectin levels and non‐alcoholic fatty liver disease (NAFLD) susceptibility.Methods: Ninety‐six patients with NAFLD and 96 healthy controls were included. The single nucleotide polymorphisms (SNPs) of C161T PPAR‐γand Gly482Ser PGC‐1α genes were analysed by polymerase chain reaction and restriction fragment length polymorphism.Result: The CC, CT and TT genotypic distributions of the NAFLD group were significantly different from those of controls (55.2, 39.6, 5.2 vs. 74.0, 25.0, 1.0%; P=0.015). The allelic frequencies of C and T were also different between the two groups (P=0.004). As for the PGC‐1α gene, there was no difference of the genotypic and allelic frequencies between the two groups (P>0.05). In NAFLD patients, the plasma adiponectin concentrations were lower in the PPAR‐γ CT/TT genotypes compared with those in the CC genotype group (3.0±0.6 vs. 4.3±0.9, P=0.02). Multivariate logistic regression analysis showed that CT/TT genotypes of PPAR‐γ, TG, waist hip ratio, hypoadiponectinaemia and homoeostasis model assessment (HOMA)‐IR were the risk factors for NAFLD.Conclusion: SNPs in the PPAR‐γ, but not PGC‐1α, gene are associated with NAFLD susceptibility possibly through the adiponectin pathway.
Persistent hepatitis B viral replication affects recurrence of hepatocellular carcinoma after curative resection
Authors: Kim Beom Kyung , Park Jun Yong , Kim Do Young , Kim Ja Kyung , Kim Kyung Sik , Choi Jin Sub , Moon Byung Soo , Han Kwang Hyub , Chon Chae Yoon , Moon Young Myoung , Ahn Sang Hoon 
Published: August 2010

AbstractBackground: Elevated serum hepatitis B virus (HBV) DNA increases the development of hepatocellular carcinoma (HCC). Rather than instantaneous DNA level, the duration of persistent HBV replication is more important in carcinogenesis. Nevertheless, most investigators evaluated the DNA level at study entry. We assessed the effects of persistently detectable serum HBV DNA on HCC recurrence.Patients and methods: We included 230 consecutive patients undergoing curative resection between 2000 and 2006. Patients who had antiviral therapy (at diagnosis or during follow‐up), fluctuating DNA (cut‐off value: 100 000 copies/ml) or recurrence within 12 months of resection were excluded. Ultimately, 157 were enrolled: 89 (non‐viraemia group) had consistently negative DNA (<100 000 copies/ml), while 68 (viraemia group) had consistently positive DNA (>100 000copies/ml). Serum DNA level, biochemical tests, α‐foetoprotein (AFP) and liver dynamic computed tomography were obtained every 3 months after surgery.Results: There were no significant differences in age, gender, liver function, histology, AFP, tumour stages or follow‐up duration between the two groups. During follow‐up (median: 35 months), patients in the non‐viraemia group had a lower 5‐year cumulative recurrence rate (54.7%) than those in the viraemia group (72.9%; P=0.043). In multivariate analysis, sustained viraemia (P=0.041) increased recurrence independently.Conclusions: Persistent viraemia increased recurrence independently after surgery. To prevent long‐term recurrences, antiviral therapy should be initiated in those with detectable serum HBV DNA.
High hepatitis C viral load is associated with insulin resistance in patients with chronic hepatitis C
Authors: Hsu Ching‐Sheng , Liu Chun‐Jen , Liu Chen‐Hua , Wang Chia‐Chi , Chen Chi‐Ling , Lai Ming‐Yang , Chen Pei‐Jer , Kao Jia‐Horng , Chen Ding‐Shinn 
Published: August 2010

AbstractBackground and Aims:Although insulin resistance affects liver fibrosis progression and treatment response in chronic hepatitis C (CHC), the relationship between chronic hepatitis C virus (HCV) infection and insulin resistance (IR) remains to be firmly established. We thus studied the impact of host, metabolic and viral factors on IR in CHC patients.Methods:A total of 162 CHC patients with complete clinical data were enrolled. Among them, 94 received histological examinations. Quantitative HCV RNA was assayed by a real‐time polymerase chain reaction (PCR) assay. Genotyping was performed by reverse transcription PCR with type‐specific primers. The pretreatment IR index was determined using homeostasis model assessment (HOMA), and an index value of more than 2.4 was designated IR. Unadjusted and adjusted association of the HCV RNA level and IR was further analysed.Results:In multivariate linear regression analysis, a dose–response relationship was observed between the log10 HCV RNA level and the presence of IR. IR was positively correlated with body mass index, triglyceride, HCV RNA and alanine aminotransferase levels, but negatively correlated with adiponectin level. Subgroup analysis stratified by HCV genotype showed that there was a trend towards a higher HOMR‐IR index value and lower adiponectin levels in genotype 1 patients. Histological analysis showed that IR was positively associated with the severity of hepatic steatosis.Conclusions:Our data indicate that higher HCV RNA levels are associated with the presence of IR in CHC patients. Further studies are needed to clarify the interplays between HCV infection, IR and adiponectin in an attempt to develop new adjuvant therapy for CHC.
Transforming growth factor‐β induces epithelial to mesenchymal transition by down‐regulation of claudin‐1 expression and the fence function in adult rat hepatocytes
Authors: Kojima Takashi , Takano Ken‐ichi , Yamamoto Toshinobu , Murata Masaki , Son Seiichi , Imamura Masafumi , Yamaguchi Hiroshi , Osanai Makoto , Chiba Hideki , Himi Tetsuo , Sawada Norimasa 
Published: August 2010

AbstractBackground/Aims: Transforming growth factor‐β (TGF‐β) initiates and maintains epithelial–mesenchymal transition (EMT), which causes disassembly of tight junctions and loss of epithelial cell polarity. In mature hepatocytes during EMT induced by TGF‐β, changes in the expression of tight junction proteins and the fence function indicated that epithelial cell polarity remains unclear.Methods: In the present study, using primary cultures of adult rat hepatocytes at day 10 after plating, in which epithelial cell polarity is well maintained by tight junctions, we examined the effects of 0.01–20 ng/ml TGF‐β on the expression of the integral tight junction proteins, claudin‐1, ‐2 and occludin, as well as the fence function.Results: In adult rat hepatocytes, TGF‐β induced EMT, which was indicated as upregulation of Smad‐interacting protein‐1 (SIP1) and Snail and down‐regulation of E‐cadherin. Down‐regulation of claudin‐1 and upregulation of occludin were observed beginning from a low dose of TGF‐β, whereas upregulation of claudin‐2 was observed at a high dose of TGF‐β. Furthermore, treatment with TGF‐β caused disruption of the fence function, which was closely associated with the expression of claudin‐1 via p38 mitogen‐activated protein kinase (MAPK), phosphoinositide‐3 kinase and protein kinase C but not MAPK signalling pathways.Conclusion: These results suggest that in mature hepatocytes in vitro, TGF‐β induces EMT by down‐regulation of claudin‐1 and the fence function via distinct signalling pathways.
Evaluation of hepatotropic targeting properties of allogenic and xenogenic erythrocyte ghosts in normal and liver‐injured rats
Authors: Gressner Olav A. , Lahme Birgit , Koch Martin , Gressner Axel M. 
Published: August 2010

AbstractBackground/Aims: Haemoglobin‐depleted erythrocyte ghosts have been recommended as vesicle carriers of drugs with hepatotropic properties. However, the influence of liver injury on ghost elimination and targeting has not been reported so far.Methods: Human and rat ghosts were prepared and loaded with model substances, and the basic parameters were characterized. Ghosts were injected intravenously into rats with acute, subacute and chronic liver injuries. Elimination from circulation, organ distribution and cellular targeting was measured. The uptake of ghosts by liver macrophages/Kupffer cells was determined in cell culture.Results: Ghosts are strong hepatotropic carriers with a recovery of 90% in normal liver. Kupffer cells are the almost exclusive target cell type. Hepatotropic properties remain in rats with chronic liver diseases, but are reduced by 60–70% in acute liver damage as a result of decline of phagocytosis of macrophages/Kupffer cells. Although the uptake of ghosts per gram liver tissue in chronic liver injury was also reduced by about 40%, the increase of liver mass and of macrophages/Kupffer cells compensated for the reduced phagocytotic activity. In subacute injury, the uptake per gram liver tissue was only moderately reduced.Conclusion: Drug targeting with ghosts might be feasible in chronic and subacute liver injuries, e.g. fibrogenesis and tumours, because the content of ingested ghosts is released by Kupffer cells into the micro‐environment, providing the uptake by and pharmacological effects on adjacent cells.