bluuebunny/crossref_metadata_2025_split huggingface dataset:
Protective effect of Kalpaamruthaa in combating the oxidative stress posed by aflatoxin B1‐induced hepatocellular carcinoma with special reference to flavonoid structure–activity relationship
Authors: Umarani Mohanasundaram , Shanthi Palanivelu , Sachdanandam Panchanadham 
Published: August 2010

AbstractAims/Background: Aflatoxin B1(AFB1) is a potent hepatotoxic and hepatocarcinogenic mycotoxin. It has been postulated to play a major role in the aetiology of primary human liver cancer. Lipid peroxidation (LPO) is one of the main manifestations of oxidative damage and has been found to play an important role in the toxicity and carcinogenesis of many carcinogens. The present investigation aimed at assessing the effect of Kalpaamruthaa (KA), a modified Siddha preparation, on AFB1‐mediated hepatocellular carcinoma (HCC).Methods: The drug was administered orally (300 mg/kg body weight/day) for 28 days to HCC‐bearing rats. The level of lipid peroxides, antioxidant enzymes, glutathione and glutathione‐metabolizing enzyme activity were determined in the plasma, haemolysate and liver homogenate of control and experimental rats.Results: Rats subjected to AFB1showed a decline in the thiol capacity of the cell, accompanied by high malondialdehyde levels along with lowered activities of enzymic and non‐enzymic antioxidant and glutathione‐metabolizing enzyme levels. KA treatment restored the deranged LPO and enzyme activities almost to control levels, thereby suggesting hepatoprotection.Conclusion: This study highlighted the beneficial effect of KA in reversing the damage posed by AFB1and thereby bringing about an improvement in the antioxidant status to combat the oxidative stress.
Prevalence of diabetes mellitus and insulin resistance in patients with chronic hepatitis C: comparison with hepatitis B virus‐infected and hepatitis C virus‐cleared patients
Authors: Imazeki Fumio , Yokosuka Osamu , Fukai Kenichi , Kanda Tatsuo , Kojima Hiroshige , Saisho Hiromitsu 
Published: August 2010

AbstractBackground/Aims: Our aim was to evaluate the relationship between hepatitis C virus (HCV) infection and development of diabetes mellitus (DM) or insulin resistance (IR) in comparison with hepatitis B virus (HBV) infection and eradication of HCV infection by interferon treatment.Methods: This study consisted of 952 outpatients, including 544 HCV‐infected (HCV+chronic), 286 HBV‐infected (HBV+chronic) and 122 patients whose HCV was cleared by interferon treatment (HCV+cleared) (diabetes study). Among 849 without overt DM, IR was assessed in 423 patients, including 232 HCV‐infected (HCV+chronic), 135 HBV‐infected (HBV+chronic) and 56 HCV‐eradicated patients (HCV+cleared) (IR substudy).Results: The prevalence of DM in the HBV+chronic, HCV+chronic and HCV+cleared groups was 6.3, 13.6 and 9.0%, respectively (HBV+chronic vs HCV+chronic, P<0.005), in the diabetes study, and the prevalence of IR in the HCV+chronic group (54.3%) was also higher than that in the HBV+chronic (36.3%) (P<0.005) and HCV+cleared groups (35.7%) (P<0.05) in the IR substudy. However, HCV infection was not shown to be independently associated with DM development [odds ratio (OR) 1.669; P=0.0936] and with IR (OR 1.531; P=0.2154) by multivariate analysis in comparison with HBV infection as control.Conclusions: HCV‐infected patients showed a higher prevalence of DM and IR than those with HBV infection. However, in Japan, other confounding factors appeared to be more important risk factors for the development of disturbance in glucose metabolism.
An enormous hepatitis B virus‐related liver disease burden projected in Vietnam by 2025
Authors: Nguyen Van Thi Thuy , Law Matthew G. , Dore Gregory J. 
Published: August 2010

AbstractBackground: Hepatitis B virus (HBV) is the major cause of chronic liver disease in Vietnam. This study aimed to estimate and project chronic HBV prevalence and HBV‐related liver cirrhosis (LC) and hepatocellular carcinoma (HCC) for the period 1990–2025.Method: The Vietnamese population for the period 1990–1999 was derived from census data to 1999 and from 2000 to 2025 based on projection data from the United States Census Bureau. Population chronic HBV prevalence for males and females was estimated based on age‐specific HBV prevalence from Vietnamese community‐based studies. Universal infant HBV vaccination from 2003 was assumed to reduce HBV infection by 90% in subsequent birth cohorts. Incidences of HBV‐related LC and HCC by HBV DNA levels from the Taiwanese REVEAL studies were applied to the chronic HBV population to estimate and project HBV‐related liver disease burden.Results: Estimated chronic HBV prevalence increased from 6.4 million cases in 1990 to around 8.4 million cases in 2005 and was projected to decrease to 8.0 million by 2025. Estimated HBV‐related LC and HCC incidence increased linearly from 21 900 and 9400 in 1990 to 58 650 and 25 000 in 2025. Estimated HBV‐related mortality increased from 12 600 in 1990 to 40 000 in 2025.Conclusion: Over the next two decades, universal infant HBV vaccination will reduce chronic HBV prevalence in Vietnam but HBV‐related liver disease burden will continue to rise. A national HBV strategy is required to address this expanding burden of liver disease.
Antimitochondrial antibody‐negative primary biliary cirrhosis: a subset of primary biliary cirrhosis
Authors: Liu Bin , Shi Xu Hua , Zhang Feng Chun , Zhang Wen , Gao Li Xia 
Published: August 2010

AbstractObjective: Antimitochondrial antibodies (AMA) are the hallmark in primary biliary cirrhosis (PBC); nevertheless, it has long been recognized that 5–10% patients with typical features compatible with PBC do not have detectable AMA, and they were referred to as ‘AMA‐negative PBC’. This study aimed to evaluate whether AMA‐negative/positive PBC represents different clinical entities.Methods: We compared the clinical, laboratory, percentage of regulatory T cells (Tregs) in peripheral blood, liver biopsy features and response to treatment of the two groups of patients. The first group was comprised of 12 patients with ‘AMA‐negative PBC’. The second was made up of another 12 PBC patients with positive AMA.Results: Antimitochondrial antibodies‐negative/positive patients were remarkably similar in terms of clinical manifestations, liver biochemistries and histological findings. The frequency of anti‐nuclear antibodies, anti‐smooth‐muscle antibody, anti‐gp210 and anti‐sp100 antibody showed no significant difference between the two groups. A significantly lower mean percentage of CD4+CD25high T cells was observed in peripheral blood mononuclear cells of AMA‐negative/positive PBC patients compared with that of the 12 control subjects (5.8±1.8 and 5.4±1.4% vs. 7.6±1.7% respectively; P=0.014 and 0.004). However, no difference could be found between AMA‐negative and AMA‐positive PBC patients (P=0.599). After 1 year treatment with ursodeoxycholic acid, the two groups showed similar response.Conclusion: Antimitochondrial antibody‐negative/positive PBC patients are similar in clinical, laboratory, percentage of Treg in peripheral blood, liver biopsy features and response to treatment. This suggests that AMA‐negative PBC may be a variant of AMA‐positive PBC rather than a separate clinical entity.
Renal hepatitis C in the absence of detectable serum or hepatic virus
Authors: Fowell Andrew J. , Sheron Nicholas , Rosenberg William M. C. 
Published: August 2010

AbstractWe report an apparently unique case where hepatitis C virus (HCV) RNA was identified in renal tissue from a patient with membranoproliferative glomerulonephritis and treated chronic hepatitis C, despite the absence of detectable virus in the serum or liver (COBAS Amplicor qualitative assay, lower limit of detection 50 IU/ml). The implications of this finding are discussed, with particular reference to current concepts regarding ‘occult’ hepatitis C infection.
Zinc modulates lithium‐induced hepatotoxicity in rats
Authors: Chadha Vijayta Dani , Bhalla Punita , Dhawan Devinder Kumar 
Published: August 2010

AbstractAim: The present study explored the hepatoprotective role of zinc in lithium‐induced hepatotoxicity.Methods: Rats received either lithium treatment in diet at a dose level of 1.1 g/kg diet, zinc alone at a dose level of 227 mg/L in drinking water, and combined lithium plus zinc or drinking water alone for different time durations of 1, 2 and 4 months. This study explored the hepatic marker enzymes, antioxidant status and histopathological investigations in the liver of rats following different treatments.Results: The activities of glutamic oxaloacetic transaminase, glutamic pyruvic transaminase and alkaline phosphatase were found to be elevated significantly following 2 and 4 months of lithium treatment. Lithium‐treated rats showed a significant increase in the levels of lipid peroxidation and superoxide dismutase and a significant inhibition in the levels of reduced glutathione, catalase and glutathione‐S‐transferase, following 2 and 4 months of treatment. However, zinc co‐administration revealed significant improvement in the altered activities of hepatic marker and antioxidant enzymes in comparison with lithium‐treated animals. Lithium‐treated rats also indicated drastic alterations in hepatic histoarchitecture and zinc co‐administration resulted in improvement in the structure of hepatocytes.Conclusion: The present study suggests the protective potential of zinc in lithium‐induced hepatotoxicity.
Atorvastatin induces apoptosis by a caspase‐9‐dependent pathway: an in vitro study on activated rat hepatic stellate cells
Authors: Aprigliano Isabella , Dudas Joszef , Ramadori Giuliano , Saile Bernhard 
Published: August 2010

AbstractBackground: Statins are shown to have cholesterol‐independent properties such as anti‐inflammation and immunomodulation. Activated hepatic stellate cells (HSCs) acquire the capacity to synthesize matrix proteins in damaged liver. We tested the hypothesis that atorvastatin may be capable of inducing apoptosis in HSCs.Methods: Primary cultures of rat HSCs were exposed to atorvastatin, mevalonic acid and U0126. Quantification of living, apoptotic and necrotic HSCs was performed by flow cytometry and laser‐scan microscopy. Cell‐cycle analysis was performed by flow cytometry. Pro‐ and anti‐apoptotic factors were investigated by Western blot and electrophoresis mobility shift assay. Protease activity of caspases was calculated using a colorimetric kit.Results: Atorvastatin leads to a G2‐arrest and induces apoptosis in activated HSCs. Atorvastatin‐mediated apoptosis could be blocked by co‐administration of mevalonic acid and U0126. No effects of atorvastatin on gene expression of CD95, CD95L, NF‐κB, p53 and p21WAF1 could be observed. Atorvastatin‐induced apoptosis in activated HSCs is related to an increased protease activity of caspase‐9 and ‐3. Gene expression of the major proteins of the bcl‐system shows that truncated Bid is involved in apoptosis mediated by atorvastatin. By blocking the extracellular signal‐regulated protein kinase (ERK1/2) activation by adding U0126, we could prevent the apoptosis induced by atorvastatin. By Western blot we could not detect any change in the activation of c‐jun N‐terminal kinase (JNK).Conclusions: Atorvastatin induces apoptosis in activated HSCs acting through an ERK‐dependent cleavage of Bid and a highly increased protease activity of caspase‐9 and ‐3. JNK is not involved in atorvastatin‐mediated apoptosis in HSCs.
Cardiotrophin‐1 enhances regeneration of cirrhotic liver remnant after hepatectomy through promotion of angiogenesis and cell proliferation
Authors: Yang Zhen Fan , Lau Chi Keung , Ngai Patricia , Lam Shuk Pik , Ho David W. , Poon Ronnie Tung‐Ping , Fan Sheung Tat 
Published: August 2010

AbstractBackground/Aim: Hepatic resection is not applicable to a certain proportion of hepatocellular carcinoma patients owing to an insufficient liver function reserve. The present study was designed to investigate the effects of cardiotrophin‐1 (CT‐1) on improving the function of CCl4‐induced cirrhotic liver remnant after major hepatectomy.Methods: CT‐1 was administered to rats after hepatectomy according to different protocols.Results: A double‐dose CT‐1 protocol improved liver function, enlarged the volume of liver remnant, upregulated the expression of von Willebrand factor and increased the number of BrdU+ or Ki‐67+ hepatocytes. Administration of CT‐1 enhanced the expression of nuclear factor‐κB (P65), vascular endothelial growth factor (VEGF), CyclinD1 and p42/44 in the liver remnant. However, the effects of CT‐1 were blocked by a VEGF receptor blocker, PTK787. Although the expression of gp130, a receptor of CT‐1, was downregulated in the diseased hepatocytes isolated from the cirrhotic liver, CT‐1 could still stimulate the cell proliferation. CT‐1 administration enhanced the expression of P65 and VEGF in the diseased hepatocytes, but the augmented P65 and VEGF expression was blocked by PTK787 administration.Conclusion: Short‐term administration of CT‐1 could improve the function of cirrhotic liver remnant and stimulate liver regeneration through promotion of angiogenesis and cell proliferation.
Utilization rates, complications and costs of percutaneous liver biopsy: a population‐based study including 4275 biopsies
Authors: Myers Robert P. , Fong Andrew , Shaheen Abdel Aziz M. 
Published: August 2010

AbstractBackground: Liver biopsy is an important tool in the management of patients with liver disease. Because biopsy practices may be changing, we studied patterns of use in a large Canadian Health Region. We aimed to describe trends in biopsy utilization and the incidence and costs of complications from a population‐based perspective.Methods: Administrative databases were used to identify percutaneous liver biopsies performed between 1994 and 2002. Significant complications were identified by reviewing medical records of patients hospitalized within 7 days of a biopsy and those with a diagnostic code indicative of a procedural complication. Analyses of biopsy rates employed Poisson regression.Results: Between 1994 and 2002, 3627 patients had 4275 liver biopsies (median 1 per patient; range 1–12). Radiologists performed the majority (90%), particularly during the latter years (1994 vs. 2002: 73 vs. 98%; P<0.0001). The overall annual biopsy rate was 54.8 per 100 000 population with a 41% (95% CI 23–61%) increase between 1994 and 2002. Annual increases were greatest in males and patients 30–59 years. Thirty‐two patients (0.75%) had significant biopsy‐related complications (1994–1997 vs. 1998–2002: 1.28 vs. 0.44%; P=0.003). Pain requiring admission (0.51%) and bleeding (0.35%) were most common. Six patients (0.14%) died; all had malignancies. The median direct cost of a hospitalization for complications was $4579 (range $1164–29 641).Conclusions: Liver biopsy rates are increasing likely owing to the changing epidemiology and management of common liver diseases. The similarity of the complication rate in our population‐based study with estimates from specialized centres supports the safety of this important procedure.
Intra‐operative application of real‐time tissue elastography for the diagnosis of liver tumours
Authors: Kato Koichi , Sugimoto Hiroyuki , Kanazumi Naohito , Nomoto Shuji , Takeda Shin , Nakao Akimasa 
Published: August 2010

AbstractObjective: Real‐time tissue elastography (RTE) has made it possible to visualize tissue elasticity. The aim of this study was to evaluate the usefulness of RTE for the differential diagnosis of liver tumours during surgical exploration.Methods: Fifty‐five liver tumours in 44 patients were examined with RTE, concomitant with routine intra‐operative ultrasonography. Elasticity images were classified into four types, from type A (even strain) to type D (no strain), according to the distribution and the degree of the strain contrasted with that of the surrounding liver [elasticity type of liver tumour (ETLT)]. We evaluated the consistency of the findings of RTE with the pathological diagnosis as a reference standard.Results: All malignant lesions showed various degrees of strain reduction in the tumour tissue. Twenty‐one of 22 hepatocellular carcinomas (HCCs) were classified as type B with a sensitivity of 95.5%, a specificity of 90.9% and an accuracy of 92.7%, while all 24 metastatic adenocarcinomas were classified as either type C or type D with a sensitivity of 100%, a specificity of 80.6% and an accuracy of 89.1%.Conclusion: Application of RTE in surgical exploration provided significant information about the elasticity of liver tumours. RTE, using a new criterion, ETLT, enabled us to distinguish rather accurately between two common malignancies: HCC and metastatic adenocarcinoma.
Hepatic fat and adenosine triphosphate measurement in overweight and obese adults using 1H and 31P magnetic resonance spectroscopy
Authors: Solga Steven F. , Horska Alena , Hemker Susanne , Crawford Stephen , Diggs Charalett , Diehl Anna Mae , Brancati Frederick L. , Clark Jeanne M. 
Published: August 2010

AbstractBackground/Aims: Magnetic resonance spectroscopy (MRS) measures hepatic fat and adenosine triphosphate (ATP), but magnetic resonance studies are challenging in obese subjects. We aimed to evaluate the inter‐ and intrarater reliability and stability of hepatic fat and ATP measurements in a cohort of overweight and obese adults.Methods: We measured hepatic fat and ATP using proton MRS (1H MRS) and phosphorus MRS (31P MRS) at baseline in adults enrolled in the Action for Health in Diabetes (Look AHEAD) clinical trial at one site. Using logistic regression, we determined factors associated with successful MRS data acquisition. We calculated the intra‐ and inter‐rater reliability for hepatic fat and ATP based on 20 scans analysed twice by two readers. We also calculated the stability of these measures three times on five healthy volunteers.Results: Of 244 participants recruited into our ancillary study, 185 agreed to MRS. We obtained usable hepatic fat data from 151 (82%) and ATP data from 105 (58%). Obesity was the strongest predictor of failed data acquisition; every unit increase in the body mass index reduced the likelihood of successful fat data by 11% and ATP data by 14%. The inter‐ and intrarater reliability were excellent for fat (intraclass correlation coefficient=0.99), but substantially more variable for ATP. Fat measures appeared relatively stable, but this was less true for ATP.Conclusions: Obesity can hinder 1H and 31P MRS data acquisition and subsequent analysis. This impact was greater for hepatic ATP than hepatic fat.
Macaca radiata (bonnet monkey): a spontaneous model of nonalcoholic fatty liver disease
Authors: Nagarajan Perumal , Venkatesan Ramasamy , Kumar Mahesh , Usmani Abul , Majumdar Subeer S. 
Published: August 2010

AbstractBackground: Nonalcoholic fatty liver disease (NAFLD) is a well‐recognized condition that includes a spectrum of clinicopathology conditions ranging from steatotosis to cirrhosis and liver failure. Available animal models are not ideal as they show only a partial resemblance to characteristic human NAFLD.Objective: This study was aimed at identifying a nonhuman primate model of NAFLD resembling features of human NAFLD, which will be useful in understanding the mechanism of the onset of this disease and for developing novel therapeutic modalities.Methods: The histological status of the liver and serum levels of triglycerides (TG), cholesterol, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) of aged bonnet monkeys were compared with that of the aged rhesus and adult bonnet monkeys. Histopathology and immunostaining of liver sections and oil red ‘O’ confirmed NAFLD in aged bonnet monkeys.Results: Aged bonnet monkeys showed a significant (P<0.01) increase in serum TG, AST and ALT compared with aged rhesus and adult bonnet monkeys. Histopathology of the liver of aged bonnet macaques showed diffused microvesicular and macrovesicular fatty changes, perivenular and portal and perisinusoidal fibrosis with fatty degeneration of hepatocytes, and immunostaining of liver sections was suggestive of NAFLD.Conclusion: The spontaneous occurrence of NAFLD in normal animals is rare, but aged bonnet monkeys may serve as a unique animal model for studies related to NAFLD because they mimic pathophysiological features of human NAFLD.
Inflammatory change of fatty liver induced by intraportal low‐dose lipopolysaccharide infusion deteriorates pancreatic insulin secretion in fructose‐induced insulin‐resistant rats
Authors: Hsieh Po‐Shiuan 
Published: August 2010

AbstractBackground: This study tested whether subacute inflammatory change of fatty liver induced by portal endotoxaemia is detrimental to pancreatic insulin secretion in fructose‐fed rats (FFRs) with fatty liver.Methods: Rats were randomly assigned into two groups with a regular or fructose‐enriched diet for 8 weeks. Rats, after fructose feeding for 4 weeks, were further divided into three subgroups: on fructose diet alone, on fructose diet combined with intraportal saline or lipopolysaccharide (LPS) infusion (n=8 per group) for the next 4 weeks. In another set of experiments, the liver and pancreatic tissues were obtained for histological examination in these four groups. Pancreatic insulin secretion was evaluated by in vivo hyperglycaemic clamp study.Results: Fasting plasma insulin concentrations and homoeostasis model assessment‐insulin resistance, an insulin resistance score, were significantly increased in FFRs but failed to change in rats with LPS treatment. The 4‐week intraportal LPS infusion significantly increased circulating aspartate transaminase, alanine transaminase and C‐reactive protein levels but did not alter endotoxin levels in FFRs. The increased white blood cell count was also noted in rats after intraportal LPS infusion for 2 and 4 weeks. The attenuated first‐phase and second‐phase insulin responses in FFRs shown in hyperglycaemic clamp were further deteriorated in those with intraportal LPS infusion. Increased histopathological scores of liver and pancreas shown in FFRs were further increased in those combined with portal endotoxaemia.Conclusion: This study demonstrates that the chronic subacute inflammatory change of fatty liver induced by mild portal endotoxaemia could deteriorate insulin secretion in a rodent model of metabolic syndrome and fatty liver.
Prevention of paracentesis‐induced circulatory dysfunction: midodrine vs albumin. A randomized pilot study
Authors: Appenrodt Beate , Wolf Andrea , Grünhage Frank , Trebicka Jonel , Schepke Michael , Rabe Christian , Lammert Frank , Sauerbruch Tilman , Heller J. 
Published: August 2010

AbstractBackground/Aims: Large‐volume paracentesis in patients with cirrhosis and ascites induces arterial vasodilatation and decreases effective arterial blood volume, termed paracentesis‐induced circulatory dysfunction (PICD), which can be prevented by costly intravenous albumin. Vasoconstrictors, e.g. terlipressin, may also prevent PICD. The aim was to compare the less expensive vasoconstrictor midodrine, an α‐adrenoceptor agonist, with albumin in preventing PICD.Methods: Twenty‐four patients with cirrhosis and ascites were randomly assigned to be treated with either midodrine (n=11) (12.5 mg three times per day; over 2 days) or albumin (n=13) (8 g/L of removed ascites) after large‐volume paracentesis. Effective arterial blood volume was assessed indirectly by measuring plasma renin and aldosterone concentration on days 0 and 6 after paracentesis; renal function and haemodynamic changes were also measured. PICD was defined as an increase in plasma renin concentration on day 6 by more than 50% of the baseline value.Results: PICD developed in six patients of the midodrine group (60%) and in only four patients (31%) of the albumin group. Six days after paracentesis, the aldosterone concentration increased significantly in the midodrine group, but not in the albumin group.Conclusions: This pilot study suggests that midodrine is not as effective as albumin in preventing circulatory dysfunction after large‐volume paracentesis in patients with cirrhosis and ascites.