bluuebunny/crossref_metadata_2025_split huggingface dataset:
Consumer understanding and use of nutrition labelling: a systematic review
Authors: Cowburn Gill , Stockley Lynn 
Published: February 2005

AbstractObjectiveTo explore published and unpublished research into consumer understanding and use of nutrition labelling which is culturally applicable in Europe.DesignA systematic review undertaken between July 2002 and February 2003.ResultsOne hundred and three papers were identified that reported on consumer understanding or use of nutrition labelling, most originating from North America or northern Europe. Only a few studies (9%) were judged to be of high or medium–high quality. We found that reported use of nutrition labels is high but more objective measures suggest that actual use of nutrition labelling during food purchase may be much lower. Whether or not consumers can understand and use nutrition labelling depends on the purpose of the task. Available evidence suggests that consumers who do look at nutrition labels can understand some of the terms used but are confused by other types of information. Most appear able to retrieve simple information and make simple calculations and comparisons between products using numerical information, but their ability to interpret the nutrition label accurately reduces as the complexity of the task increases. The addition of interpretational aids like verbal descriptors and recommended reference values helps in product comparison and in putting products into a total diet context.ConclusionsImprovements in nutrition labelling could make a small but important contribution towards making the existing point-of-purchase environment more conducive to the selection of healthy choices. In particular, interpretational aids can help consumers assess the nutrient contribution of specific foods to the overall diet.
In vivo expression patterns of survivin and its splicing variants in chronic liver disease and hepatocellular carcinoma
Authors: Takashima Hidetaka , Nakajima Tomoki , Moriguchi Michihisa , Sekoguchi Satoru , Nishikawa Taichiro , Watanabe Tadashi , Katagishi Tatsuo , Kimura Hiroyuki , Minami Masahito , Itoh Yoshito , Kagawa Keizo , Okanoue Takeshi 
Published: February 2005

Abstract: Aim: Our aim was to clarify the significance of expression levels and post‐transcriptional splicing patterns of survivin during multistep hepatocarcinogenesis and tumor progression.Methods: Using immunohistochemistry, we first elucidated the expression of survivin protein in tissues of hepatocellular carcinoma (HCC) and the adjacent non‐cancerous tissues. Furthermore, we investigated survivin gene expression patterns in these tissues.Results: Survivin protein was expressed not only in most HCC tissues but also in some cirrhotic nodules. In non‐cancerous regions, the levels of survivin mRNA increased in proportion to their stage of progression. Survivin protein was expressed mainly in periportal areas, where proliferating cells were localized. In HCC, mRNA levels of survivin and survivin ΔEx3 correlated with high proliferative activity, whereas the levels of surviving 2B did not.Discussion: These findings of mRNA and protein expressions of survivin in chronically injured avers indicate that it has an important role in hepatocarcinogenesis. A lack of correlation between proliferative activity and survivin 2B mRNA levels in HCC is suggestive of a previous hypothesis that this variant decreases sruvivin function in a dominan negative manner. Thus, our data suggest different functions of these splicing variants and their important roles in tumor progression.
Hepatocellular carcinoma – survival and clinical characteristics in relation to various histologic molecular markers in Western patients
Authors: Schöniger‐Hekele Maximilian , Hänel Sabine , Wrba Fritz , Müller Christian 
Published: February 2005

Abstract: Background:Many genes participate in the regulation of cell proliferation and growth of tumor cells. Altered expression and loss of function of some of these gene products have been found in malignant tumors and correlated with progression and poor prognosis.Aims:Our aim was to correlate the expression of various molecular histologic markers with tumor characteristics and survival time of patients with hepatocellular carcinoma (HCC).Patients and methods:Tumor tissues of 81 patients with HCC were investigated immunohistochemically for the expression of cellular proliferation markers Mib1 (Ki67) and c‐erbB‐2 (HER2/neu), cellcycle markers (p53, mdm2 and p21), CD81 (TAPA1), a marker shown to be associated with metastasis, and human leukocyte antigen (HLA)‐DR expression, involved in immunological antigen presentation.Results:p21 was expressed in a higher percentage (83.3 vs. 50%,P=0.014) in undifferentiated histological tumor grades (Edmondson Steiner G3 vs. G1/G2). HCC in patients with enlarged lymph nodes expressed HLA‐DR in a higher percentage (28.6%) than tumors without lymph node enlargement (5.7%,P=0.006). Patients with distant metastases were less likely to express CD 81 (11.1%) on tumor cells than patients without distant metastases (38.3%,P=0.0335). No other correlation with clinical or tumor characteristics or molecular histologic markers investigated was found. P53 accumulating patients showed a worse survival than patients with tumors p53 non‐accumulating (median 4.1 months vs. median 9.3 months,P=0.01798). Neither the expression nor the non‐expression of proliferation, cell cycle, immunologic or cell adhesion markers was associated with differences in survival. However, patients with a low expression of cell cycle marker mdm2 survived significantly longer (median 9.4 months) as compared with patients with high expression (median 3.9 months).Conclusion:Our results suggest that p53 nuclear accumulation and mdm2 high expression are associated with poor survival in patients withHCC. Furthermore, patients with enlarged lymph nodes had HLA‐DR‐positive tumors more frequently and patients with distant metastases had tumors with CD81 expression less often.
Decreased expression of peroxisome proliferator‐activated receptor α and liver fatty acid binding protein after partial hepatectomy of rats and mice
Authors: Skrtic Stanko , Carlsson Linda , Ljungberg Anna , Lindén Daniel , Michalik Liliane , Wahli Walter , Oscarsson Jan 
Published: February 2005

Abstract:
Background Aims: Marked changes in metabolism, including liver steatosis and hypoglycemia, occur after partial hepatectomy. Peroxisome proliferator‐activated receptor α (PPARα) is a nuclear hormone receptor that is activated by fatty acids and involved in hepatic fatty acid metabolism and regeneration. Liver fatty acid binding protein (LFABP) is an abundant protein in liver cytosol whose expression is regulated by PPARα. It is involved in fatty acid uptake and diffusion and in PPARα signaling. The aim of this study was to investigate the expression of PPARα and LFABP during liver regeneration.Methods: Male Sprague–Dawley rats and male C57 Bl/6 mice were subjected to 2/3 hepatectomy and LFABP and PPARα mRNA and protein levels were measured at different time points after surgery. The effect of partial hepatectomy was followed during 48 h in rats and 72 h in mice.Results: PPARα mRNA and protein levels were decreased 26 h after hepatectomy of rats. The LFABP mRNA and protein levels paralleled those of PPARα and were also decreased 26 h after hepatectomy. In mice, the mRNA level was decreased after 36 and 72 h after hepatectomy. In this case, LFABP mRNA levels decreased more slowly after partial hepatectomy than in rats.Conclusions: A marked decrease in PPARα expression may be important for changed gene expression, e.g. LFABP, and metabolic changes, such as hypoglycemia, during liver regeneration.
Nitric oxide synthases inhibition results in renal failure improvement in cirrhotic rats
Authors: Islas‐Carbajal M. C. , Covarrubias A. , Grijalva G. , Alvarez‐Rodríguez A. , Armendáriz‐Borunda J. , Rincón‐Sánchez A. R. 
Published: February 2005

Abstract: Nitric oxide (NO) has been implicated in cirrhosis and might be implicated in renal failure end‐stage cirrhosis.Aim: Our aim was to evaluate NO role in renal failure induced during decompensated cirrhosis, using the following inhibitors: aminoguanidine (AG), a specific inducible nitric oxide synthase (iNOS) inhibitor and NG‐nitro‐l‐arginine methyl ester (L‐NAME), a nonselective blocker of NOS isoforms.Methods: Endothelial (eNOS) and iNOS gene expression was analyzed by reverse transcriptase‐polymerase chain reaction. Cirrhotic rats received a single intragastric dose of CCl4 to induce acute liver damage (ALD).Results: After ALD, aspartate aminotransferase highest levels were observed in rats treated with AG and ALT in rats treated with L‐NAME. Inhibitors decreased creatinine serum levels to normal values and serum sodium levels re‐established after the third day of ALD. L‐NAME diminished (P<0.05) eNOS RNA renal expression. Renal iNOS with no inhibitor was overexpressed but was down‐regulated by AG treatment. Liver eNOS RNA expression had a decreased expression before ALD in cirrhotic rats, but L‐NAME treatment down‐regulated eNOS after ALD. AG induced an important iNOS liver decrease.Conclusion: Both inhibitors improved renal function, although AG displayed a better effect and did not aggravate liver function. We concluded that NOS isoforms are implicated in the renal pathophysiologic events induced by ALD.
Decreased risk of hepatocellular carcinoma in patients with chronic hepatitis C whose serum alanine aminotransferase levels became less than twice the upper limit of normal following interferon therapy
Authors: Moriyama Mitsuhiko , Matsumura Hiroshi , Aoki Hiroshi , Shimizu Toshihiro , Yamagami Hiroaki , Shioda Atsuo , Kaneko Miki , Goto Iori , Tanaka Naohide , Arakawa Yasuyuki 
Published: February 2005

Abstract: Aim: The incidence of hepatocellular carcinoma (HCC) in C‐viral chronic hepatitis (CH) and liver cirrhosis (LC) patients after interferon (IFN) therapy was evaluated according to alanine aminotransferase (ALT) levels.Patients: Two hundred sixty‐nine patients with C‐viral CH and LC were treated with natural IFN‐α. The efficacy of IFN therapy was evaluated based on virologic response and ALT levels using the following groups: virologic‐sustained responders (VSR); biochemical‐sustained responders (BSR); partial responders (PR), which consisted of BSR patients whose serum ALT levels later relapsed; non‐responders (NR)1, which included patients with serum ALT levels that were usually less than 80 IU/l; and NR2, NR with ALT levels persistently more than 80 IU/l.Results: Of the 269 patients, 22 (8.2%) developed HCC after IFN therapy. The incidence of HCC (%/patient/year) was 0.78%, 0%, 0%, 0.17%, 4.68% in VSR, BR, PR, NR1, NR2, respectively. Multivariate analysis revealed that an increase in ALT levels to more than 80 IU/l is an important risk factor for the occurrence of HCC.Conclusions: We concluded that the patients with ALT levels less than twice the upper limit of normal after IFN therapy have a reduced risk of progression to HCC from C‐viral chronic liver disease.
Normal liver regeneration and liver cell apoptosis after partial hepatectomy in tumor necrosis factor‐α‐deficient mice
Authors: Hayashi Hideki , Nagaki Masahito , Imose Motoaki , Osawa Yosuke , Kimura Kiminori , Takai Shinji , Imao Motohiro , Naiki Takafumi , Kato Tomohiro , Moriwaki Hisataka 
Published: February 2005

Abstract: Aims/Background: Tumor necrosis factor‐α (TNF‐α) is known as a proinflammatory cytokine that has been implicated as a contributing factor in a number of disease processes. TNF‐α also influences liver repair following hepatotoxic damage, and regeneration following partial hepatectomy (PH). The aim of this study was to assess the mechanism by which TNF‐α influences liver cell apoptosis and regeneration following PH in TNF‐α‐deficient (TNF‐α−/−) mice.Methods: PH was performed in wild mice and TNF‐α−/− mice.Results: In both groups, serum alanine aminotransferase and serum total bilirubin levels comparably peaked at 6 and 48 h after PH, respectively. No differences were observed in hepatocyte proliferation, as determined by mitotic and the proliferating cell nuclear antigen labeling indices, between TNF‐α+/+ and TNF‐α−/− mice. Few terminal deoxynucleotidyl transferase nick end‐labeling‐positive hepatocytes were seen in either type of mice. Nuclear factor‐κB DNA binding activity in the remaining liver of TNF‐α−/− mice after PH was similar to that of control mice. Ribonuclease protection assay showed that transforming growth factor β1 mRNA was up‐regulated comparably in the livers of the two groups, and that other cytokines were hardly seen in either. Interleukin‐6/ signal transducer and activator of transcription‐3‐dependent pathway was not affected in TNF‐α−/− mice.Conclusions: These findings suggest that TNF‐α has little influence on liver regeneration and liver cell apoptosis after PH in mice.
Outcome after orthotopic liver transplantation in five HIV‐infected patients with virus hepatitis‐induced cirrhosis
Authors: Radecke Klaus , Frühauf Nils R. , Miller Michael , Ross Birgit , Köditz Roland , Malagó Massimo , Broelsch Christoph E. , Gerken Guido , Treichel Ulrich 
Published: February 2005

Abstract: Background: We report on our experiences with orthotopic liver transplantation (OLT) in HIV‐infected patients. Between July 1998 and October 2001, five HIV‐infected patients underwent OLT because of virus‐induced liver cirrhosis. One patient suffered from hepatitis B virus (HBV)‐, three patients from hepatitis C virus (HCV)‐ and one patient from HCV/HBV/HDV‐related cirrhosis (HDV, hepatitis D virus). The mean duration of HIV infection was 15 years. Patients were prospectively followed up with a mean duration of 25.6 months.Results: Three patients died 3, 10 and 31 months after OLT, respectively, due to graft failure. The causes of graft failure were: recurrent thrombosis of the hepatic artery, HCV‐associated cholestatic hepatitis and chemotherapy‐induced liver damage due to Hodgkin's disease, which was diagnosed 17 months after OLT, in addition to chronic HCV disease. The two survivors show a stable liver function and non‐progredient HIV infection under antiretroviral therapy 61 and 23 months after OLT, respectively.Conclusions: A medium‐ or even long‐term survival after OLT can be achieved in HIV‐infected patients without progression of HIV disease under antiretroviral therapy. However, in our study three out of five patients died due to graft failure. Therefore, prognostic criteria have to be defined for the selection of HIV‐infected patients, who may benefit from OLT.
Hepatic microcirculation assessed by positron emission tomography of first‐pass ammonia metabolism in porcine liver
Authors: Keiding Susanne , Munk Ole Lajord , Vilstrup Hendrik , Nielsen Dennis Tønner , Roelsgaard Klaus , Bass Ludvik 
Published: February 2005

Abstract: Aims/Background: Intrahepatic branching of the hepatic artery (HA) to liver microcirculatory units, the acini, is more heterogeneous than that of the portal vein (PV). Furthermore, part of HA blood enters the sinusoid partially downstream between the in‐ and outlets. We examined the effects of these vascular variations on porcine hepatic first‐pass ammonia metabolism, which is characterised by high uptake and separate periportal urea and perivenous glutamine formations.Methods: 13NH3 was given via the PV, HA or caval vein, followed by 22 min dynamic liver positron emission tomography (PET) recordings in six pigs. Heterogeneity of liver 13N‐metabolism was quantified by the coefficient of variation of tissue 13N‐radioactivity measured 10 min after tracer infusion. Sinusoidal zonal clearances of 13NH3 into 13N‐urea and 13N‐glutamine were calculated by kinetic PET modelling.Results: Liver metabolic heterogeneity was 0.65±0.20 (mean±SD, n=6) following 13NH3‐infusion into HA, 0.34±0.17 into PV and 0.10±0.02 into the caval vein. Clearance of 13NH3 to 13N‐urea was of similar magnitude following 13NH3 administration into HA and PV: 0.27±0.11 ml/min/g (mean±SD) and 0.29±0.09 ml/min/g, respectively. Clearances of 13NH3 to 13N‐glutamine when 13NH3 was given into HA and PV were also similar: 0.47±0.18 and 0.50±0.13 ml/min/g, respectively.Conclusions: The present measurements of the hepatic metabolism of 13NH3 showed metabolic heterogeneity compatible with variation of the HA supply of the acini. Second, results of PET modelling of the sinusoidal zonation metabolism of 13NH3 to 13N‐urea and to 13N‐glutamine did not indicate metabolically important partial downstream arterial entry into the sinusoids.
The influence of brain death on liver function
Authors: Olinga Peter , Van Der Hoeven Joost A. B. , Merema Marjolijn T. , Freund Rennie L. , Ploeg Rutger J. , Groothuis Geny M. M. 
Published: February 2005

Abstract: Background: In this study, we investigated the influence of brain death on inflammatory response and the effects of brain death on liver function both directly after explantation and after reoxygenation.Methods: The influence of brain death on liver function was studied in rats using a brain death model and the liver slice model to mimic reoxygenation. Liver function was assessed by measuring the ATP content and the ATP‐driven urea synthesis. The activation of non‐parenchymal cells was studied by measuring mRNA levels of IL‐10, cytokine production (IL‐10 and IL‐1β) and inducible nitric oxide synthases (iNOS) upregulation (mRNA) and protein level.Results: Brain death had no direct influence on the ATP content of the liver. However, it led to induction of several cytokines because of activation of non‐parenchymal cells, which led to upregulation of iNOS and to nitric oxide metabolites production. It is known that cytokine production may influence the drug metabolism capacity; however, no influence of brain death on drug metabolism was observed. An explanation may be the relatively short experimental period.Conclusions: Kupffer cells seem to be activated during the onset of brain death induction; however, they become quiescent when liver slices of brain dead rats were reoxygenated during incubation. Other non‐parenchymal cells, possibly the endothelial cells, remain activated during incubation and reoxygenation in slices from brain death donors but not in slices from control livers. Future experiments in our rat liver transplantation model need to elucidate the implications of these findings.
The influence of spleen size on liver regeneration after major hepatectomy in normal and early cirrhotic liver
Authors: Shan Yan‐Shen , Hsieh Yu‐Hsiang , Sy Edgar D , Chiu Nan‐Tsing , Lin Pin‐Wen 
Published: February 2005

Abstract: Background/Purpose: The relationship between liver regeneration and spleen size after major hepatectomy in normal and cirrhotic liver was studied by single photon emission computed tomography (SPECT).Materials and methods: Twenty‐six patients, 18 patients with normal liver and eight patients with cirrhotic liver, receiving major hepatectomy were included. Liver and spleen volumes were measured by SPECT before major hepatectomy, 6 months, 1 year and 2 years after operation. The correlation of liver and spleen volume during liver regeneration was analyzed.Results: In both groups, the residual liver volume increased within the first year and decreased in the second year. No difference in regeneration ability was found. The spleen volume in cirrhotic liver was increased, with a trend similar to normal liver during the first year. In contrast, the increased spleen volume persisted up to the second year in cirrhotic patients. Age per year, the female sex, and body surface index had a positive correlation with increased percentage of liver volume. The spleen volume per 100 ml with time played a significantly negative role in increasing percentage of liver volume, confidence interval: −2.16 to −27.92, P=0.011.Conclusion: In early cirrhotic liver within normal functional limits, the liver still could regenerate as a normal liver after major hepatectomy in 1 year. Age, the female sex, and body surface index had positive correlation but the size of spleen volume played a negative role to regenerative liver volume.
Effect of lipopolysaccharide on in vivo and genetic regulation of rat urea synthesis
Authors: Nielsen Susanne Schouw , Grøfte Thorbjørn , Tygstrup Niels , Vilstrup Hendrik 
Published: February 2005

Abstract: Background: The acute phase response causes a negative nitrogen balance. It is unknown whether this involves regulation of hepatic urea synthesis.Methods: We examined the in vivo capacity of urea nitrogen synthesis (CUNS), mRNA levels of urea cycle enzyme genes and galactose elimination capacity (GEC) during moderate and severe acute phase response induced by low‐ and high‐dose lipopolysaccharide (LPS) in rats.Results: Low‐dose LPS doubled CUNS (P<0.05), decreased the mRNA level of the rate‐limiting urea cycle enzyme (arginino succinate synthetase (ASS) by 26% (P<0.05) and did not change GEC. High‐dose LPS did not change CUNS, decreased the mRNA level of the flux‐generating enzyme carbamoyl phosphate synthetase (CPS) by 11% (P<0.05) and the rate‐limiting urea cycle enzyme (ASS) by 27% (P<0.05) and almost halved GEC (P<0.05).Conclusion: The moderate acute phase response up‐regulated in vivo urea synthesis but had the opposite effect on gene level. The severe acute phase response decreased the functional liver mass that attenuated the increase in urea synthesis.
Malignant transformation of the cultured human hepatocytes induced by hepatitis C virus core protein
Authors: Shan Yu , Chen Xi‐gu , Huang Bing , Hu An‐bin , Xiao Dong , Guo Zhong‐min 
Published: February 2005

Abstract: Background/Aim: Hepatitis C virus core protein (HCV‐C) has been known to play an important role in hepatocarcinogenesis. But, up to now there is no certain evidence in pathomorphology directly supporting this standpoint. In this study, a human hepatocytes model expressing HCV‐C was established for investigating the influence of HCV‐C on hepatocytes biological properties.Methods: The HCV‐C expression plasmid, PcDNA3‐C, was transfected into Chang‐liver cells to establish HCV‐C expressing cells. Proliferation rate and variation index of DNA content of these cells were measured by MTT and FCM. The malignant transformation of these cells was observed by electron microscope. Furthermore, these cells were subcutaneous injected into nude mice to observed their tumor genesis.Results: Proliferation rate and variation index of DNA content of these cells markedly increased. 10/10 of BALB/c‐nu/nu nude mice generated tumors at 3 weeks after subcutaneous inoculation of the HCV‐C expressing cells. And, histological structure of the tumors coincided with that of hepatocarcinoma.Conclusions: The HCV‐C may play a key role in hepatocarcinogenesis resulting from HCV infection.