bluuebunny/crossref_metadata_2025_split huggingface dataset:
Specific effect of high-pressure treatment of milk on cheese proteolysis
Authors: Buffa Martín , Guamis Buenaventura , Trujillo Antonio J 
Published: October 2005

The extent of primary and secondary proteolysis of cheeses made from raw (RA), pasteurized (PA, 72 °C, 15 s) or pressure-treated (PR, 500 MPa, 15 min, 20 °C) goats' milk was assessed. Modifications in cheese-making technology were introduced to obtain cheeses with the same moisture content, and thus studied per se the effect of milk treatment on cheese proteolysis.The PR milk cheese samples were differentiated from RA and PA milk cheeses by their elevated β-lg content, and by the faster degradation of αs1-, αs2- and β-CN throughout ripening. Non-significant differences were found in either pH 4·6 soluble-nitrogen or trichloracetic acid soluble-nitrogen contents of cheeses. However, the pasteurization of milk decreased the free amino acid production in cheese. The RA milk cheeses had the highest amount of proline and the lowest concentrations of serine, tyrosine, arginine and α-aminobutyric acid, whereas PR milk cheese showed higher levels of arginine.
Suffix-tree analyser (STAN): looking for nucleotidic and peptidic patterns in chromosomes
Authors: Nicolas Jacques , Durand Patrick , Ranchy Grégory , Tempel Sébastien , Valin Anne-Sophie 
Published: October 2005

Abstract
Summary: We have developed STAN (suffix-tree analyser), a tool to search for nucleotidic and peptidic patterns within whole chromosomes. Pattern syntax uses a string variable grammar-like formalism which allows the description of complex patterns including ambiguities, insertions/deletions, gaps, repeats and palindromes. STAN is based on a reduction to multipart matching on a suffix-tree data structure and can handle large DNA sequences, whether assembled or not.
Availability: STAN is accessible online at
Contact: stan@irisa.fr
Athena: a resource for rapid visualization and systematic analysis of Arabidopsis promoter sequences
Authors: O'Connor Timothy R. , Dyreson Curtis , Wyrick John J. 
Published: October 2005

Abstract
Summary: To better understand the regulatory networks that control plant gene expression, tools are needed to systematically analyze and visualize promoter regulatory sequences in Arabidopsis thaliana. We have developed the Athena database, which contains 30 067 predicted Arabidopsis promoter sequences and consensus sequences for 105 previously characterized transcription factor (TF) binding sites. Athena provides four novel tools to facilitate the analysis of promoter sequences: a promoter visualization tool to enable the rapid inspection of key regulatory sequences in multiple promoters; a TF binding site enrichment tool to identify statistically over-represented TF sites occurring in a user-selected subset of promoters; a data-mining tool to rapidly select promoter sequences containing the specified combination of TF binding sites; and a tool to display the distribution of TF binding site positions in a selected set of promoter sequences.
Availability:
Contact: jwyrick@wsu.edu
Dose‐dependence of promotion of 2‐amino‐3,8‐dimethylimidazo[4,5‐f]quinoxaline‐induced rat hepatocarcinogenesis by ethanol: Evidence for a threshold
Authors: Kushida Masahiko , Wanibuchi Hideki , Morimura Keiichirou , Kinoshita Anna , Kang Jin Seok , Puatanachokchai Rawiwan , Wei Min , Funae Yoshihiko , Fukushima Shoji 
Published: October 2005

Although ethanol is thought to be a tumor‐promoter, there are conflicting results concerning its effects on experimental hepatocarcinogenesis. Furthermore, the relationship between the amount of ethanol consumed and tumor promoting effects has hitherto not been investigated in detail. In the present study, 21‐day‐old F344/DuCrj rats were fed 200 p.p.m. 2‐amino‐3,8‐dimethylimidazo[4,5‐f]quinoxaline (MeIQx) in their diet for 8 weeks and thereafter received ethanol at doses of 0, 0.1, 0.3, 1, 3, 10 and 20% in drinking waterad libitumfor 16 weeks. The incidences of hepatocellular adenoma and total tumors increased dose‐dependently with statistical significance at doses of 10% and 20%, compared to the initiated control value. Similarly, dose dependence was observed for the incidence of hepatocellular carcinoma, which was elevated significantly at the dose of 20%. No alteration in development of preneoplastic glutathione‐S‐transferase placental form positive foci or tumors was observed with 0.1–1%. Cell proliferation also increased dose‐dependently and CYP2E1 protein induction was recognized in centrilobular regions without alteration in mRNA levels, but no effects were evident on formation of 8‐hydroxy‐2′‐deoxyguanosine, an oxidative DNA damage marker, or lipid peroxidation in any of the initiated groups. The mRNA expression of cyclin D1 increased dose dependently. The results demonstrated that ethanol dose‐dependently promotes hepatocarcinogenesis induced by MeIQx, but with no adverse influence at doses of 1% or less, comparable to sensible drinking levels in humans. (Cancer Sci2005; 96: 747–757)
Review article: diabetes, genetics and ethnicity
Authors: CARULLI L. , RONDINELLA S. , LOMBARDINI S. , CANEDI I. , LORIA P. , CARULLI N. 
Published: October 2005

SummaryThe prevalence of insulin resistance and diabetes has increased in the past decades at an alarming rate in all Western countries and in those countries which are adopting a ‘western life style’. This trend suggests the impact of environmental factors such as diet, obesity and physical activity on the pathogenesis of diabetes. However it is known that the prevalence and variation of prevalence, as consequence of environmental changes, it is different in various ethnic groups. Studies conducted in multiethnic populations suggest that some ethnic groups, such as Hispanics or Asian Indians, might have a particular predisposition, possibly on genetic basis, to develop insulin resistance and diabetes, when exposed to adverse conditions. According to the ‘thrifty gene’ hypothesis, a clustering of different genetic defects or polymorphisms, developed as genetic advantage in some populations, could predispose some ethnic groups to insulin resistance and diabetes in presence of an increased food supply. Multiple mutations, associated with small changes in insulin sensitivity, when combined, may induce a significant reduction in insulin sensitivity. This review deals with the possible relevance of genetic factors in the expression of insulin resistance and diabetes in relation to ethnicity.
Review article: the metabolic syndrome and non‐alcoholic fatty liver disease
Authors: LORIA P. , LONARDO A. , CARULLI L. , VERRONE A. M. , RICCHI M. , LOMBARDINI S. , RUDILOSSO A. , BALLESTRI S. , CARULLI N. 
Published: October 2005

SummaryMetabolic syndrome represents a common risk factor for premature cardiovascular disease and cancer whose core cluster includes diabetes, hypertension, dyslipidaemia and obesity. The liver is a target organ in metabolic syndrome patients in which it manifests itself with non‐alcoholic fatty liver disease spanning steatosis through hepatocellular carcinoma via steatohepatitis and cirrhosis. Given that metabolic syndrome and non‐alcoholic fatty liver disease affect the same insulin‐resistant patients, not unexpectedly, there are amazing similarities between metabolic syndrome and non‐alcoholic fatty liver disease in terms of prevalence, pathogenesis, clinical features and outcome. The available drug weaponry for metabolic syndrome includes aspirin, metformin, peroxisome proliferator‐activated receptor agonists, statins, ACE (angiotensin I‐converting enzyme) inhibitors and sartans, which are potentially or clinically useful also to the non‐alcoholic fatty liver disease patient. Studies are needed to highlight the grey areas in this topic. Issues to be addressed include: diagnostic criteria for metabolic syndrome; nomenclature of non‐alcoholic fatty liver disease; enlargement of the clinical spectrum and characterization of the prognosis of insulin resistance‐related diseases; evaluation of the most specific clinical predictors of metabolic syndrome/non‐alcoholic fatty liver disease and assessment of their variability over the time; characterization of the importance of new risk factors for metabolic syndrome with regard to the development and progression of non‐alcoholic fatty liver disease.
Review article: the treatment of fatty liver disease associated with the metabolic syndrome
Authors: MARCHESINI G. , NATALE S. , MANINI R. , AGOSTINI F. 
Published: October 2005

SummaryThe treatment of non‐alcoholic fatty liver disease may be worthwhile to prevent progression to advanced liver failure, but no therapy is definitely evidence‐based. Weight loss or lifestyle modifications remain the primary line of intervention, particularly in overweight or obese subjects. In adult non‐alcoholic fatty liver disease, they are effective in the short‐term, but require a multidisciplinary team approach that is rarely available in liver units. Insulin‐sensitizing agents are probably the treatment of choice. They definitely reduce the insulin resistance that promotes steatosis. Several uncontrolled and controlled studies have documented an improvement in liver biochemistry and in histology, but the long‐term results remain unsettled. This is an area where significant advances are expected in the next few years.
Review article: steatosis, the metabolic syndrome and cancer
Authors: BUGIANESI E. 
Published: October 2005

SummaryThe incidence of hepatocellular carcinoma is increasing, but the temporal changes of risk factors remain unclear. A significant proportion of hepatocellular carcinoma (7–30%) develops in cryptogenic cirrhosis, and may represent the most worrisome complication of non‐alcoholic steatohepatitis. Non‐alcoholic steatohepatitis is tightly related to insulin resistance and several features of the metabolic syndrome, i.e obesity, type 2 diabetes and dyslipidaemia. Nearly two‐thirds of adults in the United States and an increasing percentage of the population worldwide are overweight or obese. Diabetes prevalence is increasing as well. The rising prevalence of risk factors associated with non‐alcoholic steatohepatitis can partially account for the increasing incidence of cryptogenic cirrhosis and subsequent hepatocellular carcinoma. Moreover, recent evidence demonstrates that both obesity and diabetes are per se associated with an increased cancer risk. Large prospective studies show a significant association with obesity for several cancers, including cancers of the colon, female breast, endometrium, kidney, oesophagus and liver (hepatocellular carcinoma). Type 2 diabetes is also related with increased risks of colon, endometrial, kidney, pancreatic cancer and hepatocellular carcinoma. In western countries, the insulin resistance syndrome is emerging as a risk factor for a wide variety of cancers, including hepatocellular carcinoma.
Review article: non‐alcoholic fatty liver disease and hepatitis C – risk factors and clinical implications
Authors: SANYAL A. J. 
Published: October 2005

SummaryHepatitis C and non‐alcoholic fatty liver disease (NAFLD) are the two most common liver diseases in the Western hemisphere. It is therefore natural that these conditions often co‐exist in the same individual. Hepatitis C, especially genotype 3, is often associated with hepatic steatosis. In subjects with genotype 3 infection, a sustained virologic response to treatment is associated with improvement in hepatic steatosis. The diagnosis of NAFLD in a subject with hepatitis C infection is based on the presence of hepatic steatosis. Most investigators require the presence of at least grade II steatosis to warrant a diagnosis of concomitant NAFLD because the significance of minimal steatosis is uncertain. The presence of steatohepatitis is surmised by the additional presence of Mallory bodies, cytologic ballooning and pericellular fibrosis. It is of paramount importance to exclude alcohol as a cause of these histologic findings in this population before a diagnosis of NAFLD is made. The presence of NAFLD in subjects with hepatitis C genotype 1 infection is most strongly associated with the presence of the metabolic syndrome and insulin resistance. The degree of hepatic steatosis correlates with the degree of hepatic fibrosis and the presence of concomitant steatosis is associated with more advanced fibrosis. The presence of cytologic ballooning confers an additional risk for increased fibrosis. Insulin resistance and hyperinsulinemia have been associated with increased collagen production by hepatic stellate cells. Subjects with hepatitis C and NAFLD are more likely to be virologic nonresponders following anti‐HCV therapy. The value of treating insulin resistance and NAFLD prior to antiviral therapy remains to be experimentally verified.
Review article: hepatitis C virus‐associated steatosis – pathogenic mechanisms and clinical implications
Authors: ADINOLFI L. E. , DURANTE‐MANGONI E. , ZAMPINO R. , RUGGIERO G. 
Published: October 2005

SummarySteatosis is a common feature of chronic hepatitis C, and may be caused directly by the virus, as in genotype 3 infection, or be associated with host metabolic factors. The interaction of hepatitis C virus core protein with the lipoprotein secretion pathways causes the characteristic alterations of lipid metabolism observed in hepatitis C virus‐related steatosis. Several pathogenic mechanisms are likely involved into the pathogenesis of hepatitis C virus‐related steatosis, including hyper‐homocysteinaemia, hypoadiponectinaemia and insulin resistance. Steatosis is a major determinant of the liver damage progression in chronic hepatitis C (CHC), and negatively affects the response rate to the interferon (IFN)‐based anti‐viral treatment. Moreover, recent evidence suggests that steatosis may contribute to liver carcinogenesis. Chronic hepatitis C is a recognized risk factor for type 2 diabetes and it could be implicated into the pathogenesis of atherosclerosis. The role of hepatitis C virus (HCV)‐related steatosis in these epidemiological associations remains to be determined.
Review article: hepatic steatosis and insulin resistance
Authors: LONARDO A. , LOMBARDINI S. , RICCHI M. , SCAGLIONI F. , LORIA P. 
Published: October 2005

SummaryHepatic steatosis may be both an adaptive phenomenon and an example of lipotoxicity. Its prevalence ranks in the same order of magnitude of insulin resistance in the general population. Studies support the finding that hepatic steatosis is secondary to insulin resistance and not vice versa. A steatotic liver will further contribute to the development of insulin resistance through impaired clearance of insulin from the portal blood, creating a vicious cycle. Insulin resistance is the leading force in the pathogenesis and natural history of non‐alcoholic fatty liver disease. Dysfunction of energetic homeostasis and the interaction of adiponectin, leptin and tumour necrosis factor‐α are key events in the pathogenesis of steatosis and insulin resistance. Insulin resistance represents the frame within which hepatic and extrahepatic non‐alcoholic fatty liver disease‐related clinical manifestations are to be anticipated and interpreted.
Review article: role of oxidative stress in the progression of non‐alcoholic steatosis
Authors: ALBANO E. , MOTTARAN E. , OCCHINO G. , REALE E. , VIDALI M. 
Published: October 2005

SummaryThe mechanisms responsible for the progression of nonalcoholic fatty liver disease (NAFLD) to more severe liver injury are still poorly understood. Data from animal models suggest that oxidative stress contributes to steatohepatitis and an increase of lipid peroxidation has been documented in human NAFLD. By measuring the titers of circulating antibodies against lipid peroxidation products as markers of oxidative stress we have observed that NAFLD patients have titers of these antibodies significantly higher than in controls. Moreover, the titers of lipid peroxidation‐related antibodies are associated with a 3‐fold increase in the risk of developing advanced fibrosis/cirrhosis. Although the mechanisms causing oxidative stress in NAFLD have not been elucidated, these results support the involvement of lipid peroxidation in the processes leading to liver fibrosis associated with NAFLD.
Review article: chronic hepatitis C – natural history and cofactors
Authors: ALBERTI A. , VARIO A. , FERRARI A. , PISTIS R. 
Published: October 2005

SummaryChronic hepatitis C is highly heterogeneous in clinical presentation and outcomes.This heterogeneity is largely related to host factors that have been clearly proven to affect the severity and rapidity of disease progression. The most relevant factors that have been shown to accelerate progression to cirrhosis include age at infection, alcohol abuse and the metabolic syndrome with insulin resistance, obesity and hepatic steatosis.Co‐infection with HIV and/or HBV also increases the risk of progression to cirrhosis and to hepatocellular carcinoma.Surprisingly enough, viral related factors appear as less important and neither the virus genotype and load have been found to exert a clear influence on disease severity and progression, although more data in this field, and particularly on the role of different viral proteins in causing cytopathic effects, are awaited and may change this view in the near future.
HCV liver infection and liver steatosis: evidence for indirect mechanisms in genotype 3?
Authors: GRASSI A. , BALLARDINI G. , SUSCA M. , BIANCHINI F. , BONOLI S. , BIANCHI F. B. , LENZI M. 
Published: October 2005

SummaryBackground : Hepatitis C virus (HCV) infection is associated with the appearance of liver steatosis.Aim : To search for a correlation between the number of HCV infected hepatocytes and the presence, amount and distribution of steatosis.Methods : A total of 124 frozen liver biopsies from HCV patients (genotype 3 = 21) were studied. HCV‐antigens were detected on frozen liver sections using a four steps immunoperoxidase technique. Steatosis was graded by haematoxilin‐eosin counterstaining on a serial section.Results : Steatosis was detected in 82 of 124 (66.1%) patients without differences between different genotypes. Uric acid, body mass index, γGT levels significantly correlated with steatosis in non‐3 (P < 0.01, P < 0.05, P < 0.01, respectively) but not in genotype 3 patients. HCV‐antigens were detected in 95 of 124 (76.6%) cases. A positive correlation between steatosis and the number of infected hepatocytes was observed only in genotype 3 patients (P = 0.06). In most cases the number of cells with steatosis greatly outnumbered that of HCV infected cells.Conclusion : We confirm a possible role of the virus in the genesis of steatosis in HCV genotype 3 infected patients; however, as steatosis do not appear to be directly related to the presence of HCV‐antigens within single hepatocytes, an indirect, possibly cytokine mediated, mechanism might be operative.
Review article: diabetes and atherosclerosis – running on a common road
Authors: FEDERICI M. , LAURO R. 
Published: October 2005

SummaryInsulin resistance accounts for glucotoxicity observed in diabetes and atherosclerotic disease. Glucotoxicity depends from the shift of glucose metabolism from the glycolytic pathway to minor forms of glucose metabolism, including sorbitol, hexosamine and AGE pathways. These pathways increase oxidative stress and/or block insulin signalling so leading to a further decline of insulin action. A genetic defect of insulin action (the g972R Insulin Receptor Substrate 1 variant) may sustain endothelial dysfunction, the first defect of vascular homeostasis in the road to atherosclerosis. Furthermore, hyperglycemia even in the absence of insulin resistance, activates the hexosamine pathway in endothelial cells, affects the production of nitric oxide, increases the production and activity of metalloproteinase 2 and 9 and activates endothelium thus provoking endothelial dysfunction.Oxidative stress and inflammation through activtion of IKK‐beta could determine insulin resistance impairing IRS‐1 ability to activate the metabolic branch of insulin signalling. Furthermore, increased oxidative stress may be speculated to affect glucose metabolism in a proportion of patients with coronary artery disease.In conclusion, type 2 diabetes and atherosclerosis share vascular homeostasis and glucose metabolism and insulin resistance might be the common road where diabetes and atherosclerosis run together.
Ultrasonographic and biochemical parameters in the non‐invasive evaluation of liver fibrosis in hepatitis C virus chronic hepatitis
Authors: IACOBELLIS A. , FUSILLI S. , MANGIA A. , CLEMENTE R. , FESTA V. , GIACOBBE A. , FACCIORUSSO D. , NIRO G. , CONOSCITORE P. , ANDRIULLI A. 
Published: October 2005

SummaryBackground : Prior studies suggest that platelet counts of <140 000/μL can discriminate patients with different stages of fibrosis.Aim : To determine the added value of abdominal ultrasound analysis of morphological liver features in increasing the diagnostic accuracy of platelet counts for the prediction of liver fibrosis at histology.Methods : In a retrospective study, clinical records of 1143 chronic hepatitis C patients at their first presentation, naives to both liver biopsy and anti‐viral treatment, were reviewed. Sensitivity, specificity, positive and negative predictive values, positive and negative likelihood ratios of following indices were evaluated singularly or in combination: platelet counts <140 000/μL; nodular liver surface, spleen and portal vein size.Results : All indices had specificity rate of ≥90% in excluding bridging fibrosis/cirrhosis, whereas sensitivity was acceptable (51%) for only platelet counts <140 000/μL. None of the ultrasonographic parameters singularly evaluated and reached an acceptable sensitivity rate. For ruling cirrhosis in or out, specificity rate was ≥82% for all tests, with the highest value reported by portal vein size. Low platelet counts plus nodular liver surface had the best sensitivity.Conclusions : No additional significant predictive value was given by adding ultrasonographic parameters to low platelet counts, whereas only a mild non‐significant improvement in sensitivity was obtained combining platelet counts <140 000/μL with the presence of nodular liver surface. The platelet counts <140 000/μL showed the best predictive value for including both significant fibrosis and cirrhosis.
Oral butyrate for mildly to moderately active Crohn's disease
Authors: SABATINO A. DI , MORERA R. , CICCOCIOPPO R. , CAZZOLA P. , GOTTI S. , TINOZZI F. P. , TINOZZI S. , CORAZZA G. R. 
Published: October 2005

SummaryBackground : Butyrate exerts anti‐inflammatory effects in experimental colitis and on Crohn's disease lamina propria mononuclear cells in vitro.Aim : To explore the efficacy and safety of oral butyrate in Crohn's disease.Methods : Thirteen patients with mild–moderate ileocolonic Crohn's disease received 4 g/day butyrate as enteric‐coated tablets for 8 weeks. Full colonoscopy and ileoscopy were performed before and after treatment. Endoscopical and histological score, laboratory data, Crohn's disease activity index and mucosal interleukin (IL)‐1β, IL‐6, IL‐12, interferon‐γ, tumour necrosis factor‐α and nuclear factor‐kappa B (NF‐κB) were assessed before and after treatment.Results : One patient withdrew from the study, and three patients did not experience clinical improvement. Among the nine patients (69%) who responded to treatment, seven (53%) achieved remission and two had a partial response. Endoscopical and histological score significantly improved after treatment at ileocaecal level (P < 0.05). Leucocyte blood count, erythrocyte sedimentation rate and mucosal levels of NF‐κB and IL‐1β significantly decreased after treatment (P < 0.05).Conclusions : Oral butyrate is safe and well tolerated, and may be effective in inducing clinical improvement/remission in Crohn's disease. These data indicate the need for a large investigation to extend the present findings, and suggest that butyrate may exert its action through downregulation of NF‐κB and IL‐1β.