bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE POLITICAL ECONOMY OF AFRICA'S NATURAL RESOURCES AND THE ‘GREAT FINANCIAL CRISIS’
Authors: BÜSCHER BRAM 
Published: March 2012

ABSTRACTOver the last decade, Africa's natural resources have seen another rapid rise in political‐economic importance. The continent's abundant biodiversity underpins the fast‐growing (eco)tourism industry, while its rich energy resources have seen renewed attention from global powers. Obviously, these boom‐and‐bust cycles of interest in African natural resources have signified the continent's place in the capitalist world order for a long time. Yet, and despite the intense ambiguities and manifold negative consequences of this history, the conservation of Africa's biodiversity riches and the exploitation of its energy resources continue to be promoted in win‐win terms: beneficial to the continent and outsiders ‘consuming’ the resources. The paper reviews this ‘boom‐and bust’ cycle of interest in Africa's resources in the light of the recent ‘Great Financial Crisis’. It argues that an initial review of mainstream responses to the crisis shows a global ‘reflex’ that falls back on and so reinstates Africa's ‘natural place’ in the global order.
Evaluating the effectiveness of a web‐based intervention to promote mental wellbeing in women and partners following miscarriage, using a modified patient preference trial design: an external pilot
Authors: Klein S , Cumming GP , Lee AJ , Alexander DA , Bolsover D 
Published: March 2012

Please cite this paper as: Klein S, Cumming G, Lee A, Alexander D, Bolsover D. Evaluating the effectiveness of a web‐based intervention to promote mental wellbeing in women and partners following miscarriage, using a modified patient preference trial design: an external pilot. BJOG 2012;119:762–767.This article describes an external pilot study of a modified ‘partially randomised patient preference’ trial comparing a web‐based intervention (designed to promote mental wellbeing) with standard care post‐miscarriage. Assessment comprised an online administration of baseline measures with follow‐up at 3 months following registration. Baseline data were obtained from 60 women (and seven partners) post‐discharge from one of two Early Pregnancy Assessment Units. ‘Intention to treat’ versus a ‘per protocol’ sensitivity analysis showed the effects of introducing a ‘preference’ option post‐randomisation, and highlights the benefits compared with a randomised controlled trial design to enable a robust evaluation of the website in promoting mental wellbeing after miscarriage.
Mechanisms mediating the ability of caffeine to influence MDMA (‘Ecstasy’)‐induced hyperthermia in rats
Authors: Vanattou‐Saïfoudine N , McNamara R , Harkin A 
Published: March 2012

Background and purpose:  Caffeine exacerbates the hyperthermia associated with an acute exposure to 3,4 methylenedioxymethamphetamine (MDMA, ‘Ecstasy’) in rats. The present study investigated the mechanisms mediating this interaction.Experimental approach:  Adult male Sprague‐Dawley rats were treated with caffeine (10 mg·kg−1; i.p.) and MDMA (15 mg·kg−1; i.p.) alone and in combination. Core body temperatures were monitored before and after drug administration.Key results:  Central catecholamine depletion blocked MDMA‐induced hyperthermia and its exacerbation by caffeine. Caffeine provoked a hyperthermic response when the catecholamine releaser d‐amphetamine (1 mg·kg−1) was combined with the 5‐HT releaser d‐fenfluramine (5 mg·kg−1) or the non‐selective dopamine receptor agonist apomorphine (1 mg·kg−1) was combined with the 5‐HT2 receptor agonist DOI (2 mg·kg−1) but not following either agents alone. Pretreatment with the dopamine D1 receptor antagonist Schering (SCH) 23390 (1 mg·kg−1), the 5‐HT2 receptor antagonist ketanserin (5 mg·kg−1) or α1‐adreno‐ receptor antagonist prazosin (0.2 mg·kg−1) blocked MDMA‐induced hyperthermia and its exacerbation by caffeine. Co‐administration of a combination of MDMA with the PDE‐4 inhibitor rolipram (0.025 mg·kg−1) and the adenosine A1/2 receptor antagonist 9‐chloro‐2‐(2‐furanyl)‐[1,2,4]triazolo[1,5‐C]quinazolin‐5‐amine 15943 (10 mg·kg−1) or the A2A receptor antagonist SCH 58261 (2 mg·kg−1) but not the A1 receptor antagonist DPCPX (10 mg·kg−1) exacerbated MDMA‐induced hyperthermia.Conclusions and implications:  A mechanism comprising 5‐HT and catecholamines is proposed to mediate MDMA‐induced hyperthermia. A combination of adenosine A2A receptor antagonism and PDE inhibition can account for the exacerbation of MDMA‐induced hyperthermia by caffeine.
A systematic review on prognostic indicators of acute on chronic liver failure and their predictive value for mortality
Authors: Wlodzimirow Kama A. , Eslami Saeid , Abu‐Hanna Ameen , Nieuwoudt Martin , Chamuleau Robert A. F. M. 
Published: March 2012

AbstractBackgroundAn early and proper diagnosis of acute on chronic liver failure (ACLF), together with the identification of indicators associated with disease severity is critical for outcome prediction and therapy.ObjectiveTo systematically identify and summarize prognostic indicators for patients with ACLF and to evaluate the predictive value of these indicators.MethodsEmbase and Ovid‐Medline were searched for English‐language articles. The search criteria focused on identifying clinical trials and observational studies reporting on indicators used for prediction of mortality in patients with ACLF.ResultsOf 2382 studies identified, 19 were included for detailed analysis. Thirteen different definitions of ACLF were found. The main differences were related to acute deterioration in liver function, coagulopathy and hyperbilirubinaemia/jaundice. Seventy three prognostic indicators and their association with mortality were extracted and categorized into seven categories: general markers (n = 13), viral markers (n = 6), bio‐markers (n = 22), hemodynamics (n = 1), morphology/histology (n = 17), scoring systems (n = 10) and treatments (n = 4).ConclusionsThe ambiguity and variability in the definition of ACLF and in its predictive indicators hampers comparability among studies. There is a need for a single uniform definition of ACLF. Also absence of a gold standard is an obstacle to render one indicator superior to another. The age, hepatic encephalopathy, model for end‐stage liver disease score, total bilirubin and International normalized ratio (prothrombin time) appeared to be promising candidates for evaluation in future studies. The result of this review may be useful as a starting point in developing a standard list of indicators for clinical outcome that concur with the clinicians' subjective views on prognosis in ACLF.
MicroRNA profiling of hepatocarcinogenesis identifies C19MC cluster as a novel prognostic biomarker in hepatocellular carcinoma
Authors: Augello Claudia , Vaira Valentina , Caruso Luca , Destro Annarita , Maggioni Marco , Park Young Nyun , Montorsi Marco , Santambrogio Roberto , Roncalli Massimo , Bosari Silvano 
Published: March 2012

AbstractBackground and aimsProgressive hepatocarcinogenesis is a stepwise process that drives liver transformation. However, the molecular mechanisms of early liver transformation are far from clear. A role for microRNAs (miRNA) as diagnostic and prognostic factors in human tumours, including hepatocellular carcinoma (HCC), is promising. We aimed to identify novel miRNA as biomarkers for differential diagnosis and predictors of disease progression.MethodsWe used a low‐density array platform to profile the expression of 664 mature miRNA in a cohort of 60 hepatitis C virus‐positive liver lesions representative of all stages of progressive hepatocarcinogenesis. We validated selected miRNA in two independent patient series by qPCR and we characterized the genomic status of the miRNA cluster C19MC by fluorescent in situ hybridization and copy‐number variation analyses.ResultsA 18‐miRNA signature distinguished cirrhosis, dysplastic nodules and HCC lesions. Four miRNAs overexpressed in HCCs belonged to chromosome 19 miRNA cluster (C19MC). Significant overexpression of C19MC in early HCC compared to dysplastic nodules could be confirmed in a second series of hepatitis B virus‐related liver lesions (n = 30). In a third series of 61 HCCs, C19MC cluster was overexpressed in HCCs compared to matched cirrhotic parenchyma and regardless of the type of viral infection. High C19MC miRNA levels were correlated with poor clinico‐pathological features, increased risk of tumour recurrence and shorter overall survival time. HCCs overexpressing the C19MC cluster showed genetic amplification of the corresponding locus.ConclusionsC19MC cluster is a novel molecular alteration characteristic of liver cancer and predictor of poor prognosis. C19MC is an attractive candidate for novel HCC therapies.
The Association Between Barrett’s Esophagus and Helicobacter pylori Infection: A Meta‐Analysis
Authors: Fischbach Lori A. , Nordenstedt Helena , Kramer Jennifer R. , Gandhi Subi , Dick‐Onuoha Sam , Lewis Anthony , El‐Serag Hashem B. 
Published: March 2012

AbstractObjective:  The effect of Helicobacter pylori on Barrett’s esophagus is poorly understood. We conducted a meta‐analysis to summarize the existing literature examining the effect that H. pylori has on Barrett’s esophagus.Design:  We performed a comprehensive search to identify studies pertaining to the association between H. pylori and Barrett’s esophagus. We conducted meta‐regression analyses to identify sources of variation in the effect of H. pylori on Barrett’s esophagus.Results:  Our analysis included a total of 49 studies that examined the effect of H. pylori on Barrett’s esophagus and seven studies that examined the effect of cag A positivity on Barrett’s esophagus. Overall, H. pylori, and even more so cag A, tended to be protective for Barrett’s esophagus in most studies; however, there was obvious heterogeneity across studies. The effect of H. pylori on Barrett’s esophagus varied by geographic location and in the presence of selection and information biases. Only four studies were found without obvious selection and information bias, and these showed a protective effect of H. pylori on Barrett’s esophagus (Relative risk = 0.46 [95% CI: 0.35, 0.60]).Conclusions:  Estimates for the effect of H. pylori on Barrett’s esophagus were heterogeneous across studies. We identified selection and information bias as potential sources of this heterogeneity. Few studies without obvious selection and information bias have been conducted to examine the effect of H. pylori on Barrett’s esophagus, but in these, H. pylori infection is associated with a reduced risk of Barrett’s esophagus.
Expression of Adhesion and Activation Molecules on Circulating Monocytes in Children with Helicobacter pylori Infection
Authors: Helmin‐Basa Anna , Czerwionka‐Szaflarska Mieczyslawa , Bala Grazyna , Szaflarska‐Poplawska Anna , Mierzwa Grazyna , Gackowska Lidia , Kubiszewska Izabela , Eljaszewicz Andrzej , Marszalek Andrzej , Michalkiewicz Jacek 
Published: March 2012

AbstractObjectives:  The aim of this study was to assess the cell surface expression of adhesion (CD11a, CD11b, CD11c, CD18, CD54, and CD58) and activation (CD14, HLA‐DR, and CD16) molecules on the circulating monocytes in Helicobacter pylori (H. pylori)‐infected and noninfected children with gastritis, with the goal of comparing the results with those obtained from the controls.Materials and Methods:  Ninety‐four children were studied: 47 of them with H. pylori infection (of those 25 children after the failure of eradication therapy) and 26 children with gastritis where H. pylori infection was excluded, as well as 21 controls. H. pylori infection status was assessed based on [13C] urea breath test, rapid urease test, and histology. Analysis of the monocyte surface molecule expression was carried out by flow cytometry.Results:  H. pylori‐infected children and children who experienced a failure of the eradication therapy differed significantly in the expression of adhesion and activation molecule on circulating monocytes. A decrease, both in the proportion of CD11c‐ and CD14‐bearing monocytes, and the expression of CD11c and CD14 molecules on circulating monocytes, was found in children in whom the eradication therapy failed (p < .05). Low expression of CD11b (p = .04) and CD18 (p = .02) integrins on monocytes was also observed. Additionally, the percentage of HLA‐DR‐bearing monocytes was decreased (p = .04), while the CD16 density receptor was increased (p = .02). Compared with the controls, low percentage of CD16‐positive monocytes was noted in noninfected children with gastritis (p = .01).Conclusion:  H. pylori eradication therapy in children causes inhibition of inflammatory response via a reduction in CD11b, CD11c, and CD18 beta2 integrin monocyte expression.
Single Nucleotide Polymorphisms of Helicobacter pylori dupA that Lead to Premature Stop Codons
Authors: Moura Sílvia B. , Costa Rafaella F. A. , Anacleto Charles , Rocha Gifone A. , Rocha Andreia M. C. , Queiroz Dulciene M. M. 
Published: March 2012

AbstractBackground:  The detection of the putative disease‐specific Helicobacter pylori marker duodenal ulcer promoting gene A (dupA) is currently based on PCR detection of jhp0917 and jhp0918 that form the gene. However, mutations that lead to premature stop codons that split off the dupA leading to truncated products cannot be evaluated by PCR.Methods:  We directly sequence the complete dupA of 75 dupA‐positive strains of H. pylori isolated from patients with gastritis (n = 26), duodenal ulcer (n = 29), and gastric carcinoma (n = 20), to search for frame‐shifting mutations that lead to stop codon.Results:  Thirty‐four strains had single nucleotide mutations in dupA that lead to premature stop codon creating smaller products than the predicted 1839 bp product and, for this reason, were considered as dupA‐negative. Intact dupA was more frequently observed in strains isolated from duodenal ulcer patients (65.5%) than in patients with gastritis only (46.2%) or with gastric carcinoma (50%). In logistic analysis, the presence of the intact dupA independently associated with duodenal ulcer (OR = 5.06; 95% CI = 1.22–20.96, p = .02).Conclusion:  We propose the primer walking methodology as a simple technique to sequence the gene. When we considered as dupA‐positive only those strains that carry dupA gene without premature stop codons, the gene was associated with duodenal ulcer and, therefore, can be used as a marker for this disease in our population.
Helicobacter pylori‐Associated Regulation of Forkhead Transcription Factors FoxO1/3a in Human Gastric Cells
Authors: Tabassam Fazal H. , Graham David Y. , Yamaoka Yoshio 
Published: March 2012

AbstractBackground:  Interaction of Helicobacter pylori with gastric mucosa leads to marked cellular and humoral host immunologic responses. The signaling pathways initiated by bacteria–host interaction that result in perturbations in cell structure and function remain unclear. Forkhead transcription factors of class O (FoxO) are implicated in the regulation of apoptosis, cell survival, and pathogenesis. H. pylori infection of gastric epithelial cells induces phosphoinositide‐3 kinase (PI3K)‐dependent Akt activation and cell survival signaling. We investigated the role of H. pylori‐activated PI3K/Akt in the regulation of FoxO1/3a in gastric cells.Methods:  Immunoblot, immunoprecipitation, and fluorescence microscopy were used to assess the effect of infection of gastric epithelial cells with wild‐type H. pylori and their isogenic cag pathogenicity island (PAI) or oipA mutants on the FoxO1/3a signaling pathways. Interleukin‐8 release was determined by enzyme‐linked immunosorbent assays.Results:  H. pylori infection resulted in activation of the PI3K p85 subunit and inactivation of FoxO1 and FoxO3a by their phosphorylation and translocation of from the nucleus to the cytoplasm. Inhibition of PI3K or Akt kinase activity reduced FoxO1/3a phosphorylation. Akt, FoxO1, or FoxO3a siRNA reduced H. pylori‐induced interleukin‐8 production. Infection with oipA mutants reduced PI3K/Akt activation and inhibited FoxO1/3a phosphorylation, whereas infection with cag PAI mutants reduced PI3K/Akt activity but did not inhibit FoxO1/3a activation.Conclusions:  FoxO1 and FoxO3a are novel nuclear substrates of H. pylori‐induced PI3K/Akt cell survival signaling pathways that partially control interleukin‐8 production. OipA‐regulated interleukin‐8 release through PI3K/Akt is dependent on FoxO1/3a inactivation, whereas cag PAI‐mediated interleukin‐8 production employs FoxO1/3‐independent signaling.
Probiotics‐Containing Yogurts Suppress Helicobacter pylori Load and Modify Immune Response and Intestinal Microbiota in the Helicobacter pylori‐Infected Children
Authors: Yang Yao‐Jong , Sheu Bor‐Shyang 
Published: March 2012

AbstractBackground:  The benefits of probiotics to the pediatric Helicobacter pylori infection remain uncertain. We tested whether the H. pylori‐infected children have an altered gut microflora, and whether probiotics‐containing yogurt can restore such change and improve their H. pylori‐related immune cascades.Methods:  We prospectively included 38 children with H. pylori infection confirmed by a positive 13C‐urea breath test (UBT) and 38 age‐ and sex‐matched noninfected controls. All of them have provided the serum and stool samples before and after 4‐week ingestion of probiotics‐containing yogurt. The serum samples were tested for the TNF‐α, IL‐10, IL‐6, immunoglobulin (Ig) A, G, E, pepsinogens I and II levels. The stool samples were tested for the colony counts of Bifidobacterium spp. and Escherichia coli. The follow‐up UBT indirectly assessed the H. pylori loads after yogurt usage.Results:  The H. pylori‐infected children had lower fecal Bifidobacterium spp. count (p = .009), Bifidobacterium spp./E. coli ratio (p = .04), serum IgA titer (p = .04), and pepsinogens I/II ratio (p < .001) than in controls. In the H. pylori‐infected children, 4‐week yogurt ingestion reduced the IL‐6 level (p < .01) and H. pylori loads (p = .046), but elevated the serum IgA and pepsinogen II levels (p < .001). Moreover, yogurt ingestion can improve the childhood fecal Bifidobacterium spp./E. coli ratio (p = .03).Conclusions:  The H. pylori‐infected children have a lower Bifidobacterium microflora in gut. The probiotics‐containing yogurt can offer benefits to restore Bifidobacterium spp./E. coli ratio in children and suppress the H. pylori load with increment of serum IgA but with reduction in IL‐6 in H. pylori‐infected children.
Eradication of Helicobacter pylori Infection Reduces the Incidence of Peptic Ulcer Disease in Patients using Nonsteroidal Anti‐Inflammatory Drugs: A Meta‐Analysis
Authors: Tang Chun‐Li , Ye Feng , Liu Wei , Pan Xiao‐Lin , Qian Juan , Zhang Guo‐Xin 
Published: March 2012

AbstractAim:  To investigate the association between use of nonsteroidal anti‐inflammatory drugs (NSAID) and Helicobacter pylori infection, interactive effect of H. pylori infection and NSAID use on the development of peptic ulcer disease (PUD), and the effect of H. pylori eradication therapy on PUD development.Material and Methods:  We performed a systematic literature search in EMBASE and PubMed for relevant articles published in English between January 1989 and August 2010, with the following MeSH and/or key words: non‐steroidal anti‐inflammatory drugs, or NSAIDs, Helicobacter pylori, or H. pylori, peptic ulcer disease or PUD, and randomized‐control study or clinical trial. The meta‐analysis was conducted using the Review Manager 4.2.2.Results:  In the analysis of five studies, the pooled prevalence of H. pylori infection was 74.5% and 71.1% in NSAID users and non‐NSAID users, respectively, (OR = 0.65; 95% CI: 0.35–1.20, p = .170). In the analysis of nine studies, the pooled prevalence of PUD in NSAID users was 31.2% and 17.9% in the presence and absence of H. pylori infection, respectively, (OR = 3.08; 95% CI: 1.26–7.55, p = .010). Moreover, in the analysis of seven studies, PUD developed in 6.4% and 11.8% of NSAID users with and without eradication therapy, respectively (OR = 0.50; 95% CI: 0.36–0.74, p < .001). The preventive effect of the eradication therapy was further revealed in NSAID‐naive users (OR = 0.26; 95% CI: 0.14–0.49, p < .0001) and in the Asian population (OR = 0.30; 95% CI: 0.16–0.56, p < .001).Conclusion:  NSAID use is not associated with H. pylori infection in patients with PUD. PUD is more common in H. pylori positive than in negative NSAID users. Moreover, H. pylori eradication therapy reduces PUD incidence in NSAID users, especially in naive users and in the Asian population.
Helicobacter pylori Infection in Clinical Practice: Probiotics and a Combination of Probiotics + Lactoferrin Improve Compliance, But Not Eradication, in Sequential Therapy
Authors: Manfredi Marco , Bizzarri Barbara , Sacchero Roberto Igino , Maccari Sergio , Calabrese Lorenzo , Fabbian Fabio , de’Angelis Gian Luigi 
Published: March 2012

AbstractBackground:  Sequential therapy (ST) seems to offer higher success rates than triple therapy (TT) in the eradication of Helicobacter pylori (H. pylori) infection. However, from the standpoint of therapeutic compliance, there is no difference between the two treatments. Adjuvant treatment (especially with probiotics (PB) and lactoferrin (LF)) has often improved compliance and eradication rates in patients subjected to TT, while ST had never been used in association with adjuvants.Methods:  Over a period of 2 years, we randomized and divided 227 consecutive adult patients with H. pylori infection into three groups. The patients were given ST with the addition of adjuvants, as follows: group A (ST + placebo), group B (ST + LF + PB), and group C (ST + PB). Our goal was to assess therapeutic compliance, so we prepared a questionnaire to help determine the severity of the side effects. We also determined the eradication rates for the groups.Results:  Patients with ST + placebo had the worst compliance as compared with the other two groups in terms of the absence of symptoms (p < .001 between B and A; p = .001 between C and A) and the presence of intolerable symptoms (p = .016 between B and A; p = .046 between C and A). The differences between the values for the treated groups and those for the placebo group were statistically significant. On the other hand, there was no statistically significant difference in compliance between groups B and C. The eradication rate was similar for the three groups.Conclusions:  Probiotics associated with ST provide optimum therapeutic compliance compared with the placebo and, despite the need to take a larger number of tablets, they should be taken into consideration as an adjuvant to therapy for H. pylori infection. The addition of LF to the PB did not bring about any further improvements in compliance. As compared with the placebo, the eradication rate of ST did not improve by adding LF + PB or by using PB alone.