bluuebunny/crossref_metadata_2025_split huggingface dataset:
Islamic Alternatives to Purely Capitalist Modes of Finance: A Study of Malaysian Banks from 1999 to 2006
Authors: ElGindi Tamer , Said Mona , Salevurakis John William 
Published: September 2009

Like Western financial markets, Islamic modes of finance offer services characterized by profit-and-loss sharing while also providing certain debt-based instruments. Unlike traditional capitalist modes of finance, however, Islamic finance places a unique emphasis upon the former, thus prompting many comparisons between the performance of Islamic banks and conventional ones. Given the mixed results of these studies, our paper analyzes eight banks in Malaysia offering both conventional and Islamic banking operations. Our comparison is conducted via discussions of profitability, liquidity, and asset quality. It is illustrated via this micro-level analysis that Islamic modes of finance may generally equal or surpass the quantitative measures of performance describing traditional capitalist finance systems and simultaneously encourage higher levels of social equity and economic stability in the era of financialization. JEL classification: B25, D33, D63, E44, N25
Low dietary sodium intake is associated with enhanced vascular endothelial function in middle-aged and older adults with elevated systolic blood pressure
Authors: Jablonski Kristen L. , Gates Phillip E. , Pierce Gary L. , Seals Douglas R. 
Published: September 2009

Background: Age and increasing systolic blood pressure (BP) are associated with vascular endothelial dysfunction, but the factors involved are incompletely understood. We tested the hypothesis that vascular endothelial function is related to dietary sodium intake among middle-aged and older adults (MA and O) with elevated systolic BP. Methods: Data were analyzed on 25 otherwise healthy adults aged 48—73 years with high normal systolic BP or stage I systolic hypertension (130—159 mmHg). Self-reported sodium intake was <100 mmol/d in 12 (7 M) subjects (low sodium, 73±6 mmol/d) and between 100 and 200 mmol/d in 13 (9 M) subjects (normal sodium, 144±6 mmol/d). Results: Groups did not differ in other dietary factors, age, body weight and composition, BP, metabolic risk factors, physical activity and maximal aerobic capacity. Plasma concentrations of norepinephrine, endothelin-1, oxidized low-density lipoproteins (LDL), antioxidant status and inflammatory markers did not differ between groups. Brachial artery flow-mediated dilation (FMD) was 42% (mm Δ) to 52% (% Δ) higher in the low versus normal sodium group ( p < 0.05). In all subjects, brachial artery FMD was inversely related to dietary sodium intake (FMD mm Δr =—0.40, p < 0.05; %Δr =—0.53, p < 0.01). Brachial artery FMD was not related to any other variable. In contrast, endothelium-independent dilation did not differ between groups ( p ≥ 0.24) and was not related to sodium intake in the overall group ( p ≥ 0.29). Conclusions: Low sodium intake is associated with enhanced brachial artery FMD in MA and O with elevated systolic BP. These results suggest that dietary sodium restriction may be an effective intervention for improving vascular endothelial function in this high-risk group.
Depletion of endogenous tumor-associated regulatory T cells improves the efficacy of adoptive cytotoxic T-cell immunotherapy in murine acute myeloid leukemia
Authors: Zhou Qing , Bucher Christoph , Munger Meghan E. , Highfill Steven L. , Tolar Jakub , Munn David H. , Levine Bruce L. , Riddle Megan , June Carl H. , Vallera Daniel A. , Weigel Brenda J. , Blazar Bruce R. 
Published: September 2009

Abstract
Tumor-induced immune suppression can permit tumor cells to escape host immune resistance. To elucidate host factors contributing to the poor response of adoptively transferred tumor-reactive cytotoxic T lymphocytes (CTLs), we used a systemic model of murine acute myeloid leukemia (AML). AML progression resulted in a progressive regulatory T-cell (Treg) accumulation in disease sites. The adoptive transfer of in vitro–generated, potently lytic anti–AML-reactive CTLs failed to reduce disease burden or extend survival. Compared with non–AML-bearing hosts, transferred CTLs had reduced proliferation in AML sites of metastases. Treg depletion by a brief course of interleukin-2 diphtheria toxin (IL-2DT) transiently reduced AML disease burden but did not permit long-term survival. In contrast, IL-2DT prevented anti-AML CTL hypoproliferation, increased the number of transferred CTLs at AML disease sites, reduced AML tumor burden, and resulted in long-term survivors that sustained an anti-AML memory response. These data demonstrated that Tregs present at AML disease sites suppress adoptively transferred CTL proliferation, limiting their in vivo expansion, and Treg depletion before CTL transfer can result in therapeutic efficacy in settings of substantial pre-existing tumor burden in which antitumor reactive CTL infusion alone has proven ineffective.
Relationship of erythropoietin, fetal hemoglobin, and hydroxyurea treatment to tricuspid regurgitation velocity in children with sickle cell disease
Authors: Gordeuk Victor R. , Campbell Andrew , Rana Sohail , Nouraie Mehdi , Niu Xiaomei , Minniti Caterina P. , Sable Craig , Darbari Deepika , Dham Niti , Onyekwere Onyinye , Ammosova Tatiana , Nekhai Sergei , Kato Gregory J. , Gladwin Mark T. , Castro Oswaldo L. 
Published: September 2009

AbstractHydroxyurea and higher hemoglobin F improve the clinical course and survival in sickle cell disease, but their roles in protecting from pulmonary hypertension are not clear. We studied 399 children and adolescents with sickle cell disease at steady state; 38% were being treated with hydroxyurea. Patients on hydroxyurea had higher hemoglobin concentration and lower values for a hemolytic component derived from 4 markers of hemolysis (P ≤ .002) but no difference in tricuspid regurgitation velocity compared with those not receiving hydroxyurea; they also had higher hemoglobin F (P < .001) and erythropoietin (P = .012) levels. Hemoglobin F correlated positively with erythropoietin even after adjustment for hemoglobin concentration (P < .001). Greater hemoglobin F and erythropoietin each independently predicted higher regurgitation velocity in addition to the hemolytic component (P ≤ .023). In conclusion, increase in hemoglobin F in sickle cell disease may be associated with relatively lower tissue oxygen delivery as reflected in higher erythropoietin concentration. Greater levels of erythropoietin or hemoglobin F were independently associated with higher tricuspid regurgitation velocity after adjustment for degree of hemolysis, suggesting an independent relationship of hypoxia with higher systolic pulmonary artery pressure. The hemolysis-lowering and hemoglobin F–augmenting effects of hydroxyurea may exert countervailing influences on pulmonary blood pressure in sickle cell disease.
How I treat EBV lymphoproliferation
Authors: Heslop Helen E. 
Published: September 2009

Abstract
Epstein-Barr virus (EBV)–associated B-cell lymphoproliferation is a life-threatening complication after hematopoietic stem cell or solid organ transplantation resulting from outgrowth of EBV-infected B cells that would normally be controlled by EBV-cytotoxic T cells. During the past decade, early detection strategies, such as serial measurement of EBV-DNA load in peripheral blood samples, have helped to identify high-risk patients and to diagnose early lymphoproliferation. Treatment options include manipulation of the balance between outgrowing EBV-infected B cells and the EBV cytotoxic T lymphocyte response and targeting the B cells with monoclonal antibodies or chemotherapy. Major challenges remain for defining indications for preemptive therapies and integrating novel and conventional therapies.
Increased ATP generation in the host cell is required for efficient vaccinia virus production
Authors: Chang Chia-Wei , Li Hui-Chun , Hsu Che-Fang , Chang Chiao-Yen , Lo Shih-Yen 
Published: September 2009

Abstract
To search for cellular genes up-regulated by vaccinia virus (VV) infection, differential display-reverse transcription-polymerase chain reaction (ddRT-PCR) assays were used to examine the expression of mRNAs from mock-infected and VV-infected HeLa cells. Two mitochondrial genes for proteins that are part of the electron transport chain that generates ATP, ND4 and CO II, were up-regulated after VV infection. Up-regulation of ND4 level by VV infection was confirmed by Western blotting analysis. Up-regulation of ND4 was reduced by the MAPK inhibitor, apigenin, which has been demonstrated elsewhere to inhibit VV replication. The induction of ND4 expression occurred after viral DNA replication since ara C, an inhibitor of poxviral DNA replication, could block this induction. ATP production was increased in the host cells after VV infection. Moreover, 4.5 μM oligomycin, an inhibitor of ATP production, reduced the ATP level 13 hr after virus infection to that of mock-infected cells and inhibited viral protein expression and virus production, suggesting that increased ATP production is required for efficient VV production. Our results further suggest that induction of ND4 expression is through a Bcl-2 independent pathway.
Comparative study of gene set enrichment methods
Authors: Abatangelo Luca , Maglietta Rosalia , Distaso Angela , D'Addabbo Annarita , Creanza Teresa Maria , Mukherjee Sayan , Ancona Nicola 
Published: September 2009

Abstract

Background
The analysis of high-throughput gene expression data with respect to sets of genes rather than individual genes has many advantages. A variety of methods have been developed for assessing the enrichment of sets of genes with respect to differential expression. In this paper we provide a comparative study of four of these methods: Fisher's exact test, Gene Set Enrichment Analysis (GSEA), Random-Sets (RS), and Gene List Analysis with Prediction Accuracy (GLAPA). The first three methods use associative statistics, while the fourth uses predictive statistics. We first compare all four methods on simulated data sets to verify that Fisher's exact test is markedly worse than the other three approaches. We then validate the other three methods on seven real data sets with known genetic perturbations and then compare the methods on two cancer data sets where our a priori knowledge is limited.

Results
The simulation study highlights that none of the three method outperforms all others consistently. GSEA and RS are able to detect weak signals of deregulation and they perform differently when genes in a gene set are both differentially up and down regulated. GLAPA is more conservative and large differences between the two phenotypes are required to allow the method to detect differential deregulation in gene sets. This is due to the fact that the enrichment statistic in GLAPA is prediction error which is a stronger criteria than classical two sample statistic as used in RS and GSEA. This was reflected in the analysis on real data sets as GSEA and RS were seen to be significant for particular gene sets while GLAPA was not, suggesting a small effect size. We find that the rank of gene set enrichment induced by GLAPA is more similar to RS than GSEA. More importantly, the rankings of the three methods share significant overlap.

Conclusion
The three methods considered in our study recover relevant gene sets known to be deregulated in the experimental conditions and pathologies analyzed. There are differences between the three methods and GSEA seems to be more consistent in finding enriched gene sets, although no method uniformly dominates over all data sets. Our analysis highlights the deep difference existing between associative and predictive methods for detecting enrichment and the use of both to better interpret results of pathway analysis. We close with suggestions for users of gene set methods.
Weighted gene co-expression network analysis of the peripheral blood from Amyotrophic Lateral Sclerosis patients
Authors: Saris Christiaan GJ , Horvath Steve , van Vught Paul WJ , van Es Michael A , Blauw Hylke M , Fuller Tova F , Langfelder Peter , DeYoung Joseph , Wokke John HJ , Veldink Jan H , van den Berg Leonard H , Ophoff Roel A 
Published: September 2009

Abstract

Background
Amyotrophic Lateral Sclerosis (ALS) is a lethal disorder characterized by progressive degeneration of motor neurons in the brain and spinal cord. Diagnosis is mainly based on clinical symptoms, and there is currently no therapy to stop the disease or slow its progression. Since access to spinal cord tissue is not possible at disease onset, we investigated changes in gene expression profiles in whole blood of ALS patients.

Results
Our transcriptional study showed dramatic changes in blood of ALS patients; 2,300 probes (9.4%) showed significant differential expression in a discovery dataset consisting of 30 ALS patients and 30 healthy controls. Weighted gene co-expression network analysis (WGCNA) was used to find disease-related networks (modules) and disease related hub genes. Two large co-expression modules were found to be associated with ALS. Our findings were replicated in a second (30 patients and 30 controls) and third dataset (63 patients and 63 controls), thereby demonstrating a highly significant and consistent association of two large co-expression modules with ALS disease status. Ingenuity Pathway Analysis of the ALS related module genes implicates enrichment of functional categories related to genetic disorders, neurodegeneration of the nervous system and inflammatory disease. The ALS related modules contain a number of candidate genes possibly involved in pathogenesis of ALS.

Conclusion
This first large-scale blood gene expression study in ALS observed distinct patterns between cases and controls which may provide opportunities for biomarker development as well as new insights into the molecular mechanisms of the disease.
Characterization of a salt-induced DhAHP, a gene coding for alkyl hydroperoxide reductase, from the extremely halophilic yeast Debaryomyces hansenii
Authors: Chao Hsiu-fung , Yen Yung-fu , Ku Maurice SB 
Published: September 2009

Abstract

Background

Debaryomyces hansenii is one of the most salt tolerant species of yeast and has become a model organism for the study of tolerance mechanisms against salinity. The goal of this study was to identify key upregulated genes that are involved in its adaptation to high salinity.

Results
By using forward subtractive hybridization we have cloned and sequenced DhAHP from D. hansenii that is significantly upregulated during salinity stress. DhAHP is orthologous to the alkly hydroperoxide reductase of the peroxiredoxin gene family, which catalyzes the reduction of peroxides at the expense of thiol compounds. The full-lengthed cDNA of DhAHP has 674 bp of nucleotide and contains a 516 bp open reading frame (ORF) encoding a deduced protein of 172 amino acid residues (18.3 kDa). D. hansenii Ahp is a cytosolic protein that belongs to the Ahp of the 1-Cys type peroxiredoxins. Phylogentically, the DhAhp and Candida albicans Ahp11 (Swiss-Prot: Q5AF44) share a common ancestry but show divergent evolution. Silence of its expression in D. hansenii by RNAi resulted in decreased tolerance to salt whereas overexpression of DhAHP in D. hansenii and the salt-sensitive yeasts Saccharomyces cereviasiae and Pichia methanolica conferred a higher tolerance with a reduced level of reactive oxygen species.

Conclusion
In conclusion, for the first time our study has identified alkly hydroperoxide reductase as a key protein involved in the salt tolerance of the extremely halophilic D. hansenii. Apparently, this enzyme plays a multi-functional role in the yeast's adaptation to salinity; it serves as a peroxidase in scavenging reactive oxygen species, as a molecular chaperone in protecting essential proteins from denaturation, and as a redox sensor in regulating H2O2-mediated cell defense signaling.
Optimal strategy to identify incidence of diagnostic of diabetes using administrative data
Authors: Asghari Shabnam , Courteau Josiane , Carpentier André C , Vanasse Alain 
Published: September 2009

Abstract

Background
Accurate estimates of incidence and prevalence of the disease is a vital step toward appropriate interventions for chronic disease like diabetes. A growing body of scientific literature is now available on producing accurate information from administrative data. Advantages of use of administrative data to determine disease incidence include feasibility, accessibility and low cost, but straightforward use of administrative data can produce biased information on incident cases of chronic disease like diabetes. The present study aimed to compare criteria for the selection of diabetes incident cases in a medical administrative database.

Methods
An exhaustive retrospective cohort of diabetes cases was constructed for 2002 using the Canadian National Diabetes Surveillance System case definition (one hospitalization or two physician claims with a diagnosis of diabetes over a 2-year period) with the Quebec health service database. To identify previous occurrence of diabetes in the database, a five-year observation period was evaluated using retrograde survival function and kappa agreement. The use of NDSS case definition to identify incident cases was compared to a single occurrence of an ICD-9 code 250 in the records using the McNemar test.

Results
Retrograde survival function showed that the probability of being a true incident case after a 5-year diabetes-free observation period was almost constant and near 0.14. Agreement between 10 years (maximum period) and 5 years and more diabetes-free observation periods were excellent (kappa > 0.9). Respectively 41,261 and 37,473 incident cases were identified using a 5-year diabetes-free observation period with NDSS definition and using a single ICD-9 code 250.

Conclusion
A 5-year diabetes-free observation period was a conservative time to identify incident cases in an administrative database using one ICD-9 code 250 record.
Microsatellites and SNPs linkage analysis in a Sardinian genetic isolate confirms several essential hypertension loci previously identified in different populations
Authors: Mocci Evelina , Concas Maria P , Fanciulli Manuela , Pirastu Nicola , Adamo Mauro , Cabras Valentina , Fraumene Cristina , Persico Ivana , Sassu Alessandro , Picciau Andrea , Prodi Dionigio A , Serra Donatella , Biino Ginevra , Pirastu Mario , Angius Andrea 
Published: September 2009

Abstract

Background
A multiplicity of study designs such as gene candidate analysis, genome wide search (GWS) and, recently, whole genome association studies have been employed for the identification of the genetic components of essential hypertension (EH). Several genome-wide linkage studies of EH and blood pressure-related phenotypes demonstrate that there is no single locus with a major effect while several genomic regions likely to contain EH-susceptibility loci were validated by multiple studies.

Methods
We carried out the clinical assessment of the entire adult population in a Sardinian village (Talana) and we analyzed 16 selected families with 62 hypertensive subjects out of 267 individuals. We carried out a double GWS using a set of 902 uniformly spaced microsatellites and a high-density SNPs map on the same group of families.

Results
Three loci were identified by both microsatellites and SNP scans and the obtained linkage results showed a remarkable degree of similarity. These loci were identified on chromosome 2q24, 11q23.1–25 and 13q14.11–21.33. Further support to these findings is their broad description present in literature associated to EH or related phenotypes. Bioinformatic investigation of these loci shows several potential EH candidate genes, several of whom already associated to blood pressure regulation pathways.

Conclusion
Our search for major susceptibility EH genetic factors evidences that EH in the genetic isolate of Talana is due to the contribution of several genes contained in loci identified and replicated by earlier findings in different human populations.
Frequency of single nucleotide polymorphisms in NOD1gene of ulcerative colitis patients: a case-control study in the Indian population
Authors: Verma Ravi , Ahuja Vineet , Paul Jaishree 
Published: September 2009

Abstract

Background
Epidemiological studies have provided enough evidence that genetic factors have an important role in determining susceptibility to IBD. The most significant finding in the IBD research has been identification of mutations in the gene that encodes Nod2 (nucleotide-binding oligomerization domain 2) protein in a subgroup of patients with Crohn's disease. However, a very similar gene encoding Nod1 protein still has not been well documented for its association with Ulcerative colitis patients. Detection of polymorphism in NOD1 gene using SNP analysis has been attempted in the present study. We evaluated frequency and significance of mutations present in the nucleotide-binding domain (NBD) of NOD1 gene in context to Indian population.

Methods
A total of 95 patients with ulcerative colitis and 102 controls enrolled in the Gastroenterology department of All India Institute of Medical Sciences, New Delhi were screened for SNPs by DHPLC and RFLP techniques. Exon 6 locus in the NBD domain of NOD1 gene was amplified and sequenced. Genotype and allele frequencies of the patients and controls were calculated by the Pearson's χ2 test, Fisher's exact test and ANOVA with Bonferroni's correction using SPSS software version 12.

Results
We have demonstrated DHPLC screening technique to show the presence of SNPs in Exon 6 locus of NBD domain of NOD1 gene. The DHPLC analysis has proven suitable for rapid detection of base pair changes. The data was validated by sequencing of clones and subsequently by RFLP analysis. Analyses of SNP data revealed 3 significant mutations (W219R, p = 0.002; L349P, p = 0.002 and L370R, p = 0.039) out of 5 in the Exon 6 locus of NBD domain of the gene that encompasses ATP and Mg2+binding sites. No significant association was observed within different sub phenotypes.

Conclusion
We propose that the location of mutations in the Exon 6 spanning the ATP and Mg2+ binding site of NBD in NOD1 gene may affect the process of oligomerization and subsequent function of the LRR domain. Further studies are been conducted at the protein level to prove this possibility.