bluuebunny/crossref_metadata_2025_split huggingface dataset:
Encoding dysfunctions in a dynamic–static paradigm for visuospatial working memory in first‐episode psychosis patients: a 2‐year follow‐up study
Authors: Cocchi Luca , Debbané Martin , Vianin Pascal , Bircher Romaine , Roulin Sacha , Conus Philippe , Sarrasin‐Bruchez Pascale , Bovet Pierre , Volken Henri , Wood Stephen J. , Schenk Françoise 
Published: February 2009

AbstractAim: To investigate static and dynamic visuospatial working memory (VSWM) processes in first‐episode psychosis (FEP) patients and explore the validity of such measures as specific trait markers of schizophrenia.Methods: Twenty FEP patients and 20 age‐, sex‐, laterality‐ and education‐matched controls carried out a dynamic and static VSWM paradigm. At 2‐year follow up 13 patients met Diagnostic and Statistical Manual (of Mental Health Disorders) – Fourth Edition (DSM‐IV) criteria for schizophrenia, 1 for bipolar disorder, 1 for brief psychotic episode and 5 for schizotypal personality disorder.Results: Compared with controls, the 20 FEP patients showed severe impairment in the dynamic VSWM condition but much less impairment in the static condition. No specific bias in stimulus selection was detected in the two tasks. Two‐year follow‐up evaluations suggested poorer baseline scores on the dynamic task clearly differentiated the 13 FEP patients who developed schizophrenia from the seven who did not.Conclusions: Results suggest deficits in VSWM in FEP patients. Specific exploratory analyses further suggest that deficit in monitoring‐manipulation VSWM processes, especially involved in our dynamic VSWM task, can be a reliable marker of schizophrenia.
Early intervention for cognitive decline: is there a role for multiple medical or behavioural interventions?
Authors: Naismith Sharon L. , Glozier Nick , Burke David , Carter Phoebe E. , Scott Elizabeth , Hickie Ian B. 
Published: February 2009

AbstractAim: Early medical or behavioural intervention to slow cognitive decline might be a viable strategy for reducing disability and rates of institutional care in older persons. This paper details the published work supporting cross‐sectional and longitudinal associations between vascular risk factors, depressive symptoms and progressive cognitive decline. Evidence for the beneficial effects of providing relevant interventions is assessed.Methods: Relevant published work from the areas of dementia research, ‘vascular depression’ and the cognitive benefits that might result from treating vascular risk factors, managing depression or promoting nutrition, cognitive or physical exercise was ascertained from electronic database searches and recent reviews of key areas.Results: The existing published work does not provide many examples of early intervention strategies that target vascular strategies or active treatment of depression to reduce the rate of cognitive decline. Most studies have major limitations including the evaluation of only single‐risk‐factor interventions, the observational designs and the inadequate measurement of cognition. An optimal early intervention strategy might be to target multiple risk factors within relevant experimental or health service frameworks.Conclusions: Early identification and multifaceted reduction of vascular risk factors, active management of depression, engagement in cognitive activity and physical exercise and promotion of better nutrition might together help to slow some forms of cognitive decline or progression to dementia. This health services approach now requires systematic evaluation.
MEASURING THE OPERATIONAL EFFICIENCY OF COMMERCIAL BANKS IN NAMIBIA
Authors: Ikhide Sylvanus I. 
Published: February 2009

AbstractThis paper examines the efficiency of commercial banks in Namibia using the standard econometric frontier approach. Although two aspects of efficiency (scale and scope) receive our attention, the emphasis is on the latter which pertains to whether a firm produces as efficiently as it possibly can, given its size.Our results indicate that substantial economies of scale exist in commercial banking in Namibia. This will tend to suggest that commercial banks in Namibia can increase their efficiency by increasing their current scale of operation. The results for scope economies show that the current level of input combination does not make for maximum efficiency as sufficient scope exists for a more efficient combination of inputs. We believe this will reduce operating costs in the industry and stimulate efficiency.
AN ECONOMIC APPRAISAL OF THE IMPACT OF TRAFFIC DIVERSION – THE N1 TOLL ROAD AND ITS ALTERNATIVE
Authors: Meyer N.g. , Breitenbach M. , Kekana R.d. 
Published: February 2009

AbstractThis paper investigates two alternative roads running parallel to one another; one being a double‐carriageway national road that was tolled 4 years ago and the other being an inter‐city single‐carriageway road. The purpose of the paper is to test the application of the World Bank‐developed Road Economic Decision (RED) model for assessing the economic impact of traffic diversion between two existing alternative roads. In order to do so, the RED model is first used to conduct a cost–benefit analysis of each road in isolation. Thereafter, the model is used to do a scenario analysis followed by a sensitivity analysis. The results show that the RED model is a useful tool for evaluating the impact on society of diverted traffic between alternative roads elsewhere in South Africa.
Atlantic cod (Gadus morhua) from cold and warm environments differ in their maximum growth capacity at low temperatures
Authors: Dutil Jean-Denis , Jabouin Coraline , Larocque Richard , Desrosiers Gaston , Blier Pierre U. 
Published: February 2009

Maximum growth rate of Atlantic cod (Gadus morhua) was determined at a range of temperatures representative of cod benthic habitats (1–13 °C) using wild animals obtained from a cold environment (southern Gulf of St. Lawrence stock, SG) and a mild environment (Bay of Fundy stock, BF). SG cod performed well over a broader range of temperatures than BF cod. Growth in mass was greater for SG than BF cod at any temperature below 7 °C. SG cod consumed twice as much food as BF cod at 1 and 3 °C. At 1 °C, growth in mass was positive for SG cod but negative for BF cod, whereas growth in length did not differ from 0 for both SG and BF cod. Liver size represented a larger proportion of body mass in SG cod at both low and high temperatures, and citrate synthase activity in the intestine exhibited a strong inverse relationship to temperature. The maximum growth capacity of SG cod was comparable with that of cod of similar size in various other stocks in the Atlantic. These observations are not consistent with the view that intensive size-selective fishing practices have resulted in a significant loss of innate growth capacity in SG cod.
Acoustic characterization of Mysis relicta at multiple frequencies
Authors: Rudstam Lars G. , Knudsen Frank R. , Balk Helge , Gal Gideon , Boscarino Brent T. , Axenrot Thomas 
Published: February 2009

We measured acoustic backscattering from Mysis relicta , a common invertebrate in northern lakes, using five frequencies (38, 120, 200, 430, and 710 kHz). Acoustic backscattering from mysids was highest at 430 kHz and lowest at 38 kHz (19 dB lower). Maximum difference between the four other frequencies was 5.2 dB. Mysid target strength (TS) ranged from –80.1 dB at 430 kHz to –99.4 dB at 38 kHz (12 mm average length, range 5–21 mm). A theoretical scattering model (Stanton’s fluid-like, bent-cylinder model) predicted TS within 0.3–1.9 dB of observed TS for the different frequencies. The detection range was lowest at 38 and 710 kHz and greatest at 120 and 200 kHz. Fish were common above the mysid layer and produced higher acoustic backscattering at 38 kHz than at the other frequencies. A combination of 38 kHz and 120 or 200 kHz provides a strong contrast between mysid and fish acoustic backscattering that would help separate these groups using acoustic data.
High Speed 3D Tomography on CPU, GPU, and FPGA
Authors: GAC Nicolas , Mancini Stéphane , Desvignes Michel , Houzet Dominique 
Published: February 2009

AbstractBack-projection (BP) is a costly computational step in tomography image reconstruction such as positron emission tomography (PET). To reduce the computation time, this paper presents a pipelined, prefetch, and parallelized architecture for PET BP (3PA-PET). The key feature of this architecture is its original memory access strategy, masking the high latency of the external memory. Indeed, the pattern of the memory references to the data acquired hinders the processing unit. The memory access bottleneck is overcome by an efficient use of the intrinsic temporal and spatial locality of the BP algorithm. A loop reordering allows an efficient use of general purpose processor's caches, for software implementation, as well as the 3D predictive and adaptive cache (3D-AP cache), when considering hardware implementations. Parallel hardware pipelines are also efficient thanks to a hierarchical 3D-AP cache: each pipeline performs a memory reference in about one clock cycle to reach a computational throughput close to 100%. The 3PA-PET architecture is prototyped on a system on programmable chip (SoPC) to validate the system and to measure its expected performances. Time performances are compared with a desktop PC, a workstation, and a graphic processor unit (GPU).
Antitumoral Immune Response by Recruitment and Expansion of Dendritic Cells in Tumors Infected with Telomerase-Dependent Oncolytic Viruses
Authors: Ramakrishna Edukulla , Woller Norman , Mundt Bettina , Knocke Sarah , Gürlevik Engin , Saborowski Michael , Malek Nisar , Manns Michael P. , Wirth Thomas , Kühnel Florian , Kubicka Stefan 
Published: February 2009

Abstract
Virotherapy can potentially be used to induce tumor-specific immune responses and to overcome tumor-mediated tolerance mechanisms because apoptotic tumor cells are exposed together with viral danger signals during oncolysis. However, insufficient numbers of dendritic cells (DC) present at the site of oncolysis can limit a tumor-specific immune response and the resulting therapeutic benefit. We investigated MHC class I peptide–specific immune responses against model antigens ovalbumin (OVA) and hemagglutinin (HA) in mouse tumor models that support efficient replication of the oncolytic adenovirus hTert-Ad. Virotherapy resulted in peptide-specific cytotoxic T-cell responses against intracellular tumor antigens. Triggering of DC and T-cell infiltration to the oncolytic tumors by macrophage inflammatory protein 1α (MIP-1α, CCL3) and Fms-like tyrosine kinase-3 ligand (Flt3L) enhanced both antitumoral and antiviral immune responses. Although immune-mediated clearance of the virus can restrict therapeutic efficacy of virotherapy, MIP-1α/FLT3L–augmented hTert-Ad virotherapy inhibited local tumor growth more effectively than virotherapy alone. In agreement with the hypothesis that immune-mediated mechanisms account for improved outcome in MIP-1α/FLT3L virotherapy, we observed systemic antitumoral effects by MIP-1α/FLT3L virotherapy on uninfected lung metastasis in immunocompetent mice but not in nude mice. Furthermore, MIP-1α/FLT3L virotherapy of primary tumors was strongly synergistic with tumor DC vaccination in inhibition of established lung metastasis. Combined viroimmunotherapy resulted in long-term survival of 50% of treated animals. In summary, improvement of cross-presentation of tumor antigens by triggering of DC and T-cell infiltration during virotherapy enhances antitumoral immune response that facilitates an effective viroimmunotherapy of primary tumors and established metastases. [Cancer Res 2009;69(4):1448–58]
Epidermal Growth Factor Receptor Signaling Synergizes with Hedgehog/GLI in Oncogenic Transformation via Activation of the MEK/ERK/JUN Pathway
Authors: Schnidar Harald , Eberl Markus , Klingler Stefan , Mangelberger Doris , Kasper Maria , Hauser-Kronberger Cornelia , Regl Gerhard , Kroismayr Renate , Moriggl Richard , Sibilia Maria , Aberger Fritz 
Published: February 2009

Abstract
Persistent activation of the Hedgehog (HH)/GLI signaling pathway has been implicated in the development of a number of human cancers. The GLI zinc finger transcription factors act at the end of the HH signaling cascade to control gene expression, and recent studies have shown that the activity of GLI proteins can be additionally modified by integration of distinct signals, such as the MEK/extracellular signal-regulated kinase (ERK) and phosphinositide-3 kinase (PI3K)/AKT pathway. However, little is known about the identity of the upstream activators of these HH/GLI interacting signaling pathways in cancer. Here, we provide evidence that integration of the HH/GLI and epidermal growth factor receptor (EGFR) pathway synergistically induces oncogenic transformation, which depends on EGFR-mediated activation of the RAS/RAF/MEK/ERK but not of the PI3K/AKT pathway. EGFR/MEK/ERK signaling induces JUN/activator protein 1 activation, which is essential for oncogenic transformation, in combination with the GLI activator forms GLI1 and GLI2. Furthermore, pharmacologic inhibition of EGFR and HH/GLI efficiently reduces growth of basal cell carcinoma (BCC) cell lines derived from mice with activated HH/GLI signaling. The results identify the synergistic integration of GLI activator function and EGFR signaling as a critical step in oncogenic transformation and provide a molecular basis for therapeutic opportunities relying on combined inhibition of the HH/GLI and EGFR/MEK/ERK/JUN pathway in BCC. [Cancer Res 2009;69(4):1284–92]
TMPRSS2-ERG Gene Fusion Is Not Associated with Outcome in Patients Treated by Prostatectomy
Authors: Gopalan Anuradha , Leversha Margaret A. , Satagopan Jaya M. , Zhou Qin , Al-Ahmadie Hikmat A. , Fine Samson W. , Eastham James A. , Scardino Peter T. , Scher Howard I. , Tickoo Satish K. , Reuter Victor E. , Gerald William L. 
Published: February 2009

Abstract
A significant number of prostate cancers have been shown to have recurrent chromosomal rearrangements resulting in the fusion of the androgen-regulated TMPRSS2 promoter to a member of the ETS transcription factor family, most commonly ERG. This results in ERG overexpression, which may have a direct causal role in prostate tumorigenesis or progression. However, the clinical significance of the rearrangement is unclear, and in particular, relationship to outcome has been inconsistent in recent reports. We analyzed TMPRSS2-ERG gene rearrangement status by fluorescence in situ hybridization in 521 cases of clinically localized surgically treated prostate cancer with 95 months of median follow-up and also in 40 unmatched metastases. Forty-two percent of primary tumors and 40% of metastases had rearrangements. Eleven percent had copy number increase (CNI) of the TMPRRS2-ERG region. Rearrangement alone was associated with lower grade, but not with stage, biochemical recurrence, metastases, or death. CNI with and without rearrangement was associated with high grade and advanced stage. Further, a subgroup of cancers with CNI and rearrangement by deletion, with two or more copies of the deleted locus, tended to be more clinically aggressive. DNA index assessment revealed that the majority of tumors with CNI of TMPRSS2-ERG had generalized aneuploidy/tetraploidy in contrast to tumors without TMPRSS2-ERG CNI, which were predominantly diploid. We therefore conclude that translocation of TMPRSS2-ERG is not associated with outcome, and the aggressive clinical features associated with CNI of chromosome 21 reflect generalized aneuploidy and are not due to CNI specifically of rearranged TMPRSS2-ERG. [Cancer Res 2009;69(4):1400–6]
Wilms' Tumor 1 Gene Expression in Hepatocellular Carcinoma Promotes Cell Dedifferentiation and Resistance to Chemotherapy
Authors: Perugorria Maria J. , Castillo Josefa , Latasa M. Ujue , Goñi Saioa , Segura Victor , Sangro Bruno , Prieto Jesús , Avila Matías A. , Berasain Carmen 
Published: February 2009

Abstract
The Wilms' tumor 1 gene (WT1) encodes a transcription factor involved in cell growth and development. As we previously reported, WT1 expression is hardly detectable in normal hepatic tissue but is induced in liver cirrhosis. Although WT1 has been found to be overexpressed in a number of malignancies, the role of WT1 in hepatocarcinogenesis has not been clarified. We found that WT1 is expressed in several human hepatocellular carcinoma (HCC) cell lines, including PLC/PRF/5 and HepG2, and in HCC tumor tissue in 42% of patients. WT1 small interfering RNAs did not affect proliferation rate of HCC cells but abrogated their resistance to anoikis. Transcriptome analysis of PLC/PRF/5 cells after WT1 knockdown showed up-regulation of 251 genes and down-regulation of 321. Ninety percent of the former corresponded to metabolic genes, mostly those characterizing the mature hepatocyte phenotype. On the contrary, genes that decreased upon WT1 inhibition were mainly related to defense against apoptosis, cell cycle, and tumor progression. In agreement with these findings, WT1 expression increased the resistance of liver tumor cells to doxorubicin, a compound used to treat HCC. Interestingly, doxorubicin strongly enhanced WT1 expression in both HCC cells and normal human hepatocytes. Among different chemotherapeutics, induction of WT1 transcription was restricted to topoisomerase 2 inhibitors. When WT1 expression was prohibited, doxorubicin caused a marked increase in caspase-3 activation. In conclusion, WT1 is expressed in a substantial proportion of HCC contributing to tumor progression and resistance to chemotherapy, suggesting that WT1 may be an important target for HCC treatment. [Cancer Res 2009;69(4):1358–67]
Altered Proliferation and Differentiation Properties of Primary Mammary Epithelial Cells from BRCA1 Mutation Carriers
Authors: Burga Laura N. , Tung Nadine M. , Troyan Susan L. , Bostina Mihnea , Konstantinopoulos Panagiotis A. , Fountzilas Helena , Spentzos Dimitrios , Miron Alexander , Yassin Yosuf A. , Lee Bernard T. , Wulf Gerburg M. 
Published: February 2009

Abstract
Female BRCA1 mutation carriers have a nearly 80% probability of developing breast cancer during their life-time. We hypothesized that the breast epithelium at risk in BRCA1 mutation carriers harbors mammary epithelial cells (MEC) with altered proliferation and differentiation properties. Using a three-dimensional culture technique to grow MECs ex vivo, we found that the ability to form colonies, an indication of clonality, was restricted to the aldehyde dehydrogenase 1–positive fraction in MECs but not in HCC1937 BRCA1-mutant cancer cells. Primary MECs from BRCA1 mutation carriers (n = 9) had a 28% greater ability for clonal growth compared with normal controls (n = 6; P = 0.006), and their colonies were significantly larger. Colonies in controls and BRCA1 mutation carriers stained positive for BRCA1 by immunohistochemistry, and 79% of the examined single colonies from BRCA1 carriers retained heterozygosity for BRCA1 (ROH). Colonies from BRCA1 mutation carriers frequently showed high epidermal growth factor receptor (EGFR) expression (71% EGFR positive versus 44% in controls) and were negative for estrogen receptor (ERα; 32% ER negative, 44% mixed, 24% ER positive versus 90% ER positive in controls). Expression of CK14 and p63 were not significantly different. Microarray studies revealed that colonies from BRCA1-mutant PMECs anticipate expression profiles found in BRCA1-related tumors, and that the EGFR pathway is up-regulated. We conclude that BRCA1 haploinsufficiency leads to an increased ability for clonal growth and proliferation in the PMECs of BRCA1 mutation carriers, possibly as a result of EGFR pathway activation. These altered growth and differentiation properties may render BRCA1-mutant PMECs vulnerable to transformation and predispose to the development of ER-negative, EGFR-positive breast cancers. [Cancer Res 2009;69(4):1273–8]
Telomere Attrition in Cancer Cells and Telomere Length in Tumor Stroma Cells Predict Chromosome Instability in Esophageal Squamous Cell Carcinoma: A Genome-Wide Analysis
Authors: Zheng Yun-Ling , Hu Nan , Sun Qing , Wang Chaoyu , Taylor Philip R. 
Published: February 2009

Abstract
Previous studies showed that chromosomal instability was common in esophageal squamous cell carcinoma (ESCC); however, the mechanisms underlying this instability are unknown. Individuals with deficiencies in telomere maintenance are susceptible to enhanced telomere loss during cell proliferation; such deficiencies could result in telomere dysfunction and genomic instability. We investigated the association between genome-wide chromosomal changes in cancer cells and telomere length/attrition in cancer/stroma cells in 47 ESCC patients. Genome-wide detection of loss of heterozygosity was performed using the Affymetrix GeneChip single nucleotide polymorphism arrays. Telomere length was assessed separately for cancer cells, carcinoma-associated fibroblasts (CAF), infiltrative lymphocytes, and adjacent normal epithelial cells by quantitative fluorescent in situ hybridization using paraffin-embedded sections. Telomere length differed significantly among cell types, such that length in infiltrative lymphocytes &gt; CAFs &gt; cancer cells. Shortened telomeres were observed in cancer cells in 44 of 47 (94%) of the tumors examined. Telomere length in CAFs was significantly associated with chromosomal instability on 4q and 13q and lymphocyte telomere length was significantly associated with instability on chromosomal arms 15q. Although telomere length in cancer cells was not associated with chromosome arm instability, telomere attrition in cancer cells, defined as the telomere length in CAFs minus the telomere length in cancer cells, was significantly associated with chromosomal instability on 13q and 15q. This study provides evidence that telomere shortening is a common genetic alteration in ESCC and that chromosome arm instability is related to both telomere attrition in cancer cells and telomere length in tumor stroma cells. [Cancer Res 2009;69(4):1604–14]