bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characteristics of children with positive coeliac serology and normal villous morphology: potential coeliac disease
Authors: Tanpowpong Pornthep , Broder‐Fingert Sarabeth , Katz Aubrey J. , Camargo Carlos A. 
Published: August 2012

Positive coeliac serology with normal villous morphology (NVM) indicates potential coeliac disease (CD). Few studies have compared characteristics of NVM vs villous atrophy in patients with positive serology. Our aim was to determine the independent clinical predictors of NVM in children with positive CD serology. We performed a structured medical record review of patients aged 1–19 years who presented for an initial CD evaluation between 2000 and 2010 at a large teaching hospital. Data collection included demographics, medical history, prior history of gluten avoidance, CD‐specific serology, oesophagogastroduodenoscopy and histopathology. Predictors of NVM (vs Marsh III) were determined using multivariable logistic regression. Among 320 patients with positive serology, we identified 62 patients (19%, 95% CI 15–24) with NVM (i.e. potential CD). Younger children may have been more likely to exhibit NVM (p = 0.06). Three significant predictors of NVM were prior gluten avoidance (OR 4.17, 95% CI 1.02–17.13), positive tissue transglutaminase antibody but <100 U/mL (OR 14.75, 95% CI 3.33–65.30), and absence of gross duodenal abnormalities (OR 3.48, 95% CI 1.51–8.03). Among children with positive CD serology, prior gluten avoidance predicts NVM. Future studies are warranted on the impact of gluten intake and CD testing in children without prior established CD diagnosis.
The evaluation of enteric viruses in asymptomatic free‐ranging non‐human primates (Alouatta guariba clamitans, Alouatta caraya, Callithrix spp., Callithrix penicillata, and Leontopithecus caissara) in southern Brazil
Authors: Souza Fabiana , Alfieri Amauri A. , Alfieri Alice F. , Lorenzetti Elis , Headley Selwyn A. , Passos Fernando , Silvestre Thiago , Zago Luciana , Mottin Viviane , Montiani‐Ferreira Fabiano , Lange Rogério , Svoboda Walfrido , Gomes Eliane 
Published: August 2012

AbstractBackgroundThis study evaluated the presence of rotavirus groups A, B, and C (RV‐A, RV‐B, and RV‐C), sapovirus (SaV), and norovirus (NoV) in asymptomatic non‐human primates (NHP).MethodsFecal samples were collected from 19 recently captured (Red‐howler, Alouatta guariba clamitans, n = 18; Howler, Alouatta caraya, n = 1) and 43 free‐ranging NHP (Marmosets, Callithrix spp., Callithrix penicillata, n = 30; Black‐faced lion tamarin, Leontopithecus caissara, n = 12, Red‐howler, Alouatta guariba clamitans, n = 1) that were maintained in southern Brazil without manifestation of diarrhea. Screening was performed by a combination of silver‐stained polyacrylamide gel electrophoresis (ss‐PAGE) and RT‐PCR analyses.ResultsAll samples were negative for RV‐A, RV‐B, RV‐C, SaV, and NoV by both assays.ConclusionThe negative results obtained might be due to the absence of clinical manifestations of disease in the population of NHP evaluated.
Determinants of tree species turnover in a southern Amazonian rain forest
Authors: Guèze Maximilien , Paneque‐Gálvez Jaime , Luz Ana C. , Pino Joan , Orta‐Martínez Marti , Reyes‐García Victoria , Macía Manuel J. 
Published: August 2012

AbstractQuestionsWhat is the relative importance of environmental variables and geographical distances to explain tree species turnover? Are these patterns consistent for different tree categories, i.e. all trees (DBH ≥ 2.5 cm), large trees (DBH ≥ 10 cm), small trees sensu lato (DBH < 10 cm) and small trees sensu stricto (strictly understorey species, DBH < 10 cm)?LocationDepartment of Beni, Bolivia, southwestern Amazon.MethodsA total of 55 0.1‐ha plots were inventoried in old‐growth terra firme forest in seven sites. Composite soil samples from each plot were analysed for physical and chemical properties. Environmental and geographical influences on tree species turnover were quantified with Mantel correlations and variation partitioning based on multiple regressions on distance matrices.ResultsFloristic differences between sites yielded significant correlations with both geographical distances and environmental variables (pH, Ca, Mg, exchangeable acidity, C:N ratio, sand content) for all tree categories. Phosphorus was correlated with floristic patterns only for small trees sensu stricto. Together, geographical distances and environmental variables explained 62% of the floristic variation for all trees. Environmental variables explained more variation for large trees than for small trees sensu stricto.ConclusionsThe results support the hypothesis that species distributions are driven by both geographical distances (as quantifiers of dispersal processes) and environmental variables (niche factors) in similar proportions. Spatial floristic patterns of large trees and small trees sensu stricto were in general terms congruent.
Parliamentary Inquiry Into Health Promoting Schools in Victoria: Analysis of Stakeholder Views
Authors: Bruce Emma , Klein Ruth , Keleher Helen 
Published: August 2012

BACKGROUND: In 2009, the Victorian Parliament Legislative Assembly of Australia commissioned a Parliamentary Inquiry into the opportunities for schools to become a focus for promoting healthy community living. Submissions to the Inquiry varied widely in their positions about school health promotion. The aim of this review is to analyze the submissions to identify core themes in the debates about school health promotion and how stakeholders saw schools becoming a focus for promoting healthy communities.METHODS: Submissions (N = 159) were downloaded from the Inquiry website. Open coding was used to code the data. The codes were then refined into conceptual categories to create themes. The Inquiry's terms of reference were used as an organizing framework.RESULTS: Emergent themes included barriers and enablers to school health promotion including the need for stronger leadership from the Departments of Health (DoH) and Education and Early Childhood Development (DEECD).CONCLUSION: Rather than supporting the idea that schools could have a wider role in communities, submissions pointed to the acute need for increased resource allocation to support health promotion in schools, and for coordinated approaches with stronger leadership from the health and education sectors. Without these structures, schools can only address health in an ad hoc manner with limited resources, capacity, and outcomes.
Characterization of Thorn‐Shaped Astrocytes in White Matter of Temporal Lobe in Alzheimer's Disease Brains
Authors: López‐González Irene , Carmona Margarita , Blanco Rosa , Luna‐Muñoz José , Martínez‐Mandonado Alejandra , Mena Raúl , Ferrer Isidre 
Published: August 2012

AbstractThorn‐shaped astrocytes (TsA) are mainly localized in the periventricular white matter of the temporal lobe in a subgroup of aged individuals usually in the context of Alzheimer's disease (AD). Immunohistochemistry of TsA shows 4Rtau deposition, tau phosphorylation at different sites recognized with phosphospecific anti‐tau antibodies Thr181, Ser202, Ser214, Thr231, Ser396, Ser422, and clones AT8 and PHF‐1, and conformational changes revealed with Alz50 and MC‐1 antibodies; TsA are also immunostained with antibodies to active tau kinases MAPK/ERK‐P, SAPK/JNK‐P, p38‐P and GSK‐3β. These findings are common to neurofibrillary tangles in AD. However, TsA are not stained with 3Rtau antibodies, and they are seldom stained or not at all with phosphospecific tauSer262 and with Tau‐C3 antibody, which recognizes the latter tau truncation at aspartic acid 421. Previous studies have shown that tau phosphorylation at Ser262 reduces tau binding to microtubules and increases caspase‐3 activity, whereas tau truncation at aspartic acid 421 is associated with tau ubiquitination, and toxic effects of tau. In this line, ubiquitin is not accumulated in TsA, and in situ end‐labeling of nuclear DNA fragmentation shows absence of degeneration in TsA. These observations support the concept that tau lesions in neurons differ from those seen in TsA in AD.
Seroprevalence of Japanese Encephalitis Virus and Risk Factors Associated with Seropositivity in Pigs in Four Mountain Districts in Nepal*
Authors: Thakur K. K. , Pant G. R. , Wang L. , Hill C. A. , Pogranichniy R. M. , Manandhar S. , Johnson A. J. 
Published: August 2012

SummaryJapanese encephalitis was recently reported from individuals in the mountain districts of Nepal without travel history to Japanese encephalitis virus (JEV) endemic areas. We performed a cross‐sectional study to estimate the seroprevalence of JEV in pigs and subsequently conducted a survey of farmers to identify risk factors associated with seropositivity. In July and August, 2010, 454 pig serum samples were collected and tested by competitive ELISA. Data from a 35‐question survey of 109 pig owners were analysed using multivariate logistic regression. Seventy‐six (16.7, 95% CI 13.6–20.4) pigs tested positive for anti‐JEV antibodies, none of which had been vaccinated against JEV or sourced from JEV endemic areas. Risk factors associated with JEV seropositivity were ‘summer abortion’, ‘wells as a water source’, ‘urban location’, ‘reported presence of mosquitoes’ and ‘lower elevation’. Our results suggest that JEV is likely circulating in the mountain districts of Nepal, and that locally acquired JEV should be considered a risk for residents and travellers in these areas.
Abstract 1081: Expression of TGFβ3 and its effects on migratory and invasive behavior in prostate cancer cells: Involvement of PI3K/Akt pathway
Authors: Walker Lindsey , Millena Ana Cecilia , Strong Nicole , Khan Shafiq 
Published: August 2012

Abstract
Transforming Growth Factor-β (TGFβ) is a secreted protein that is involved in the regulation of many cellular processes and has been implicated as a factor in cancer cell invasion and metastasis. Studies have indicated that different TGFβ isoforms may exert differential effects on cancer cells during different stages of the disease, however very little is known about the expression patterns of the 3 isoforms in prostate cancer. Non-traditional signaling pathways including PI3-kinase have been associated with TGFβ-mediated effects on cancer cell invasion and metastasis. Whether or not TGFβ isoforms play a differential role in migration and invasion of prostate cancer, and act through PI3-Kinase, has not been investigated. In the present study, we have carried out expression analysis of TGFβ isoforms and signaling components in cell line models representing different stages of prostate cancers and studied the differential effects of specific isoforms on migratory, invasive behavior and induction of the PI3-Kinase and MAPK/ERK pathways. TGFβ1 and TGF-β3 were expressed in all cell lines, with TGFβ3 increasing in metastatic cell lines. TGFβ1 and TGFβ3 induced motility and invasive behavior in PC3 cells, with TGFβ3 being more potent in inducing invasive behavior. TGF-β3 caused a significant increase in the phosphorylation of AKT (pAKT), a downstream target of PI3-Kinase, in PC3 cells. LY294002, a PI3-kinase inhibitor, blocked this induced migration and phosphorylation of AKT. Inhibitors of TGFβRI (SB431524) and Smad-3 (SIS3) blocked TGF-β induced motility and TGFβ isoform induced pAKT. There was no differential isoform effect on the phosphorylation of ERK (pERK). PD98059, a MAPK/ERK inhibitor, did inhibit any TGFβ induced migration and pERK, but did not affect isoform induced pAKT. Furthermore, TGFβ isoforms may be differentially phosphorylating Smad-2 and Smad-3 in PC3 cells. Based on these results, we conclude that TGFβ3 is expressed in metastatic prostate cancer cell lines and is involved in induction of invasive behavior in these cells. Furthermore, these effects of TGFβ3 are mediated via the PI3-Kinase pathway and are TGFβRI and Smad-3 dependent. Grant support: MBRS-RISE 2R25GM060414, NIH 1P20MD002285-02 and RCMI G12RR03602
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1081. doi:1538-7445.AM2012-1081
Abstract 1085: TGFBR2-dependent alterations of glycosylation in MSI colorectal cancer
Authors: Lee Jennifer , Schoenig Kai , Ball Claudia R. , Glimm Hanno , Kopitz Juergen , Gebert Johannes 
Published: August 2012

Abstract
Aberrant glycosylation is a common feature of many malignancies including colorectal cancers. About 15% of colorectal cancers show the microsatellite instability (MSI) phenotype that is associated with a high frequency of biallelic frameshift mutations in the exon 3 coding mononucleotide microsatellite of the Transforming growth factor beta receptor 2 (TGFBR2) gene. If and how disruption of normal TGFBR2 signaling in these MSI colorectal cancer cells is linked to altered glycan pattern is largely unexplored. To address this issue we used the TGFBR2-deficient MSI colon carcinoma cell line HCT116 as a model system. Stable clones enabling doxycycline-inducible expression of wildtype TGFBR2 transgene were generated by recombinase-mediated cassette exchange (RMCE). In two independent clones dox-inducible expression of wildtype TGFBR2 protein and functional reconstitution of TGFBR2-mediated signal transduction as recognized by target gene regulation (SMAD7, SERPINE, c-myc) and Phospho-SMAD2 analysis was confirmed by Western blot and qRT-PCR analysis. Metabolic labeling experiments using the sialic acid precursor 3H-N-acetyl-mannosamine revealed a significant decline of 30% and hence newly synthesized sialoglycoproteins in TGFBR2 expressing cells. Therefore, our findings demonstrate that this model system can be used as a versatile tool to study TGFBR2-dependent effects. Furthermore, our data reveal a TGFBR2 gene-dependent aberrant glycosylation pattern in the MSI colon cell line HCT116.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1085. doi:1538-7445.AM2012-1085
Abstract 1095: Comprehensive miRNA profiling of taxane-resistant human breast and ovarian cancer cell lines using the SmartChip real-time PCR system
Authors: Duran George E. , Wang Cindy Y. , Francisco E. Brian , Wong Kee , Robinson Nicole , Sikic Branimir I. 
Published: August 2012

Abstract
MiRNAs are post-transcriptional regulators of cell proliferation, tissue differentiation, embryonic development and apoptosis. We profiled the expression of miRNAs in a panel of taxane-resistant human breast and ovarian cancer cell lines using the recently developed WaferGen SmartChip System. Four breast cancer cell lines (MCF-7, BT-549, MDA-MB-231 and T-47D) and four ovarian cancer cell lines (1A9/A2780, ES-2, MES-OV and OVCAR-3) were selected for resistance to either docetaxel or paclitaxel alone or co-selected with taxane in the presence of the P-glycoprotein inhibitor, PSC-833 (valspodar, 2 µM). All of the variants established by exposure to taxanes alone are MDR1/ABCB1(+), whereas the resistance observed in the co-selected variants is not transporter-mediated. We have previously reported elevated class III β-tubulin (TUBB3) content, reduced BRCA1 and elevated CDKN1A (p21) in the majority of the non-MDR1 taxane variants relative to parental controls. For miRNA profiling, total RNA was analyzed using the SmartChip Human MicroRNA Panel version 2.0 containing 1,150 unique real-time PCR reactions in quadruplicate for a total of ∼4,600 reactions per sample. Following ligation to a miRNA cloning linker (Integrated DNA Technology, Coraville, IA), the equivalent of 500 ng of starting RNA per sample was added to a one-step cDNA and real-time PCR cocktail (Applied Biosystems, Foster City, CA). The total volume per reaction was 100 nL containing an equivalent of 96 pg of RNA. Forty cycles of real-time PCR were performed on the SmartChip Cycler and a quality screen was performed to remove any outlier data. MiRNA profiling is complete and an analysis of these data revealed a clear separation between the two sets of non-MDR1 variants based on tumor type (breast vs. ovarian), and selection conditions (non-MDR1 vs. parental). We observed reduced miR-200 family expression in the majority of these taxane-resistant variants, consistent with published findings that miR-200c directly targets and suppresses TUBB3. Furthermore, Significance Analysis of Microarrays (SAM) software identified reduced miR-635, miR-296-3P, and let-7B in both MDR1(+) and MDR1(-) variants of breast origin, and elevated let-7 family (let-7B, let-7F and let-7I) and reduced miR-1225-5P and miR-4286 in the ovarian cell lines relative to parental controls. The functional significance of these observations will be studied by introducing miRNA inhibitors or mimics specific to key alterations with the goal of sensitizing cells to taxanes.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1095. doi:1538-7445.AM2012-1095
Abstract 1096: Loss of miR-200 family of microRNAs confers resistance to tamoxifen in human breast cancer cells
Authors: Manavalan Tissa T. , Klinge Carolyn M. 
Published: August 2012

Abstract
MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level. MiR-200 family includes two clusters i.e. miR-200 a/200b/ 429 and miR-200c/141 encoded on chromosome 1 and chromosome 12, respectively. Previous studies have demonstrated that miR-200 family targets ZEB1, a transcription factor that promotes epithelial-to-mesenchymal transition (EMT). Previous reports demonstrated a loss of miR-200a, b and c in MDA-MB-231 breast cancer cells resulted in EMT. These studies also showed a concomitant increase in ZEB1 protein. We observed lower miR-200a, b and c expression in estrogen-independent LCC1 and endocrine-resistant LCC2, LCC9, and LY2 compared to the parental, endocrine-sensitive MCF-7 human breast cancer cell line. We found that ZEB1 protein is expressed in tamoxifen-resistant LY2 cells but not in tamoxifen-sensitive MCF-7 cells. LY2 cells did not express E-cadherin, a ZEB1 target which is also a marker for epithelial phenotype. This is the first demonstration that LY2 cells have undergone EMT as part of their endocrine-resistant phenotype. These studies indicate that loss of miR-200 and a corresponding increase in ZEB1 protein is an indicator of tamoxifen-resistance in breast cancer cells. Further, in concordance with higher miR-221/222, there was decreased expression of estrogen receptor alpha (ERα) mRNA and protein in LY2 cells when compared to MCF-7 cells. We hypothesize that ERα expression is decreased in cells that have undergone EMT and this subsequently leads to endocrine-resistance and an invasive phenotype. Future studies will determine whether re-expression of ERα or knockdown of ZEB1 restores TAM-sensitivity in LY2 cells. By evaluating the expression of E-cadherin, it will be possible to determine whether restoration of ERα or knockdown of ZEB1 can revert cells from a mesenchymal to an epithelial phenotype. If validated, loss of miR-200 could be used as a marker of poor prognosis in TAM-resistant breast cancer.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1096. doi:1538-7445.AM2012-1096
Abstract 1100: RNA aptamers as highly specific inhibitors of three human RTKs including Axl, EGFR and PDGFR
Authors: Esposito Carla Lucia , Camorani Simona , Iaboni Margherita , Condorelli Gerolama , de Franciscis Vittorio , Cerchia Laura 
Published: August 2012

Abstract
Aptamers are single-stranded oligonucleotides able to bind with high affinity to specific protein or non-protein targets by folding into complex tertiary structures. They have proven useful as reagents for identifying cell surface proteins and for cell typing. Further, their high specificity and low toxicity render them a valid alternative to antibodies for in vivo targeted recognition as therapeutics or delivery agents for nanoparticles, small interfering RNAs, chemotherapeutics and molecular imaging probes. We have generated aptamers as biologically active ligands for cancer cell surface proteins. The approach has been applied to different tumor systems with the generation of different 2′fluoro-pyrimidines containing RNA aptamers that specifically bind to the ectodomain of human receptor tyrosine kinases (RTKs). Three of these aptamers (named GL21, CL4 and M4) bind at high affinity and high specificity to Axl, EGFR and PDGFR, respectively. Following binding, the aptamers hamper ligand-dependent receptor dimerization and autophosphorylation. All the selected aptamers bind to the correspondent protein target with Kd values in the order of 10 nM and show excellent correlation between cell surface binding and the expression of the target on the cell surface. The anti-Axl GL21 aptamer strongly inhibits cell migration and invasion in vitro, reduces the number of colonies in soft agar colony formation assay and interferes with spheroid formation by malignant glioma U87MG cells. Furthermore, it strongly inhibits tumor growth in mouse xenograft models of human cancer. The anti-EGFR CL4 aptamer strongly induces apoptosis of EGFR-positive cells and at low doses it works even on cells that are resistant to the most frequently used EGFR-inhibitors, as gefitinib and cetuximab. In addition, the combined treatment of cetuximab with the aptamer shows clear synergy in vitro and in vivo. Moreover, we demonstrated that GL21 and M4 aptamer not only bind to Axl and PDGFR, respectively, but also internalize within the target cell thus they can be used as cargoes for tissue specific internalization. The generation of RNA-chimeras (aptamer/miRNA) is on going in our laboratory.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1100. doi:1538-7445.AM2012-1100