bluuebunny/crossref_metadata_2025_split huggingface dataset:
T‐bet protects against exacerbation of schistosome egg‐induced immunopathology by regulating Th17‐mediated inflammation
Authors: Rutitzky Laura I. , Smith Patrick M. , Stadecker Miguel J. 
Published: August 2009

AbstractC57BL/6 mice infected with Schistosoma mansoni naturally develop mild CD4+ T‐cell‐mediated immunopathology characterized by small hepatic granulomas around parasite eggs. However, immunization with soluble egg Ag in CFA markedly exacerbates the lesions by inducing a potent proinflammatory environment with high levels of IFN‐γ and IL‐17, which are signature cytokines of distinct Th1‐ versus Th17‐cell lineages. To determine the relative role of these subsets in disease exacerbation, we examined mice deficient in T‐bet (T‐bet−/−), which is required for Th1 differentiation and IFN‐γ production. We now report that immunization with soluble egg Ag in CFA caused a significantly greater enhancement of egg‐induced hepatic immunopathology in T‐bet−/− mice compared with WT controls, and analysis of their granulomas disclosed a higher proportion of activated DC and CD4+ T cells, as well as a marked influx of neutrophils. The absence of IFN‐γ in the T‐bet−/− mice correlated with a marked increase in IL‐23p19, IL‐17 and TNF‐α in granulomas and MLN. In contrast, T‐bet−/− mice had lower levels of IL‐4, IL‐5 and IL‐10 and a reduction in FIZZ1 and FoxP3 expression, suggesting diminished regulatory activity, respectively, by alternatively activated macrophages and Treg. These findings demonstrate that T‐bet‐dependent signaling negatively regulates Th17‐mediated immunopathology in severe schistosomiasis.
Central tolerance: Essential for preventing autoimmune disease?
Authors: von Boehmer Harald 
Published: August 2009

AbstractRecessive central tolerance of developing T cells is caused by antigen‐induced deletion of immature cortical double positive and medullary single positive thymocytes in the absence of TCR editing. There are few examples where it can be convincingly shown that recessive tolerance plays an essential role in preventing autoimmune disease. This is in part due to the fact that genetic factors predisposing to autoimmune disease could conceivably contribute to both recessive tolerances in the thymus and antigen‐induced generation of Treg. Of considerable interest is the notion that several epitopes recognized by disease‐causing T‐cell clones exhibit poor class II MHC binding consistent with the notion that the limited availability of such epitopes in the thymus could lead to failing recessive tolerance, while more abundant quantities in peripheral lymphoid tissues could result in activation of T cells that have escaped central tolerance.
Tolerance checkpoints in B‐cell development: Johnny B good
Authors: Tussiwand Roxane , Bosco Nabil , Ceredig Rhodri , Rolink Antonius G. 
Published: August 2009

AbstractB‐cell development up to the immature B‐cell stage takes place in the bone marrow, while final maturation into mature B cells occurs in the spleen. During differentiation, the precursor and immature B cells have to pass several checkpoints, including those in which they are censored for being auto‐reactive, and therefore being potentially dangerous. Numerous studies have shown that the immature B‐cell stage in the bone marrow and the transitional B‐cell stages in the spleen comprise distinct checkpoints at which auto‐reactivity is censored. Recently, evidence has been provided that the large pre‐BII stage in the bone marrow, at which the pre‐BCR is expressed, is yet another B‐cell tolerance checkpoint. Here, we review these findings and speculate on directions for possible further experimentation.
E3 ubiquitin ligases in T‐cell tolerance
Authors: Paolino Magdalena , Penninger Josef M. 
Published: August 2009

AbstractThe immune system uses several mechanisms of central and peripheral tolerance in order to prevent the activation of T lymphocytes toward self‐antigens. Although the importance of immune self‐tolerance has been established for a long time, some essential cellular and molecular mechanisms of T‐cell tolerance have only been recently revealed. Once thought to be a recycling system, protein ubiquitylation by E3 ligases has now emerged as a regulated and crucial modulator of immune responses, and more importantly as a key signaling pathway involved in T‐cell tolerance. In this review, we highlight our current understanding of the transcriptional and molecular signaling mechanisms involved in ubiquitylation‐mediated T‐cell tolerance.
Cover Picture: Eur. J. Immunol. 9/09
Authors: Iwanami Norimasa , Okada Minoru , Hoa Vu Q. , Seo Yasuhito , Mitani Hiroshi , Sasaki Takashi , Shimizu Nobuyoshi , Kondoh Hisato , Furutani‐Seiki Makoto , Takahama Yousuke 
Published: August 2009

AbstractThis cover is specifically designed to celebrate the 2nd European Congress of Immunology (www.eci‐berlin2009.com), to be held September 13–16, 2009 in Berlin. The cover consists of a collage of images from Iwanami et al. (pp 2606–2616) with Berlin's historic Bradenburg Gate, Brandenburger Tor, in the forefront (image of the Brandenburg Gate r ImageState'. Iwanami et al.'s elegant study shows that, in addition, to defective thymus development, teleosts with mutations in KIAA1440, TRRAP, and SKIV2L2 also exhibit defective development of multiple organs, thus identifying previously unknown roles of these genes in organ development.
Spatial modelling of left censored water quality data
Authors: Toscas Peter J. 
Published: August 2009

AbstractEnvironmental monitoring data is often spatially correlated and left censored. In this paper a previously proposed Bayesian approach to handling spatially correlated data is modified so that bias corrected estimates of variance and spatial correlation parameters are attained. The methodology is applied to a water quality data set from the Ecosystem Health Monitoring Program (EHMP) in south‐east Queensland, and the results are contrasted with those from uncorrected for bias variance estimates to show that the latter can lead to unreliable inferences. A simulation study is conducted which shows that the bias corrected estimates of variance and correlation parameters are less biased than uncorrected estimates of these parameters and that the credible intervals for the parameters from bias corrected analyses are wider than those from the uncorrected analyses. The simulation also suggests that predictions of below detection values are generally overestimated by both bias corrected and uncorrected analyses, but the latter predictions are more biased. For predictions of detectable concentrations the simulations suggest that bias corrected and uncorrected analyses are equally biased and both underestimate the true values. Copyright © 2009 John Wiley & Sons, Ltd.
Regulation of GSK‐3β by calpain in the 3‐nitropropionic acid model
Authors: Crespo‐Biel N. , Camins A. , Gutiérrez‐Cuesta J. , Melchiorri D. , Nicoletti F. , Pallàs M. , Canudas A.M. 
Published: August 2009

AbstractGlycogen synthase kinase‐3β (GSK‐3β) is a crucial component in the cascade of events that culminate in a range of neurodegenerative diseases. It is controlled by several pathways, including calpain‐mediated cleavage. Calpain mediates in cell death induced by 3‐nitropropionic acid (3‐NP), but GSK‐3β regulation has not been demonstrated. Here we studied changes in total GSK‐3β protein levels and GSK‐3β phosphorylation at Ser‐9 in this model. The 3‐NP treatment induced GSK‐3β truncation. This regulation was dependent on calpain activation, since addition of calpeptin to the medium prevented this cleavage. While calpain inhibition prevented 3‐NP‐induced neuronal loss, inhibition of GSK‐3β by SB‐415286 did not. Furthermore, inhibition of cdk5, a known target of calpain involved in 3‐NP‐induced cell death, also failed to rescue neurons in our model. Our results point to a new target of calpain and indicate possible cross‐talk between calpain and GSK‐3β in the 3‐NP toxicity pathway. On the basis of our findings, we propose that calpain may modulate 3‐NP‐induced neuronal loss. © 2009 Wiley‐Liss, Inc.
Effects of brain‐derived neurotrophic factor Val66Met polymorphism on hippocampal volume change in schizophrenia
Authors: Koolschijn P. Cédric M.P. , van Haren Neeltje E.M. , Bakker Steven C. , Hoogendoorn Mechteld L.C. , Pol Hilleke E. Hulshoff , Kahn René S. 
Published: August 2009

AbstractA functional polymorphism of the brain‐derived neurotrophic factor (BDNF) gene (Val66Met) has been associated with the risk for schizophrenia and volume differences in the hippocampus. However, little is known about the association between progressive brain volume change in schizophrenia and BDNF genotype. The aim of this study was to investigate the relationship between hippocampal volume change in patients with schizophrenia and healthy control subjects and BDNF genotype. Two structural magnetic resonance imaging brain scans were acquired of 68 patients with schizophrenia and 83 healthy subjects with an interval of approximately 5 yrs. Hippocampal volume change was measured and related to BDNF genotype in patients and healthy controls. BDNF genotype was not associated with hippocampal volume change over time in patients or healthy controls, nor could we replicate earlier findings on smaller hippocampal volume in Met‐carriers. However, we did find a genotype‐by‐diagnosis interaction at baseline demonstrating smaller hippocampal volumes in patients homozygous for the Val‐allele relative to healthy Val‐homozygotes. In addition, irrespective of genotype, patients showed smaller hippocampal volumes compared with healthy controls at baseline. In summary, our results suggest that the BDNF Val66Met polymorphism is not associated with hippocampal volume change over time. Nevertheless, our findings may support the possibility that BDNF affects brain morphology differently in schizophrenia patients and healthy subjects. © 2009 Wiley‐Liss, Inc.
Stromal cell‐derived CSF‐1 blockade prolongs xenograft survival of CSF‐1‐negative neuroblastoma
Authors: Abraham Dietmar , Zins Karin , Sioud Mouldy , Lucas Trevor , Schäfer Romana , Stanley E. Richard , Aharinejad Seyedhossein 
Published: August 2009

AbstractThe molecular mechanisms of tumor–host interactions that render neuroblastoma (NB) cells highly invasive are unclear. Cancer cells upregulate host stromal cell colony‐stimulating factor‐1 (CSF‐1) production to recruit tumor‐associated macrophages (TAMs) and accelerate tumor growth by affecting extracellular matrix remodeling and angiogenesis. By coculturing NB with stromal cells in vitro, we showed the importance of host CSF‐1 expression for macrophage recruitment to NB cells. To examine this interaction in NB in vivo, mice bearing human CSF‐1‐expressing SK‐N‐AS and CSF‐1‐negative SK‐N‐DZ NB xenografts were treated with intratumoral injections of small interfering RNAs directed against mouse CSF‐1. Significant suppression of both SK‐N‐AS and SK‐N‐DZ NB growth by these treatments was associated with decreased TAM infiltration, matrix metalloprotease (MMP)‐12 levels and angiogenesis compared to controls, while expression of tissue inhibitors of MMPs increased following mouse CSF‐1 blockade. Furthermore, Tie‐2‐positive and ‐negative TAMs recruited by host CSF‐1 were identified in NB tumor tissue by confocal microscopy and flow cytometry. However, host‐CSF‐1 blockade prolonged survival only in CSF‐1‐negative SK‐N‐DZ NB. These studies demonstrated that increased CSF‐1 production by host cells enhances TAM recruitment and NB growth and that the CSF‐1 phenotype of NB tumor cells adversely affects survival.
Chemotherapy‐induced apoptosis in hepatocellular carcinoma involves the p53 family and is mediated via the extrinsic and the intrinsic pathway
Authors: Seitz Sarah J. , Schleithoff Elisa Schulze , Koch Andreas , Schuster André , Teufel Andreas , Staib Frank , Stremmel Wolfgang , Melino Gerry , Krammer Peter H. , Schilling Tobias , Müller Martina 
Published: August 2009

AbstractWe investigated the downstream mechanisms by which chemotherapeutic drugs elicit apoptosis in hepatocellular carcinoma (HCC). Genomic signatures of HCC cell lines treated with different chemotherapeutic drugs were obtained. Analyses of apoptosis pathways were performed and RNA interference was used to evaluate the role of the p53 family. Endogenous p53, p63 and p73 were upregulated in response to DNA damage by chemotherapeutic drugs. Blocking p53 family function led to chemoresistance in HCC. Stimulation and blocking experiments of the CD95‐, the TNF‐ and the TRAIL‐receptor systems revealed that cytotoxic drugs, via the p53 family members as transactivators, can trigger expression of each of these death receptors and consequently sensitize HCC cells toward apoptosis. Furthermore, our findings demonstrate a link between chemotherapy, the p53 family and the mitochondrial apoptosis pathway in HCC. Chemotherapeutic treatment induces expression of proapoptotic Bcl‐2 family members like Bax and BCL2L11 and the expression of Apaf1, BNIP1, Pdcd8 and RAD. Thus, upon DNA damage, p53, p63 and p73 promote apoptosis via the extrinsic and the intrinsic signaling pathway. In addition, not only proapoptotic genes were upregulated, but also genes known to exert antiapoptotic functions. Bleomycin‐induced upregulation of BCL‐XL/BCLXL1 and MDM2 suggests that it is the ratio of proapoptotic and antiapoptotic proteins that regulates the apoptosis response of HCC cells toward chemotherapy, thereby playing a decisive role between treatment sensitivity vs. drug resistance. The clinical importance of these data is evidenced by our finding that the bleomycin target gene signature can predict the prognosis of patients suffering from HCC.
Cancer stem/progenitor cells are highly enriched in CD133+CD44+ population in hepatocellular carcinoma
Authors: Zhu Zheng , Hao Xiangfang , Yan Mingxia , Yao Ming , Ge Chao , Gu Jianren , Li Jinjun 
Published: August 2009

AbstractBoth our previous study and other reports have suggested that CD133, originally classified as a hematopoietic stem cell marker, could be used for enrichment of cancer stem cells (CSCs) in human hepatocellular carcinoma (HCC). It was also noted that not all of CD133+ cells were representative of CSCs. Further identification and characterization of CSCs or tumor‐initiating cells in HCC are necessary to better understand hepatocarcinogenesis. In present study, we demonstrated that CSC phenotype could be precisely defined by co‐expression of CD133 and CD44 cell surface markers. CD133+CD44+ HCC cells showed stem cell properties, including extensive proliferation, self‐renewal, and differentiation into the bulk of cancer cells. In vivo xenograft experiments revealed that, actually, the highly tumorigenic capacity of CD133+ cells as previously described was primarily attributed to CD133+CD44+ cell subpopulation, instead of their CD133+CD44− counterparts. Moreover, cells double‐positive for CD133 and CD44 exhibited preferential expression of some stem cell‐associated genes and were more resistant to chemotherapeutic agents due to the upregulation of ATP‐binding cassette (ABC) superfamily transporters, including ABCB1, ABCC1, and ABCG2, further supporting these cells as HCC cell origin. Our findings suggest that CD133+CD44+ cells might represent true cancer stem/progenitor cells in HCC, which could allow a better understanding of HCC initiation and progression, as well as establish a precise target for the development of more effective therapies.
A framework of view‐dependent planar scene active camouflage
Authors: Lin Huei‐Yung , Lie Wen‐Nung , Wang Min‐Liang 
Published: August 2009

AbstractActive camouflage is a technique for occluding objects disappear from the observer. Current implementations make assumptions on the viewpoints of both the observer and the camouflaged target. In this work, we present a framework of view‐dependent planar scene camouflage. The cameras representing the observer and the occluding object are placed in general positions. The images captured by the object camera are transformed to the observer viewpoint to generate globally consistent visual data for transparent camouflage. Experimental results are presented for real scene images. © 2009 Wiley Periodicals, Inc. Int J Imaging Syst Technol, 19, 167–174, 2009
EM algorithm‐based adaptive custom thresholding for image denoising in wavelet domain
Authors: Raja S. Selvakumar , John Mala 
Published: August 2009

AbstractIn this article, a novel denoising technique based on custom thresholding operating in the wavelet transform domain is proposed. The denoising process is spatially adaptive and also sub‐band adaptive. To render the denoising algorithm space adaptive, a Vector Quantization (VQ)‐based algorithm is used. The design of the VQ is based on Expectation Maximization (EM) algorithm. The results of the algorithm is demonstrated on SAR images corrupted by speckle noise. Experimental results show that Custom thresholding function outperforms the traditional soft, hard, and Bayes threshoding functions, improving the denoised results significantly in terms of Peak Signal to Noise Ratio (PSNR). © 2009 Wiley Periodicals, Inc. Int J Imaging Syst Technol, 19, 175–178, 2009
Texture‐based parametric active contour for target detection and tracking
Authors: Vard Ali Reza , Moallem Payman , Nilchi Ahmad Reza Naghsh 
Published: August 2009

AbstractIn recent years, active contour models (ACM) have been considered as powerful tools for image segmentation and object tracking in computer vision and image processing applications. This article presents a new tracking method based on parametric active contour models. In the proposed method, a new pressure energy called “texture pressure energy” is added to the energy function of the parametric active contour model to detect and track a texture target object in a texture background. In this scheme, the texture features of the contour are calculated by a moment‐based method. Then, by comparing these features with texture features of the target object, the contour curve is expanded or contracted to be adapted to the object boundaries. Experimental results show that the proposed method is more efficient and accurate in the tracking of objects compare to the traditional ones, when both object and background are textures in nature. © 2009 Wiley Periodicals, Inc. Int J Imaging Syst Technol, 19, 187–198, 2009
Visual data association for real‐time video tracking using genetic and estimation of distribution algorithms
Authors: Patricio Miguel A. , García Jesús , Berlanga Antonio , Molina José M. 
Published: August 2009

AbstractIn this article, an efficient and novel approach for video data association is developed. This new method is formulated as a search across the hypotheses space defined by the possible association among tracks and detections, carried out for each frame of a video sequence. The full data association problem in visual tracking is formulated as a combinatorial hypotheses search with a heuristic evaluation function taking into account structural and specific information such as distance, shape, color, etc. To guarantee real‐time performance, a time limit is set for the search process explore alternative solutions. This time limit defines the upper bound of the number of evaluations depending on search algorithm efficiency. Estimation distribution algorithms are proposed as an efficient evolutionary computation technique to search in this hypothesis space. Finally, an exhaustive comparison of the performance of alternative algorithms is carried out considering complex representative situations in real video sets. © 2009 Wiley Periodicals, Inc. Int J Imaging Syst Technol, 19, 208–220, 2009
An acidic extracellular pH disrupts adherens junctions in HepG2 cells by Src kinases‐dependent modification of E‐cadherin
Authors: Chen Ying , Chen Chia‐Huei , Tung Po‐Yuan , Huang Shih‐Horng , Wang Seu‐Mei 
Published: August 2009

AbstractWe have previously shown that culturing HepG2 cells in pH 6.6 culture medium increases the c‐Src‐dependent tyrosine phosphorylation of β‐catenin and induces disassembly of adherens junctions (AJs). Here, we investigated the upstream mechanism leading to this pH 6.6‐induced modification of E‐cadherin. In control cells cultured at pH 7.4, E‐cadherin staining was linear and continuous at cell–cell contact sites. Culturing cells at pH 6.6 was not cytotoxic, and resulted in weak and discontinuous junctional E‐cadherin staining, consistent with the decreased levels of E‐cadherin in membrane fractions. pH 6.6 treatment activated c‐Src and Fyn kinase and induced tyrosine phosphorylation of p120 catenin (p120ctn) and E‐cadherin. Inhibition of Src family kinases by PP2 attenuated the pH 6.6‐induced tyrosine phosphorylation of E‐cadherin and p120ctn, and prevented the loss of these proteins from AJs. In addition, E‐cadherin was bound to Hakai and ubiquitinated. Furthermore, pH 6.6‐induced detachment of E‐cadherin from AJs was blocked by pretreatment with MG132 or NH4Cl, indicating the involvement of ubiquitin‐proteasomal/lysosomal degradation of E‐cadherin. An early loss of p120ctn prior to E‐cadherin detachment from AJs was noted, concomitant with a decreased association between p120ctn and E‐cadherin at pH 6.6. PP2 pretreatment prevented the dissociation of these two proteins. In conclusion, pH 6.6 activated Src kinases, resulting in tyrosine phosphorylation of E‐cadherin and p120ctn and a weakening of the association of E‐cadherin with p120ctn and contributing to the instability of E‐cadherin at AJs. J. Cell. Biochem. 108: 851–859, 2009. © 2009 Wiley‐Liss, Inc.
Regenerative medicine in the treatment of peripheral arterial disease
Authors: Sneider Erica B. , Nowicki Philip T. , Messina Louis M. 
Published: August 2009

AbstractThe last decade has witnessed a dramatic increase in the mechanistic understanding of angiogenesis and arteriogenesis, the two processes by which the body responds to obstruction of large conduit arteries. This knowledge has been translated into novel therapeutic approaches to the treatment of peripheral arterial disease, a condition characterized by progressive narrowing of lower extremity arteries and heretofore solely amenable to surgical revascularization. Clinical trials of molecular, genetic, and cell‐based treatments for peripheral artery obstruction have generally provided encouraging results. J. Cell. Biochem. 108: 753–761, 2009. © 2009 Wiley‐Liss, Inc.
Transitive partitions in realizations of tournament score sequences
Authors: Busch Arthur H. , Chen Guantao , Jacobson Michael S. 
Published: August 2009

AbstractA tournament is an oriented complete graph, and one containing no
directed cycles is called transitive. A tournament
T=(V, A) is called m‐partition
transitive if there is a partition
such that the subtournaments induced by each Xi are all transitive, and T is m‐partition k‐transitive if max|Xi|=k. Two tournaments are equivalent if they have the same out‐degree sequence. We show that for any m and k, T is equivalent to an m‐partition k‐transitive tournament T′ whenever T is equivalent to any tournament which contains a transitive subtournament of order at least k. This generalizes results of Guiduli et al. and Acosta et al., who proved the claim for m=2 and k=⌈n/2⌉, and m>2 and k⩽⌈n/2⌉, respectively. © 2009 Wiley Periodicals, Inc. J Graph Theory 64: 52–62, 2010