bluuebunny/crossref_metadata_2025_split huggingface dataset:
CXCR2-Dependent Mucosal Neutrophil Influx Protects against Colitis-Associated Diarrhea Caused by an Attaching/Effacing Lesion-Forming Bacterial Pathogen
Authors: Spehlmann Martina E. , Dann Sara M. , Hruz Petr , Hanson Elaine , McCole Declan F. , Eckmann Lars 
Published: August 2009

Abstract
Enteropathogenic Escherichia coli (EPEC) is a major cause of diarrheal disease in young children, yet symptoms and duration are highly variable for unknown reasons. Citrobacter rodentium, a murine model pathogen that shares important functional features with EPEC, colonizes mice in colon and cecum and causes inflammation, but typically little or no diarrhea. We conducted genome-wide microarray studies to define mechanisms of host defense and disease in C. rodentium infection. A significant fraction of the genes most highly induced in the colon by infection encoded CXC chemokines, particularly CXCL1/2/5 and CXCL9/10, which are ligands for the chemokine receptors CXCR2 and CXCR3, respectively. CD11b+ dendritic cells were the major producers of CXCL1, CXCL5, and CXCL9, while CXCL2 was mainly induced in macrophages. Infection of gene-targeted mice revealed that CXCR3 had a significant but modest role in defense against C. rodentium, whereas CXCR2 had a major and indispensable function. CXCR2 was required for normal mucosal influx of neutrophils, which act as direct antibacterial effectors. Moreover, CXCR2 loss led to severe diarrhea and failure to express critical components of normal ion and fluid transport, including ATPase β2-subunit, CFTR, and DRA. The antidiarrheal functions were unique to CXCR2, since other immune defects leading to increased bacterial load and inflammation did not cause diarrhea. Thus, CXCR2-dependent processes, particularly mucosal neutrophil influx, not only contribute to host defense against C. rodentium, but provide protection against infection-associated diarrhea.
HLA-DR Alleles in Amyloid β-Peptide Autoimmunity: A Highly Immunogenic Role for the DRB1*1501 Allele
Authors: Zota Victor , Nemirovsky Anna , Baron Rona , Fisher Yair , Selkoe Dennis J. , Altmann Daniel M. , Weiner Howard L. , Monsonego Alon 
Published: August 2009

Abstract
Active amyloid β-peptide (Aβ) immunization of patients with Alzheimer’s disease (AD) caused meningoencephalitis in ∼6% of immunized patients in a clinical trial. In addition, long-term studies of AD patients show varying degrees of Aβ Ab responses, which correlate with the extent of Aβ clearance from the brain. In this study, we examined the contribution of various HLA-DR alleles to these immune-response variations by assessing Aβ T cell reactivity, epitope specificity, and immunogenicity. Analysis of blood samples from 133 individuals disclosed that the abundant DR haplotypes DR15 (found in 36% of subjects), DR3 (in 18%), DR4 (12.5%), DR1 (11%), and DR13 (8%) were associated with Aβ-specific T cell responses elicited via distinct T cell epitopes within residues 15–42 of Aβ. Because the HLA-DRB1*1501 occurred most frequently, we examined the effect of Aβ challenge in humanized mice bearing this allele. The observed T cell response was remarkably strong, dominated by secretion of IFN-γ and IL-17, and specific to the same T cell epitope as that observed in the HLA-DR15-bearing humans. Furthermore, following long-term therapeutic immunization of an AD mouse model bearing the DRB1*1501 allele, Aβ was effectively cleared from the brain parenchyma and brain microglial activation was reduced. The present study thus characterizes HLA-DR alleles directly associated with specific Aβ T cell epitopes and demonstrates the highly immunogenic properties of the abundant allele DRB1*1501 in a mouse model of AD. This new knowledge enables us to explore the basis for understanding the variations in naturally occurring Aβ-reactive T cells and Aβ immunogenicity among humans.
Memory-Like CD8+ T Cells Generated during Homeostatic Proliferation Defer to Antigen-Experienced Memory Cells
Authors: Cheung Kitty P. , Yang Edward , Goldrath Ananda W. 
Published: August 2009

Abstract
Naive T cells proliferate in response to lymphopenia and acquire the phenotypic and functional qualities of memory T cells, providing enhanced protection against infection. How well memory-like T cells generated during lymphopenia-induced homeostatic proliferation (HP)-memory differentiate into secondary memory cells and compete with Ag-experienced true-memory cells is unknown. We found that CD8+ HP-memory T cells generated robust responses upon infection and produced a secondary memory population comparable to true-memory cells in the absence of competition. However, when true-memory and HP-memory T cells competed during infection, HP-memory cells contributed less to the effector population, contracted earlier, and formed fewer secondary memory cells. Furthermore, HP- and true-memory cells demonstrated distinct chemokine receptor expression and localization within the spleen during infection, indicating differential access to signals necessary for secondary memory formation. Thus, HP-memory T cells provide protection without compromising the true-memory population. Differences in HP- and true-memory T cells may reveal the basis of competition for limited resources within the memory-T cell compartment.
Phosphorylation of Nur77 by the MEK-ERK-RSK Cascade Induces Mitochondrial Translocation and Apoptosis in T Cells
Authors: Wang Aibo , Rud Jonathan , Olson Chris M. , Anguita Juan , Osborne Barbara A. 
Published: August 2009

Abstract
Nur77, an orphan nuclear receptor, plays a key role in apoptosis in T cells. In cancer cell lines, Nur77 can induce apoptosis through the intrinsic apoptotic pathway, but the mechanism by which Nur77 kills T cells remains controversial. In this study, we provide biochemical, pharmacological, and genetic evidence demonstrating that Nur77 induces apoptosis through the activation of the intrinsic pathway in T cells. We also show that Nur77 is a physiological substrate of the MEK-ERK-RSK cascade. Specifically, we demonstrate that RSK phosphorylates Nur77 at serine 354 and this modulates Nur77 nuclear export and intracellular translocation during T cell death. Our data reveal that Nur77 phosphorylation and mitochondrial targeting, regulated by RSK, defines a role for the MEK1/2-ERK1/2 cascade in T cell apoptosis.
Organic Superconductors
Authors: Jacobsen Claus Schelde 
Published: August 2009

Abstract
The old dream of organic superconductivity was finally realized in 1980, but hopes for high transition temperatures have not been fulfilled as yet. We review the phenomenon of superconductivity and the present understanding of the microscopic theory with emphasis on molecular conductors. The historical development is briefly described. We discuss how the common approach to making molecular conductors almost invariably leads to materials that are highly anisotropic, in some cases even quasi‐one‐dimensional. Quasi‐one‐dimensional conductors are susceptible to various instabilities and up till now superconductivity has only been found in two groups of related materials with a maximum superconducting temperature around 12 K. The structure and the physical properties of the materials are presented in relation to the occurrence of superconductivity.
Emergence of New Mechanical Functionality in Materials via Size Reduction
Authors: Greer Julia R. , Jang Dongchan , Kim Ju‐Young , Burek Michael J. 
Published: August 2009

AbstractJulia R. Greer received her S.B. in Chemical Engineering from the Massachusetts Institute of Technology (1997) and a Ph.D. in Materials Science from Stanford University, where she worked on the nanoscale plasticity of gold with W. D. Nix (2005). She also worked at Intel Corporation in Mask Operations (2000–03) and was a post‐doctoral fellow at the Palo Alto Research Center (2005–07), where she worked on organic flexible electronics with R. A. Street. Greer is a recipient of TR‐35, Technology Review's Top Young Innovator award (2008), a NSF CAREER Award (2007), a Gold Materials Research Society Graduate Student Award (2004), and an American Association of University Women Fellowship (2003). Julia joined Caltech's Materials Science department in 2007 where she is developing innovative experimental techniques to assess mechanical properties of nanometer‐sized materials. One such approach involves the fabrication of nanopillars with different initial microstructures and diameters between 25 nm and 1 µm by using focused ion beam and electron‐beam lithography microfabrication. The mechanical response of these pillars is subsequently measured in a custom‐built in situ mechanical deformation instrument, SEMentor, comprising a scanning electron microscope and a nanoindenter. Read our interview with Prof. Greer on MaterialsViews.commagnified image
Stochastic mixed integer nonlinear programming using rank filter and ordinal optimization
Authors: Wen Chengtao , Ydstie B. Erik , Ma Xiaoyan 
Published: August 2009

AbstractA rank filter algorithm is developed to cope with the computational‐difficulty in solving stochastic mixed integer nonlinear programming (SMINLP) problems. The proposed approximation method estimates the expected performance values, whose relative rank forms a subset of good solutions with high probability. Suboptimal solutions are obtained by searching the subset using the accurate performances. High‐computational efficiency is achieved, because the accurate performance is limited to a small subset of the search space. Three benchmark problems show that the rank filter algorithm can reduce computational expense by several orders of magnitude without significant loss of precision. The rank filter algorithm presents an efficient approach for solving the large‐scale SMINLP problems that are nonconvex, highly combinatorial, and strongly nonlinear. © 2009 American Institute of Chemical Engineers AIChE J, 2009
Base‐free catalytic aerobic oxidation of mercaptans for gasoline sweetening over HTLcs‐derived CuZnAl catalyst
Authors: Gao Lida , Xue Qingsong , Liu Ye , Lu Yong 
Published: August 2009

AbstractAn aerobic oxidative removal of mercaptans from gasoline in the absence of liquid base has been demonstrated for gasoline sweetening over CuZnAl catalyst. This process could proceed at large WHSV of gasoline (50–70 h−1) with >95% mercaptan conversion at 150°C (or 300°C) using an O2/S molar ratio of 20–40. At 150°C, dimerization of mercaptans occurred dominantly to form their disulfides. At 300°C, deep oxidation of the mercaptans to SO2 was the dominant process in the first tens of hours, but it decreased then with prolonged time on stream and meanwhile the dimerization increased. The spent catalyst could be restored to its fresh activity level only through a calcination treatment in air. This process was also demonstrated to be effective and efficient for sweetening of a real cracking gasoline. © 2009 American Institute of Chemical Engineers AIChE J, 2009
Agglomeration detection based on attractor comparison in horizontal stirred bed reactors by acoustic emission sensors
Authors: Cao Yijia , Wang Jingdai , He Yijun , Liu Wei , Yang Yongrong 
Published: August 2009

AbstractIn industrial propylene polymerization technology of Innovene and Chisso, agglomeration of polymer particles in horizontal stirred bed reactors (HSBR) has significant negative impacts on the reactor efficiency. If the hydrodynamic change could be detected early enough, then large chunks may not be formed nor cause an unscheduled shutdown of the plant. A novel non‐invasive acoustic emission (AE) technique combined with an attractor comparison method is presented. It is based on the comparison of the time series of AE signals acquired from a normal state with the time series measured during operation of the bed. The nature of the method is to determine whether or not two time series are generated by the same mechanism. A statistical characteristic S is used to test the null hypothesis that the two multidimensional probability distributions are identical. Experiments were carried out at room temperature in a 475 mm i.d. laboratory HSBR. The results demonstrated that the method is sensitive to small changes in the particle size distribution. It is, therefore, indicated that the proposed method not only can offer “early and accurate warning,” but also has the potential to locate the agglomeration in HSBR with multiple AE sensors. © 2009 American Institute of Chemical Engineers AIChE J, 2009
Performance improvement of a combined double‐way thermochemical sorption refrigeration cycle with reheating process
Authors: Li Tingxian , Wang Ruzhu , Chen Heng , Wang Liwei , Kiplagat Jeremiah K. 
Published: August 2009

AbstractA reheating process is proposed aimed at improving the system performance of a combined double‐way thermochemical sorption thermodynamic cycle based on adsorption and resorption refrigeration. The reheating process causes an increase in the driving equilibrium temperature difference, which promotes the reaction rate and thus improves the global conversion of sorbent. Experimental results showed that the proposed reheating process is an effective technique for improving the performance of the combined double‐way cycle. The improvement in the COP ranged between 12 and 48% in the different cycle conditions, when compared with the combined double‐way cycle without reheating. The low pseudo‐evaporation temperature and high heat sink temperature can further improve the system performance. The COP obtained with the combined double‐way cycle without reheating was 0.57, when the heat sink, evaporation, and pseudo‐evaporation temperatures were 25, 10, and 10°C, respectively. However, at the same cycle conditions, the COP increased to 0.64 when the proposed reheating process was introduced in the combined double‐way sorption cycle. © 2009 American Institute of Chemical Engineers AIChE J, 2010
Oral findings in ankyloblepharon‐ectodermal dysplasia‐cleft lip/palate (AEC) syndrome
Authors: Farrington Frank , Lausten Leonard 
Published: August 2009

AbstractThis article outlines the dental conditions and treatment findings of individuals ranging in age from 4 months to 30 years of age diagnosed with ankyloblepharon‐ectodermal dysplasia‐cleft lip/palate (AEC) syndrome. The average number of permanent teeth present is 4.75 with a range of 0–12 teeth. The most frequently present permanent teeth are first molars, canines and maxillary incisors. The dentition of AEC‐affected individuals in our study is similar to reports in other ectodermal dysplasia syndromes. The dental treatment findings, including those necessitated by the cleft palate defect seen in the syndrome, are also similar to age appropriate treatment seen in other cases of ectodermal dysplasia syndromes. Only 22% of subjects had prosthetic replacement of missing teeth. History indicated that issues related to treatment of the palatal cleft and lack of recognition of the oral defects as a part of the underlying medical problem were factors in receiving comprehensive tooth replacement care. © 2009 Wiley‐Liss, Inc.
ΔNp63 knockdown mice: A mouse model for AEC syndrome
Authors: Koster Maranke I. , Marinari Barbara , Payne Aimee S. , Kantaputra Piranit N. , Costanzo Antonio , Roop Dennis R. 
Published: August 2009

AbstractDominant mutations in TP63 cause ankyloblepharon ectodermal dysplasia and clefting (AEC), an ectodermal dysplasia characterized by skin fragility. Since ΔNp63α is the predominantly expressed TP63 isoform in postnatal skin, we hypothesized that mutant ΔNp63α proteins are primarily responsible for skin fragility in AEC patients. We found that mutant ΔNp63α proteins expressed in AEC patients function as dominant‐negative molecules, suggesting that the human AEC skin phenotype could be mimicked in mouse skin by downregulating ΔNp63α. Indeed, downregulating ΔNp63 expression in mouse epidermis caused severe skin erosions, which resembled lesions that develop in AEC patients. In both cases, lesions were characterized by suprabasal epidermal proliferation, delayed terminal differentiation, and basement membrane abnormalities. By failing to provide structural stability to the epidermis, these defects likely contribute to the observed skin fragility. The development of a mouse model for AEC will allow us to further unravel the genetic pathways that are normally regulated by ΔNp63 and that may be perturbed in AEC patients. Ultimately, these studies will not only contribute to our understanding of the molecular mechanisms that cause skin fragility in AEC patients, but may also result in the identification of targets for novel therapeutic approaches aimed at treating skin erosions. © 2009 Wiley‐Liss, Inc.
Dermatologic findings of ankyloblepharon‐ectodermal defects‐cleft lip/palate (AEC) syndrome
Authors: Julapalli Meena R. , Scher Richard K. , Sybert Virginia P. , Siegfried Elaine C. , Bree Alanna F. 
Published: August 2009

AbstractHay–Wells syndrome, caused by mutations in the p63 gene, is an autosomal dominant ectodermal dysplasia with the main features of ankyloblepharon filiforme adnatum, ectodermal defects, and cleft lip/palate, from which the disorder's other name, AEC syndrome, is derived. The National Foundation for Ectodermal Dysplasias convened the International Research Symposium for AEC Syndrome on November 8–10, 2006, at Texas Children's Hospital/Baylor College of Medicine, Houston, TX with appropriate IRB approval. This multidisciplinary conference was the largest gathering of such patients to date and allowed us to further characterize dermatologic features of AEC syndrome, which included: sparse and wiry hair, nail changes, past or present scalp erosions, decreased sweat production, palmar/plantar changes, and unique pigmentary anomolies. Early recognition of the features of AEC syndrome and subsequent early diagnosis is important in minimizing invasive diagnostic studies, improving morbidity and mortality, and providing genetic counseling. Skin erosions, especially those of the scalp, were identified as the most challenging cutaneous aspect of this syndrome. Although the reasons for the skin erosions and poor healing are not known, mutations of p63 may lead to a diminished store of basal cells capable of replenishing the disrupted barrier. Therapeutic strategies currently under exploration include gene therapy, as well as epidermal stem cell therapy. Until then, gentle wound care and limiting further trauma seem to be the most prudent treatment modalities. © 2009 Wiley‐Liss, Inc.
Perspective on the classification of ectodermal dysplasia
Authors: Jorgenson Ronald J. 
Published: August 2009

AbstractThe need for revisiting the classification of ectodermal dysplasia syndromes has come. Prior to considering a new way to classify this group of disorders, however, thought should be given to some basic ideas about terminology and the process of classification. Consequently, this article reiterates the meanings of the words ectoderm, dysplasia, genetic and syndrome, and describes the process by which numeric taxonomists go about classification. In the process, a new family with the Jorgenson syndrome is described and the inheritance of the Schopf syndrome is clarified. Finally, the backgrounds of those with vested interests in the ectodermal dysplasia syndromes are described in order that all approaches to classification are covered. © 2009 Wiley‐Liss, Inc.
Molecular aspects of hypohidrotic ectodermal dysplasia
Authors: Mikkola Marja L. 
Published: August 2009

AbstractHypohidrotic (anhidrotic) ectodermal dysplasia (HED) is a congenital syndrome characterized by sparse hair, oligodontia, and reduced sweating. It is caused by mutations in any of the three Eda pathway genes: ectodysplasin (Eda), Edar, and Edaradd which encode a ligand, a receptor, and an intracellular signal mediator of a single linear pathway, respectively. In rare cases, HED is associated with immune deficiency caused by mutations in further downstream components of the Eda pathway that are necessary for the activation of the transcription factor NF‐κB. Here I present a brief research update on the molecular aspects of this evolutionarily conserved pathway. The developmental role of Eda will be discussed in light of loss‐ and gain‐of‐function mouse models with emphasis on the past few years. © 2009 Wiley‐Liss, Inc.
What the future holds for ectodermal dysplasias: Future research and treatment directions
Authors: Slavkin Harold C. 
Published: August 2009

AbstractA contrarian view suggests that the ectodermal dysplasias, including more than 200 different disorders, represent clinical variability and molecular heterogeneity as well as complex multigene heritable conditions often characterized by dysmorphogenesis of derivatives of embryonic ectoderm and beyond. Controversy exists over which syndromes do or do not belong in the classification of the clinical features that characterize ectodermal dysplasias. For example, Ellis–van Creveld syndrome is characterized by abnormalities of the teeth and hair, as well as of the skeleton and the cardiovascular system. Precision in diagnosis often is a preamble for improved patient diagnosis, treatment and desired outcomes. In tandem, molecular studies of complex epithelial–mesenchymal interactions required for ectodermal derivatives (e.g., hair, nail, skin, teeth, and exocrine glands) continue to identify and explain many signal transduction pathways and networks related to ectodermal dysplasias. Meanwhile, major international investments in fundamental biomedical research continue to yield significant benefits to the larger society. The convergence of informatics, nanotechnology, genomics, and epigenetic studies with clinical medicine and dentistry promise major progress for special needs patients such as ectodermal dysplasias. For example, investments in the molecular biology of genes and their regulation and function now provide more than 30 candidates for specific biomarkers to improve diagnosis, prognosis, treatments, therapeutics, and biomaterials for ectodermal dysplasias. Innovations in high throughput genotyping, gene mapping, single nucleotide polymorphisms (SNPs), interference RNA treatments, bioimaging, tissue engineering and related biomimetic approaches to design and fabricate biomaterials, offer enormous promise for the future of ectodermal dysplasias. © 2009 Wiley‐Liss, Inc.
Ectodermal dysplasias: Clinical and molecular review
Authors: Visinoni Átila F. , Lisboa‐Costa Toni , Pagnan Nina A.B. , Chautard‐Freire‐Maia Eleidi A. 
Published: August 2009

AbstractEctodermal dysplasias (EDs) as defined by Freire‐Maia [Freire‐Maia (1971); Hum Hered 21: 309–312; Freire‐Maia (1977); Acta Genet Med Gemellol 26: 121–131] are congenital disorders characterized by alterations in two or more ectodermal structures, at least one of these involving alterations in hair, teeth, nails, or sweat glands. Suggestions for a new definition and, consequently, for a new classification of EDs have being proposed lately, mainly with the purpose of connecting clinical knowledge with recent discoveries of gene mutations responsible for about 30% of EDs. The aim of this review was to update the clinical classification of EDs with recent molecular (64 genes and 3 chromosome regions) and clinical data, mainly of EDs of the A group (N = 186), in order to contribute information for the evaluation of the ED definition proposed by Freire‐Maia. Our conclusion is that the combination of both procedures—clinical and molecular—only brings advantages for a deeper knowledge of EDs. First, it allows a rapid diagnosis that may become even more precise whenever DNA exams are available. Secondly, the comprehension of the biological mechanisms that cause EDs is needed for the design of efficient prevention and treatment approaches. © 2009 Wiley‐Liss, Inc.