bluuebunny/crossref_metadata_2025_split huggingface dataset:
Atlas Linguistiques Roumains
Authors: Saramandu Nicolae 
Published: April 2009

Abstract
The author introduces the Romanian linguistic atlases that appeared within an interval of a hundred years. There were taken into consideration three series of linguistic atlases:
– Linguistischer Atlas des dakorumänischen Sprachgebietes (Leipzig, 1909) by Gustav Weigand,
– Atlasul lingvistic român (1938–1942) by Sever Pop and Emil Petrovici, under the guidance of Sextil Puşcariu,
– 8 regional linguistic atlases, representing the historical provinces; starting with 1967 there appeared 24 volumes up to the present moment.
– At present Atlasul lingvistic român pe regiuni. Sinteză (coordinator: Nicolae Saramandu) is being elaborated. The first volume was issued in 2005.
Largemouth Bass Virus in Texas: Distribution and Management Issues
Authors: Southard Gregory M. , Fries Loraine T. , Terre David R. 
Published: April 2009

Abstract
In response to fish kills at prominent fishing sites for largemouth bass Micropterus salmoides, such as Lake Fork and Sam Rayburn Reservoir, the Texas Parks and Wildlife Department began a systematic evaluation of state waters for the presence of largemouth bass virus (LMBV). The survey comprised 49 water bodies and 13 river basins, and a total of 2,876 adult bass were collected by electrofishing and angling during the summer and fall of 2000. The virus was initially detected by means of cell culture and its presence subsequently confirmed by polymerase chain reaction. Fourteen reservoirs in eight river basins in eastern and central Texas tested positive for LMBV. Lake Fork was also tested to determine the prevalence of infection following a 1999 LMBV fish kill. The overall prevalence was low in all of the water bodies tested (1.50 ± 2.82% (mean ± SD)) as well as those determined to contain LMBV (5.00 ± 3.02%). Largemouth bass testing positive for LMBV had a significantly higher prevalence of swim bladder anomalies, but this condition was not a good indicator of LMBV infection. No significant relationships were found between LMBV-positive fish and other factors investigated, including the presence or absence of grossly visible injury, hook marks, external parasites, known water quality problems, gender, allozyme–phenotype, method of capture, length, weight, body condition (relative weight), or age. This survey provided a means of gathering scientific information about LMBV, including its distribution in Texas. From the information gained by this survey, prior fish kills, and previous sampling efforts, a total of 19 water bodies within 9 of the 13 major river basins in the state were found to contain the virus. These results were used to guide a statewide fish stocking strategy aimed at preventing the spread of LMBV in Texas and to contribute to a nationwide effort to understand this virus and its effects on largemouth bass fisheries.
Similarity Hypotheses for the Atmospheric Surface Layer Expressed by Non-Dimensional Characteristic Invariants – A Review
Authors: Kramm Gerhard , Herbert Fritz 
Published: April 2009

In this paper, similarity hypotheses for the atmospheric surface layer (ASL) are reviewed using nondimensional characteristic invariants, referred to as π-numbers. The basic idea of this dimensional π-invariants analysis (sometimes also called Buckingham’s π-theorem) is described in a mathematically generalized formalism. To illustrate the task of this powerful method and how it can be applied to deduce a variety of reasonable solutions by the formalized procedure of non-dimensionalization, various instances are represented that are relevant to the turbulence transfer across the ASL and prevailing structure of ASL turbulence. Within the framework of our review we consider both (a) Monin- Obukhov scaling for forced-convective conditions, and (b) Prandtl-Obukhov-Priestley scaling for free-convective conditions. It is shown that in the various instances of Monin-Obukhov scaling generally two π-numbers occur that result in corresponding similarity functions. In contrast to that, Prandtl-Obukhov-Priestley scaling will lead to only one π number
in each case usually considered as a non-dimensional universal constant.
Since an explicit mathematical relationship for the similarity functions cannot be obtained from a dimensional π- invariants analysis, elementary laws of π-invariants have to be pointed out using empirical or/and theoretical findings. To evaluate empirical similarity functions usually considered within the framework flux-profile relationships, so-called integral similarity functions for momentum and sensible heat are presented and assessed on the basis of the friction velocity and the vertical component of the eddy flux densities of sensible and latent heat directly measured during the GREIV I 1974 field campaign.
Prevalence of Hip Symptoms and Radiographic and Symptomatic Hip Osteoarthritis in African Americans and Caucasians: The Johnston County Osteoarthritis Project
Authors: JORDAN JOANNE M. , HELMICK CHARLES G. , RENNER JORDAN B. , LUTA GHEORGHE , DRAGOMIR ANCA D. , WOODARD JANICE , FANG FANG , SCHWARTZ TODD A. , NELSON AMANDA E. , ABBATE LAUREN M. , CALLAHAN LEIGH F. , KALSBEEK WILLIAM D. , HOCHBERG MARC C. 
Published: April 2009

Objective.To report contemporary estimates of the prevalence of hip-related osteoarthritis (OA) outcomes in African Americans and Caucasians aged ≥ 45 years.Methods.Weighted prevalence estimates and their corresponding 95% confidence intervals for hip symptoms, radiographic hip OA, symptomatic hip OA, and severe radiographic hip OA were calculated using SUDAAN® for age, race, and sex subgroups among 3068 participants (33% African Americans, 38% men) in the baseline examination (1991–97) of The Johnston County Osteoarthritis Project, a population-based study of OA in North Carolina. Radiographic hip OA was defined as Kellgren-Lawrence radiographic grade ≥ 2, moderate/severe radiographic hip OA as grades 3 and 4, and symptomatic hip OA as hip symptoms in a hip with radiographic OA.Results.Hip symptoms were present in 36%; 28% had radiographic hip OA; nearly 10% had symptomatic hip OA; and 2.5% had moderate/severe radiographic hip OA. Prevalence of all 4 outcomes was higher in older individuals; most outcomes were higher for women and African Americans.Conclusion.African Americans in this population do not have a lower prevalence of hip-related OA outcomes as previous studies suggested. Increasing public and health system awareness of the relatively high prevalence of these outcomes, which can be disabling, may help to decrease their effects and ultimately prevent them.
Rabbit Polyclonal Mouse Antithymocyte Globulin Administration Alters Dendritic Cell Profile and Function in NOD Mice to Suppress Diabetogenic Responses
Authors: Huang Yanfei , Parker Matthew , Xia Changqing , Peng Ruihua , Wasserfall Clive , Clarke Tracy , Wu Lizhen , Chowdhry Tayseer , Campbell-Thompson Martha , Williams John , Clare-Salzler Michael , Atkinson Mark A. , Womer Karl L. 
Published: April 2009

Abstract
Mouse antithymocyte globulin (mATG) prevents, as well as reverses, type 1 diabetes in NOD mice, through mechanisms involving modulation of the immunoregulatory activities of T lymphocytes. Dendritic cells (DC) play a pivotal role in the generation of T cell responses, including those relevant to the autoreactive T cells enabling type 1 diabetes. As Abs against DC are likely generated during production of mATG, we examined the impact of this preparation on the phenotype and function of DC to elucidate novel mechanisms underlying its beneficial activities. In vivo, mATG treatment transiently induced the trafficking of mature CD8− predominant DC into the pancreatic lymph node of NOD mice. Splenic DC from mATG-treated mice also exhibited a more mature phenotype characterized by reduced CD8 expression and increased IL-10 production. The resultant DC possessed a potent capacity to induce Th2 responses when cultured ex vivo with diabetogenic CD4+ T cells obtained from BDC2.5 TCR transgenic mice. Cotransfer of these Th2-deviated CD4+ T cells with splenic cells from newly diabetic NOD mice into NOD.RAG−/− mice significantly delayed the onset of diabetes. These studies suggest the alteration of DC profile and function by mATG may skew the Th1/Th2 balance in vivo and through such actions, represent an additional novel mechanism by which this agent provides its beneficial activities.
Brief Residence at the Plasma Membrane of the MHC Class I-Related Chain B Is Due to Clathrin-Mediated Cholesterol-Dependent Endocytosis and Shedding
Authors: Agüera-González Sonia , Boutet Philippe , Reyburn Hugh T. , Valés-Gómez Mar 
Published: April 2009

AbstractRecognition of MHC class I-related chain (MIC) molecules on the surface of target cells by the activating receptor NKG2D leads to their lysis by immune effector cells. Up-regulation of NKG2D ligands is broadly related to stress, although the detailed molecular mechanisms that control the presence of these molecules at the plasma membrane are unclear. To investigate the posttranslational mechanisms that control surface expression of the human NKG2D ligand MICB, we studied the subcellular localization and trafficking of this molecule. We found that in several cellular systems, the expression of MICB molecules on the cell surface is accompanied by an intracellular accumulation of the molecule in the trans-Golgi network and late endosome-related compartments. Surprisingly, MICB has a much shorter half-life at the plasma membrane than MHC molecules and this depends on both recycling to internal compartments and shedding to the extracellular medium. Internalization of MICB depends partially on clathrin, but importantly, the lipid environment of the membrane also plays a crucial role in this process. We suggest that the brief residence of MICB at the plasma membrane modulates, at least in part, the function of this molecule in the immune system.
Drak2 Is Upstream of p70S6 Kinase: Its Implication in Cytokine-Induced Islet Apoptosis, Diabetes, and Islet Transplantation
Authors: Mao Jianning , Luo Hongyu , Han Bing , Bertrand Richard , Wu Jiangping 
Published: April 2009

Abstract
Drak2 is a member of the death-associated protein family and a serine threonine kinase. In this study, we investigated its role in β cell survival and diabetes. Drak2 mRNA and protein were rapidly induced in islet β cells after stimulation by inflammatory lymphokines known to be present in type 1 diabetes. Drak2 up-regulation was accompanied by increased β cell apoptosis. β cell apoptosis caused by the said stimuli was inhibited by Drak2 knockdown using small interfering RNA. Conversely, transgenic Drak2 overexpression led to aggravated β cell apoptosis triggered by the stimuli. Further in vivo experiments demonstrated that Drak2 transgenic islets were more vulnerable to streptozocin insult. We established that inducible NO synthase was upstream and caspase-9 was downstream of Drak2 in its signaling pathway. Purified Drak2 could phosphorylate ribosomal protein S6 (p70S6) kinase in an in vitro kinase assay. Drak2 overexpression in NIT-1 cells led to enhanced p70S6 kinase phosphorylation, whereas Drak2 knockdown in these cells reduced it. These mechanistic studies proved that p70S6 kinase was a bona fide Drak2 substrate.
N-Glycosylation Enhances Presentation of a MHC Class I-Restricted Epitope from Tyrosinase
Authors: Ostankovitch Marina , Altrich-VanLith Michelle , Robila Valentina , Engelhard Victor H. 
Published: April 2009

Abstract
We recently demonstrated that the mechanism of processing of an HLA-A*0201-restricted peptide epitope, Tyr369(D), derived from the membrane protein tyrosinase, involves retrotranslocation of glycosylated molecules from the endoplasmic reticulum to the cytosol, removal of an N-linked carbohydrate from Asn371 by peptide N-glycanase, proteolysis by the proteasome and other proteases, and retransport of the resulting peptides into the endoplasmic reticulum for association with HLA-A*0201. Carbohydrate removal results in deamidation of Asn371 to aspartic acid. The asparagine-containing homolog of this peptide, Tyr369(N), is not presented by tyrosinase-expressing cells, and this has been presumed to be due to quantitative glycosylation of Asn371. Although examining cytosolic intermediates that accumulated in human melanoma cells treated with proteasome inhibitors, we were surprised to find both molecules that had been deglycosylated by peptide N-glycanase and a large number of molecules that had not been previously glycosylated. The failure of Tyr369(N) to be processed and presented from these latter molecules may be partially due to a process of deamidation independent of glycosylation. However, we also established that proteasomes degrade tyrosinase molecules that are still glycosylated, giving rise to a set of discrete intermediates that are not observed when unglycosylated molecules are degraded. We propose that Tyr369(N) fails to be presented because unglycosylated tyrosinase is degraded rapidly and relatively nonselectively. In contrast, glycosylation alters the selectivity of tyrosinase processing by the proteasome, enhancing the production or survival of Tyr369(D).
A Novel Hybrid Yeast-Human Network Analysis Reveals an Essential Role for FNBP1L in Antibacterial Autophagy
Authors: Huett Alan , Ng Aylwin , Cao Zhifang , Kuballa Petric , Komatsu Masaaki , Daly Mark J. , Podolsky Daniel K. , Xavier Ramnik J. 
Published: April 2009

Abstract
Autophagy is a conserved cellular process required for the removal of defective organelles, protein aggregates, and intracellular pathogens. We used a network analysis strategy to identify novel human autophagy components based upon the yeast interactome centered on the core yeast autophagy proteins. This revealed the potential involvement of 14 novel mammalian genes in autophagy, several of which have known or predicted roles in membrane organization or dynamics. We selected one of these membrane interactors, FNBP1L (formin binding protein 1-like), an F-BAR-containing protein (also termed Toca-1), for further study based upon a predicted interaction with ATG3. We confirmed the FNBP1L/ATG3 interaction biochemically and mapped the FNBP1L domains responsible. Using a functional RNA interference approach, we determined that FNBP1L is essential for autophagy of the intracellular pathogen Salmonella enterica serovar Typhimurium and show that the autophagy process serves to restrict the growth of intracellular bacteria. However, FNBP1L appears dispensable for other forms of autophagy induced by serum starvation or rapamycin. We present a model where FNBP1L is essential for autophagy of intracellular pathogens and identify FNBP1L as a differentially used molecule in specific autophagic contexts. By using network biology to derive functional biological information, we demonstrate the utility of integrated genomics to novel molecule discovery in autophagy.
Activin A Promotes the TGF-β-Induced Conversion of CD4+CD25− T Cells into Foxp3+ Induced Regulatory T Cells
Authors: Huber Samuel , Stahl Felix R. , Schrader Jörg , Lüth Stefan , Presser Katrin , Carambia Antonella , Flavell Richard A. , Werner Sabine , Blessing Manfred , Herkel Johannes , Schramm Christoph 
Published: April 2009

Abstract
TGF-β induces the conversion of CD4+CD25− T cells into CD4+CD25+Foxp3+ regulatory T cells (Treg). Activin A is a pleiotropic TGF-β family member and is expressed in response to inflammatory signals. In this study, we report on the effects of activin A on the conversion of CD4+CD25− T cells into Foxp3-expressing induced Treg (iTreg). Activin A was able to promote the conversion of CD4+CD25− T cells into iTreg in a dose-dependent manner in vitro. Activin A together with TGF-β1 had synergistic effects on the rate of iTreg conversion in vitro. Intact TGF-β1 signaling seemed to be essential for the effects of activin A on iTreg generation because cells overexpressing a dominant negative TGF-β type II receptor could not be converted by activin A in vitro. In vivo, the frequency of peripheral, but not central, Treg was increased in transgenic mice with elevated activin A serum levels and the in vivo conversion rate of CD4+CD25− T cells into Foxp3-expressing iTreg was increased as compared with wild type mice. These data suggest a role for activin A as a promoter of the TGF-β dependent conversion of CD4+CD25− T cells into iTreg in vitro and in vivo. Therefore, besides promoting inflammation, activin A may contribute to the regulation of inflammation via the expansion of peripheral Treg.
Cutting Edge: A Critical Role of B and T Lymphocyte Attenuator in Peripheral T Cell Tolerance Induction
Authors: Liu Xikui , Alexiou Maria , Martin-Orozco Natalia , Chung Yeonseok , Nurieva Roza I. , Ma Li , Tian Qiang , Kollias George , Lu Sijie , Graf Daniel , Dong Chen 
Published: April 2009

Abstract
T cell activation and tolerance are delicately regulated by costimulatory molecules. Although B and T lymphocyte attenuator (BTLA) has been shown as a negative regulator for T cell activation, its role in peripheral T cell tolerance induction in vivo has not been addressed. In this study, we generated a novel strain of BTLA-deficient mice and used three different models to characterize the function of BTLA in controlling T cell tolerance. In an oral tolerance model, BTLA-deficient mice were found resistant to the induction of T cell tolerance to an oral Ag. Moreover, compared with wild-type OT-II cells, BTLA−/− OT-II cells were less susceptible to tolerance induction by a high-dose OVA peptide administered i.v. Finally, BTLA−/− OT-I cells caused autoimmune diabetes in RIP-mOVA recipient mice. Our results thus demonstrate an important role for BTLA in the induction of peripheral tolerance of both CD4+ and CD8+ T cells in vivo.
Differential Requirements for Protection against Mucosal Challenge withFrancisella tularensisin the Presence versus Absence of Cholera Toxin B and InactivatedF. tularensis
Authors: Bitsaktsis Constantine , Rawool Deepak B. , Li Ying , Kurkure Nitin V. , Iglesias Bibiana , Gosselin Edmund J. 
Published: April 2009

AbstractFrancisella tularensis is a category A biothreat agent for which there is no approved vaccine and the correlates of protection are not well understood. In particular, the relationship between the humoral and cellular immune response to F. tularensis and the relative importance of each in protection is controversial. Yet, understanding this relationship will be crucial to the development of an effective vaccine against this organism. We demonstrate, for the first time, a differential requirement for humoral vs cellular immunity in vaccine-induced protection against F. tularensis infection, and that the requirement for Ab observed in some protection studies, may be overcome through the induction of enhanced cellular immunity. Specifically, following intranasal/mucosal immunization of mice with inactivated F. tularensis organisms plus the cholera toxin B subunit, we observe increased production of IgG2a/2c vs IgG1 Ab, as well as IFN-γ, indicating induction of a Th1 response. In addition, the requirement for F. tularensis-specific IgA Ab production, observed in studies following immunization with inactivated F. tularensis alone, is eliminated. Thus, these data indicate that enhanced Th1 responses can supersede the requirement for anti-F. tularensis-specific IgA. This observation also has important ramifications for vaccine development against this organism.
Acidic Mammalian Chitinase Regulates Epithelial Cell Apoptosis via a Chitinolytic-Independent Mechanism
Authors: Hartl Dominik , He Chuan Hua , Koller Babara , Da Silva Carla A. , Kobayashi Yasushi , Lee Chun Geun , Flavell Richard A. , Elias Jack A. 
Published: April 2009

Abstract
Acidic mammalian chitinase (AMCase) is produced during and plays an important role in the pathogenesis of Th2-mediated diseases and antiparasite responses. However, the effector responses of AMCase in these settings have not been adequately defined and the relationship(s) between its chitinolytic and other biologic properties have not been investigated. In these studies, we demonstrate that AMCase protects airway epithelial cells from Fas ligand- and growth factor withdrawal-induced apoptosis. This cytoprotection was associated with Akt phosphorylation and abrogated when the PI3K/Akt pathway was inhibited. Comparable cytoprotection was also seen in experiments comparing wild-type AMCase and mutant AMCase that lacked chitinolytic activity. Importantly, the apoptosis-inhibiting effect of enzymatically active and inactive AMCase was abrogated by treatment with allosamidin. These studies demonstrate that secreted AMCase feeds back in an autocrine and/or paracrine manner to protect pulmonary epithelial cells from growth factor withdrawal- and Fas ligand-induced apoptosis. They also demonstrate that the cytoprotection is mediated via a PI3K/Akt-dependent and allosamidin-sensitive pathway that is independent of the chitinolytic activity of this chitinase.
CD30 Is Required for CCL21 Expression and CD4 T Cell Recruitment in the Absence of Lymphotoxin Signals
Authors: Bekiaris Vasileios , Gaspal Fabrina , Kim Mi-Yeon , Withers David R. , McConnell Fiona M. , Anderson Graham , Lane Peter J. L. 
Published: April 2009

Abstract
Lymphoid tissue inducer cells express a diverse array of tumor necrosis family ligands, including those that bind CD30 and the lymphotoxin β receptor. Both of these signaling pathways have been linked with B/T segregation in the spleen. In this study, we have dissected a lymphotoxin-independent CD30-dependent signal for the induction of expression of the T zone chemokine, CCL21. Reduced expression of CCL21 due to CD30 deficiency was functionally significant: mice deficient in both lymphotoxin and CD30 (dKO) signals had significantly smaller accumulations of lymphocytes in their splenic white pulp areas, with no evidence of focal aggregation of T cells. Furthermore, recruitment of wild-type CD4 T cells was poor in dKO mice compared with both wild-type or lymphotoxin-deficient mice. Phylogeny suggests that CD30 signals predated those through the lymphotoxin β receptor. We suggest that CD30 signals from lymphoid tissue inducer cells were a primitive mechanism to recruit and prime CD4 T cells. This would have been a stepping stone in the evolution of the highly organized lymphotoxin dependent B and T white pulp areas within which CD4-dependent memory Ab responses now develop.
NK Cell Responsiveness Is Tuned Commensurate with the Number of Inhibitory Receptors for Self-MHC Class I: The Rheostat Model
Authors: Joncker Nathalie T. , Fernandez Nadine C. , Treiner Emmanuel , Vivier Eric , Raulet David H. 
Published: April 2009

Abstract
Inhibitory receptors that engage self-MHC class I molecules enable NK cells to detect disease-associated loss of MHC class I on surrounding cells. Previous studies showed that some NK cells lack all receptors for self-MHC class I, yet fail to exhibit autoimmunity because they are generally hyporesponsive to stimulation. We asked whether NK cells exist in only two states, responsive and hyporesponsive, corresponding to cells that express or fail to express inhibitory receptors for self-MHC class I. The alternative model is that NK cells vary continuously in their responsiveness, based on variations in the number of different inhibitory and stimulatory receptors they express, which is known to vary. In this study, we show in the murine system that NK cell responsiveness increases quantitatively with each added self-MHC-specific inhibitory receptor. Genetic analysis demonstrated that interactions of each of the receptors with self-MHC class I were necessary to observe augmented responsiveness. These findings suggest that NK cell responsiveness is comparable to a rheostat: it is tuned to an optimal set point depending on the inhibitory and stimulatory interactions encountered in the normal environment, so as to ensure self-tolerance and yet optimize sensitivity to changes in normal cells.