bluuebunny/crossref_metadata_2025_split huggingface dataset:
Swelling behavior of poly(acrylamide)/clay nanocomposite hydrogels in acrylamide aqueous solution
Authors: Jiang Yongmei , Zhu Meifang , Li Biao , Liu Yang , Qin Zongyi , Chen Long , Chen Yanmo 
Published: December 2008

AbstractThe swelling behaviors of poly(acrylamide) (PAAm)/clay nanocomposite hydrogels (hereinafter abbreviated as NC gels) in acrylamide (AAm) aqueous solution have been investigated. As‐prepared PAAm/clay hydrogels (S‐M gels) were posttreated by immersing them in AAm aqueous solution. It was found that the swelling ratio of the NC gels increased greatly when the concentration of the solution is below a critical concentration (c*), whereas the gels were disintegrated in the solution when the concentration of the solution is above the c*. Some disc‐like particles were found in the AAm solution accompanying with the unusual swelling behaviors. This unusual swelling behavior is resulted from the change of network structure of the NC gels in AAm aqueous solution, which was further convinced by transmission electron microscopy and element analyses. © 2008 Wiley Periodicals, Inc. J Appl Polym Sci, 2009
Electrical conductivity of carbon‐filled polypropylene‐based resins
Authors: King Julia A. , Johnson Beth A. , Via Michael D. , Ciarkowski Charles J. 
Published: December 2008

AbstractAdding conductive carbon fillers to insulating thermoplastic resins increases composite electrical conductivity. Often, as much of a single type of carbon filler is added to achieve the desired conductivity and still allow the material to be molded into a bipolar plate for a fuel cell. In this study, various amounts of three different carbons (carbon black, synthetic graphite particles, and carbon nanotubes) were added to polypropylene resin. The resulting single‐filler composites were tested for electrical resistivity (1/electrical conductivity). The effects of single fillers and combinations of the different carbon fillers were studied via a factorial design. The percolation threshold was 1.4 vol % for the composites containing only carbon black, 2.1 vol % for those containing only carbon nanotubes, and 13 vol % for those containing only synthetic graphite particles. The factorial results indicate that the composites containing only single fillers (synthetic graphite followed closely by carbon nanotubes and then carbon black) caused a statistically significant decrease in composite electrical resistivity. All of the composites containing combinations of different fillers had a statistically significant effect that increased the electrical resistivity. © 2008 Wiley Periodicals, Inc. J Appl Polym Sci, 2009
Preparation and characterization of petroleum‐pitch‐based carbon aerogels
Authors: Zeng Xianhua , Wu Dingcai , Fu Ruowen 
Published: December 2008

AbstractCarbon aerogels were prepared by the sol–gel polymerization of petroleum pitches followed by ambient‐pressure drying and then carbonization. Furfural and sulfuric acid were found to be the best crosslinking agent and best catalyst for the reaction system, respectively. It was necessary to add acetic acid as a cosolvent, and the volume ratio of toluene to acetic acid played an important role in the mass densities of the samples. The average diameters of the nanonetwork particles of the typical carbon aerogels thus obtained were about 30–40 nm, and their surface areas were over 360 m2/g. © 2008 Wiley Periodicals, Inc. J Appl Polym Sci, 2009
Preservation causes shrinkage in seahorses: implications for biological studies and for managing sustainable trade with minimum size limits
Authors: Nadeau Julie L. , Curtis Janelle M.R. , Lourie Sara A. 
Published: December 2008

AbstractThe implications of shrinkage associated with desiccation and ethanol preservation for seahorses (genusHippocampus) were investigated usingHippocampus guttulatus(European long‐snouted seahorse) as a model. Specifically, this research addressed the implications of preservation for taxonomy and life history studies and the application of minimum size limits (MSL) for managing seahorse trade.In 2004, the Convention on International Trade in Endangered Species of Wild Fauna and Flora (CITES) listed all seahorse species on its Appendix II, and recommended a 10 cm MSL as an interim means of ensuring sustainable international trade. Inconsistencies in seahorse measurement methods and repeatability posed challenges for applying the MSL. Moreover, the shrinking effect of desiccation on body length observed in other fish was assumed to be negligible for seahorses because of their high degree of ossification.Changes in seahorse sizes were measured following immersion in ethanol and desiccation.H. guttulatusshrank on average by 0.1–2.3% when preserved in ethanol and 3.0–6.4% when dried, depending on the trait measured. Similar trends were observed in a sample ofH. kuda(yellow seahorse). Specimen posture during drying, and measurement methods also influenced estimates of size.Based on the shrinkage observed, 14–44% of captured seahorses that are dried could shrink to below the recommended MSL, even if all seahorses were longer than the MSL at capture. This demonstrates that small changes in body lengths can have significant implications for trade of species managed with size limits.Recommendations are to (1) standardize seahorse measurement methods, (2) consider the effects of preservation and measurement technique on body lengths, and apply appropriate corrections in comparative studies and when developing fisheries management strategies, and (3) adjust size limits at the point of capture to ensure retained seahorses comply with the CITES recommended MSL.Copyright © 2008 John Wiley & Sons, Ltd.
Habitat diversity relative to wave action on rocky shores: implications for the selection of marine protected areas
Authors: Blamey Laura K. , Branch George M. 
Published: December 2008

Abstract
Current selection of marine protected areas in South Africa is based on objective criteria including biogeographic representation and habitat heterogeneity. This paper specifically examines rocky shores on the west coast of South Africa to determine whether they are divisible into discrete ‘habitats’ that need independent conservation.
Seventeen rocky shores spanning the full spectrum of wave exposure were compared in terms of maximum wave forces, biomass, species richness and diversity among zones and sites. Three biotic assemblages were identified, characterizing sheltered, semi‐exposed to exposed, and very exposed habitats. Differences among these were clear‐cut low on the shore but disappeared at the top of the shore where wave action was attenuated and desiccation uniformly intense.
The recognition of three discrete biologically‐defined habitats means that rocky shores cannot be regarded as a uniform habitat for conservation purposes. All three components need protection if the full spectrum of rocky‐shore communities is to be conserved.
It is argued that this approach allows habitats to be defined in an objective manner, and that once this has been done, habitat heterogeneity constitutes a better measure of conservation value of an area than a ‘hotspot’ approach based on species richness and endemism.
Copyright © 2008 John Wiley & Sons, Ltd.
Status, ecology and conservation of an endemic fish, Oreochromis niloticus baringoensis, in Lake Baringo, Kenya
Authors: Britton J.R. , Jackson M.C. , Muchiri M. , Tarras‐Wahlberg H. , Harper D.M. , Grey J. 
Published: December 2008

Abstract
The tilapia Oreochromis niloticus baringoensis is a genetically and morphologically distinct sub‐species of Oreochromis niloticus endemic to Lake Baringo, Kenya. In recent years, concern has been expressed as to its status. Recent declines in catch returns suggest the population may be threatened, with conservation action required to safeguard it.
Catch returns from the Baringo fishery since 1964 have shown considerable fluctuations for all species, but especially O. n. baringoensis. From a peak of 712 t in 1970, their total catch was only 5 t in 2005, despite a 2 year period of closure in 2002 and 2003. Changes in fishery catch and relative abundance were independent of exploitation in the fishery but were significantly correlated with lake level.
Few individuals were captured at lengths >250 mm, with no fish sampled >284 mm. During periods of high lake level, individuals matured at smaller sizes and were capable of growing to larger ultimate sizes. With maturity at lengths <130 mm and fishery regulations preventing removal of fish <180 mm, there was a relatively large proportion of mature fish that was below exploitation size each year (19 to 44%). In most years, the proportion of fish available for exploitation was <10%.
Stable isotope analyses revealed O. n. baringoensis was reliant upon planktonic basal resources and zooplankton carbon. There was only minimal trophic overlap with other fish species in the lake, indicating little potential for competition for food resources.
These data suggest that the population status of O. n. baringoensis is not threatened per se, but subject to an unpredictable and unstable environment that strongly influences their life‐history traits and, ultimately, their population abundance, and should be managed accordingly.
Copyright © 2008 John Wiley & Sons, Ltd.
Ablation of Lung Epithelial Cells Deregulates FGF‐10 Expression and Impairs Lung Branching Morphogenesis
Authors: Kim Namjin , Yamamoto Hiroaki , Pauling Michelle Haynes , Lorizio Walter , Vu Thiennu H. 
Published: December 2008

AbstractEpithelial‐mesenchymal interactions are essential for tissue patterning during organogenesis. Distal lung epithelium and its adjacent mesenchyme comprise the epithelial‐mesenchymal signaling unit that regulates lung branching morphogenesis. Tissue recombination experiments have demonstrated the importance of mesenchymal signals in inducing lung epithelial differentiation and branching, but the role of the epithelium in regulating mesenchymal signals has not been well characterized. Using transgenic mice, we ablated distal lung epithelial cells during lung development by inducing the expression of a constitutively active proapoptotic Bax protein under the surfactant protein C (SP‐C) promoter. We found that epithelial cell ablation results in impaired lung branching morphogenesis, which progresses to emphysematous airspaces in the adults. Mesenchymal expression of fibroblast growth factor 10 (Fgf‐10), whose strict spatial and temporal expression is critical for proper lung branching morphogenesis, is disrupted and loses its localized pattern. Interestingly, the expression of sonic hedgehog (Shh), an epithelial gene known to modulate Fgf‐10 expression, is unchanged, indicating the existence of other distal epithelial signals that regulate mesenchymal Fgf‐10expression. We propose that distal SP‐C expressing lung epithelial cells provide essential signals for the downregulation of Fgf‐10expression in the distal mesenchyme during lung development. 292:123–130, 2009. © 2008 Wiley‐Liss, Inc.
A case–control study to assess sensitivity and specificity of a questionnaire for the detection of hip and knee osteoarthritis
Authors: Morvan J. , Roux C. H. , Fautrel B. , Rat A. C. , Euller‐Ziegler L. , Loeuille D. , Banal F. , Mazieres B. , Coste J. , Saraux A. , Guillemin F. 
Published: December 2008

AbstractObjectiveTo assess the performance of a telephone‐administered questionnaire suitable for use in 2‐phase surveys in the detection of symptomatic hip and knee osteoarthritis (OA) cases.MethodsA questionnaire was designed based on typical symptoms and self‐reported OA diagnosis. Three groups of subjects were consecutively enrolled from rheumatology units at French university hospitals. The disease status, based on American College of Rheumatology criteria, was first confirmed by a rheumatologist. Subjects then completed the screening questionnaire administered by interviewers unaware of the diagnosis and the clinical examination results. Three screening strategies were evaluated.ResultsIn all, 119 subjects with hip OA, 137 with knee OA, and 111 subjects with other rheumatic diseases with lower extremity symptoms were recruited. The highest sensitivity for both hip and knee OA was obtained with the strategy based on reporting the presence or absence of symptoms (>96%). The specificity of this strategy was low (42% for both joints). When taking into account the self‐reported OA diagnosis, the sensitivity slightly decreased (>91%), and the specificity increased greatly, from 76% to 78%. The highest specificity was obtained with the third strategy, requiring a rheumatologist opinion (from 82% to 85%) at the expense of lower sensitivity (>90%).ConclusionThe questionnaire tested in this study is a simple, valid, and reliable instrument to screen symptomatic hip and knee OA. As such, it fails to reach complete accuracy and clinical examination and radiographs remain necessary for complete ascertainment procedure.
Role of the NOD2 genotype in the clinical phenotype of Blau syndrome and early‐onset sarcoidosis
Authors: Okafuji Ikuo , Nishikomori Ryuta , Kanazawa Nobuo , Kambe Naotomo , Fujisawa Akihiro , Yamazaki Shin , Saito Megumu , Yoshioka Takakazu , Kawai Tomoki , Sakai Hidemasa , Tanizaki Hideaki , Heike Toshio , Miyachi Yoshiki , Nakahata Tatsutoshi 
Published: December 2008

AbstractObjectiveBlau syndrome and its sporadic counterpart, early‐onset sarcoidosis (EOS), share a phenotype featuring the symptom triad of skin rash, arthritis, and uveitis. This systemic inflammatory granulomatosis is associated with mutations in the NOD2 gene. The aim of this study was to describe the clinical manifestations of Blau syndrome/EOS in Japanese patients and to determine whether the NOD2 genotype and its associated basal NF‐κB activity predict the Blau syndrome/EOS clinical phenotype.MethodsTwenty Japanese patients with Blau syndrome/EOS and NOD2 mutations were recruited. Mutated NOD2 was categorized based on its basal NF‐κB activity, which was defined as the ratio of NF‐κB activity without a NOD2 ligand, muramyldipeptide, to NF‐κB activity with muramyldipeptide.ResultsAll 9 mutations, including E383G, a novel mutation that was identified in 20 patients with Blau syndrome/EOS, were detected in the centrally located NOD region and were associated with ligand‐independent NF‐κB activation. The median age of the patients at disease onset was 14 months, although in 2 patients in Blau syndrome families (with mutations R334W and E383G, respectively) the age at onset was 5 years or older. Most patients with Blau syndrome/EOS had the triad of skin, joint, and ocular symptoms, the onset of which was in this order. Clinical manifestations varied even among familial cases and patients with the same mutations. There was no clear relationship between the clinical phenotype and basal NF‐κB activity due to mutated NOD2. However, when attention was focused on the 2 most frequent mutations, R334W and R334Q, R334W tended to cause more obvious visual impairment.ConclusionNOD2 genotyping may help predict disease progression in patients with Blau syndrome/EOS.
Genetic association of the major histocompatibility complex with rheumatoid arthritis implicates two non‐DRB1 loci
Authors: Vignal Charlotte , Bansal Aruna T. , Balding David J. , Binks Michael H. , Dickson Marion C. , Montgomery Doug S. , Wilson Anthony G. 
Published: December 2008

AbstractObjectiveThe HLA–DRB1 locus within the major histocompatibility complex (MHC) at 6p21.3 has been identified as a susceptibility gene for rheumatoid arthritis (RA); however, there is increasing evidence of additional susceptibility genes in the MHC region. The aim of this study was to estimate their number and location.MethodsA case–control study was performed involving 977 control subjects and 855 RA patients. The HLA–DRB1 locus was genotyped together with 2,360 single‐nucleotide polymorphisms in the MHC region. Logistic regression was used to detect DRB1‐independent effects.ResultsAfter adjusting for the effect of HLA–DRB1, 18 markers in 14 genes were strongly associated with RA (P < 10−4). Multivariate logistic regression analysis of these markers and DRB1 led to a model containing DRB1 plus the following 3 markers: rs4678, a nonsynonymous change in the VARS2L locus, ∼1.7 Mb telomeric of DRB1; rs2442728, upstream of HLA–B, ∼1.2 Mb telomeric of DRB1; and rs17499655, located in the 5′‐untranslated region of DQA2, only 0.1 Mb centromeric of DRB1. In‐depth investigation of the DQA2 association, however, suggested that it arose through cryptic linkage disequilibrium with an allele of DRB1. Two non–shared epitope alleles were also strongly associated with RA (P < 10−4): *0301 with anti– cyclic citrullinated peptide–negative RA and *0701 independently of autoantibody status.ConclusionThese results confirm the polygenic contribution of the MHC to RA and implicate 2 additional non‐DRB1 susceptibility loci. The role of the HLA–DQ locus in RA has been a subject of controversy, but in our data, it appears to be spurious.
Novel markers of inflammation identified in tumor necrosis factor receptor–associated periodic syndrome (TRAPS) by transcriptomic analysis of effects of TRAPS‐associated tumor necrosis factor receptor type I mutations in an endothelial cell line
Authors: Rebelo Susana L. , Amel‐Kashipaz Mohammad R. , Radford Paul M. , Bainbridge Susan E. , Fiets Roel , Fang Johnny , McDermott Elizabeth M. , Powell Richard J. , Todd Ian , Tighe Patrick J. 
Published: December 2008

AbstractObjectiveTo analyze the effects of tumor necrosis factor receptor–associated periodic syndrome (TRAPS)–associated mutant tumor necrosis factor receptor type I (TNFRI) expression in a cell type directly relevant to the inflammation in TRAPS, and to identify novel markers associated with mutant TNFRI expression.MethodsTranscriptome analysis on 30,000 human genes was performed on SK‐Hep‐1 human endothelial cells transfected with either wild‐type (WT) or TRAPS‐associated mutant TNFRI. Quantitative reverse transcriptase–polymerase chain reaction and protein expression levels measured by enzyme‐linked immunosorbent assay verified transcriptional changes for selected genes both in supernatants from cells expressing mutant TNFRI and in patient plasma.ResultsCells expressing mutant TNFRI showed up‐regulation of multiple proinflammatory genes relative to WT transfectants, including genes for pentraxin 3, granulocyte–macrophage colony‐stimulating factor, granulocyte colony‐stimulating factor, CCL2, and CCL5, which were also expressed as proteins. In addition, the expression of most of these markers was increased in the plasma and peripheral blood mononuclear cells from TRAPS patients relative to those from healthy controls. The cysteine mutations (C33Y and C52F), which are associated with a more severe clinical phenotype, induced more genes than the low‐penetrance mutation R92Q, which is associated with a milder phenotype. The expression of most genes was induced by a death domain (DD)–dependent mechanism, since they were not induced by expression of TNFRI mutants with an inactivated DD.ConclusionTRAPS‐associated TNFRI mutants induce the expression of multiple genes encoding inflammatory molecules, cellular receptors, transcription factors, and regulators of apoptosis in endothelial cells that require the cytoplasmic signaling properties of the receptor. Different mutants have specific expression profiles, indicating mutation‐specific effects. The expression of some of these markers was also elevated in samples from TRAPS patients.
Independent association of rheumatoid arthritis with increased left ventricular mass but not with reduced ejection fraction
Authors: Rudominer Rebecca L. , Roman Mary J. , Devereux Richard B. , Paget Stephen A. , Schwartz Joseph E. , Lockshin Michael D. , Crow Mary K. , Sammaritano Lisa , Levine Daniel M. , Salmon Jane E. 
Published: December 2008

AbstractObjectiveRheumatoid arthritis (RA) is a chronic inflammatory disease associated with premature atherosclerosis, vascular stiffening, and heart failure. This study was undertaken to investigate whether RA is associated with underlying structural and functional abnormalities of the left ventricle (LV).MethodsEighty‐nine RA patients without clinical cardiovascular disease and 89 healthy matched controls underwent echocardiography, carotid ultrasonography, and radial tonometry to measure arterial stiffness. RA patients and controls were similar in body size, hypertension and diabetes status, and cholesterol level.ResultsLV diastolic diameter (4.92 cm versus 4.64 cm; P < 0.001), mass (136.9 gm versus 121.7 gm; P = 0.004 or 36.5 versus 32.9 gm/m2.7; P = 0.01), ejection fraction (71% versus 67%; P < 0.001), and prevalence of LV hypertrophy (18% versus 6.7%; P = 0.023) were all higher among RA patients versus controls. In multivariate analysis, presence of RA was an independent correlate of LV mass (P = 0.004). Furthermore, RA was independently associated with presence of LV hypertrophy (odds ratio 4.14 [95% confidence interval 1.24, 13.80], P = 0.021). Among RA patients, age at diagnosis and disease duration were independently related to LV mass. RA patients with LV hypertrophy were older and had higher systolic pressure, damage index scores, C‐reactive protein levels, homocysteine levels, and arterial stiffness compared with those without LV hypertrophy.ConclusionThe present results demonstrate that RA is associated with increased LV mass. Disease duration is independently related to increased LV mass, suggesting a pathophysiologic link between chronic inflammation and LV hypertrophy. In contrast, LV systolic function is preserved in RA patients, indicating that systolic dysfunction is not an intrinsic feature of RA.
Systems biology analysis of sjögren's syndrome and mucosa‐associated lymphoid tissue lymphoma in parotid glands
Authors: Hu Shen , Zhou Michael , Jiang Jiang , Wang Jianghua , Elashoff David , Gorr Sven , Michie Sara A. , Spijkervet Fred K. L. , Bootsma Hendrika , Kallenberg Cees G. M. , Vissink Arjan , Horvath Steve , Wong David T. 
Published: December 2008

AbstractObjectiveTo identify key target genes and activated signaling pathways associated with the pathogenesis of Sjögren's syndrome (SS) by conducting a systems analysis of parotid glands manifesting primary SS or primary SS/mucosa‐associated lymphoid tissue (MALT) lymphoma phenotypes.MethodsA systems biology approach was used to analyze parotid gland tissue samples obtained from patients with primary SS, patients with primary SS/MALT lymphoma, and subjects without primary SS (non–primary SS controls). The tissue samples were assessed concurrently by gene‐expression microarray profiling and proteomics analysis, followed by weighted gene‐coexpression network analysis.ResultsGene‐coexpression modules related to primary SS and primary SS/MALT lymphoma were significantly enriched with genes known to be involved in the immune/defense response, apoptosis, cell signaling, gene regulation, and oxidative stress. Detailed functional pathway analyses indicated that primary SS–associated modules were enriched with genes involved in proteasome degradation, apoptosis, signal peptides of the class I major histocompatibility complex (MHC), complement activation, cell growth and death, and integrin‐mediated cell adhesion, while primary SS/MALT lymphoma–associated modules were enriched with genes involved in translation, ribosome biogenesis and assembly, proteasome degradation, class I MHC signal peptides, the G13 signaling pathway, complement activation, and integrin‐mediated cell adhesion. Combined analyses of gene expression and proteomics data implicated 6 highly connected “hub” genes for distinguishing primary SS from non–primary SS, and 8 hub genes for distinguishing primary SS/MALT lymphoma from primary SS.ConclusionSystems biology analyses of the parotid glands from patients with primary SS and those with primary SS/MALT lymphoma revealed pathways and molecular targets associated with disease pathogenesis. The identified gene modules/pathways provide further insights into the molecular mechanisms of primary SS and primary SS/MALT lymphoma. The identified disease‐hub genes represent promising targets for therapeutic intervention, diagnosis, and prognosis.