bluuebunny/crossref_metadata_2025_split huggingface dataset:
Influence of KOH solution on the tensile strength and chemical stability of carbon fiber‐reinforced epoxy resin composites
Authors: Wazzan A. A. , Al‐Turaif H. A. , Daous M. A. 
Published: March 2005

AbstractThe effect of a relatively high concentration of KOH solution (4M) on the mechanical properties and chemical stability of carbon fiber‐reinforced epoxy resin composites, prepared with different volume fractions of reinforcement, were investigated. Upon treatment of specimens of such composites with the KOH solution at different temperature and for different durations, their tensile strengths were adversely affected to varying degrees, depending on treatment conditions and volume percent of carbon fiber reinforcement used. Surfaces of treated specimens were examined for matrix stability, fiber disruption, and debonding. Optical microscopy, scanning electron microscopy (SEM), and X‐ray photoelectron spectroscopy (XPS) were used to evaluate chemical and mechanical degradation of these composites. Results clearly showed that prolonged exposure of composite specimens to such aggressive environments markedly increased the degradation of their mechanical properties. On the other hand, these results also showed that increasing the volume fraction of the carbon fiber reinforcement reduced the severity of degradation of these composite and enhanced their mechanical stability. © 2005 Wiley Periodicals, Inc. J Appl Polym Sci 96: 1682–1690, 2005
Degradation of low‐density polyethylene during extrusion. VI. Effects of oxygen content in air gap
Authors: Andersson Thorbjörn , Wesslén Bengt 
Published: March 2005

AbstractIn our previous papers polyethylene degradation during extrusion coating has been studied and the type of degradation products that are formed and from which step they originate have been discussed. A trained sensory panel has rated the off‐flavor intensities in water samples that have been in contact with various extruded films. Encouraged by the results from these investigations and the documented synergism between aldehydes and ketones and aldehydes and carboxylic acids in off‐flavor intensity, the present study was aimed at confirming the belief that the off‐flavor depends on the presence of oxidative degradation products that have migrated from the film into the water. By decreasing the oxygen concentration in the atmosphere surrounding the extruded melt presence of the highly oxidized species (i.e., carbonyl compounds and carboxylic acids) would decrease and thus the off‐flavor in the water should decline. From this study it could be concluded that the extrusion temperature and the oxygen content in the atmosphere nearest the molten film before quenching are the most important parameters for oxidative degradation and residence time in the air gap influence the amount of oxidative degradation products formed. Furthermore we concluded that the off‐flavor intensity is strongly correlated to the surface oxidation index of the film. Carboxylic acids are present in the water extracts of extruded films and are related to the off‐flavor intensities. © 2005 Wiley Periodicals, Inc. J Appl Polym Sci 96: 1767–1775, 2005
The needs of terminally ill cancer patients versus those of caregivers for information regarding prognosis and end‐of‐life issues
Authors: Clayton Josephine M. , Butow Phyllis N. , Tattersall Martin H. N. 
Published: March 2005

AbstractBACKGROUNDThe difficulty of negotiating the concerns of family members while also respecting the needs of the patient adds complexity to the task of discussing prognosis and end‐of‐life (EOL) issues with terminally ill cancer patients. The informational needs of caregivers may be different from those of the patients themselves with regard to these topics. However, to the authors' knowledge, this issue has received relatively little research attention.METHODSThe authors conducted focus groups and individual interviews with 19 patients with far advanced cancer and 24 caregivers from 3 palliative care (PC) services in Sydney and 22 PC health professionals (HPs) from around Australia. The focus groups and individual interviews were audiotaped and fully transcribed. Additional focus groups or individual interviews were conducted until no additional topics were raised. The participants' narratives were analyzed using qualitative methodology.RESULTSThe participants had varying views regarding whether patients and caregivers should be told different information concerning prognosis and EOL issues. Three themes were identified from the transcripts regarding meeting the informational needs of both the patients and caregivers: 1) the importance of consistency and openness, 2) the specific information needed to care for the patient, and 3) the value of having separate discussions with the patient and caregiver. A desire to restrict the patient's access to information by the caregiver or vice versa was reported by the HPs to be one of the most challenging issues when discussing prognosis and EOL issues. Three themes were identified with regard to this issue: 1) autonomy versus protection, 2) negotiating family dynamics, and 3) difficulty using interpreters.CONCLUSIONSThe results of the current study emphasized the importance of considering the distinct informational needs of caregivers, as well as those of the patient, when discussing prognosis and EOL issues. Cancer 2005. © 2005 American Cancer Society.
Connexin36 mediates gap junctional coupling of alpha‐ganglion cells in mouse retina
Authors: Schubert Timm , Degen Joachim , Willecke Klaus , Hormuzdi Sheriar G. , Monyer Hannah , Weiler Reto 
Published: March 2005

AbstractAlpha‐ganglion cells are present in all vertebrate retinae and are subdivided into ON and OFF types according to their level of dendritic ramification within the inner plexiform layer. They have large dendritic fields and usually a good responsiveness to moving stimuli. They were the first ganglion cells in which tracer coupling was observed, suggesting the presence of gap junctions composed of unknown connexins. Here we show that ON‐alpha‐ganglion cells in the mouse retina are coupled to amacrine cells, whereas OFF‐alpha‐ganglion cells are coupled to other OFF‐alpha‐ganglion cells and to amacrine cells. These tracer coupling patterns were completely absent in mice deficient in connexin36 (Cx36). The expression of Cx36 protein in alpha‐ganglion cells but not in coupled amacrine cells was confirmed in mice in which the Cx36 coding DNA was replaced by the lacZ reporter gene. The dendritic localization and the distribution pattern of Cx36 patches, analyzed in mice in which the enhanced green fluorescent protein (EGFP) was linked to the C‐terminal region of the Cx36 protein, revealed a rather small number of fluorescent plaques and different patterns for ON‐ and OFF‐alpha‐ganglion cells. Furthermore, tracer coupling between OFF‐alpha‐ganglion cells could be inhibited by quinine, a gap junctional blocker with a slight preference for gap junctions formed by Cx36. These data strongly suggest that Cx36 gap junction channels are functional not only in interneurons but also in output neurons of the retina and are responsible for distinct coupling patterns of ganglion cells. J. Comp. Neurol. 485:191–201, 2005. © 2005 Wiley‐Liss, Inc.
Prior elevation of IL‐18 promotes rapid early IFN‐γ production during staphylococcal infection
Authors: Culshaw Shauna , Leung Bernard P. , Gracie J. Alastair , Campbell Carol C. , Thomson Duncan , Gemmell Curtis , Liew Foo Y. , McInnes Iain B. 
Published: March 2005

AbstractSystemic Staphylococcus aureus infection is associated with significant morbidity and mortality arising from both bacterial and host immune factors. IL‐18 is a pro‐inflammatory cytokine of the IL‐1 superfamily that exhibits broad functional effects in innate and acquired immune responses and which has been found in high levels in several chronic inflammatory and autoimmune diseases. Over‐expression of IL‐18 may promote early resolution of infection or could promote a detrimental exaggerated immune response. This was explored in a model of S. aureus infection. We report increased mortality in Swiss mice that were given recombinant IL‐18 prior to inoculation with S. aureus LS‐1. IL‐18 administration prior to infection induced preferentially enhanced IFN‐γ mRNA expression in peripheral blood leukocytes and spleen, especially splenic NK cells. This correlated with increased IFN‐γ protein detection in serum, and leukocyte and spleen cultures at subsequent discrete time points. These data suggest that increased mortality following gram‐positive infection in autoimmune diseases could in part reflect the impact of high levels of pleiotropic pro‐inflammatory cytokines such as IL‐18 present prior to the onset of infection.
Extracellular lysosome‐associated membrane protein‐1 (LAMP‐1) mediates autoimmune disease progression in the NOD model of type 1 diabetes
Authors: De Carvalho Bittencourt Marcelo , Herren Suzanne , Graber Pierre , Vilbois Francis , Pasquali Christian , Berney Claude , Plitz Thomas , Nicoletti Ferdinando , Kosco‐Vilbois Marie H. 
Published: March 2005

AbstractTreatment (from 5 to 25 weeks of age) with a novel blocking monoclonal antibody, mAb I‐10, directed against the plasma membrane (pm) form of LAMP‐1, protected against development of autoimmune diabetes in the NOD mouse. A shorter course of treatment, i.e. from 5 to 12 weeks of age, significantly reduced the occurrence of insulitis as well as disease onset. Interfering with pm‐LAMP‐1 required continuous treatment as tolerance was not observed when treatment was stopped, and no higher proportion of cells with a T regulatory phenotype (e.g. CD4+CD25+) were induced. The mechanism appears to involve modulating a proinflammatory cytokine, as the proportion of pancreatic‐infiltrating IFN‐γ‐positive cells was significantly reduced in the mAb I‐10‐treated group. These results demonstrate an unexpected role for pm‐LAMP‐1 in autoimmune disease progression, and suggest that further investigation should be performed to understand how this molecule modulates IFN‐γ‐driven responses.
Discovery and characterization of highly immunogenic and broadly recognized mimics of the HIV‐1 CTL epitope Gag77–85
Authors: Boggiano César , Moya Rosa , Pinilla Clemencia , Bihl Florian , Brander Christian , Sidney John , Sette Alessandro , Blondelle Sylvie E. 
Published: March 2005

AbstractHuman immunodeficiency virus (HIV)‐specific cytotoxic T lymphocytes (CTL) play an important role in HIV infection. Given the viral genetic diversity, the selection of suitable antigens and epitope variants will be important in the design of an effective vaccine. We have previously shown that combinatorial libraries are useful tools to identify epitope mimics as well as potentially cross‐reactive natural sequences in protein databases. We have applied this approach to the HIV Gag p17‐derived epitope SL9 (SLYNTVATL) to identify broadly recognized SL9 mimics and to assess the cross‐recognition of naturally occurring SL9 variants. Nine nonapeptides were identified that were up to one order of magnitude more effective than SL9 in stimulating CTL responses in PBMC from HIV‐infected subjects. Using transgenic mice, we demonstrate that a number of these epitope mimics were able to generate de novo T cell responses that cross‐reacted with the original SL9 sequence. Particularly, mimics with changes at the relatively conserved F‐pocket anchor residue were frequently cross‐recognized. This approach may lead to vaccine candidates with higher in vivo immunogenicity and increased potential for cross‐recognition of naturally occurring SL9 variants.
Increased inflammation in mice deficient for the chemokine decoy receptor D6
Authors: de la Torre Yeny Martinez , Locati Massimo , Buracchi Chiara , Dupor Jana , Cook Donald N. , Bonecchi Raffaella , Nebuloni Manuela , Rukavina Daniel , Vago Luca , Vecchi Annunciata , Lira Sergio A. , Mantovani Alberto 
Published: March 2005

AbstractChemokines are chemotactic cytokines with a key role in the control of cell trafficking and positioning under homeostatic and inflammatory conditions. D6 is a promiscuous 7‐transmembrane‐domain receptor expressed on lymphatic vessels which recognizes most inflammatory, but not homeostatic, CC chemokines. In vitro experiments demonstrated that D6 is unable to signal after ligand engagement, and it is structurally adapted to sustain rapid and efficient ligand internalization and degradation. These unique functional properties lead to the hypothesis that D6 may be involved in the control of inflammation by acting as a decoy and scavenger receptor for inflammatory chemokines. Consistent with this hypothesis, here we report that D6–/– mice showed an anticipated and exacerbated inflammatory response in a model of skin inflammation. Moreover, the absence of D6 resulted in increase cellularity and inflammatory‐chemokine levels in draining lymph nodes. Thus, D6 is a decoy receptor structurally adapted and strategically located to tune tissue inflammation and control transfer of inflammatory chemokines to draining lymph nodes.
A propensity score approach to estimating the cost–effectiveness of medical therapies from observational data
Authors: Mitra Nandita , Indurkhya Alka 
Published: March 2005

AbstractHealth summary measures are commonly used by policy makers to help make decisions on the allocation of societal resources for competing medical treatments. The net monetary benefit is a health summary measure that overcomes the statistical limitations of a popular measure namely, the cost–effectiveness ratio. We introduce a linear model framework to estimate propensity score adjusted net monetary benefit. This method provides less biased estimates in the presence of significant differences in baseline measures and demographic characteristics between treatment groups in quasi‐randomized or observational studies. Simulation studies were conducted to better understand the utility of propensity score adjusted estimates of net monetary benefits when important covariates are unobserved. The results indicated that the propensity score adjusted net monetary benefit provides a robust measure of cost–effectiveness in the presence of hidden bias. The methods are illustrated using data from SEER‐Medicare for the treatment of bladder cancer. Copyright © 2005 John Wiley & Sons, Ltd.
What caused the early millennium slowdown? Evidence based on vector autoregressions
Authors: Peersman Gert 
Published: March 2005

AbstractThis paper uses a simple VAR for the USA and Euro area to analyse the underlying shocks of the early millennium slowdown, i.e. supply, demand, monetary policy and oil price shocks. The results of two identification strategies are compared. One is based on traditional zero restrictions and, as an alternative, an identification scheme based on more recent sign restrictions is proposed. The main conclusion is that the recent slowdown is caused by a combination of several shocks: negative aggregate supply and aggregate spending shocks, the increase of oil prices in 1999, and restrictive monetary policy in 2000. These shocks are more pronounced in the USA than the Euro area. The results are somewhat different depending on the identification strategy. It is illustrated that traditional zero restrictions can have an influence on the estimated impact of certain shocks. Copyright © 2005 John Wiley & Sons, Ltd.
Comparing shocks and frictions in US and euro area business cycles: a Bayesian DSGE Approach
Authors: Smets Frank , Wouters Raf 
Published: March 2005

AbstractThis paper estimates a DSGE model with many types of shocks and frictions for both the US and the euro area economy over a common sample period (1974–2002). The structural estimation methodology allows us to investigate whether differences in business cycle behaviour are due to differences in the type of shocks that affect the two economies, differences in the propagation mechanism of those shocks, or differences in the way the central bank responds to those economic developments. Our main conclusion is that each of these characteristics is remarkably similar across both currency areas. Copyright © 2005 John Wiley & Sons, Ltd.
Racial differences in adolescent distress: Differential effects of the family and community for blacks and whites
Authors: Wickrama K.A.S. , Noh Samuel , Bryant Chalandra M. 
Published: March 2005

AbstractUsing a sample of 15,885 adolescents derived from the National Longitudinal Study of Adolescent Health, this study examined (1) unique additive influences of race, family, and community and (2) various multiplicative influences among race, family, and community factors on adolescent distress. Community characteristics such as community poverty and ethnic composition were included in the analysis. Community poverty, family poverty, single parenthood, family size, and race/ethnicity all uniquely contributed to adolescent distress. There were significant black–white differences in additive and multiplicative influences of these predictors. The detrimental influence of family poverty was stronger for whites than for blacks. Among blacks, the detrimental influence of community poverty is greater for poor families than for nonpoor families. In contrast, among whites, the detrimental influence of community adversity is greater for nonpoor families than for poor families. Although ethnic composition had no significant impact on adolescent distress for the total sample, it showed a beneficial effect for black adolescents, after controlling for the poverty levels of the communities. Seemingly, community poverty and ethnic composition influence adolescent distress differently through different mechanisms. Understanding these complex processes raise some practical questions about programs aimed at minorities. For example, do black children fare better if their family overcomes persistent poverty and moves out of adverse communities? © 2005 Wiley Periodicals, Inc. J Comm Psychol 33: 261–282, 2005.
Polyaniline with Two Types of Functional Groups: Preparation and Characteristics
Authors: Mu Shaolin 
Published: March 2005

AbstractSummary: Polyaniline with two types of functional groups (sulfonated poly(aniline‐co‐o‐aminophenol), s‐copolymer) has been prepared by the electrochemical copolymerization of aniline and o‐aminophenol in sulfuric acid solution followed by sulfonation of the copolymer in the concentrated sulfuric acid. There are SO3H groups and OH groups in the s‐copolymer. The presence of SO3H groups on the polymer chain enables the s‐copolymer to possess intrinsic protonic doping ability. The OH group on the polymer chain can be oxidized and reduced reversibly. The shape of the cyclic voltammogram of the s‐copolymer is very similar to that of polyaniline in 0.2 M H2SO4 solution, in the potential range −0.20 to 0.80 V (vs. SCE). The results from cyclic voltammograms indicate only 22.8 and 31.6% decay of the electrochemical activity that was observed when the s‐copolymer electrode was transferred from the solution of pH 5.0 to the solutions of pH 10.0 and 11.0, respectively. Especially, there are still two pairs of redox peaks on the cyclic voltammogram of the s‐copolymer in 0.3 M Na2SO4 solution of pH 11.0 at the scan rate of 6 mV s−1. In this case, its usable potential range is 0.0–0.60 V. The s‐copolymer has a conductivity of 0.85 S cm−1, which is slightly dependent on pH when equilibrated with water. The spectra of FTIR, XPS, and ESR of the s‐copolymer are represented here.The cyclic voltammograms of (1) poly(aniline‐co‐o‐aminophenol) and (2) s‐copolymer in H2SO4 solution.magnified imageThe cyclic voltammograms of (1) poly(aniline‐co‐o‐aminophenol) and (2) s‐copolymer in H2SO4 solution.
Involvement of protein kinase PKN1 in G2/M delay caused by arsenite
Authors: Isagawa Takayuki , Takahashi Mikiko , Kato Tomohisa , Mukai Hideyuki , Ono Yoshitaka 
Published: March 2005

AbstractPKN1 is a serine/threonine protein kinase that has been reported to mediate cellular response to stress. We show here that in response to arsenite exposure, PKN1 kinase activity was stimulated, which was associated with increased binding of PKN1 to Cdc25C and delayed mitotic entry. A role for PKN1 in mediating arsenite‐induced G2/M delay was supported by the finding that expression of a constitutively active form of PKN1 (PKN1AF3) in HeLa cells delayed the mitotic entry of cell cycle. Further experiments indicate that PKN1 directly phosphorylated serine 216 (Ser216) in Cdc25C, which then facilitated association between Cdc25C and 14‐3‐3. Significantly, expression of a phosphorylation mutant of Cdc25C (S216A) partially abrogated the cell‐cycle arrest in response to arsenite. Together, our results suggest that PKN1 mediates arsenite‐induced delay of the G2/M transition by binding to and phoshorylating Cdc25C. © 2005 Wiley‐Liss, Inc.
Differential inhibition of UVB‐induced AP‐1 and NF‐κB transactivation by components of the jun bZIP domain
Authors: Cooper Simon , Ranger‐Moore James , Bowden Tim G. 
Published: March 2005

AbstractPotential targets for chemoprevention of nonmelanoma skin cancer include UV‐induced nuclear factor κB (NF‐κB) and activator protein‐1 (AP‐1) activation in keratinocytes. Inhibition of both these ultraviolet light B (UVB)‐induced transcription factors has been shown with the dominant‐negative c‐jun mutant, TAM67; however, its mechanism of action has not yet been determined. Here we demonstrated that transient transfection of a mouse keratinocyte cell line (308) with a dominant‐negative phosphorylation mutant of c‐Jun before exposure to 250 J/m2 UVB inhibits transactivation mediated by both AP‐1 and NF‐κB transcription factors to levels below those of UVB exposed controls. Through the utilization of immunoprecipitation techniques, protein‐protein interactions between NF‐κB family members IκBα, IκBβ, p50, and p65 (Rel‐A) were identified with an Xpress tagged dominant‐negative c‐Jun (TAM67) protein. Expression of the leucine zipper domain of the TAM67 protein inhibited UVB‐induced NF‐κB transactivation but not AP‐1 transactivation. Expression of the bZIP domain of the TAM67 protein was able to inhibit transactivation mediated by both transcription factors. These data demonstrate that TAM67 is able to inhibit two significant UVB‐induced molecular targets AP‐1 and NF‐κB, and that the inhibition of these two transcription factor families is potentially due to protein‐protein interactions between different regions of the dominant‐negative c‐Jun protein. © 2005 Wiley‐Liss, Inc.
Effects of serotonin 5‐HT1A agonist in advanced Parkinson's disease
Authors: Bara‐Jimenez William , Bibbiani Francesco , Morris Michael J. , Dimitrova Tzvetelina , Sherzai Abdullah , Mouradian Maral M. , Chase Thomas N. 
Published: March 2005

AbstractIntermittent stimulation of striatal dopaminergic receptors seems to contribute to motor dysfunction in advanced Parkinson's disease (PD). With severe dopaminergic denervation, exogenous levodopa is largely decarboxylated to dopamine in serotonergic terminals. If 5‐HT1A autoreceptors regulate dopamine as well as serotonin release, in parkinsonian patients inhibition of striatal serotonergic neuron firing might help maintain more physiological intrasynaptic dopamine concentrations and thus ameliorate motor fluctuations and dyskinesias. To evaluate this hypothesis, effects of a selective 5‐HT1A agonist, sarizotan, given orally at 2 and 5 mg twice daily to 18 relatively advanced parkinsonian patients, were compared with baseline placebo function during a 3‐week, double‐blind, placebo‐controlled, proof‐of‐concept study. Sarizotan alone or with intravenous levodopa had no effect on parkinsonian severity. But at safe and tolerable doses, sarizotan coadministration reduced levodopa‐induced dyskinesias and prolonged its antiparkinsonian response (P ≤ 0.05). Under the conditions of this study, our findings suggest that 5‐HT1A receptor stimulation in levodopa‐treated parkinsonian patients can modulate striatal dopaminergic function and that 5‐HT1A agonists may be useful as levodopa adjuvants in the treatment of PD. © 2005 Movement Disorder Society