bluuebunny/crossref_metadata_2025_split huggingface dataset:
Influence of orthopedic particulate biomaterials on inflammation and synovial microcirculation in the murine knee joint
Authors: Zysk Stefan P. , Gebhard Harry , Plitz Wolfgang , Buchhorn G.H. , Sprecher Christoph M. , Jansson Volkmar , Messmer Konrad , Veihelmann Andreas 
Published: May 2004

AbstractThe purpose of the present study was to examine changes in the synovial microcirculation as well as synovial tissue responses to exposure to titanium, polymethylmethacrylate (PMMA), ceramic (Al2O3), cobalt–chromium alloy (Co–Cr), and polyethylene (PE) particles in an in vivo model. The particulate biomaterials were injected into the left knee joint of female Balb/c mice and assessment of the synovial microcirculation using intravital fluorescence microscopy as well as histological evaluation of the synovial tissue response were performed on day 7 after particle administration. Intravital microscopic measurements revealed that all tested biomaterials caused significantly (p < 0.05) enhanced leukocyte–endothelial cell interactions and an increase of functional capillary density compared to controls. In the histological examination PMMA, Al2O3, PE, and Co–Cr particles provoked significantly (p < 0.05) enhanced inflammatory tissue responses in comparison to tissue from control animals. Titanium particles showed significantly (p < 0.05) less leukocyte–endothelial cell interactions than the other particulate biomaterials and caused significantly (p < 0.05) minor membrane thickening compared to PE and PMMA particles. In conclusion, all tested particulate biomaterials were capable of inducing inflammatory responses in the present study. Our data suggest that titanium particles may cause less leukocyte activation and inflammatory tissue responses than other particulate biomaterials used in total joint arthroplasty. © 2004 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 71B: 108–115, 2004
Differential activation of ERK1,2 MAP kinase signaling pathway in mesenchymal stem cell from control and osteoporotic postmenopausal women
Authors: Rodríguez J. Pablo , Ríos Susana , Fernández Mireya , Santibañez J. Francisco 
Published: May 2004

AbstractOsteoblasts, the cells responsible for bone formation, derive from mesenchymal stem cells (MSCs) in bone marrow. To acquire a new cell phenotype, uncommitted MSCs must undergo several proliferation and differentiation changes. Although, it is known that extracellular signal‐regulated protein kinases (ERKs) mitogen‐activated protein (MAP) kinase pathway signaling is involved in the proliferation and differentiation processes, the role of ERKs in osteogenic differentiation it is controversial, at present. In addition, the function that ERK could play in MSCs derived from osteoporotic patients it is not well documented. In this study, we analyze whether previously observed differences in the dynamic response of MSCs from normal and osteoporotic postmenopausal women can be explained by changes in the activation of this signal transduction pathway. Levels of ERK phosphorylation and their correlation with osteogenic differentiation were evaluated in cultures of MSCs derived from osteoporotic postmenopausal women and “healthy” controls. The results show that, under basal conditions, MSCs derived from osteoporotic donors show a level of ERK phosphorylation 2.5 times higher than MSCs derived from control donors. The addition of the osteogenic stimulus only slightly increases the p‐ERK level in cells derived from osteoporotic donors, and is higher in cells derived from control women. Important differences in the ability of PD98059 to inhibit phosphorylation of ERK in both types of cells were also observed, as well as the effect that this inhibition produced on calcium deposition. We conclude that the MAP kinase pathway signaling is differentially activated in MSCs derived from osteoporotic postmenopausal women. The high p‐ERK levels in MSC derived from osteoporotic donors could determine the unresponsiveness of these cells to the osteogenic differentiation stimulus. © 2004 Wiley‐Liss, Inc.
Consultation and interprofessional collaboration: Modeling for the future
Authors: Arredondo Patricia , Shealy Craig , Neale Michael , Winfrey LaPearl Logan 
Published: May 2004

AbstractConsultation and interprofessional collaboration by psychologists occur with individuals, groups, programs, and organizations. The practice of consultation and interprofessional collaboration involves interdisciplinary relationships, preparation, and advanced skill development within specialty areas of psychology (e.g., clinical, counseling, industrial‐organizational, and school). The Workgroup on Consultation and Interdisciplinary Relationships engaged in a planning process at the Competencies Conference: Future Directions in Education and Credentialing in Professional Psychology to address fundamental issues regarding consultation and interprofessional collaboration in professional psychology. The Workgroup articulated working definitions, consensus points about psychologists as consultants and interprofessional collaborators, a consulting and interprofessional competency blueprint for preparation and assessment strategies, and future directions. This is one of a series of articles published in this issue of the Journal of Clinical Psychology. Several other articles that resulted from the Competencies Conference will appear in Professional Psychology: Research and Practice and The Counseling Psychologist. © 2004 Wiley Periodicals, Inc. J Clin Psychol.
Community resilience and the impact of stress: Adult response to Israel's withdrawal from Lebanon
Authors: Kimhi Shaul , Shamai Michal 
Published: May 2004

AbstractAgainst the background of the Israeli withdrawal from Lebanon, we investigated the relationship between perceived community resilience and the effect of stress and life satisfaction. The research sample included 741 adults, aged 18–85. The participants were divided into four groups, three of which live close to the Israel–Lebanon border and were directly exposed to the threat created by war and terror. The fourth group was considered as a control group and included subjects from the central region of Israel, who were not directly exposed to the war with Lebanon and to the possible outcomes of withdrawal. Questionnaires were distributed to the participants immediately after the withdrawal from Lebanon and were completed by them between 1 and 3 weeks after the withdrawal. The items were designed to measure perceived community resilience, the effects of stress, and life satisfaction, and demographic background. The results show that the level of threat has a significant impact on community resilience, namely, that living in situations with a high level of threat over a long period of time results in a lower level of community resilience. In addition, community resilience serves as a partial mediator between the level of threat and the effect of stress and life satisfaction. The results highlight the importance of perceived community resilience as an individual resource for coping with the threat created by war and terror, thereby connecting between micro‐ and macro‐levels in events related to political violence. © 2004 Wiley Periodicals, Inc. J Comm Psychol 32: 439–451, 2004.
PDGF and FGF induce focal adhesion kinase (FAK) phosphorylation at Ser‐910: Dissociation from Tyr‐397 phosphorylation and requirement for ERK activation
Authors: Hunger‐Glaser Isabel , Fan Robert S. , Perez‐Salazar Eduardo , Rozengurt Enrique 
Published: May 2004

AbstractA rapid increase in the tyrosine phosphorylation of focal adhesion kinase (FAK) has been extensively documented in cells stimulated by multiple signaling molecules, but very little is known about the regulation of FAK phosphorylation at serine residues. Stimulation of Swiss 3T3 cells with platelet‐derived growth factor (PDGF) promoted a striking increase in the phosphorylation of FAK at Ser‐910, as revealed by site‐specific antibodies that recognized the phosphorylated state of this residue. FAK phosphorylation at Ser‐910 could be distinguished from that at Tyr‐397 in terms of dose‐response relationships and kinetics. Furthermore, the selective phosphoinositide 3‐kinase (PI 3‐kinase) inhibitors wortmannin and LY 294002 abrogated FAK phosphorylation at Tyr‐397 but did not interfere with PDGF‐induced FAK phosphorylation at Ser‐910. Conversely, treatment with U0126, a potent inhibitor of MEK‐mediated ERK activation, prevented FAK phosphorylation at Ser‐910 induced by PDGF but did not interfere with PDGF‐induced FAK phosphorylation at Tyr‐397. These results were extended using growth factors that either stimulate, fibroblast growth factor (FGF), or do not stimulate (insulin) the ERK pathway activation in Swiss 3T3 cells. FGF but not insulin promoted a striking ERK‐dependent phosphorylation of FAK at Ser‐910. Our results indicate that FAK phosphorylation at Tyr‐397 and FAK phosphorylation at Ser‐910 are induced in response to PDGF stimulation through different signaling pathways, namely PI 3‐kinase and ERK, respectively. © 2004 Wiley‐Liss, Inc.
Chimeric molecule IL‐6/soluble IL‐6 receptor is a potent mitogen for fetal hepatocytes
Authors: Zvibel Isabel , Brill Shlomo , Kariv Revital , Traister Alexandra , Golan Talia , Chebath Judith , Halpern Zamir , Revel Michel , Oren Ran 
Published: May 2004

AbstractA novel recombinant molecule, termed IL‐6c and consisting of a chimera of interleukin 6 (IL‐6) and its soluble receptor is extremely potent in stimulating proliferation of hematopoietic progenitors. We investigated the effect of the IL‐6c on the proliferation and differentiation of E14 fetal hepatocytes. IL‐6c, in a dose‐dependent manner, stimulated proliferation of E14 fetal rat hepatocytes. Adult hepatocyte mitogens together with IL‐6c showed no further effect on proliferation. Hematopoietic stem cells mitogens SCF and flt3 ligand (FL) were also mitogenic for fetal hepatocytes, but did not further enhance the effect of IL‐6c on cell proliferation. IL‐6c decreased expression of fetal markers α‐fetoprotein (AFP) and gamma‐glutamyltranspeptidase, and induced expression of adult enzyme glucose‐6‐phosphatase (Gluc‐6‐P) in E14 hepatocytes. On the other hand, IL‐6c strongly reduced, in a dose‐dependant manner, expression of albumin and tyrosine aminotransferase (TAT). However, when the cells were grown for 3 days with IL‐6c, and IL‐6c was removed for the next 5 days, expression of albumin and TAT returned to levels found in control cultures. In conclusion, IL‐6c stimulated proliferation and affected gene expression in fetal hepatocytes in culture. © 2004 Wiley‐Liss, Inc.
Role of LRP in TGFβ2‐mediated neuronal uptake of Aβ and effects on memory
Authors: Harris‐White Marni E. , Balverde Zerlinde , Lim Giselle P. , Kim Peter , Miller Sheryl A. , Hammer Heidi , Galasko Doug , Frautschy Sally A. 
Published: May 2004

AbstractThere is increasing evidence that soluble amyloid‐β peptide (Aβ) uptake into neurons is an early event in the pathogenesis of Alzheimer's disease (AD). Identification of the early events leading to neuronal dysfunction is key to developing therapeutic strategies, but relative roles of receptors and factors modulating uptake are poorly understood. Studies have shown that transforming growth factor β (TGFβ), particularly TGFβ2, can influence the targeting of Aβ to cells in vitro. TGFβ2 can target Aβ to neurons in organotypic hippocampal slice cultures (OHSC). We examine a specific mechanism for TGFβ2‐mediated targeting of Aβ to neurons. The receptor‐associated protein (RAP), a low‐density lipoprotein receptor‐related protein (LRP) antagonist, can attenuate the cellular targeting of Aβ both in vitro and in vivo and prevent Aβ/TGFβ2‐induced memory retention deficits. Using both in vitro and in vivo methods, we identify LRP as playing a role in TGFβ2‐mediated Aβ uptake, neurodegeneration, and spatial memory impairment. © 2004 Wiley‐Liss, Inc.
Activation of adenosine A2A receptor protects sympathetic neurons against nerve growth factor withdrawal
Authors: Ramirez Servio H. , Fan Shongshan , Maguire Casey A. , Perry Seth , Hardiek Kathy , Ramkumar Vickram , Gelbard Harris A. , Dewhurst Stephen , Maggirwar Sanjay B. 
Published: May 2004

AbstractAdenosine mediates a range of effects in the central nervous system (CNS), including the promotion of neuronal survival, but its actions on sympathetic neurons are less well characterized. We therefore sought to understand the role of endogenous adenosine in contributing to the survival of neurotrophin‐dependent sympathetic neurons. Rat superior cervical ganglion (SCG) cultures were maintained in the continuous presence of nerve growth factor (NGF) and then exposed to adenosine deaminase (ADA), to deplete endogenous adenosine. This resulted in a marked increase in cellular apoptosis, to a level that approximated the effect of NGF withdrawal. Furthermore, the addition of exogenous adenosine to NGF‐deprived SCG neurons resulted in enhanced cell survival. Analysis of adenosine receptor (AR) subtypes on these neurons, using real‐time RT‐PCR and receptor binding analyses, revealed that the A2A receptor was the major subtype present. Accordingly, the A2A receptor agonist CGS21680 significantly reduced both ADA‐induced and NGF‐withdrawal‐induced neuronal apoptosis, whereas the A1 receptor agonist R‐PIA had no such effect. The survival‐promoting effect of CGS21680 was eliminated when cells were coincubated with a molar excess of an A2A receptor antagonist. Finally, follow‐up experiments revealed that CGS21680 prevented the induction of early apoptotic events, such as changes in mitochondrial integrity and caspase activation, and that it also triggered an increase in ERK activation, which was essential for neurotrophin‐independent cell survival. Taken together, these findings provide evidence that endogenous adenosine may be important in mediating protection of sympathetic neurons and that it may act via the A2A receptor subtype. © 2004 Wiley‐Liss, Inc.
Effect of the peroxisome proliferator‐activated receptor β activator GW0742 in rat cultured cerebellar granule neurons
Authors: Smith Steven A. , Monteith Gregory R. , Robinson Jodie A. , Venkata Nagaraj Gopisetty , May Fiona J. , Roberts‐Thomson Sarah J. 
Published: May 2004

AbstractThe ligand‐activated transcription factor peroxisome proliferator‐activated receptor β (PPARβ) is present in the brain and is implicated in the regulation of genes with potential roles in neurotoxicity. We sought to examine the role of PPARβ in neuronal cell death by using the PPARβ ligand GW0742. Primary cultures of rat cerebellar granule neurons were prepared from 7‐day‐old pups. Reverse transcriptase‐polymerase chain reaction and in situ hybridization were used to verify that PPARβ mRNA was present in neurons. After 10–12 days in culture, the neuronal cells were incubated in the presence of GW0742, and cell death was measured with a lactate dehydrogenase release (LDH) assay. After 24 hr of exposure, PPARβ activation by GW0742 was not inherently toxic to cerebellar granule neurons. However, toxicity was observed after 48 hr, with cell death mediated via an apoptotic mechanism. In an effect opposite to that observed with PPARα‐activating ligands, PPARβ activation exhibited neuroprotective properties. Treatment with GW0742 significantly reduced cell death during a 12‐hr exposure to low‐KCl media. These results clearly reinforce very specific roles for the PPAR isoforms in neurons and suggest that PPARβ is worthy of further investigation regarding its potential role as a therapeutic target in neurodegenerative states. © 2004 Wiley‐Liss, Inc.
Cyclic AMP/protein kinase a signal attenuates Ca2+‐induced fibroblast growth factor‐1 synthesis in rat cortical neurons
Authors: Kinukawa Hideki , Jikou Takahiro , Nitta Atsumi , Furukawa Yoshiko , Hashimoto Manabu , Fukumitsu Hidefumi , Nomoto Hiroshi , Furukawa Shoei 
Published: May 2004

AbstractFibroblast growth factor (FGF)‐1 is increased in particular brain regions after birth, suggesting an involvement of some regulatory neuronal circuits. To address the neuronal activity responsible for FGF‐1 synthesis, effects of various neurotransmitter receptor activation on cellular FGF‐1 content were examined using cultured rat cortical neurons. Histamine, glutamate, carbachol, serotonin or γ‐aminobutyric acid (GABA) caused an increase of FGF‐1 content. Because this effect was mimicked by (1) N‐methyl‐D‐aspartate, a glutamatergic agonist; (2) Ca2+ ionophore; (3) depolarization with high concentration of KCl, but was abolished in Ca2+‐free medium, Ca2+ influx was thought to trigger FGF‐1 synthesis. Such Ca2+‐mediated enhancement of FGF‐1 synthesis, however, did not occur in the presence of norepinephrine (NE), but was restored by KT‐5720, an inhibitor of protein kinase A (PKA), suggesting an interplay between Ca2+‐activated and cAMP/PKA signals for neuronal FGF‐1 synthesis. This mechanism was proved to function in vivo by stimulation of FGF‐1 expression in neurons of the cerebral cortex after intracerebral administration of propranolol, an antagonist of adrenergic β receptors. This demonstrates that FGF‐1 synthesis is essentially upregulated by Ca2+ influx through excitatory neuronal activities, but such an effect is abolished by neurotransmission that evokes cAMP/PKA signals. FGF‐1 produced is thought to act on establishment and maintenance of particular neuronal circuits in the brain, which may be one of the ways neurotransmitters regulate brain function. © 2004 Wiley‐Liss, Inc.
Activity‐regulated cytoskeleton‐associated protein arc is targeted to dendrites and coexpressed with mu‐opioid receptors in postnatal rat caudate‐putamen nucleus
Authors: Wang Hong , Pickel Virginia M. 
Published: May 2004

AbstractDendritic expression of the activity‐regulated cytoskeleton‐associated protein (Arc) is dramatically enhanced by increased synaptic activity in adult brain. We used immunocytochemical electron microscopy to determine whether the subcellular localization of Arc in developing dendrites corresponds to the peak period of synaptogenesis in the postnatal rat caudate‐putamen nucleus (CPN). The distribution was compared with that of mu‐opioid receptors (MORs), whose localization in dendritic spines closely parallels excitatory synapse formation during postnatal development (Wang et al. [2003] Neuroscience 118:695–708). Sections were processed for immunocytochemical detection of antisera against Arc or MORs at the beginning (postnatal day 15; P15) and the end (P30) of the peak period of synaptogenesis in rat CPN. At P15, immunolabeling for Arc showed a punctate distribution in the cytoplasm of dendritic shafts, some of which was associated with polyribosomes. In some spiny dendrites, Arc immunoreactivity was more intensely localized in putative spines than in their parental dendrites, whereas, in other spiny dendrites, Arc labeling was restricted in the shafts. Many dendritic shafts and spines also showed immunoreactivity for MORs, although dually labeled spines were less numerous than the shafts. At P30, the proportion of singly and dually labeled spines significantly increased from 2.0% to 7.5% and from 9.5% to 21%, respectively. Arc labeling in spines was more detectable beneath the postsynaptic density or at extrasynaptic sites on the plasma membrane. Our results suggest a correlation between Arc expression in dendritic spines during postnatal development and the onset of synaptogenesis in opioid‐responsive neurons in the rat CPN. © 2004 Wiley‐Liss, Inc.
Interplay among platelet‐activating factor, oxidative stress, and group I metabotropic glutamate receptors modulates neuronal survival
Authors: Zhu Peimin , DeCoster Mark A. , Bazan Nicolas G. 
Published: May 2004

AbstractPlatelet‐activating factor (PAF) is a potent phospholipid messenger in the nervous system that participates in synaptic plasticity and in pathologic processes, including neurodegeneration. Oxidative stress plays important roles in neuronal cell death. To define the interaction between PAF and oxidative radicals in neuronal death, we studied the effects of PAF in the presence of oxidative radicals in primary neurons in culture. Exogenous PAF (50 μM) caused PAF receptor‐independent injury to neurons. A nonneurotoxic PAF concentration (500 nM) potentiated neuronal death caused by hydrogen peroxide as determined by lactate dehydrogenase (LDH) assay, Hoechst staining, and TUNEL analysis, but it did not potentiate neuronal death caused by menadione, a superoxide donor, or by the nitric oxide donors 3‐morpholino‐sydnonimine (SIN‐1) and sodium nitroprusside (SNP). This potentiation of the hydrogen peroxide effect was selectively blocked by a PAF membrane‐receptor antagonist, BN52021 (5 μM). The neurotoxic effect of PAF and hydrogen peroxide was also completely blocked by ebselen and partially decreased by pretreatment with (S)‐3,5‐dihydroxyphenylglycine (DHPG), a group I metabotropic glutamate receptor (mGluR) agonist. This study suggests that PAF‐receptor antagonists may be useful for neuroprotection. A similar effect might also be obtained with group I mGluR agonists, probably by way of a different underlying mechanism. © 2004 Wiley‐Liss, Inc.
Effect of foliar sprays containing calcium, magnesium and titanium on peach (Prunus persica L) fruit quality
Authors: Alcaraz‐López Carlos , Botía María , Alcaraz Carlos F , Riquelme Fernando 
Published: May 2004

AbstractSprays containing Ca2+, Mg2+ or Ti4+ were applied to peach trees in several combinations. Effects of treatments on the commercial quality of fruits, especially focused on improving their mechanical properties, are discussed. All treatments containing titanium increased tree performance (branch elongation, flowering and fruit set intensities) and fruit size. At harvest, fruits from Ti‐treated trees showed improved resistance to compression and penetration, as well as a decrease in weight loss during postharvest storage. A similar response was obtained for external colour, though all treatments seemed to delay somewhat the apparent ripening status. Nevertheless, fruits from Ti‐treated trees showed better behaviour in the evolution of colour parameters during storage than did control fruits. Titanium application showed significant increases in iron, copper and zinc concentrations in the peel and calcium concentration in the peel and flesh. This improvement in calcium absorption is explained as a consequence of the beneficial effect of titanium on the absorption, translocation and assimilation processes. Copyright © 2004 Society of Chemical Industry