bluuebunny/crossref_metadata_2025_split huggingface dataset:
Acute effects of caffeine in volunteers with different patterns of regular consumption
Authors: Hewlett Paul , Smith Andrew 
Published: March 2006

AbstractRationaleThe effects of caffeine on mood and performance are well established. One explanation of these effects is that caffeine removes negative effects induced by prior caffeine withdrawal. This was tested here by comparing effects of caffeine in withdrawn consumers and non‐consumers (who by definition were not withdrawn).ObjectivesThe present study aimed to determine whether caffeine withdrawal influenced mood and performance by comparing regular consumers who had been withdrawn from caffeine overnight with non‐consumers. Following this the effects of acute caffeine challenges were compared in withdrawn consumers and non‐consumers. In addition, comparisons were made between those with higher and lower caffeine consumption.MethodsOne hundred seventy‐six volunteers participated in the study. Regular caffeine consumption was assessed by questionnaire and this showed that 56 of the sample did not regularly consume caffeinated beverages. Volunteers were instructed to abstain from caffeine overnight and then completed a baseline session measuring mood and a range of cognitive functions at 08.00 the next day. Following this approximately half of the volunteers were given 1 mg/kg caffeine in a milkshake or water (in the ‘no caffeine’ condition they were given just the milkshake or water) and the test battery repeated one hour later. A second test battery was carried out at 12.00 and a second caffeine challenge at 13.00. A final test session was carried out at 15.00.ResultsThe baseline data revealed little evidence of effects of caffeine withdrawal on performance and mood. In contrast to this, caffeine produced a number of significant improvements in performance. There were some differences in the effects of caffeine on regular and non‐consumers, with caffeine tending to reduce reaction time in regular consumers while the opposite was true for non‐consumers.ConclusionsThe present results show little evidence of effects of caffeine withdrawal on performance. In contrast, caffeine challenge produced improvements in aspects of performance and these were often not modified by regular caffeine consumption patterns. The differences in effects of caffeine that were observed between non‐consumers and regular consumers were in functions that were unaffected by caffeine withdrawal. These findings show that the observed beneficial effects of caffeine cannot be interpreted in terms of a reversal of caffeine withdrawal. Copyright © 2006 John Wiley & Sons, Ltd.
Intertemporal pricing and price discrimination: a semiparametric hedonic analysis of the personal computer market
Authors: Stengos T. , Zacharias E. 
Published: March 2006

AbstractWe apply a smooth coefficient semiparametric model to a unique high‐frequency data set to examine the intertemporal pricing of personal computers. Furthermore, we test whether firms charge differential component prices for their top performance personal computers and whether premium firms charge both a premium for all their computers and a premium for their top performance ones. We find nonlinear effects in the pricing of personal computer components. We also find that firms in general do not charge differential prices for the components of their top performance computers. In addition, high‐quality firms charge higher premia only for their most advanced products. Copyright © 2006 John Wiley & Sons, Ltd.
Magazine prices revisited
Authors: Willis Jonathan L. 
Published: March 2006

AbstractThis paper examines price adjustment behaviour in the magazine industry. In a frequently cited study, Cecchetti (1986) constructs a reduced‐form (S, s) model for firms. Cecchetti assumes that a firm's pricing rules are fixed for non‐overlapping three‐year intervals and estimates the model using a conditional logit specification from Chamberlain (1980). The estimates are inconsistent, however, due to the duration‐dependent specification of the model. Two alternative specifications are used to obtain consistent estimation. The consistent estimates continue to provide strong evidence in favour of state‐dependent pricing models, but only weak evidence on the behaviour of price adjustment costs. Copyright © 2006 John Wiley & Sons, Ltd.
Brain, mind, and dyadic change processes
Authors: Neborsky Robert J. 
Published: March 2006

AbstractFor many individuals attachment trauma is at the core of psychoneurosis and personality disorder. Combining theoretical aspects of psychodynamic therapy, developmental neuroscience, and attachment styles provides a useful framework for intensifying emotion and accelerating the course of treatment. A bihemispheric model is considered. The model addresses the challenge in treating the implicit trauma, which resides in the right hemisphere. This is achieved without resorting to interpretation, which is largely a left hemispheric process. The article presents a patient who benefits from a brief emotionally based psychotherapy that was completed after a course of a 20‐year psychoanalysis. © 2006 Wiley Periodicals, Inc. J Clin Psychol: In Session 62: 523–538, 2006.
Emotional processing in the treatment of psychosomatic disorders
Authors: Coughlin Della Selva Patricia 
Published: March 2006

AbstractResearch has supported a hypothesis that was clinically suggested decades ago: that those who have functional disorders exhibit significant deficits in emotional processing. Studies have systematically documented that patients who habitually repress their emotions simultaneously suppress their immune response, rendering them vulnerable to physical illness and early death. Conversely, those who are encouraged to experience and express their feelings demonstrate improvement in immune function, physical condition, and psychological well‐being. This article describes a psychotherapy designed to interrupt defensive processes and facilitate the direct experience of previously disavowed feelings in the treatment of patients who have physical ailments. Verbatim transcripts from the treatment of a woman who had a life‐threatening illness illustrate the therapeutic techniques designed to facilitate emotional processing and restore health. Data from 14 years of follow‐up interviews reveal a sustained remission in her disease. © 2006 Wiley Periodicals, Inc. J Clin Psychol: In Session 62: 539–550, 2006.
Quantum transformation in trauma and treatment: Traversing the crisis of healing change
Authors: Fosha Diana 
Published: March 2006

AbstractThree ideas are discussed from the vantage point of accelerated experiential dynamic psychotherapy (AEDP): Quantum changes operate not only in trauma, but also in healing; attachment plays a major role in whether fear or excitement is the response to novelty; experientially exploring the experience of transformation can itself lead to quantum change. Vignettes from an AEDP session show a patient's grappling with the startling novelty of experience that the transformational process, particularly when occurring in quantum leaps, evokes, and illustrate the phenomenology of cascading transformations. They illustrate how the therapist's emotional engagement and attachment orientation, experiential techniques, and metatherapeutic processing activate state transformations and entrain adaptive healing processes. © 2006 Wiley Periodicals, Inc. J Clin Psychol: In Session 62: 569–583, 2006.
Adhesion and proliferation of fibroblasts on RF plasma‐deposited nanostructured fluorocarbon coatings: Evidence of FAK activation
Authors: Rosso Francesco , Marino Gerardo , Muscariello Livio , Cafiero Gennaro , Favia Pietro , D'Aloia Erica , d'Agostino Riccardo , Barbarisi Alfonso 
Published: February 2006

AbstractWe used combined plasma‐deposition process to deposit smooth and nanostructured fluorocarbon coatings on polyethylenethereftalate (PET) substrates, to obtain surfaces with identical chemical composition and different roughness, and investigate the effect of surface nanostructures on adhesion and proliferation of 3T3 Swiss Albino Mouse fibroblasts. Untreated PET and polystyrene (PS) were used as controls for cell culture. We have found that the statistically significant increase of cell proliferation rate and FAK (a nonreceptor tyrosine kinase) activation detected on ROUGH fluorocarbon surfaces is due to the presence of nanostructures. Changes in cytoskeletal organization and phospho FAK (tyr 397) localization were evident after 60 min on cells adhering to ROUGH surfaces. This change was characterized by the formation of actin stress fibers along lamellar membrane protrusion instead of usual focal contacts. Also the morphology of the adhering fibroblasts (60 min) adhering on ROUGH surfaces was found quite different compared to cells adhering on smooth ones. J. Cell. Physiol. © 2006 Wiley‐Liss, Inc.
cDNA‐array profiling of melanomas and paired melanocyte cultures
Authors: Mischiati Carlo , Natali Pier Giorgio , Sereni Alessia , Sibilio Leonardo , Giorda Ezio , Cappellacci Sandra , Nicotra Maria Rita , Mariani Giustino , Di Filippo Franco , Catricalà Caterina , Gambari Roberto , Grammatico Paola , Giacomini Patrizio 
Published: March 2006

AbstractThree paired (from the same donor) sets of melanoma cells and normal melanocytes, established as early‐passage cultures from metastatic lesions and the uninvolved skin of three patients, were comparatively cDNA profiled by macroarrays (approximately 1,200 genes) and reverse transcription (RT)‐PCR. While 145 gene products were significantly (at least twofold) upregulated or downregulated in at least 1 pair, and 23 were in at least 2 pairs, only 3 (the signal transducer and activator of transcription STAT2, collagen type VI, and CD9) were concordantly modulated (downregulation) in all 3 pairs. Array results were validated by RT‐PCR on a small panel of surgically removed nevocellular nevi and metastatic melanoma lesions, and by immunohistochemistry on a large panel of benign and malignant lesions of the nevomelanocytic lineage. The three gene products were downregulated at different stages of melanoma progression. STAT2 was detectable in nevi (5/5) and most primary melanomas (11/12), but was lost in 10/15 metastatic lesions. Collagen type VI was expressed in nevi (5/5) and primary melanomas below a Breslow thickness of 1 mm (3/3), but was lost in 24/24 primary melanomas above this threshold, and in metastatic melanomas (10/10). The tetraspanin CD9 molecule was expressed in 18/18 nevi, but was lost in 20/28 primary melanomas (including thin lesions), and in 24/52 metastatic lesions. These data provide the proof of principle that cDNA profiling of paired melanocyte/melanoma cultures sorts out novel, early signatures of melanocyte transformation that could contribute to the clinical management of patients at high risk of metastatic disease. J. Cell. Physiol. © 2006 Wiley‐Liss, Inc.
Expression and regulation of CReMM, a chromodomain helicase‐DNA‐binding (CHD), in marrow stroma derived osteoprogenitors
Authors: Marom R. , Shur I. , Hager G.L. , Benayahu D. 
Published: March 2006

AbstractThis study follows the expression of CReMM, a new CHD family member, in osteoprogenitors. CReMM expression was analyzed in primary cultured mesnchymal cells from rat and human. Analysis in ex vivo cultured marrow stromal cells (MSC) from rats revealed higher level of CReMM in cells from young (3 months), when compared to cells from old (15 months) rats. CReMM level was higher in human MSC then in mature trabecular bone cells (TBC). Within the MSC population, osteogenic clones showed higher levels of CReMM then non‐osteogenic ones. We used bone marrow derived osteogenic cell line (MBA‐15) to elaborate on the regulation of CReMM expression in correlation with cell proliferation and co‐expression with alkaline phosphatase (ALK). CReMM is highly expressed in proliferating cells and is inversely related to expression of ALK. MBA‐15 cells were challenged with dexamethasone (Dex) or 17β‐estradiol and quantification of CReMM at the protein (ELISA) and mRNA (RT‐PCR) levels had shown that Dex upregulated CReMM levels. Since CReMM is regulated by Dex, we analyzed the interaction of CReMM with the glucocorticoid receptor (GR), which mediates Dex action. Co‐immunopercipitation (Co‐IP) demonstrated an association between CReMM and GR. In summary, CReMM is a CHD protein expressed by osteoprogenitors, and we suggest it plays a role in mediating transcriptional response to hormones that coordinate osteoblast function. J. Cell. Physiol. © 2006 Wiley‐Liss, Inc.
Downregulation of Akt activity contributes to the growth arrest induced by FGF in chondrocytes
Authors: Priore Riccardo , Dailey Lisa , Basilico Claudio 
Published: March 2006

AbstractUnregulated FGF signaling produced by activating FGFR3 mutations causes several forms of dwarfism‐associated chondrodysplasias in humans and mice. FGF signaling inhibits chondrocyte proliferation by activating multiple signal transduction pathways that all contribute to chondrocyte growth arrest and induction of some aspects of differentiation. Previous studies had identified the Stat1 pathway, dephosphorylation of the Rb family proteins p107 and p130, induction of p21 expression and sustained activation of MAP kinases as playing a role in the FGF response of chondrocytes. We have examined the role of Akt (PKB) in the response of chondrocytes to FGF signaling. Differently from what is observed in many other cell types, FGF does not activate Akt in chondrocytes, and Akt phosphorylation is actually downregulated after FGF treatment. By expressing a constitutively activated, myristylated form of Akt (myr‐Akt) in the RCS chondrosarcoma cell line, we show that Akt activation partially counteracts the inhibitory effect of FGF signaling. The response of myr‐Akt expressing cells to FGF is identical to parental RCS in the first few hours after treatment, but then diverges as myr‐Akt cells show decreased p130 phosphorylation, increased cyclin E/cdk2 activity and continue to proliferate at a slow rate. Constitutive Akt activation does not affect p21 expression but appears to influence directly cdk/cyclin activity. On the other hand, the induction of differentiation‐related genes is unchanged in myr‐Akt cells. These results identify Akt downregulation as an important aspect of the response of chondrocytes to FGF that, however, only affects chondrocyte proliferation and not the ability of FGF to induce differentiation genes. J. Cell. Physiol. © 2006 Wiley‐Liss, Inc.
Functions of human replication protein A (RPA): From DNA replication to DNA damage and stress responses
Authors: Zou Yue , Liu Yiyong , Wu Xiaoming , Shell Steven M. 
Published: March 2006

AbstractHuman replication protein A (RPA), a heterotrimeric protein complex, was originally defined as a eukaryotic single‐stranded DNA binding (SSB) protein essential for the in vitro replication of simian virus 40 (SV40) DNA. Since then RPA has been found to be an indispensable player in almost all DNA metabolic pathways such as, but not limited to, DNA replication, DNA repair, recombination, cell cycle, and DNA damage checkpoints. Defects in these cellular reactions may lead to genome instability and, thus, the diseases with a high potential to evolve into cancer. This extensive involvement of RPA in various cellular activities implies a potential modulatory role for RPA in cellular responses to genotoxic insults. In support, RPA is hyperphosphorylated upon DNA damage or replication stress by checkpoint kinases including ataxia telangiectasia mutated (ATM), ATR (ATM and Rad3‐related), and DNA‐dependent protein kinase (DNA‐PK). The hyperphosphorylation may change the functions of RPA and, thus, the activities of individual pathways in which it is involved. Indeed, there is growing evidence that hyperphosphorylation alters RPA–DNA and RPA–protein interactions. In addition, recent advances in understanding the molecular basis of the stress‐induced modulation of RPA functions demonstrate that RPA undergoes a subtle structural change upon hyperphosphorylation, revealing a structure‐based modulatory mechanism. Furthermore, given the crucial roles of RPA in a broad range of cellular processes, targeting RPA to inhibit its specific functions, particularly in DNA replication and repair, may serve a valuable strategy for drug development towards better cancer treatment. J. Cell. Physiol. 208: 267–273, 2006. © 2006 Wiley‐Liss, Inc.
Proteasome inhibitors shorten replicative life span and induce a senescent‐like phenotype of human fibroblasts
Authors: Torres Claudio , Lewis Lindsey , Cristofalo Vincent J. 
Published: March 2006

AbstractThe proteasome constitutes the main non‐lysosomal cellular protease activity, and plays a crucial role not only in the disposal of unwanted material, but also in the regulation of numerous cellular processes. Previously, we have reported that during the replicative senescence of WI‐38 fibroblasts there is a significant impairment in proteasome activity, which probably has important implications in the control of MAPK signaling and cellular proliferation. In this study, we report the potential role of the proteasome in the generation of the senescent phenotype in WI‐38 fibroblasts. Our results indicate that inhibition of proteasome activity leads to an impairment in cell proliferation, and a shortening of the life span. The results also indicate that inhibition of the proteasome in young cells induces a premature senescent‐like phenotype, as indicated by the increase in senescence‐associated β‐galactosidase (SA β‐gal) activity and the abundance of both p21 and collagenase mRNAs, as well as a decreased level of EPC‐1 mRNA known markers of cellular senescence, not previously shown to depend on proteasome activity. Together, our results suggest a molecular mechanism for the lack of responsiveness of human cells to growth factors, and point towards a role for the proteasome in the control of the life span of both cells and organisms. J. Cell. Physiol. © 2006 Wiley‐Liss, Inc.
Consequences of point mutations in trout anion exchanger 1 (tAE1) transmembrane domains: Evidence that tAE1 can behave as a chloride channel
Authors: Martial Sonia , Guizouarn Hélène , Gabillat Nicole , Pellissier Bernard , Borgese Franck 
Published: February 2006

AbstractIn this study, we have shown that, when expressed in Xenopus oocytes, trout anion exchanger 1 (tAE1) was able to act as a bifunctional protein, either an anion exchanger or a chloride conductance. Point mutations of tAE1 were carried out and their effect on Cl− conductance and Cl− unidirectional flux were studied. We have shown that mutations made in transmembrane domain 7 had dramatic effects on tAE1 function. Indeed, when these residues were mutated, either individually or together (mutants E632K, D633G, and ED/KG), Cl− conductance was reduced to 28–44% that of wild‐type tAE1. Moreover, ion substitution experiments showed that anion selectivity was altered. However, the exchanger function was unchanged, as evidenced by the fact that Cl− influx and Km were identical for each of these mutants and similar to the wild‐type protein parameters. By contrast, mutations made in the C‐terminal domains of the protein (R819M, Q829K) affected both transport functions. Cl− conductance was increased by ∼200% with respect to tAE1 and anion selectivity was impaired. Likewise, Cl− influx was increased by ∼260% and was no longer saturable. These and other mutations carried out in transmembrane domains 7, 8, 12–14 of tAE1 allow us to demonstrate without doubt that, in addition to its anion exchanger activity, tAE1 can also function as a chloride channel. Above all, this work led us to identify amino acids involved in this double function organization. J. Cell. Physiol. © 2006 Wiley‐Liss, Inc.
Activation of smooth muscle and myenteric plexus cells of jejunum via toll‐like receptor 4
Authors: Rumio Cristiano , Besusso Dario , Arnaboldi Francesca , Palazzo Marco , Selleri Silvia , Gariboldi Silvia , Akira Shizuo , Uematsu Satoshi , Bignami Paola , Ceriani Valerio , Ménard Sylvie , Balsari Andrea 
Published: March 2006

AbstractThe cell types of the gut expressing Toll‐like receptor 4, which recognizes specifically bacterial lipopolysaccharides, as well as the functionality of this receptor, have remained controversial. We aimed to clarify these issues. Mouse and human intestinal specimens were stained immunohistochemically to detect Toll‐like receptor 4 expression. Smooth muscle and myenteric plexus cells but not enterocytes revealed receptor expression. Murine intestinal smooth muscle and myenteric plexus cells but not enterocytes showed nuclear translocation of nuclear factor‐kappaB after in vivo stimulation with lipopolysaccharide. Moreover, lipopolysaccharide added to human jejunum biopsies free of epithelial cells induced release of interleukin‐8 (IL‐8). We can conclude that Toll‐like receptor 4 is not expressed in epithelial layer, but rather on smooth muscle and myenteric plexus cells and that expression is functional. The expression of Toll‐like receptor 4 on smooth muscle and myenteric plexus cells is consistent with the possibility that these cells are involved in intestinal immune defense; the low or absent expression of Toll‐like receptor 4 on enterocytes might explain the intestinal epithelium hyporesponsiveness to the abundance of LPS in the intestinal lumen. J. Cell. Physiol. © 2006 Wiley‐Liss, Inc.
Differential activity of the FGF‐4 enhancer in F9 and P19 embryonal carcinoma cells
Authors: Boer Brian , Bernadt Cory T. , Desler Michelle , Wilder Phillip J. , Kopp Janel L. , Rizzino Angie 
Published: March 2006

AbstractTranscription factors Oct‐3/4 and Sox2 behave as global regulators during mammalian embryogenesis. They work together by binding co‐operatively to closely spaced HMG and POU motifs (HMG/POU cassettes). Recently, it was suggested that a critical Sox2:Oct‐3/4 target gene, FGF‐4, is expressed at lower levels in P19 than in F9 embryonal carcinoma (EC) cells, due to lower levels of Sox2 in P19 than in F9 cells. We tested this possibility to better understand how FGF‐4 expression is modulated during development. Although we found that P19 EC cells express ∼10‐fold less FGF‐4 mRNA than F9 EC cells, we determined that Sox2 levels do not differ markedly in F9 and P19 EC cells. We also determined that Sox2 and Oct‐3/4 work together equally well in both EC cell lines. Moreover, in contrast to an earlier prediction based on in vitro binding studies, we demonstrate that the function of the HMG/POU cassettes of the FGF‐4 and UTF1 genes does not differ significantly in these EC cell lines when tested in the context of a natural enhancer. Importantly, we determined that the FGF‐4 promoter is highly responsive to a heterologous enhancer in both EC cell lines; whereas, the FGF‐4 enhancer is 7‐ to 10‐fold less active in P19 than in F9 EC cells. Because F9 and P19 EC cells are likely to represent cells at different stages of mammalian development, we suggest that this difference in FGF‐4 enhancer activity may reflect a mechanism used to decrease, but not abolish, FGF‐4 expression as the early embryo develops. J. Cell. Physiol. © 2006 Wiley‐Liss, Inc.