bluuebunny/crossref_metadata_2025_split huggingface dataset:
Seeing old friends from a different angle: Novel properties of hematopoietic growth factors in the healthy and diseased brain
Authors: Diederich Kai , Schäbitz Wolf‐Rüdiger , Minnerup Jens 
Published: December 2010

AbstractHematopoietic growth factors are known for their bolstering effects on the growth, survival, and differentiation of blood progenitor cells. Several of these cytokines also influence the proliferation of neural stem/progenitor cells, paralleling cellular mechanisms in analogy to their function in the hematopoietic system. Erythropoietin (EPO), granulocyte‐colony stimulating factor (G‐CSF), thrombopoietin (TPO), and their respective receptors are all expressed in the hippocampus of the mammalian brain. Recent studies have confirmed EPO and G‐CSF as vital neurotrophic and neuroprotective factors, and ascertained their role in neuroprotection and neuroregeneration as pertaining to the most prominent neurodegenerative diseases. The aims of this review are to discuss newly discovered properties of G‐CSF, EPO, and TPO beyond their known functions in the hematopoietic system, to create an overview of the accumulating data on the role of these factors in hippocampal function, and to highlight any potential clinical implications. © 2010 Wiley Periodicals, Inc.
Calpain‐1 expression is associated with relapse‐free survival in breast cancer patients treated with trastuzumab following adjuvant chemotherapy
Authors: Storr Sarah J. , Woolston Caroline M. , Barros Fabricio F.T. , Green Andrew R. , Shehata Mohamed , Chan Stephen Y. , Ellis Ian O. , Martin Stewart G. 
Published: December 2010

AbstractThe calpain family, and their endogenous inhibitor calpastatin, has been implicated in cancer progression, and recent in vitro data have indicated a role in trastuzumab resistance. The aims of our study were to examine expression levels of calpastatin, calpain‐1 and calpain‐2 in breast tumours from patients treated with trastuzumab following adjuvant chemotherapy to determine their potential as biomarkers to predict therapeutic response. The expression of calpastatin, calpain‐1 and calpain‐2 was determined, using immunohistochemistry (IHC), in tumours from a series of 93 patients with primary breast cancer treated with surgery and adjuvant chemotherapy with or without trastuzumab followed by trastuzumab to complete 1 year of therapy. IHC was performed using tissue microarrays constructed from cores taken from intratumour and peripheral tumour areas. Expression was correlated with clinicopathologic variables and patient outcome. Calpastatin expression was correlated with Nottingham prognostic index (p = 0.003) and lymph node status (p = 0.007). Trastuzumab resistance was defined as disease relapse during therapy. Calpain‐1 expression is associated with relapse‐free survival (p = 0.001) and remained significant in multivariate analysis accounting for confounding pathological and treatment variables (hazard ratio 4.60, 95% confidence interval 1.05–20.25; p = 0.043). Calpain‐1 may be a useful biomarker to predict relapse‐free survival in breast cancer patients treated with adjuvant trastuzumab and chemotherapy. A larger verification study is warranted.
Sequential Processes in Palladium‐Catalyzed Silicon‐Based Cross‐Coupling
Authors: Denmark Scott E. , Liu Jack Hung‐Chang 
Published: December 2010

AbstractAlthough developed somewhat later, silicon‐based cross‐coupling has become a viable alternative to the more conventional Suzuki–Miyaura, Stille–Kosugi–Migita, and Negishi cross‐coupling reactions because of its broad substrate scope, high stability of silicon‐containing reagents, and low toxicity of waste streams. An empowering and yet underappreciated feature unique to silicon‐based cross‐coupling is the wide range of sequential processes available. In these processes, simple precursors are first converted to complex silicon‐containing cross‐coupling substrates, and the subsequent silicon‐based cross‐coupling reaction affords an even more highly functionalized product in a stereoselective fashion. In so doing, structurally simple and inexpensive starting materials are quickly transformed into value‐added and densely substituted products. Therefore, sequential processes are often useful in constructing the carbon backbones of natural products. In this review, studies of sequential processes involving silicon‐based cross‐coupling are discussed. Additionally, the total syntheses that utilize these sequential processes are also presented.
Determination of fentanyl, metabolite and analogs in urine by GC/MS
Authors: Strano‐Rossi Sabina , Álvarez Iván , Tabernero María Jesús , Cabarcos Pamela , Fernández Purificación , Bermejo Ana María 
Published: December 2010

AbstractA rapid and sensitive method for the simultaneous determination of alfentanyl, sufentanyl and fentanyl (and its major metabolite norfentanyl) in urine was developed and validated. The method involved a liquid–liquid extraction in alkaline conditions, derivatization with pentafluoropropionic anhydride to improve the sensitivity for norfentanyl and subsequent analysis in GC/MS. The LODs are 0.08 ng ml−1 for all substances (0.04 ng ml−1 for alfentanyl). Intra‐ and inter‐day precision coefficient of variation was always below 15%; mean relative error (accuracy) was always below 15%. The method was linear for all analytes, with quadratic regression of calibration curves always higher than 0.99. The method was applied to real samples of subjects who had received therapeutic doses of fentanyl, showing its suitability for the determination of low levels of these substances. The method was also applied to a subject whose death was attributed to fentanyl overdose. Copyright © 2010 John Wiley & Sons, Ltd.
Genotoxic effects of (−)‐cubebin in somatic cells of mice
Authors: Maistro Edson Luis , Marcondes Natel André Vinicius , de Souza Gustavo Henrique Bianco , Perazzo Fábio Ferreira 
Published: December 2010

Abstract(−)‐Cubebin belongs to the dibenzylbutyrolactone lignan group, which is widely distributed in the plant kingdom. Because this compound shows interesting biological activities, it is extremely important to evaluate its possible genotoxic activity to allow its safe use in humans. Thus, the present study was performed to investigate the genotoxicity potential activity of (−)‐cubebin assessed by two assays: micronucleus in bone marrow cells and comet test in peripheral blood leukocytes of Swiss mice. In the (−)‐cubebin dose range‐finding assays, the maximum tolerated dose was greater than 2000 mg kg−1. The compound was administered by an oral route at single doses of 250, 500 and 2000 mg kg−1 body weight. Cytotoxicity was assessed by scoring 200 consecutive total polychromatic (PCE) and normochromatic (NCE) erythrocytes (PCE/NCE ratio). Under our experimental conditions, micronucleus and comet assays, respectively, showed that (−)‐cubebin caused dose‐related clastogenic and genotoxic effects in the somatic cells investigated. PCE/NCE ratio showed no cytotoxicity for the three doses of the compound. The data suggest caution in the ingestion of (−)‐cubebin by humans, especially at high doses. Copyright © 2010 John Wiley & Sons, Ltd.
Adenylate cyclase and calmodulin-dependent kinase have opposite effects on osteoclastogenesis by regulating the PKA-NFATc1 pathway
Authors: Yoon Soo-Hyun , Ryu Ji yoon , Lee Youngkyun , Lee Zang Hee , Kim Hong-Hee 
Published: December 2010

Abstract
Nuclear factor of activated T cells c1 (NFATc1) is a transcription factor crucial for the differentiation of osteoclasts. In this study we discovered new signaling pathways involving cAMP regulators that modulate NFATc1 during osteoclastogenesis. The osteoclast differentiation factor receptor activator of NF-κB ligand (RANKL) increased the expression of adenylate cyclase 3 (AC3), accompanied by a rise in the intracellular cAMP level in osteoclasts. The knockdown of AC3 enhanced in vitro osteoclastogenesis and in vivo bone resorption, whereas cAMP-elevating agents showed opposite effects. The antiosteoclastogenic effect of the AC3-cAMP pathway was mediated by the inhibition of NFATc1 nuclear translocation and its autoamplification via a protein kinase A (PKA)–dependent mechanism. RANKL has been shown to activate Ca2+/calmodulin-dependent protein kinases (CaMKs). Knockdown or catalytic inhibition of CaMKs elevated intracellular cAMP levels in RANKL-treated osteoclast precursors and suppressed the activation of NFATc1. Taken together, our results demonstrate a pivotal role for the cAMP-PKA-NFATc1 signaling pathway during osteoclast differentiation, suggesting a mechanism by which osteoclastogenesis is fine-tuned by a balance between AC3 and CaMKs activities. © 2011 American Society for Bone and Mineral Research.
Control of RUNX3 by histone methyltransferases
Authors: Lee You Mie 
Published: December 2010

AbstractRunt‐related (RUNX) family proteins function as context‐dependent transcription factors during developmental processes such as hematopoiesis, neurogenesis, and osteogenesis. RUNX3 is involved in a variety of physiological processes including neurogenesis, thymopoiesis, and dendritic cell maturation. A large amount of information indicates that RUNX3 may be a tumor suppressor. Recent data suggest that the molecular mechanism responsible for RUNX3 deficiency in numerous cancers is a primarily epigenetic silencing. The present review focuses on the regulation of RUNX3 gene expression by histone modification, emphasizing histone methylation at the RUNX3 promoter and inactivation of protein itself. Inactivation of the promoter and protein can be the results of various chemical modifications, including methylation by histone methyltransferase. Inactivation of RUNX3 may contribute to the tumor initiation, progression and pathogenesis in specific microenvironmental contexts. Finally, this review describes the reactivation of RUNX3 by epigenetic regulatory agents. J. Cell. Biochem. 112: 394–400, 2011. © 2010 Wiley‐Liss, Inc.
Associations of saposin C, Src, and androgen receptor upregulate the expression and function of androgen receptor in human prostate cancer cells
Authors: Ding Yan , Wang Xiaoling , Xu Aihui , Xu Xia , Tian Keli , Young Charles Y.F. , Yuan Huiqing 
Published: December 2010

AbstractWe previously demonstrated that ectopic expression of neurotrophic peptide (NP) derived from saposin C promotes androgen receptor (AR) expression and transactivation in human prostate cancer cells. This prompted us to investigate how NP or saposin C can function in cells. We constructed plasmids expressing saposin C or a chimeric peptide of a viral TAT transduction domain and saposin C (TAT‐saposin C) with His‐tag. Intracellular localization of saposin C and NP was predominantly shown in transfected cells, while TAT‐saposin C was detected around membrane and in cytosol by immunofluorescence staining. Furthermore, induction of the AR expression and activation of the AR transcriptional function were observed in cells transfected with saposin C or TAT‐saposin C, compared to control cells transfected with an empty plasmid. The effects of saposin C and TAT‐saposin C on AR activity were examined in the presence of inhibitors of GPCR, MAPK1/2, and PI3K/Akt. Interestingly, we found that these inhibitors only affect AR activities in cells with TAT‐saposin C expression but not with saposin C expression. Immunostaining images showed that co‐localization of saposin C, Src, and the AR occurred in transfected cells. Physical interactions of saposin C/NP, Src, and the AR were then demonstrated by co‐immunoprecipitation assays. Blockage of Src activity by specific inhibitor led to a decrease in the saposin C‐mediated enhancement of AR transactivity, suggesting that intracellular expression of saposin C caused stimulation of AR expression and activity by associations with Src in LNCaP cells. This effect may not be mediated by GPCR. J. Cell. Biochem. 112: 818–828, 2011. © 2010 Wiley‐Liss, Inc.
Coping Style
Authors: Beutler Larry E. , Harwood T. Mark , Kimpara Satoko , Verdirame David , Blau Kathy 
Published: December 2010

AbstractThe fit of patient coping style and psychotherapy focus has been suggested as improving treatment outcome. This article reviews the definitions, measures, and previous research surrounding this hypothesis. An original meta‐analysis of 12 carefully selected studies (N = 1,291 patients) resulted in a weighted, mean effect size (d) of .55 in favor of a fit between externalizing patients and symptom‐focused treatment or, alternatively, internalizing patients and insight‐focused treatment. This medium‐size effect indicates that nondiagnostic patient factors, like coping style, are important considerations in the selection of effective therapies. Clinical examples and clinical recommendations are provided. © 2010 Wiley Periodicals, Inc. J Clin Psychol: In Session 67:176–183, 2011.
An approximation to the temporal order in endogenous circadian rhythms of genes implicated in human adipose tissue metabolism
Authors: Garaulet Marta , Ordovás José M. , Gómez‐Abellán Purificación , Martínez Jose A. , Madrid Juan A. 
Published: December 2010

AbstractAlthough it is well established that human adipose tissue (AT) shows circadian rhythmicity, published studies have been discussed as if tissues or systems showed only one or few circadian rhythms at a time. To provide an overall view of the internal temporal order of circadian rhythms in human AT including genes implicated in metabolic processes such as energy intake and expenditure, insulin resistance, adipocyte differentiation, dyslipidemia, and body fat distribution. Visceral and subcutaneous abdominal AT biopsies (n = 6) were obtained from morbid obese women (BMI ≥ 40 kg/m2). To investigate rhythmic expression pattern, AT explants were cultured during 24‐h and gene expression was analyzed at the following times: 08:00, 14:00, 20:00, 02:00 h using quantitative real‐time PCR. Clock genes, glucocorticoid metabolism‐related genes, leptin, adiponectin and their receptors were studied. Significant differences were found both in achrophases and relative‐amplitude among genes (P < 0.05). Amplitude of most genes rhythms was high (>30%). When interpreting the phase map of gene expression in both depots, data indicated that circadian rhythmicity of the genes studied followed a predictable physiological pattern, particularly for subcutaneous AT. Interesting are the relationships between adiponectin, leptin, and glucocorticoid metabolism‐related genes circadian profiles. Their metabolic significance is discussed. Visceral AT behaved in a different way than subcutaneous for most of the genes studied. For every gene, protein mRNA levels fluctuated during the day in synchrony with its receptors. We have provided an overall view of the internal temporal order of circadian rhythms in human adipose tissue. J. Cell. Physiol. 226: 2075–2080, 2011. © 2010 Wiley‐Liss, Inc.
BRG1 mutations found in human cancer cell lines inactivate Rb‐mediated cell‐cycle arrest
Authors: Bartlett Christopher , Orvis Tess J. , Rosson Gary S. , Weissman Bernard E. 
Published: December 2010

AbstractEukaryotic organisms package DNA into chromatin for compact storage in the cell nucleus. However, this process promotes transcriptional repression of genes. To overcome the transcriptional repression, chromatin remodeling complexes have evolved that alter the configuration of chromatin packaging of DNA into nucleosomes by histones. The SWI/SNF chromatin remodeling complex uses energy from ATP hydrolysis to reposition nucleosomes and make DNA accessible to transcription factors. Recent studies showing mutations of BRG1, one of two mutually exclusive ATPase subunits, in human tumor cell lines and primary tissue samples have implicated a role for its loss in cancer development. While most of the mutations lead to complete loss of BRG1 protein expression, others result in single amino acid substitutions. To better understand the role of these BRG1 point mutations in cancer development, we characterized SWI/SNF function in human tumor cell lines with these mutations in the absence of BRM expression, the other ATPase component. We found that the mutant BRG1 proteins still interacted with the core complex members and appeared at the promoters of target genes. However, while these mutations did not affect CD44 and CDH1 expression, known targets of the SWI/SNF complex, they did abrogate Rb‐mediated cell‐cycle arrest. Therefore, our results implicate that these mutations disrupt the de novo chromatin remodeling activity of the complex without affecting the status of existing nucleosome positioning. J. Cell. Physiol. 226: 1989–1997, 2011. © 2010 Wiley‐Liss, Inc.
In vivo biodistribution of stem cells using molecular nuclear medicine imaging
Authors: Welling Mick M. , Duijvestein Marjolijn , Signore Alberto , van der Weerd Louise 
Published: December 2010

AbstractStudies on stem cell are rapidly developing since these cells have great therapeutic potential for numerous diseases and has generated much promise as well as confusion due to contradictory results. Major questions in this research field have been raised as to how and in which numbers stem cells home to target tissues after administration, whether the cells engraft and differentiate, and what their long‐term fate is. To answer these questions, reliable in vivo tracking techniques are essential. In vivo molecular imaging techniques using magnetic resonance imaging, bioluminescence, and scintigraphy have been applied for this purpose in experimental studies. The aim of this review is to discuss various radiolabeling techniques for early stem cell tracking, the need for validation of viability and performance of the cells after labeling, and the routes of administration in experimental animal models. In addition, we evaluate current problems and directions related to stem cell tracking using radiolabels, including a possible role for their clinical implementation. J. Cell. Physiol. 226: 1444–1452, 2011. © 2010 Wiley‐Liss, Inc.
Modulation of intracellular glutathione affects adipogenesis in 3T3‐L1 cells
Authors: Vigilanza Paola , Aquilano Katia , Baldelli Sara , Rotilio Giuseppe , Ciriolo Maria Rosa 
Published: December 2010

AbstractImpairment of redox homeostasis has been extensively associated with obesity, as a consequence of the chronic inflammatory state present in overweight subjects. Deregulation of glutathione (GSH), the most important non‐enzymatic intracellular anti‐oxidant, induces insulin resistance in mature adipocytes, but data are lacking about its effects on adipogenesis. In this report we demonstrate that during adipogenesis of 3T3‐L1 cells the GSH/GSSG ratio decreases, shifting redox status towards oxidizing conditions. Moreover, we demonstrate that inhibition of GSH synthesis, obtained by treatment with L‐buthionine‐sulfoximine (BSO), enhances C/EBPβ LAP/LIP ratio and PPARγ expression during mitotic clonal expansion (MCE) stimulating adipogenesis. On the contrary, GSH ethyl ester (GSHest) supplementation completely abrogates this process also in the presence of BSO. GSH decrement during the first 24 h of adipogenesis is sufficient to induce higher triglyceride accumulation in differentiated adipocytes with respect to control, whereas GSHest treatment inhibits lipid droplets formation. We further demonstrate that Resveratrol (RV) could exert anti‐adipogenic properties also by increasing GSH content through γ‐glutamyl‐cysteine ligase (GCL) induction. Overall data indicate that in pre‐adipocytes the decrease of GSH accelerates adipogenesis, suggesting that the use of agents able to maintain GSH redox status in adipose tissue, such as RV, could be promising in stopping the lipogenic loop of obesity. J. Cell. Physiol. 226: 2016–2024, 2011. © 2010 Wiley‐Liss, Inc.
Association between adherens junctions and tight junctions via rap1 promotes barrier protective effects of oxidized phospholipids
Authors: Birukova Anna A. , Zebda Noureddine , Fu Panfeng , Poroyko Valery , Cokic Ivan , Birukov Konstantin G. 
Published: December 2010

AbstractPrevious studies showed that cyclopenthenone‐containing products resulting from oxidation of a natural phospholipid, 1‐palmitoyl‐2‐arachidonoyl‐sn‐glycero‐3‐phosphorylcholine (OxPAPC) exhibit potent barrier‐protective effects in the in vitro and in vivo models of lung endothelial cell (EC) barrier dysfunction, and these effects are associated with enhancement of peripheral actin cytoskeleton, cell–cell and cell–substrate contacts driven by activation of Rac and Cdc42 GTPases. Rap1 GTPase is another member of small GTPase family involved in control of cell–cell interactions; however, its involvement in EC barrier‐protective effects by OxPAPC remains unknown. This study examined a role of Rap1 in regulation of OxPAPC‐induced interactions in adherens junctions (AJ) and tight junctions (TJ) as a novel mechanism of EC barrier preservation in vitro and in vivo. Immunofluorescence analysis, subcellular fractionation, and co‐immunoprecipitation assays indicate that OxPAPC promoted accumulation of AJ proteins: VE‐cadherin, p120‐catenin, and β‐catenin; and TJ proteins: ZO‐1, occludin, and JAM‐A in the cell membrane, and induced novel cross‐interactions between AJ and TJ protein complexes, that were dependent on OxPAPC‐induced Rap1 activation. Inhibition of Rap1 function suppressed OxPAPC‐mediated pulmonary EC barrier enhancement and AJ and TJ interactions in vitro, as well as inhibited protective effects of OxPAPC against ventilator‐induced lung injury in vivo. These results show for the first time a role of Rap1‐mediated association between adherens junctions and tight junction complexes in the OxPAPC‐induced pulmonary vascular EC barrier protection. J. Cell. Physiol. 226: 2052–2062, 2011. © 2010 Wiley‐Liss, Inc.
Continuous cyclic mechanical tension inhibited Runx2 expression in mesenchymal stem cells through RhoA‐ERK1/2 pathway
Authors: Shi Yu , Li Huiwu , Zhang Xiaoling , Fu Yujie , Huang Yan , Lui Pauline Po Yee , Tang Tingting , Dai Kerong 
Published: December 2010

AbstractTensile load is known to regulate the osteogenesis of mesenchymal stem cells (MSCs) and osteogenic progenitors; therefore it is widely used in clinical treatment and tissue engineering. Meanwhile, in vitro, both published studies and our lab data demonstrate that the application of intermittent tensile loading which stimulates cells several minutes or hours each day for several days has promoted the osteogenic differentiation of MSCs. Whereas, for clinic trails, it is important to know accurately how and how long mechanical tension should be applied. Hence, it is necessary to investigate different kinds of mechanical tension on osteogenesis of MSCs. Until now, during the osteogenesis, there has been no research on the effect of continuous cyclic mechanical tension (CCMT) which provides continuous stimulation throughout the study period. We firstly figure out CCMT inhibiting the expression of osteogenic genes such as key transcription factor Runx2. It is known that RhoA regulates cell differentiation in response to mechanical stimuli. MAPK signaling acts as a downstream effector of RhoA. So, we ask in MSCs, if CCMT regulates the osteogenic master gene Runx2 through RhoA‐ERK1/2 pathway. And then, we find out there is a decrease in RhoA activity after CCMT stimulation. Pre‐treatment of CCMT‐loaded MSCs with LPA, a RhoA activator, restores ALP activity and significantly rescues Runx2 expression, while pre‐treatment with C3 toxin, a RhoA inhibitor, further decreases the activity of ALP and down‐regulates the expression of Runx2. Following results indicate that the inhibition of Runx2 expression after CCMT stimulation is mediated by RhoA‐ERK1/2 pathway. J. Cell. Physiol. 226: 2159–2169, 2011. © 2010 Wiley‐Liss, Inc.