bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immune response against Streptococcus gallolyticus in patients with adenomatous polyps in colon
Authors: Garza‐González Elvira , Ríos Merab , Bosques‐Padilla Francisco J. , Francois Fritz , Cho Ilseung , González Gloria M. , Pérez‐Pérez Guillermo I. 
Published: February 2012

AbstractOur aim was to examine the humoral immune response against Streptococcus gallolyticus subspecies gallolyticus antigens in individuals subjected to a routine colonoscopy in which colon adenomatous polyps were present or not. Serum samples from 133 individuals with adenomatous polyps and serum samples from 53 individuals with a normal colonoscopy were included. Western blot was performed in all subjects using a whole cell antigen from S. gallolyticus ATCC 9809, and rabbit antisera against the whole cell bacteria was prepared as a control. By analyzing the immune profile of the rabbit‐immunized sera by Western‐blot, at least 22 proteins were identified as immunogenic in S. gallolyticus. When we evaluated sera from human subjects, two proteins of approximately 30 and 22 kDa were most prominent. Based on this 2‐protein band pattern, Western‐blot profiles from human subjects were compared. The detection of a protein band of 22 kDa was associated with the presence of adenomatous polyps in colon [odds ratios (OR) 7.98, 95% confidence intervals (CI): 3.54–17.93], p < 0.001. When the presence of the 30 kDa protein alone or both the 22 and 30 kDa proteins were analyzed, the OR increased to 22.37 (95% CI: 3.77–131.64), p < 0.001. The specificity was 84.9 for the presence of the 22 kDa protein, and 98.1 for the presence of the 30 kDa protein alone or both 22 and 30 kDa bands. Serum from individuals with adenomatous polyps recognized two proteins from S. gallolyticus. This result confirmed the possible association of S. gallolyticus with adenomatous polyps in the colon.
p38α MAPK mediates 17β‐estradiol inhibition of MMP‐2 and ‐9 expression and cell migration in human lovo colon cancer cells
Authors: Hsu Hsi‐Hsien , Liu Chung‐Jung , Shen Chia‐Yao , Chen Yi‐Jyun , Chen Li‐Mien , Kuo Wu‐Hsien , Lin Yueh‐Min , Chen Ray‐Jade , Tsai Chang‐Hai , Tsai Fuu‐Jen , Huang Chih‐Yang 
Published: February 2012

AbstractEpidemiological studies demonstrate that the incidence and mortality rates of colorectal cancer in women are lower than in men. However, it is unknown if 17β‐estradiol (E2) treatment is sufficient to inhibit cell proliferation and cell migration in human colon cancer cells. Up‐regulation of urokinase plasminogen activator (uPA), tissue plasminogen activator (tPA), and matrix metallopeptidases (MMPs) is reported to associate with the development of cancer cell mobility, metastasis, and subsequent malignant tumor. In the present study, we treated human LoVo colon cancer cells with E2 to explore whether E2 down‐regulates cell proliferation and migration, and to identify the precise molecular and cellular mechanisms behind the down‐regulatory responses. Here, we found that E2 treatment decreased cell proliferation and cell cycle‐regulating factors such as cyclin A, cyclin D1 and cyclin E. At the same time, E2 significantly inhibited cell migration and migration‐related factors such as uPA, tPA, MMP‐2, and MMP‐9. However, E2 treatment showed no effects on upregulating expression of plasminogen activator inhibitor‐1 (PAI‐1), tissue inhibitor of metalloproteinase‐1, ‐2, ‐3, and ‐4 (TIMP‐1, ‐2, ‐3, and ‐4). After administration of inhibitors including QNZ (NFκB inhibitor), LY294002 (Akt activation inhibitor), U0126 (ERK1/2 inhibitor), SB203580 (p38 MAPK inhibitor) or SP600125 (JNK1/2 inhibitor), E2‐downregulated cell migration and expression of MMP‐2 and MMP‐9 in LoVo cells is markedly inhibited only by p38 MAPK inhibitors, SB203580. Application of specific target gene siRNA (ERα, ERβ, p38α, and p38β) to LoVo cells further confirmed that p38 MAPK mediates E2/ERs inhibition of MMP‐2 and ‐9 expression and cell motility in LoVo cells.Collectively, these results suggest that E2 treatment down‐regulates cell proliferation by modulating the expression of cyclin A, cyclin D1 and cyclin E. E2 treatment simultaneously impaired cell migration by inhibiting the expression of uPA, tPA, MMP‐2, and MMP‐9 through E2/ERs − p38α MAPK signaling pathway in human LoVo colon cancer cells. J. Cell. Physiol. 227: 3648–3660, 2012. © 2012 Wiley Periodicals, Inc.
Trop‐2 inhibits prostate cancer cell adhesion to fibronectin through the β1 integrin‐RACK1 axis
Authors: Trerotola Marco , Li Jing , Alberti Saverio , Languino Lucia R. 
Published: February 2012

AbstractTrop‐2 is a transmembrane glycoprotein upregulated in several human carcinomas, including prostate cancer (PrCa). Trop‐2 has been suggested to regulate cell–cell adhesion, given its high homology with the other member of the Trop family, Trop‐1/EpCAM, and its ability to bind the tight junction proteins claudin‐1 and claudin‐7. However, a role for Trop‐2 in cell adhesion to the extracellular matrix has never been postulated. Here, we show for the first time that Trop‐2 expression in PrCa cells correlates with their aggressiveness. Using either shRNA‐mediated silencing of Trop‐2 in cells that endogenously express it, or ectopic expression of Trop‐2 in cells that do not express it, we show that Trop‐2 inhibits PrCa cell adhesion to fibronectin (FN). In contrast, expression of another transmembrane receptor, αvβ5 integrin, does not affect cell adhesion to this ligand. We find that Trop‐2 does not modulate either protein or activation levels of the prominent FN receptors, β1 integrins, but acts through increasing β1 association with the adaptor molecule RACK1 and redistribution of RACK1 to the cell membrane. As a result of Trop‐2 expression, we also observe activation of Src and FAK, known to occur upon β1‐RACK1 interaction. These enhanced Src and FAK activities are not mediated by changes in either the activity of IGF‐IR, which is known to bind RACK1, or IGF‐IR's ability to associate with β1 integrins. In summary, our data demonstrate that the transmembrane receptor Trop‐2 is a regulator of PrCa cell adhesion to FN through activation of the β1 integrin‐RACK1‐FAK‐Src signaling axis. J. Cell. Physiol. 227: 3670–3677, 2012. © 2012 Wiley Periodicals, Inc.
Role of fibroblast growth factor 2 and wnt signaling in anabolic effects of parathyroid hormone on bone formation
Authors: Fei Yurong , Hurley Marja M. 
Published: February 2012

AbstractOsteoporosis poses enormous health and economic burden worldwide. One of the very few anabolic agents for osteoporosis is parathyroid hormone (PTH). Although great progress has been made since the FDA approved PTH in 2002, the detailed mechanisms of the bone anabolic effects of intermittent PTH treatment is still not well understood. PTH bone anabolic effect is regulated by extracellular factors. Maximal bone anabolic effect of PTH requires fibroblast growth factor 2 (FGF2) signaling, which might be mediated by transcription factor activating transcription factor 4 (ATF4). Maximal bone anabolic effect of PTH also requires Wnt signaling. Particularly, Wnt antagonists such as sclerostin, dickkopf 1 (DKK1) and secreted frizzled related protein 1 (sFRP1) are promising targets to increase bone formation. Interestingly, FGF2 signaling modulates Wnt/β‐Catenin signaling pathway in bone. Therefore, multiple signaling pathways utilized by PTH are cross talking and working together to promote bone formation. Extensive studies on the mechanisms of action of PTH will help to identify new pathways that regulate bone formation, to improve available agents to stimulate bone formation, and to identify potential new anabolic agents for osteoporosis. J. Cell. Physiol. 227: 3539–3545, 2012. © 2012 Wiley Periodicals, Inc.
Nanog regulates molecules involved in stemness and cell cycle‐signaling pathway for maintenance of pluripotency of P19 embryonal carcinoma stem cells
Authors: Choi Seung‐Cheol , Choi Ji‐Hyun , Park Chi‐Yeon , Ahn Chul‐Min , Hong Soon‐Jun , Lim Do‐Sun 
Published: February 2012

AbstractTo identify potential downstream targets of Nanog, a key transcription factor in the maintenance of pluripotency of embryonic stem (ES) and embryonal carcinoma (EC) cells, global gene expression profiles in Nanog small interfering RNA (siRNA)‐transfected P19 EC stem cells were performed using cDNA, 60‐mer, and 30‐mer microarray platforms. The putative Nanog target genes identified by Nanog silencing were verified using reverse transcription‐polymerase chain reaction after Nanog overexpression. Downregulation of Nanog in P19 cells resulted in reduction of pluripotency markers, such as Fgf4, Klf2, Mtf2, Oct‐4, Rex1, Sox1, Yes, and Zfp143, whereas overexpression of Nanog in P19 cells reversely upregulated their expression. However, expressions of pluripotency markers Cripto, germ cell nuclear factor, Sox2, and Zfp57 as well as leukemia inhibitory factor (LIF)/Stat3 pathway molecules LIF, IL6st, and Stat3 were not affected after 48 h transfection with Nanog siRNA or construct. Nanog silencing also downregulated expression of molecules involved in the p53‐ and cell cycle‐signaling pathway (Atf3, Jdp2, Cul3, Hist1hic, and Bcl6), whereas expression of E2f1, Tob1, Lyn, and Smarcc1 was upregulated by Nanog silencing. Expressions of cyclins D1, D2, D3, and E1 as well as cyclin‐dependent kinase (Cdk) 1 and Cdk6 were downregulated by Nanog silencing in P19 cells, whereas Nanog overexpression reversely increased their expressions. Taken together, examination of global transcriptional changes after Nanog silencing followed by verification by Nanog overexpression has revealed new molecules involved in the maintenance of self‐renewal and in the regulation of the p53‐ and cell cycle‐pathway of P19 cells. J. Cell. Physiol. 227: 3678–3692, 2012. © 2012 Wiley Periodicals, Inc.
Facilitated diffusion of VEGF165 through descemet's membrane with sucrose octasulfate
Authors: Fannon Michael , Forsten‐Williams Kimberly , Zhao Bing , Bach Eva , Parekh Parag P. , Chu Chia Lin , Goerges‐Wildt Adrienne L , Buczek‐Thomas Jo Ann , Nugent Matthew A. 
Published: February 2012

AbstractVascular endothelial growth factor A (VEGF‐A) is a promoter of neovascularization and thus a popular therapeutic target for diseases involving excessive growth of blood vessels. In this study, we explored the potential of the disaccharide sucrose octasulfate (SOS) to alter VEGF165 diffusion through Descemet's membrane. Descemet's membranes were isolated from bovine eyes and used as a barrier between two chambers of a diffusion apparatus to measure VEGF transport. Diffusion studies revealed a dramatic increase in VEGF165 transport in the presence of SOS, with little diffusion of VEGF165 across the membrane over a 10‐h time course in the absence of SOS. Diffusion studies with VEGF121, a non‐heparin binding variant of VEGF, showed robust diffusion with or without SOS. To determine a possible mechanism, we measured the ability of SOS to inhibit VEGF interactions with extracellular matrix (ECM), using cell‐free and cell surface binding assays. Binding studies showed SOS had no effect on VEGF165 binding to either heparin‐coated plates or endothelial cell surfaces at less than mg/ml concentrations. In contrast, we show that SOS inhibited VEGF165 binding to fibronectin in a dose dependent manner and dramatically accelerated the rate of release of VEGF165 from fibronectin. SOS also inhibited the binding of VEGF165 to fibronectin‐rich ECM deposited by vascular smooth muscle cells. These results suggest that fibronectin‐rich extracellular matrices serve as barriers to VEGF165 diffusion by providing a network of binding sites that can trap and sequester the protein. Since the content of Descemet's membrane is typical of many basement membranes it is possible that they serve throughout the body as formidable barriers to VEGF165 diffusion and tightly regulate its bioavailability and distribution within tissues. J. Cell. Physiol. 227: 3693–3700, 2012. © 2012 Wiley Periodicals, Inc.
Recapitulation of mesenchymal condensation enhances in vitro chondrogenesis of human mesenchymal stem cells
Authors: Ghone Nalinkanth V. , Grayson Warren L. 
Published: February 2012

AbstractMesenchymal condensation is a critical transitional stage that precedes cartilage formation during embryonic development. We hypothesized that “priming” hMSCs to recapitulate mesenchymal condensation events prior to inducing differentiation would enhance their subsequent chondrogenic properties. Our prior studies have suggested that exposing hMSCs to hypoxia (2% O2) induces condensation‐like effects. We therefore assessed the effect of preconditioning for different time periods on the expression of condensation specific genes by growing hMSCs in expansion medium under different normoxic (20% O2) and hypoxic conditions for up to 2 weeks, and subsequently induced chondrogenesis of preconditioned hMSCs. The total cultivation time for each group was 4 weeks and the chondrogenic properties were assessed using gene expression, biochemical analysis, and histological staining. Our results demonstrated the benefits of preconditioning were both time‐ and oxygen‐dependent. Condensation specific genes, SOX‐9 and NCAM, were significantly up‐regulated in hypoxic conditions at the end of 1 week. COL X and MMP13 expression was also lower than the normoxic samples at this time point. However, this group did not exhibit more efficient chondrogenesis after 4 weeks. Instead, hMSCs preconditioned for 1 week and subsequently differentiated, both under 20% O2, resulted in the most efficient chondrogenesis. Interestingly, while hypoxia appears to positively enhance expression of chondrogenic genes, this did not produce an enhanced matrix accumulation. The results of this study emphasize the significance of considering the timing of specific cues in developing protocols for stem cell‐based therapies and underscore the complexity in regulating stem cell differentiation and tissue formation. J. Cell. Physiol. 227: 3701–3708, 2012. © 2012 Wiley Periodicals, Inc.
Non‐classical membrane trafficking processes galore
Authors: Chua Christelle En Lin , Lim Yi Shan , Lee Min Goo , Tang Bor Luen 
Published: February 2012

AbstractDogmatic views of how proteins and other cellular components may traffic within and between eukaryotic cells have been challenged in the past few years. Beyond the classical secretory/exocytic pathway and its established players, other pathways of cell surface membrane transport, generally termed “unconventional secretion,” are now better understood. More insights have also been gleaned on the roles of secreted or shedding microvesicles, either exosomal or ectosomal in origin, in unconventional secretion. Recent works have also revealed key molecular components, particularly the Golgi reassembly stacking protein (GRASP), and the importance of stress‐induced autophagy, in unconventional exocytic transport. This GRASP and autophagy‐dependent (GAD) mode appears to underlie the unconventional exocytosis of many soluble and membrane cargoes. Likewise, recent findings have revealed transport processes that contrast the classically known mitochondria import, namely vesicular transport from the mitochondria to peroxisomes and lysosomes. Mitochondria‐peroxisomal targeting of mitochondria‐derived vesicles appears to involve the retromer complex, which was classically associated with endosome‐Golgi membrane traffic. The routes of intracellular membrane transport and communications between eukaryotic organelles now appear far more complex that one would have imagined 10 years ago. J. Cell. Physiol. 227: 3722–3730, 2012. © 2012 Wiley Periodicals, Inc.
Role of FGFs/FGFRs in skeletal development and bone regeneration
Authors: Du Xiaolan , Xie Yangli , Xian Cory J. , Chen Lin 
Published: February 2012

AbstractFibroblast growth factor (FGF)/FGF (FGFR) signaling is an important pathway involved in skeletal development. Missense mutations in FGFs and FGFRs were found clinically to cause multiple congenital skeleton diseases including chondrodysplasia, craniosynostosis, syndromes with dysregulated phosphate metabolism. FGFs/FGFRs also have crucial roles in bone fracture repair and bone regeneration. Understanding the molecular mechanisms for the role of FGFs/FGFRs in the regulation of skeletal development, genetic skeletal diseases, and fracture healing will ultimately lead to better treatment of skeleton diseases caused by mutations of FGFs/FGFRs and fracture. This review summarizes the major findings on the role of FGF signaling in skeletal development, genetic skeletal diseases and bone healing, and discusses issues that remain to be resolved in applying FGF signaling‐related measures to promote bone healing. This review has also provided a perspective view on future work for exploring the roles and action mechanisms of FGF signaling in skeletal development, genetic skeletal diseases, and fracture healing. J. Cell. Physiol. 227: 3731–3743, 2012. © 2012 Wiley Periodicals, Inc.
Patient experiences of transitioning from hospital to home: An ethnographic quality improvement project
Authors: Cain Carol H. , Neuwirth Estee , Bellows Jim , Zuber Christi , Green Jennifer 
Published: February 2012

AbstractBACKGROUND:Little is known about patient perspectives of the transition from hospital to home.OBJECTIVE:To develop a richly detailed, patient‐centered view of patient and caregiver needs in the hospital‐to‐home transition.DESIGN:An ethnographic approach including participant observation and in‐depth, semi‐structured video recorded interviews.SETTING:Kaiser Permanente's Southern California, Colorado, and Hawaii regions.PATIENTS:Twenty‐four adult inpatients hospitalized for a range of acute and chronic conditions and characterized by variety in diagnoses, illness severity, planned or unplanned hospitalization, age, and ability to self manage.RESULTS:During the hospital‐to‐home transition, patients and caregivers expressed or demonstrated experiences in 6 domains: 1) translating knowledge into safe, health‐promoting actions at home; 2) inclusion of caregivers at every step of the transition process; 3) having readily available problem‐solving resources; 4) feeling connected to and trusting providers; 5) transitioning from illness‐defined experience to “normal” life; and 6) anticipating needs after discharge and making arrangements to meet them. The work of transitioning occurs for patients and caregivers in the hours and days after they return home and is fraught with challenges.CONCLUSIONS:Reducing readmissions will remain challenging without a broadened understanding of the types of support and coaching patients need after discharge. We are piloting strategies such as risk stratification and tailoring of care, a specialized phone number for recently discharged patients, standardized same‐day discharge summaries to primary care providers, medication reconciliation, follow‐up phone calls, and scheduling appointments before discharge. Journal of Hospital Medicine 2012; © 2012 Society of Hospital Medicine
Understanding organizational diversity management programs: A theoretical framework and directions for future research
Authors: Olsen Jesse E. , Martins Luis L. 
Published: February 2012

SummaryWith the changing demographic composition of the workforce, managing diversity in organizations is an important organizational function. Organizations have employed varying approaches to diversity management (DM), resulting in varying organizational outcomes. Meanwhile, researchers have called for more theoretical development within the DM area. We present a framework rooted in social and cross‐cultural psychological research, to foster theory development and empirical testing in the area of DM. We also derive several propositions to guide future research on DM and note some boundary conditions that suggest research opportunities of their own. Our framework contributes a theoretical conceptualization that enhances our understanding of organizations' DM efforts, integrates current typologies, and suggests new directions of inquiry for management scholars as well as guidelines for practitioners in the area. Copyright © 2012 John Wiley & Sons, Ltd.
Evaluation of Akt/mTOR activity in muscle atrophy after rotator cuff tears in a rat model
Authors: Liu Xuhui , Joshi Sunil K. , Samagh Sanjum P. , Dang Yu‐Xuan , Laron Dominique , Lovett David H. , Bodine Sue C. , Kim Hubert T. , Feeley Brian T. 
Published: February 2012

AbstractAtrophy of the rotator cuff muscles is a factor that complicates the treatment of a massive rotator cuff tear (RCT). However, the molecular mechanisms that govern the development of muscle atrophy after RCTs have not been well defined. The Akt/mammalian target of rapamycin (mTOR) signaling pathway plays a central role in maintaining muscle mass in response to mechanical loading. The role of this pathway in the development of muscle atrophy after a massive RCT remains unknown. The purpose of this study was to investigate the regulation of the Akt/mTOR pathway in the development of muscle atrophy after a RCT and suprascapular nerve (SSN) injury. We evaluated the activity of the Akt/mTOR signaling pathway and how this pathway interacts with two atrophy‐related genes, MuRF‐1 and MAFbx, in supraspinatus muscles of rats that underwent unilateral complete rotator cuff tendon transection or SSN transection. Akt/mTOR activity was significantly reduced after tendon rupture, but increased after nerve injury. MuRF‐1 and MAFbx were only up‐regulated following denervation. These results suggest that tendon transection leads to a decrease in protein synthesis with down‐regulation of the Akt/mTOR signaling pathway, whereas denervation leads to an increase in protein degradation via up‐regulation of expression of MuRF‐1 and MAFbx. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 30:1440–1446, 2012
Crystallization of Poly(L‐/D‐Lactide) in the Presence of Electric Fields
Authors: Yuryev Yury , Wood‐Adams Paula M. 
Published: February 2012

AbstractWe report, for the first time, an enhancement in melt crystallization kinetics of poly(L‐/D‐lactide) (a type‐A1 polymer) in the presence of static electric fields as observed through measurement of the complex viscosity. Static electric fields of varying intensity (0–2.4 × 105 V m−1) are applied directly to the crystallizing polylactide melt at five different temperatures. The crystallization rate enhancement increases both with crystallization temperature and applied electric field intensity. An XRD analysis and optical microscopy studies allows us to attribute this to increased nucleation in the presence of an electric field. A technique allowing for the estimation of the rate of homogeneous nucleation induced by the electric field is developed.
Complexation of Tetraphenylthiophene‐Derived Ammonium Chloride to Poly(sodium vinylsulfonate) Polyelectrolytes: Aggregation‐Induced Emission Enhancement and Long‐Range Interaction
Authors: Chien Rong‐Hong , Lai Chung‐Tin , Hong Jin‐Long 
Published: February 2012

AbstractFluorescent tetraphenylthiophene (TP)‐derived ammonium cations TP‐NH3+ are synthesized and reacted with poly(sodium vinylsulfonate) (PSV) polyanions to obtain three PSV‐TP(x/y) (x/y = 4/1, 2/1 and 1/1) complexes with long‐range electrostatic interactions (LEI) and novel aggregation‐induced emission enhancement (AIEE) properties. Introduction of water into a dilute solution of PSV‐TP(x/y) in THF results in self‐aggregated particles with enhanced AIEE‐operative emission. PSV or NaCl electrolyte is applied to control the LEI forces stabilizing the aggregated particles, and the AIEE‐operative emissions can be thus manupulated. Due to the strong LEI forces, the solid PSV‐TP(4/1) has a high FL quantum yield of 0.91. The relationship between AIEE and LEI forces is evaluated.