bluuebunny/crossref_metadata_2025_split huggingface dataset:
Perceptual characteristics of tracheoesophageal speech production using the new indwelling Provox Vega voice prosthesis: A randomized controlled crossover trial
Authors: Ward Elizabeth C. , Hancock Kelli , Lawson Nadine , van As–Brooks Corina J. 
Published: April 2010

AbstractBackground.The objective of this study was to determine if the design enhancements incorporated into the new Provox Vega Indwelling Voice prostheses result in any positive benefits in vivo.Methods.Using a randomized, crossover study design, 31 participants using tracheoesophageal speech postlaryngectomy completed a 3‐week trial of the Provox Vega and a comparator device. Main outcome measures included patient perceptions of vocal effort and quality using each device, and perceptual judgments of voice quality produced.Results.The majority of patients (72%) indicated the Provox Vega gave them overall better voice quality and 52% felt they required less effort to phonate. Voice samples produced with the Provox Vega were also perceived by listeners to be significantly (p < .05) less strained, easier to understand, produced with less effort, and the better speech sample overall.Conclusion.Results support that the aerodynamic improvements incorporated in the design of the new Provox Vega facilitate enhanced voice and speech qualities. © 2010 Wiley Periodicals, Inc. Head Neck, 2011
Mechanotransduction by endothelial cells is locally generated, direction‐dependent, and ligand‐specific
Authors: Chrétien Marc L. , Zhang Ming , Jackson Moira R. , Kapus Andras , Langille B. Lowell 
Published: April 2010

AbstractVascular endothelial cells display a wide panel of responses to changes in the shear stress that is exerted on them by blood flow. How sensory mechanisms convey information about flow conditions and how this information is integrated remains poorly understood. The issue is confounded by: (1) a large number of potential force sensors, (2) difficulties in differentiating these sensors from downstream sites of signal integration, and (3) the complexities inherent in understanding how forces are transmitted from the apical surface of the cell via the cytoskeleton to intracellular sites. As a consequence, neither the structures that sense force nor the nature of the forces that loads them have been clearly defined. In this study, we employed magnetic microspheres coated with ligands that bind integrin subsets (RGD peptides or type I collagen) or PECAM‐1 to discriminate the downstream signaling effects of different sensor molecules and mechanisms for how they are loaded. We found that application of force to these transmembrane molecules elicited biologically important signaling (ERK1/2, AKT, and GSK‐3β phosphorylation), and downstream biological responses that depended on the following two factors: (1) the ligand that transmitted force and (2) the direction in which force was applied. These findings indicate that ligands locally generate different shear‐induced responses in endothelium that depend on how force is delivered. J. Cell. Physiol. 224: 352–361, 2010. © 2010 Wiley‐Liss, Inc.
Adaptation to alkalosis induces cell cycle delay and apoptosis in cortical collecting duct cells: Role of aquaporin‐2
Authors: Rivarola Valeria , Flamenco Pilar , Melamud Luciana , Galizia Luciano , Ford Paula , Capurro Claudia 
Published: April 2010

AbstractCollecting ducts (CD) not only constitute the final site for regulating urine concentration by increasing apical membrane Aquaporin‐2 (AQP2) expression, but are also essential for the control of acid–base status. The aim of this work was to examine, in renal cells, the effects of chronic alkalosis on cell growth/death as well as to define whether AQP2 expression plays any role during this adaptation. Two CD cell lines were used: WT‐ (not expressing AQPs) and AQP2‐RCCD1 (expressing apical AQP2). Our results showed that AQP2 expression per se accelerates cell proliferation by an increase in cell cycle progression. Chronic alkalosis induced, in both cells lines, a time‐dependent reduction in cell growth. Even more, cell cycle movement, assessed by 5‐bromodeoxyuridine pulse‐chase and propidium iodide analyses, revealed a G2/M phase cell accumulation associated with longer S‐ and G2/M‐transit times. This G2/M arrest is paralleled with changes consistent with apoptosis. All these effects appeared 24 h before and were always more pronounced in cells expressing AQP2. Moreover, in AQP2‐expressing cells, part of the observed alkalosis cell growth decrease is explained by AQP2 protein down‐regulation. We conclude that in CD cells alkalosis causes a reduction in cell growth by cell cycle delay that triggers apoptosis as an adaptive reaction to this environment stress. Since cell volume changes are prerequisite for the initiation of cell proliferation or apoptosis, we propose that AQP2 expression facilitates cell swelling or shrinkage leading to the activation of channels necessary to the control of these processes. J. Cell. Physiol. 224: 405–413, 2010. © 2010 Wiley‐Liss, Inc.
Inhibitive effects of Photofrin on cellular autophagy
Authors: Luo Shiming , Xing Da , Wei Yanchun , Chen Qun 
Published: April 2010

AbstractDepending on the circumstances, autophagy can be either a protective or damaging cellular process. The role of autophagy in photodynamic therapy (PDT), a photo‐chemotherapy that utilizes light to activate a photosensitizer drug to achieve localized cellular damage, has been explored in recent years. It has been reported that autophagy in PDT is significantly influenced by the treatment protocol. In this work, the role of Photofrin, a well‐established clinical photosensitizer, in regulating cellular autophagy was investigated. The effects of Photofrin on cellular autophagy induced by conventional starvation or rapamycin techniques were studied. By fluorescence imaging, Western blotting and cell viability assays, it was found that Photofrin can effectively inhibit cellular autophagy induced by starvation or rapamycin. This autophagy blocking is independent of the photosensitizing property of the drug. With Baf‐A1, a well‐established agent that inhibits autophagosome from fusing with lysosome, we also found that, the observed phenomenon is not due to accelerated degradation of existing autophagosomes, thus proving that the drug Photofrin alone, without light excitation, can truly block autophagy. J. Cell. Physiol. 224: 414–422, 2010. © 2010 Wiley‐Liss, Inc.
Constitutive activation of the mitogen‐activated protein kinase pathway impairs vitamin D signaling in human prostate epithelial cells
Authors: Zhang Zhentao , Kovalenko Pavlo , Cui Min , DeSmet Marsha , Clinton Steven K. , Fleet James C. 
Published: April 2010

AbstractWe studied the effect of prolonged activation of mitogen‐activated protein kinase (MAPK) signaling on 1,25 dihydroxyvitamin D (1,25(OH)2D3) action in the immortalized human prostate epithelial cell line RWPE1 and its Ki‐Ras transformed clone RWPE2. 1,25(OH)2D3‐treatment caused growth arrest and induced gene expression in both cell lines but the response was blunted in RWPE2 cells. Vitamin D receptor (VDR) levels were lower in RWPE2 cells but VDR over‐expression did not increase vitamin‐D‐mediated gene transcription in either cell line. In contrast, MAPK inhibition restored normal vitamin D transcriptional responses in RWPE2 cells and MAPK activation with constitutively active MEK1R4F reduced vitamin‐D‐regulated transcription in RWPE1 cells. 1,25(OH)2D3‐mediated transcription depends upon the VDR and its heterodimeric partner the retinoid X receptor (RXR) so we studied whether changes in the VDR–RXR transcription complex occur in response to MAPK activation. Mutation of putative phosphorylation sites in the activation function 1 (AF‐1) domain (S32A, T82A) of RXRα restored 1,25(OH)2D3‐mediated transactivation in RWPE2 cells. Mammalian two‐hybrid and co‐immunoprecipitation assays revealed a vitamin‐D‐independent interaction between steroid receptor co‐activator‐1 (SRC‐1) and RXRα that was reduced by MAPK activation and was restored in RWPE2 cells by mutating S32 and T82 in the RXRα AF‐1 domain. Our data show that a common contributor to cancer development, prolonged activation of MAPK signaling, impairs 1,25(OH)2D3‐mediated transcription in prostate epithelial cells. This is due in part to the phosphorylation of critical amino acids in the RXRα AF‐1 domain and impaired co‐activator recruitment. J. Cell. Physiol. 224: 433–442, 2010. © 2010 Wiley‐Liss, Inc.
Signaling pathways implicated in PGF2α effects on Fgf2+/+ and Fgf2−/− osteoblasts
Authors: Sabbieti Maria Giovanna , Agas Dimitrios , Marchetti Luigi , Santoni Giorgio , Amantini Consuelo , Xiao Liping , Menghi Giovanna , Hurley Marja M. 
Published: April 2010

AbstractProstaglandin F2α (PGF2α) regulates fibroblast growth factor‐2 (FGF‐2) and fibroblast growth factor receptor (FGFR) expression in osteoblasts. Here, the role of FGF‐2 in PGF2α‐induced proliferation and the signaling pathway involved, were determined in calvarial osteoblasts (COBs) from Fgf2+/+ and Fgf2−/− mice. The involvement of the exported FGF‐2 isoform, was determined using the FGF‐2 neutralizing antibody to alter its binding to FGFR1. PGF2α increased activity of Ras, and MAP‐kinase cascade as well as Bcl‐2 and c‐Myc levels in Fgf2+/+ but not in Fgf2−/− COBs. Moreover, in Fgf2+/+ COBs, PGF2α‐enhanced nuclear accumulation and co‐localization of Bcl‐2/c‐Myc. Although up‐regulation of multiple proliferative and survival signals were induced by PGF2α in Fgf2+/+ COBs, phospho‐p53 was unmodified while p53 was increased. Increased phospho‐p53 was, instead, found in Fgf2−/− COBs without up‐regulation of oncogenic proteins. The lack of p53 activation in wild type osteoblasts could be due in part to the overexpression of MDM2 caused by PGF2α via FGF‐2. PGF2α, also, increased cyclins D and E in Fgf2+/+ COBs and induced an expansion of Fgf2+/+ osteoblasts in G2/M phase. These data clearly show that PGF2α induces proliferation via endogenous FGF‐2 and the exported isoform mediates PGF2α effects by acting in autocrine manner. Furthermore, silencing of FGFR1 in Fgf2+/+ COBs blocked PGF2α induced increase of phospho‐MDM2 and cyclins. J. Cell. Physiol. 224: 465–474, 2010. © 2010 Wiley‐Liss, Inc.
Adiponectin increases BMP‐2 expression in osteoblasts via AdipoR receptor signaling pathway
Authors: Huang Chun‐Yin , Lee Chun‐Yi , Chen Meng‐Yi , Tsai Hsiao‐Chi , Hsu Horng‐Chaung , Tang Chih‐Hsin 
Published: April 2010

AbstractAdiponectin is a protein hormone secreted predominantly by differentiated adipocytes and involved in energy homeostasis. Bone morphogenetic protein (BMP) plays important roles in osteoblastic differentiation and bone formation. However, the effects of adiponectin on BMPs expression in cultured osteoblasts are largely unknown. Here we found that adiponectin increased mRNA expression of BMP‐2 but not other BMPs in cultured osteoblastic cells. Stimulation of osteoblasts with adiponectin also increased protein levels of BMP‐2 by Western blot and ELISA assay. Adiponectin‐mediated BMP‐2 expression was attenuated by 5′‐AMP‐activated protein kinase (AMPK) small interference RNA and AMPK inhibitor (araA and compound C). Activations of p38 and NF‐κB pathways after adiponectin treatment were demonstrated, and adiponectin‐induced expression of BMP‐2 was inhibited by the specific inhibitor and mutant of p38 and NF‐κB cascades. Taken together, our results provide evidence that adiponectin enhances BMP‐2 expression in osteoblastic cells, and AdipoR1 receptor, AMPK, p38 and NF‐κB signaling pathways may be involved in increasing BMP‐2 expression by adiponectin. J. Cell. Physiol. 224: 475–483, 2010. © 2010 Wiley‐Liss, Inc.
Cell death of prostate cancer cells by specific amino acid restriction depends on alterations of glucose metabolism
Authors: Fu Ya‐Min , Lin Huimin , Liu Xiaoyi , Fang Weigang , Meadows Gary G. 
Published: April 2010

AbstractSelective amino acid restriction targets mitochondria resulting in DU145 and PC3 prostate cancer cell death. This study shows that restriction of tyrosine and phenylalanine (Tyr/Phe), glutamine (Gln), or methionine (Met) differentially modulates glucose metabolism, glycogen synthase kinase 3β (GSK3β), p53, and pyruvate dehydrogenase (PDH) in these two cell lines. In DU145 cells, Gln and Met restriction increase glucose consumption, but Tyr/Phe restriction does not. Addition of glucose to culture media diminishes cell death induced by Tyr/Phe‐restriction. Addition of pyruvate reduces cell death due to Tyr/Phe and Gln restriction. Tyr/Phe, Gln and Met restriction increase phosphorylation of GSK3β‐Ser9, phosphorylation of p53‐Ser15 and reduce the mitochondrial localization of PDH. Addition of glucose or pyruvate to cultures significantly reverses the alterations in GSK3β, p53 and PDH induced by amino acid restriction. In p53‐null PC3 cells, Tyr/Phe, Gln and Met restriction decreases glucose consumption, reduces phosphorylation of Akt‐Ser473, and increases phosphorylation of GSK3β‐Ser9. Addition of pyruvate or glucose reduces death of Met‐restricted cells. Addition of glucose increases phosphorylation of Akt‐Ser473 in amino acid‐restricted cells reduces phosphorylation of GSK3β‐Ser9 in Tyr/Phe and Gln restricted cells and increases phosphorylation of GSK3β‐Ser9 in Met restricted cells. Addition of pyruvate reduces phosphorylation of GSK3β‐Ser9 in all amino acid‐restricted cells. In summary, cell death induced by specific amino acid restriction is dependent on or closely related to the modulation of glucose metabolism. GSK3β (DU145 and PC3) and p53 (DU145) are crucial switches connecting metabolism and these signaling molecules to cell survival during amino acid restriction. J. Cell. Physiol. 224: 491–500, 2010. © 2010 Wiley‐Liss, Inc.
Interleukin‐1β induces ICAM‐1 expression enhancing leukocyte adhesion in human rheumatoid arthritis synovial fibroblasts: Involvement of ERK, JNK, AP‐1, and NF‐κB
Authors: Yang Chuen‐Mao , Luo Shue‐Fen , Hsieh Hsi‐Lung , Chi Pei‐Ling , Lin Chih‐Chung , Wu Chi‐Chuan , Hsiao Li‐Der 
Published: April 2010

AbstractInterleukin‐1β (IL‐1β) has been shown to induce the expression of adhesion molecules on various cell types and contributes to inflammatory responses. However, the molecular mechanisms by which IL‐1β induced intercellular adhesion molecule (ICAM)‐1 expression remain unclear in human rheumatoid arthritis synovial fibroblasts (RASFs). Here, we demonstrated that IL‐1β induces ICAM‐1 gene expression via the de novo protein synthesis through transcription and translation, which is attenuated by pretreatment with actinomycin D and cycloheximide, respectively. IL‐1β‐induced ICAM‐1 expression, extracellular signal‐regulated kinase (ERK) and c‐Jun‐N‐terminal kinase (JNK) phosphorylation, AP‐1 activation, and nuclear factor‐κB (NF‐κB) p65 translocation were attenuated by the inhibitors of MEK1/2 (U0126), JNK (SP600125), AP‐1 (tanshinone IIA), and NF‐κB (helenalin) or transfection with respective short hairpin RNA plasmids. Moreover, IL‐1β‐stimulated NF‐κB p65 translocation was blocked by helenalin, but not by U0126 or SP600125, revealing that MAPKs and NF‐κB pathways were independent on these responses. IL‐1β‐stimulated AP‐1 activation was blocked by U0126 or SP600125, revealing that ERK and JNK linked to AP‐1 on these responses. IL‐1β‐stimulated ICAM‐1 gene expression was attenuated by pretreatment with U0126, SP600125, tanshinone IIA, or helenalin, revealed by ICAM‐1 promoter assay and real‐time RT‐PCR analysis. Finally, up‐regulation of ICAM‐1 enhanced the adhesion of leukocytes to RASFs exposed to IL‐1β. These results suggest that in human RASFs, activation of ERK, JNK, AP‐1, and NF‐κB are essential for IL‐1β‐induced ICAM‐1 expression and leukocyte adhesion. J. Cell. Physiol. 224: 516–526, 2010. © 2010 Wiley‐Liss, Inc.
Protection capabilities of nanostructured shells toward cell encapsulation: A saccharomyces/paramecium model
Authors: Magrassi Raffaella , Ramoino Paola , Bianchini Paolo , Diaspro Alberto 
Published: April 2010

AbstractIn this work we report the formation of nanostructured hybrid objects, made up of living cells encapsulated in a protective multilayer shell assembly of nanostructured polyelectrolyte. Such constructs can be hosted on nanostructured surfaces or can be installed around living organisms, at the right time. Their construction is based on the layer‐by‐layer (LbL) self‐assembly of two oppositely alternated charged polyelectrolytes (PEs) on cell membranes as earlier done for nanocapsules or fuzzy structured nanoshells. This communication reports the optimal conditions for cell encapsulation in terms of nanoshell design and construction. Microsc. Res. Tech. 73:931–936, 2010. © 2010 Wiley‐Liss, Inc.
Dynamics of nucleic acid/cationic polymer complexation and disassembly under biologically simulated conditions using in situ atomic force microscopy
Authors: Shim Min Suk , Wang Xi , Ragan Regina , Kwon Young Jik 
Published: April 2010

AbstractElucidating dynamic morphological changes of gene‐carrying vectors and their nucleic acid release under varying intracellular conditions has been a technical challenge. Atomic force microscopy (AFM) was used to observe nucleic acid/polymer polyplexes under endosomal and reducible cytosolic conditions. Both ketalized (acid‐degradable) and unmodified (nondegradable) polyethylenimine (PEI) in linear and branched forms were used to prepare plasmid DNA‐ or siRNA‐complexing polyplexes. Then, the polyplexes' complexation and disassembly were observed by in situ AFM in various differentially changing buffers that represent intracellular conditions. Results demonstrated obvious morphological destruction of DNA/ketalized linear PEI (KL‐PEI) polyplexes under mildly acidic endosomal conditions, whereas no morphological changes were observed by DNA/ketalized branched PEI (KB‐PEI) under the same conditions. In addition, siRNA was more efficiently dissociated from KL‐PEI than KB‐PEI under the same conditions. Nondegradable PEI did not show any evidence that DNA or siRNA was released. Anionic biomacromolecules (e.g., heparan sulfate), which was hypothesized to dissociate nucleic acids from cationic polymers, did not successfully disassemble polyplexes but appeared to be adsorbed on cationic polymers. The in situ AFM results combined with in vitro cellular transfection and gene silencing indicated that efficient endosomal escape of plasmid DNA in a compact polyplex form is required for efficient gene expression. On the contrary, rapid dissociation of siRNA from its cationic carrier is crucial for efficient gene silencing. The findings of this study may provide new insightful information for designing stimuli‐responsive nonviral gene vectors as well as expanding tools for investigating nonviral vectors in nanoscales under biologically inspired conditions. Microsc. Res. Tech. 73:845–856, 2010. © 2010 Wiley‐Liss, Inc.
Elemental composition of Physarum compressum Alb. et Schw. sporocarps and their structures cultivated on rabbit dung and agar substrates
Authors: Janik Paulina , Tylko Grzegorz , Ostachowicz Beata , Turnau Katarzyna 
Published: April 2010

AbstractThe elemental composition of spores, peridium walls, and lime nodes of Physarum compressum sporocarps, cultivated on rabbit dung as a natural growing environment for the slime mold and on artificial agar medium, was compared to evaluate differences that may be dependent on substrates. Whole fruiting bodies and samples of both experimental media were extracted with nitric acid or Parr digest bomb, respectively, and analyzed by means of total X‐ray reflection fluorescence (TXRF). Electron probe microanalysis (EPMA) of spores, peridium walls, and lime nodes structure was carried out with the scanning electron microscope equipped with energy‐dispersive spectrometer. Because of minute sizes and roughness of investigated structures, Monte Carlo simulations were utilized to establish analytical conditions of EPMA. Biological and geological standards were used in the quantification of element concentrations. According to TXRF, the fruiting bodies from agar medium revealed lower concentrations of K, Ca, Cr, Mn, and Fe in relation to fruiting bodies from the dung, reflecting elemental relationships in the experimental media. According to EPMA, the highest Ca concentration was found in the lime nodes followed by the peridium and the spores. Culturing of the slime molds on the rabbit dung indicated higher concentration of Ca in the lime nodes and peridium walls when compared with those obtained from the sporocarps grown on agar media. The opposite relation was found for the spores. The concentration of Na, Mg, P, S, and Cl was generally lower in all structures of the sporocarps harvested from the dung than from the agar medium. K was in higher concentration in analyzed structures from dung than from agar. Different element uptake (except for Ca and K) was revealed by the two methods: TXRF and EPMA. Microsc. Res. Tech. 73:1134–1142, 2010. © 2010 Wiley‐Liss, Inc.
2‐Butyl‐5‐chloro‐3H‐imidazole‐4‐carbaldehyde as a new synthon for the synthesis of fused ring heterocycles via intramolecular 1,3‐dipolar cycloaddition reactions
Authors: Gaonkar S. L. , Lokanatha Rai K. M. 
Published: April 2010

Abstract
magnified imageThe title compound 2‐butyl‐5‐chloro‐3H‐imidazole‐4‐carbaldehyde was transformed into tricyclic heterocycles by substituting the chlorine atom by an unsaturated thiolate or alkoxide and then converting aldehyde function into 1,3‐dipole. Chloramine‐T was used as an efficient reagent for the generation of 1,3‐dipoles, which resulted the formation of fused ring heterocycles via intramolecular 1,3‐dipolar cycloaddition reaction. The method is very useful for the construction of many biologically active fused heterocycles. J. Heterocyclic Chem., (2010).
Synthesis of some new pyridones, fused pyrimidines, and fused 1,2,4‐triazines
Authors: Mohamed Mahmoud A. 
Published: April 2010

Abstract
magnified imageCyclocondensation of hydrazides, 3‐aminopyrazoles, 3‐amino‐1,2,4‐triazole, 2‐aminobenzoimidazole, pyrazole‐3‐diazonium salts, 1,2,4‐triazol‐3‐diazonium salt, or benzoimidazole‐2‐diazonium salt with sodium salt of 3‐hydroxy‐1‐(2‐naphthyl)prop‐2‐en‐1‐one gave 2‐pyridones, pyrazolo[1,5‐a]pyrimidines, triazolo[1,5‐a]pyrimidine, benzo[4,5]imidazo[1,2‐a]pyrimidine, (pyrazolo[5,1‐c][1,2,4]triazin‐3‐yl)‐methanone, [1,2,4]triazolo[5,1‐c][1,2,4]triazin‐3‐yl‐methanone, or benzo[4,5]imidazo[2,1‐c] [1,2,4]triazin‐3‐yl‐methanone derivatives, respectively, which will be tested for anti‐tumor and anti‐cancer activates. J. Heterocyclic Chem., (2010).
Synthesis of imidazo[1,2‐c]quinazolin‐5(6H)‐ones and benzimidazo[1,2‐c]quinazolin‐6(5H)‐ones with the aid of low‐valent titanium reagent
Authors: Zhao Xuan , Shi Da‐Qing 
Published: April 2010

Abstract
magnified imageA short and facile synthesis of imidazo[1,2‐c]quinazolin‐5(6H)‐ones and benzimidazo[1,2‐c]quinazolin‐6(5H)‐ones was accomplished in good yields via the novel reductive cyclization of 2‐(2‐nitrophenyl)imidazoles or 2‐(2‐nitrophenyl)benzoimidazoles with isocyanates promoted by low‐valent titanium reagent. J. Heterocyclic Chem., (2010).
The reaction of 2‐dimethylaminomethylene‐3‐oxo‐N‐phenylbutyramide with active methylene nitriles
Authors: Abdelrazek Fathy M. , Sharaf Mohey F. , Metz Peter , Jaeger Anna 
Published: April 2010

Abstract
magnified image2‐Dimethylaminomethylene‐3‐oxo‐N‐phenylbutyramide 1 reacts with malononitrile 2a to afford the pent‐2‐enedioic acid 1‐amide 5‐phenylamide derivative 6, which could be cyclized to give the 6‐methylpyridone derivative 7. Compound 1 reacts with cyanoacetamide 2b to afford the same pyridone 7 and with cyanothioacetamide 2c to afford the analogous pyridinethione 12. Compound 12 reacts with DMAD to afford the pyridine derivative 15 and with N,N‐dimethylchloroacetamide 16 to afford the thieno[2,3‐d]pyridine derivative 18. Compound 18 reacts with morpholine‐4‐carboxaldehyde 19, N,N‐diemthylformamide 20, and 2,5‐dimethoxy‐tetrahydrofuran 21 to afford the fully aromatic thieno[2,3‐d]pyridine derivatives 22, 23, and 24, respectively. J. Heterocyclic Chem., (2010).