bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of the interaction of cefadroxil with different metal ions using CE
Authors: Auda Sayed H. , Mrestani Yahya , Ahmed Ahmed M. S. , Neubert Reinhard H. H. 
Published: February 2009

AbstractThe present study describes the application of CE to investigate the interaction between a cephalosporin, cefadroxil and different metal ions. This study aims at quantifying the interaction of cefadroxil with Zn2+, Al3+, Fe3+, Cu2+ and Co2+ ions using the effective electrophoretic mobility as a parameter for calculation of the reaction association constant (K). For this purpose, the electrophoretic mobilities of cefadroxil at different metal ion concentrations in citrate buffer pH 3.6 were determined. A mathematical model to calculate the association constant between cefadroxil and metal ions was used. The results showed that a strong change in the cefadroxil electrophoretic mobility was observed by increasing the metal ion concentrations. The results revealed that by increasing the concentration of metal ions in the running buffer the degree of complexation increases too. On the basis of the results, the strength of the interaction of cefadroxil with the investigated metal ions follows the order Zn2+>Cu2+>Co2+>Fe3+>Al3+. The association constant of the investigated reactions ranged from 451.57 to 1546.52 L/mmol. The results indicate that it is possible to characterize the interaction between cefadroxil and metal ions quantitatively using CE.
The Use of Fluorocarbon Surfactants to Improve the Manufacture of PEM Fuel Cell Electrodes
Authors: Wills R. G. A. , Watt‐Smith M. J. , Walsh F. C. 
Published: February 2009

AbstractFluorocarbon surfactants are used to improve surface wetting during the screen printing of carbon black inks onto PEM fuel cell electrodes. The fluorosurfactants were tested in inks that comprised a Nafion® ionomer solution with platinum‐loaded carbon black. Four commercially available fluorosurfactants (Zonyl FSO, Zonyl 1033D, Forafac 1098 and Novec FC 4430) were screened and assessed for electrochemical activity (via cyclic voltammetry), leaching and the ability to form ink layers. Good wetting characteristics were observed and the inks showed a similar specific electrochemical active area (200–430 cm2 mg–1Pt) to a standard reference ink (370 cm2 mg–1Pt), indicating that the surfactants did not adversely adsorb on the platinum catalyst surface or block the adsorption/desorption of hydrogen. Additionally, the fluorosurfactants in the cured inks were shown to be electrochemically inactive in the potential region relevant to fuel cell operation.
Intracerebral granulocyte‐macrophage colony‐stimulating factor induces functionally competent dendritic cells in the mouse brain
Authors: Mausberg Anne Kathrin , Jander Sebastian , Reichmann Gaby 
Published: February 2009

AbstractGranulocyte‐macrophage colony‐stimulating factor (GM‐CSF) is a hematopoietic growth factor and a proinflammatory cytokine. While GM‐CSF is lacking in normal brain tissue, it is expressed under pathological conditions and correlates with the presence of dendritic cells (DC). However, the role of GM‐CSF for the onset of immune responses in the brain is still unclear. To analyze the role of GM‐CSF for the induction and functional activity of immune cells in the brain, we performed chronic intracerebroventricular administration of GM‐CSF to the brains of adult mice. After GM‐CSF administration, intracerebral leukocytes (ICL) were characterized by means of flow cytometry, immunohistochemistry, and an ex vivo functional assay. GM‐CSF treatment significantly increased the number of leukocytes expressing high levels of CD45, indicative of peripheral, blood‐derived cells. The infiltrating cells were preferentially DC of the myeloid lineage (CD45high CD11c+ CD11b+) with an activated phenotype characterized by upregulated expression of MHCII and the costimulatory ligand CD80. Furthermore, DC from GM‐CSF treated mice were fully competent to activate naive allogeneic T cells in a mixed leukocyte reaction. In contrast, intracerebroventricular IFN‐γ administration stimulated MHCII expression on cells resembling resident microglia, but did not induce comparable presence of DC. Taken together, intracerebroventricular GM‐CSF treatment results in high numbers of DC in the brain. Moreover, these GM‐CSF‐induced DC display an activated phenotype and exhibit the capacity to act as fully competent DC even without a further inflammatory stimulus. © 2009 Wiley‐Liss, Inc.
Oxidative injury triggers autophagy in astrocytes: The role of endogenous zinc
Authors: Lee Sook‐Jeong , Cho Kyung Sook , Koh Jae‐Young 
Published: February 2009

AbstractWe have recently demonstrated that the accumulation of labile zinc in lysosomes during oxidative stress causes lysosomal membrane permeabilization (LMP) in cultured hippocampal neurons. Since autophagy involves fusion of autophagic vacuoles (AVs) with lysosomes, zinc accumulation may start in AVs. In the present study, we examined the role of endogenous zinc in H2O2‐induced autophagy and cell death in mouse astrocyte cultures. Live‐cell confocal imaging of astrocytes transfected with GFP‐LC3 revealed that the number of AVs positive for LC3 (microtubule‐associated protein 1 light chain 3) increased following exposure to H2O2 or ferrous chloride (FeCl2). Staining of RFP‐LC3‐transfected astrocytes with FluoZin‐3 indicated that the levels of labile zinc increased in AVs as well as in the cytosol and nuclei. The majority of AVs were double‐stained with LysoTracker, indicating that they were fused with lysosomes. Chelation of zinc with tetrakis [2‐pyridylmethyl]ethylenediamine (TPEN) decreased the number of AVs in H2O2‐treated astrocytes, whereas exposure to zinc increased their number, suggesting that dysregulation of zinc homeostasis is mechanistically linked to autophagy. Unexpectedly, inhibition of autophagy blocked the rise in labile zinc levels. Astrocytic death induced by H2O2 was accompanied by LMP. Autophagy inhibitors (3‐methyladenine, bafilomycin‐1) or TPEN attenuated LMP and cell death in astrocytes. These results support the possibility that endogenous zinc plays a key role in autophagy under oxidative stress in astrocytes, and suggest that autophagy is a necessary preceding event for LMP and cell death in oxidative injury. © 2009 Wiley‐Liss, Inc.
Amphiregulin is a factor for resistance of glioma cells to cannabinoid‐induced apoptosis
Authors: Lorente Mar , Carracedo Arkaitz , Torres Sofía , Natali Francesco , Egia Ainara , Hernández‐Tiedra Sonia , Salazar María , Blázquez Cristina , Guzmán Manuel , Velasco Guillermo 
Published: February 2009

AbstractGliomas, one of the most malignant forms of cancer, exhibit high resistance to conventional therapies. Identification of the molecular mechanisms responsible for this resistance is therefore of great interest to improve the efficacy of the treatments against these tumors. Δ9‐Tetrahydrocannabinol (THC), the major active ingredient of marijuana, and other cannabinoids inhibit tumor growth in animal models of cancer, including glioma, an effect that relies, at least in part, on the ability of these compounds to induce apoptosis of tumor cells. By analyzing the gene expression profile of two sub‐clones of C6 glioma cells with different sensitivity to cannabinoid‐induced apoptosis, we found a subset of genes with a marked differential expression in the two sub‐clones. Furthermore, we identified the epidermal growth factor receptor ligand amphiregulin as a candidate factor to mediate the resistance of glioma cells to cannabinoid treatment. Amphiregulin was highly overexpressed in the cannabinoid‐resistant cell line, both in culture and in tumor xenografts. Moreover, in vivo silencing of amphiregulin rendered the resistant tumors xenografts sensitive to cannabinoid antitumoral action. Amphiregulin expression was associated with increased extracellular signal‐regulated kinase (ERK) activation, which mediated the resistance to THC by blunting the expression of p8 and TRB3—two genes involved in cannabinoid‐induced apoptosis of glioma cells. Our findings therefore identify Amphirregulin as a factor for resistance of glioma cells to THC‐induced apoptosis and contribute to unraveling the molecular bases underlying the emerging notion that targeted inhibition of the EGFR pathway can improve the efficacy of antitumoral therapies. © 2009 Wiley‐Liss, Inc.
Exogenous Nanog alleviates but is insufficient to reverse embryonic stem cells differentiation induced by PI3K signaling inhibition
Authors: Liu Na , Lu Min , Feng Xiao Ming , Ma Feng Xia , Fang Zhi Hong , Tian Xue Mei , Ren Qian , Zhang Lei , Liu Bin , Huang Ping Ping , Liu Lin , Han Zhong Chao 
Published: February 2009

AbstractPI3K signaling pathway plays a significant role in embryonic stem cells (ES cells) self‐renewal. Overexpression of Nanog maintains mouse ES cells pluripotency independent of leukemia inhibitory factor (LIF). However, little is known about the effect of PI3K signaling pathway on ES cells with Nanog overexpression. Our experiments aimed to explore the relationship between PI3K signaling pathway and Nanog expression in ES cells. We observed the effect of LY294002, a specific inhibitor of PI3K pathway, on wild‐type J1 cells and Nanog overexpressing (Ex‐Nanog) J1 cells in the presence or absence of LIF. With LY294002 treatment, both of them lost their ES features even in the presence of LIF. But the differentiation induced by LY294002 on Ex‐Nanog J1 cells was slighter lower than that on wild‐type J1 cells. These results indicate that inhibition of PI3K pathway induces mouse ES cells differentiation. Exogenous Nanog sustains mouse ES cells pluripotency independent of LIF, and alleviates the differentiation induced by LY294002. But it is insufficient to totally reverse the differentiation. J. Cell. Biochem. 106: 1041–1047, 2009. © 2009 Wiley‐Liss, Inc.
The role of the disintegrin metalloproteinase ADAM15 in prostate cancer progression
Authors: Lucas Neali , Day Mark L. 
Published: February 2009

AbstractThe metalloproteinase ADAM15 is a multi‐domain disintegrin protease that is upregulated in a variety of human cancers. ADAM15 mRNA and protein levels are increased in prostate cancer and its expression is significantly increased during metastatic progression. It is likely that ADAM15 supports disease progression differentially through the action of its various functional domains. ADAM15 may downregulate adhesion of tumor cells to the extracellular matrix, reduce cell–cell adhesion, and promote metastasis through the activity of its disintegrin and metalloproteinase domains. Additionally, ADAM15 can influence cell signaling by shedding membrane‐bound growth factors and other proteins that interact with receptor tyrosine kinases, leading to receptor activation. There is also evidence supporting a role for ADAM15 in angiogenesis and angioinvasion of tumor cells, which are critical for unrestrained tumor growth and metastatic spread. Given its diverse functions, ADAM15 may represent a pivotal regulatory component of tumor progression, an important target for therapeutic intervention, or emerge as a biomarker of disease progression. J. Cell. Biochem. 106: 967–974, 2009. © 2009 Wiley‐Liss, Inc.
Oncogenic nucleoporin CAN/Nup214 interacts with vitamin D receptor and modulates its function
Authors: Miyauchi Yoshiteru , Sakaguchi Naoko , Okada Tomoko , Makishima Makoto , Ozono Keiichi , Michigami Toshimi 
Published: February 2009

AbstractVitamin D receptor (VDR) is a ligand‐dependent transcription factor and should be located in nucleus to transactivate target genes. To explore the molecules that interact with VDR and facilitate its nuclear localization, we screened a human kidney cDNA library using the yeast two‐hybrid approach, and found that VDR binds to the carboxy‐terminal region of an oncogenic nucleoporin, CAN/Nup214. CAN/Nup214 was originally identified through its involvement in a certain type of acute myeloid leukemia, and is a component of nuclear pore complex (NPC). Co‐immunoprecipitation experiments confirmed the interaction between VDR and the carboxy‐terminus of CAN/Nup214 containing a cluster of the phenylalanine‐glycine (FG) repeat in mammalian cells. The exogenously expressed full‐length CAN/Nup214 was localized predominantly at the nuclear envelope, suggesting its integration in the NPCs. We then examined the effects of exogenous expression of full‐length CAN/Nup214 and its carboxy‐terminal fragment on the VDR‐mediated transactivation. The overexpression of full‐length CAN/Nup214 facilitated the VDR‐mediated transactivation, while the expression of the carboxy‐terminal fragment suppressed it. The DNA‐binding domain of VDR was required for the facilitation of the VDR‐dependent transactivation by CAN/Nup214. Although the subcellular distribution of VDR was not obviously altered by the overexpression of full‐length CAN/Nup214 or the carboxy‐terminal fragment, the expression of the carboxy‐terminal fragment inhibited the interaction between full‐length CAN/Nup214 and VDR. These results indicate that CAN/Nup214 interacts with VDR and modulates its function as a transcription factor. J. Cell. Biochem. 106: 1090–1101, 2009. © 2009 Wiley‐Liss, Inc.
vOX2 glycoprotein of human herpesvirus 8 modulates human primary macrophages activity
Authors: Salata Cristiano , Curtarello Matteo , Calistri Arianna , Sartori Elena , Sette Paola , de Bernard Marina , Parolin Cristina , Palù Giorgio 
Published: February 2009

AbstractHuman herpesvirus 8 (HHV‐8) is a lymphotropic herpesvirus linked to several disorders such as Kaposi's sarcoma, primary effusion lymphoma and multicentric Castleman's disease. Several HHV‐8 proteins regulate host innate and adaptive immune response; in particular, orfK14 is expressed as an immediate early gene during the viral lytic cycle and encodes a surface glycoprotein (vOX2), significantly homologous to the cellular OX2, which delivers inhibitory signals to macrophages. Although it has been suggested that vOX2 may down‐regulate basophil and neutrophil functions, its role in macrophages, a cell type lytically infected by HHV‐8 in vivo, is still controversial. Therefore, we investigated the effect of vOX2 expression in human primary monocyte‐derived macrophages (MDMs). In this report, we demonstrate that vOX2‐expressing MDMs in basal conditions are induced to produce inflammatory cytokines and display higher phagocytic activity with respect to mock cells. By contrast, an opposite effect is exhibited by vOX2 in MDMs undergoing IFN‐γ‐activation, with a down‐modulation of the cytokine production and phagocytic activity. Moreover, we observed that, when MDMs are co‐cultured with vOX2‐expressing cells, the inflammatory cytokine release is increased, independently from the MDM activation state. Interestingly, we could correlate our results with the mRNA transcript level of the vOX2 cellular CD200R receptor. Finally, we demonstrate a down‐regulation of the MHC class I and class II molecules on the cell surface of vOX2‐transduced MDMs. Our results provide new insights into the immunomodulatory effects of HHV‐8 vOX2 protein. J. Cell. Physiol. 219: 698–706, 2009. © 2009 Wiley‐Liss, Inc.
Methodology for biomechanical testing of fresh anterior wall vaginal samples from postmenopausal women undergoing cystocele repair
Authors: Zimmern Philippe E. , Eberhart Robert C. , Bhatt Aradhana 
Published: February 2009

AbstractGoalTo explore the methodological challenges of biomechanical testing of freshly harvested human anterior vaginal wall (HAVW) samples.MethodLongitudinal full‐thickness samples of HAVW were excised during cystocele repair in postmenopausal women and age‐matched controls. Two methods of tissue storage during transport were compared. All samples were prepared for uniaxial testing within 2 hr of harvest and loaded at a rate of 0.5 mm/sec, until irreversible deformation was observed. Young's modulus and other parameters were extracted from the tensile stress–strain curves.ResultsSamples were obtained over 2 years from 42 patients. Significant differences in biomechanical parameters were noted based on the degree of hydration of the tissue, suggesting that the wetter samples were mechanically weaker.ConclusionsThis study reports on a new method for testing the biomechanical properties of freshly harvested HAVW tissues and the impact of tissue hydration during transport between the operating room and the testing lab. Neurourol. Urodynam. 28:325–329, 2009. © 2009 Wiley‐Liss, Inc.
Nocturia: An austrian study on the multifactorial etiology of this symptom
Authors: Klingler H. Christoph , Heidler Helmut , Madersbacher Helmut , Primus Guenter 
Published: February 2009

AbstractAimsTo identify the different factors contributing to nocturia in a clinical setting.Patients and MethodsThree hundred twenty‐four patients (133 women, 191 men; mean age 63 years) were entered into this multi‐institutional study. When presenting with nocturia we obtained detailed medical history and performed urine analysis, post‐void residual volume and renal ultrasonography. Bothersome score and quality of life were evaluated using visual analogue scale and Kings' Health Questionnaire (KHQ), respectively. Patients were asked to complete a 48‐hr voiding diary (VD). Nocturia and its associated problems were evaluated using KHQ and VD in conjunction with concurrent health variables.ResultsMean nocturia was 2.8 in men versus in 3.1 women. Fifty percent of patients were aged >65 years, 60% had daytime lower urinary tract symptoms (LUTS) as well as nocturia, 33% had cardiac pathologies and 7% had peripheral edema. Principal causes for nocturia were global polyuria in 17%, nocturnal polyuria (NP) in 33% and reduced functional capacity <250 ml in 16.2%; 21.2% had mixed forms of NP and reduced bladder capacity and 12.6% suffered from other causes. Mean bothersome score was higher in women (P < 0.001) and in patients with NP (P = 0.012). Quality of life was significantly lower in women (P = 0.001), in patients aged >65 years (P = 0.029) and in those with reduced functional capacity (P < 0.001). Mean voided 24‐hr urine was higher in women (P = 0.033) and in patients aged <65 years (P = 0.019).ConclusionsNocturia had a high impact on bothersome score, strong associations with poor health and other LUTS. NP was the predominant cause of nocturia. Neurourol. Urodynam. 28:427–431, 2009. © 2009 Wiley‐Liss, Inc.
Bayesian hierarchical uncertainty quantification by structural equation modeling
Authors: Jiang Xiaomo , Mahadevan Sankaran 
Published: February 2009

AbstractUncertainty quantification is playing an increasingly important role in assessing the performance, safety, and reliability of complex physical systems in the absence of adequate amount of experimental data. Simulation of a complex system involves multiple levels of modeling, such as material (lowest level) to component to subsystem to system (highest level). This paper presents a Bayesian structural equation modeling approach to quantify both epistemic and aleatoric uncertainties in hierarchical model development. A generalized structural equation modeling with latent variables is presented to model three sets of relationships in hierarchical model development, namely, model predictions vs experimental observations at each individual level, model predictions at lower vs higher levels, and experimental data at lower vs higher levels. The three sets of relationships are represented by a hierarchical Bayes network, and the influencing factors between them are estimated by a Bayesian regression approach. Both measurement and prediction errors at various levels are quantified through the Bayesian method. The variability of input variables in the computational model is updated and quantified using various levels of measurement data via Bayesian inference and the structural equation modeling parameters. The proposed methodology is illustrated with a transient heat conduction example problem. Copyright © 2009 John Wiley & Sons, Ltd.
Prolonged QTc interval in children and young adults with sickle cell disease at steady state
Authors: Liem Robert I. , Young Luciana T. , Thompson Alexis A. 
Published: February 2009

AbstractBackgroundProlongation of the QTc interval may be more common than previously believed among individuals with sickle cell disease (SCD). The clinical associations and natural history of QTc prolongation remain unclear in this population. Our objectives were to determine the prevalence of prolonged QTc and evaluate its relationship to clinical factors in children and young adults with SCD.ProceduresWe analyzed data from subjects 10 to 25 years old with SCD enrolled in our pulmonary hypertension screening protocol. Screening included echocardiography (ECHO), 12‐lead electrocardiogram (ECG) and laboratory testing at steady state. QTc interval >440 msec was considered prolonged.ResultsECG data from 76 subjects (57% male, mean age 14.2 ± 3 years old, range 10–24) were analyzed. We observed prolonged QTc in 29/76 (38%) subjects. Despite evidence of left ventricular hypertrophy (LVH) in 50/76 (66%) subjects, the frequency of LVH was not significantly different in subjects with and without QTc prolongation. When compared to subjects with normal QTc, subjects with prolonged QTc had higher mean tricuspid regurgitant jet velocity (2.51 ± 0.27 m/sec vs. 2.33 ± 0.26 m/sec, P = 0.010) as well as higher mean lactate dehydrogenase (433 ± 142 IU/L vs. 343 ± 142 IU/L, P = 0.000) and aspartate aminotransferase (48 ± 20 IU/L vs. 39 ± 15 IU/L, P = 0.026). A larger proportion of subjects with prolonged QTc also had a history of recurrent acute chest syndrome (66% vs. 38%, P = 0.038).ConclusionsWe conclude that QTc prolongation is a frequent finding in SCD not associated with LVH. Elevated pulmonary pressures, hemolysis and acute chest syndrome may represent risk factors for prolonged QTc in this population. Pediatr Blood Cancer 2009;52:842–846. © 2009 Wiley‐Liss, Inc.
Transition of patients with sickle cell disease from pediatric to adult care: Assessing patient readiness
Authors: McPherson Marianne , Thaniel Lisa , Minniti Caterina P. 
Published: February 2009

AbstractBackgroundTransfer of care from pediatric to adult‐oriented providers is challenging for adolescents with sickle cell disease (SCD). The need for transition programs is known, however many SCD patients leave pediatric care without adequate preparation. This study has two aims: to assess adolescent SCD patients' preparation for transition and to identify variables that predict patient readiness.ProcedureAdolescent patients receiving care at a pediatric SCD center received a survey regarding essential steps of the transition process. Patients' level of prior thought, interest, anticipated difficulty, and perceived importance of transition were graded on a scale of 0 to 3. Knowledge of individual transition plans was scaled 0 to 4. Responses were analyzed according to age, sex, and disease severity.ResultsSeventy patients ages 14 to 20 years (median 16.7 years) were assessed. Mean readiness scores were low, with greatest deficiencies in prior thought (mean 0.88 [0.66–1.09]), knowledge (mean 0.85 [0.61–1.09]), anticipated difficulty (mean 1.42 [1.23–1.61]), and interest (mean 1.71 [1.47–1.95]). Perceived importance of transition received the highest score (mean 2.71 [2.58–2.84]). Younger age (≤16 years) was associated with less knowledge (P = 0.003) and interest (P = 0.023); disease severity (≥3 crises/year) was associated with lower interest (P = 0.043) but greater anticipated difficulty (P = 0.001). Anticipated difficulty trended higher among females (P = 0.028).ConclusionsAdolescents with SCD acknowledge the importance but demonstrate poor preparation for transition to adult‐oriented care. Readiness improves with age but remains insufficient. This analysis highlights the need for improvements in anticipatory guidance for transition during adolescence. Pediatr Blood Cancer 2009;52:838–841. © 2009 Wiley‐Liss, Inc.