bluuebunny/crossref_metadata_2025_split huggingface dataset:
An active wound dressing for controlled convective mass transfer with the wound bed
Authors: Cabodi Mario , Cross Valerie L. , Qu Zheng , Havenstrite Karen L. , Schwartz Suzanne , Stroock Abraham D. 
Published: November 2006

AbstractConventional wound dressings—gauze, plastic films, foams, and gels—do not allow for spatial and temporal control of the soluble chemistry within the wound bed, and are thus limited to a passive role in wound healing. Here, we present an active wound dressing (AWD) designed to control convective mass transfer with the wound bed; this mass transfer provides a means to tailor and monitor the chemical state of a wound and, potentially, to aid the healing process. We form this AWD as a bilayer of porous poly(hydroxyethyl methacrylate) (pHEMA) and silicone; the pHEMA acts as the interface with the wound bed, and a layer of silicone provides a vapor barrier and a support for connecting to external reservoirs and pumps. We measure the convective permeability of the pHEMA sponge, and use this value to design a device with a spatially uniform flow profile. We quantify the global coefficient of mass transfer of the AWD on a dissolvable synthetic surface, and compare it to existing theories of mass transfer in porous media. We also operate the AWD on model wound beds made of calcium alginate gel to demonstrate extraction and delivery of low molecular weight solutes and a model protein. Using this system, we demonstrate both uniform mass transfer over the entire wound bed and patterned mass transfer in three spatially distinct regions. Finally, we discuss opportunities and challenges for the clinical application of this design of an AWD. © 2006 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 2006
Severe citrate toxicity complicating volunteer apheresis platelet donation
Authors: Bell A.M. , Nolen J.D.L. , Knudson C.M. , Raife T.J. 
Published: November 2006

AbstractWe report a case of severe citrate toxicity during volunteer donor apheresis platelet collection. The donor was a 40‐year‐old female, first‐time apheresis platelet donor. Past medical history was remarkable for hypertension, hyperlipidemia, and depression. Reported medications included bumetanide, pravastatin, and paroxetine. Thirty minutes from the start of the procedure, the donor noted tingling around the mouth, hands, and feet. She then very rapidly developed acute onset of severe facial and extremity tetany. Empirical treatment with intravenous calcium gluconate was initiated, and muscle contractions slowly subsided over approximately 10 to 15 minutes. The events are consistent with a severe reaction to calcium chelation by sodium citrate anticoagulant resulting in symptomatic systemic hypocalcemia. Upon additional retrospective analysis, it was noted that bumetanide is a loop diuretic that may cause significant hypocalcemia. We conclude that careful screening for medications and underlying conditions predisposing to hypocalcemia is recommended to help prevent severe reactions due to citrate toxicity. Laboratory measurement of pre‐procedure serum calcium levels in selected donors may identify cases requiring heightened vigilance. The case also illustrates the importance of maintaining preparedness for managing rare but serious reactions in volunteer apheresis blood donors. J. Clin. Apheresis. © 2006 Wiley‐Liss, Inc.
Approach to systematic analysis of serine/threonine phosphoproteome using Beta elimination and subsequent side effects: Intramolecular linkage and/or racemisation
Authors: Tinette Sylvette , Feyereisen René , Robichon Alain 
Published: November 2006

AbstractComplete analysis of the phosphorylation of serine and threonine residues directly from biological extracts is still at an early stage and will remain a challenging goal for many years. Analysis of phosphorylated proteins and identification of the phosphorylated sites in a crude biological extract is a major topic in proteomics, since phosphorylation plays a dominant role in post‐translational protein modification. Beta elimination of the serine/threonine‐bound phosphate by alkali action generates (methyl)dehydroalanine. The reactivity of this group susceptible of nucleophilic attacks might be used as a tool for phosphoproteome analysis. Most of the known serine/threonine kinases recognize motifs in protein targets that are rich in lysine(s) and/or arginine(s). The (methyl)dehydroalanine resulting from beta elimination of the serine/threonine‐bound phosphate by alkali action is likely to react with the amino groups of these neighboring amino acids. Furthermore, the addition reaction of dehydroalanine‐peptides with a nucleophilic group more likely generates diastereoisomers derivatives. The internal cyclic bonds and/or the stereoisomer peptide derivatives thus generated confer resistance to trypsin cleavage and/or constitute stop signals for exopeptidases such as carboxypeptidase. This might form the basis of a method to facilitate the systematic identification of phosphorylated peptides. J. Cell. Biochem. 100: 875–882, 2007. © 2006 Wiley‐Liss, Inc.
Vascular permeability induced by VEGF family members in vivo: Role of endogenous PAF and NO synthesis
Authors: Brkovic Alexandre , Sirois Martin G. 
Published: November 2006

AbstractWe previously reported that vascular endothelial growth factor (VEGF) increases vascular permeability through the synthesis of endothelial platelet‐activating factor (PAF), while others reported the contribution of nitric oxide (NO). Herein, we addressed the contribution of VEGF receptors and the role played by PAF and NO in VEGF‐induced plasma protein extravasation. Using a modified Miles assay, intradermal injection in mice ears of VEGF‐A165, VEGF‐A121, and VEGF‐C (1 µM) which activate VEGFR‐2 (Flk‐1) receptor increased vascular permeability, whereas a treatment with VEGFR‐1 (Flt‐1) analogs; PlGF and VEGF‐B (1 µM) had no such effect. Pretreatment of mice with PAF receptor antagonist (LAU8080) or endothelial nitric oxide synthase (eNOS) inhibitor (L‐NAME) abrogated protein extravasation mediated by VEGF‐A165. As opposed to PAF (0.01‐1 µM), treatment with acetylcholine (ACh; up to 100 µM; inducer of NO synthesis) or sodium nitroprusside (SNP; up to 1 µM; NO donor) did not induce protein leakage. Simultaneous pretreatment of mice with eNOS and protein kinase A (PKA) inhibitors restored VEGF‐A165 vascular hyperpermeability suggesting that endogenous NO synthesis leads to PKA inhibition, which support maintenance of vascular integrity. Our data demonstrate that VEGF analogs increase vascular permeability through VEGFR‐2 activation, and that both endogenous PAF and NO synthesis contribute to VEGF‐A165‐mediated vascular permeability. However, PAF but not NO directly increases vascular permeability per se, thereby, suggesting that PAF is a direct inflammatory mediator, whereas NO serves as a cofactor in VEGF‐A165 proinflammatory activities. J. Cell. Biochem. 100: 727–737, 2007. © 2006 Wiley‐Liss, Inc.
VDR‐mediated gene expression patterns in resting human coronary artery smooth muscle cells
Authors: Wu‐Wong J. Ruth , Nakane Masaki , Ma Junli , Ruan Xiaoan , Kroeger Paul E. 
Published: November 2006

AbstractVitamin D analogs such as paricalcitol and calcitriol that activate the vitamin D receptor (VDR) provide survival benefit for Stage 5 chronic kidney disease (CKD) patients, possibly associated with a decrease in cardiovascular (CV)‐related incidents. Phenotypic changes of smooth muscle cells play an important role in CV disease. The role of vitamin D analogs in modulating gene expression in smooth muscle cells is still not well understood. In this study, DNA microarray analysis of ∼22,000 different human genes was used to characterize the VDR‐mediated gene expression profile in human coronary artery smooth muscle cells (CASMC) at rest. Cells in serum free medium were treated with 0.1 µM calcitriol (1α,25‐dihydroxyvitamin D3) or paricalcitol (19‐nor‐1α,25‐(OH)2D2) for 30 h. A total of 181 target genes were identified, with 103 genes upregulated and 78 downregulated (>two fold changes in either drug treatment group with P < 0.01). No significant difference was observed between calcitriol and paricalcitol. Target genes fell into various categories with the top five in cellular process, cell communication, signal transduction, development, and morphogenesis. Twenty‐two selected genes linked to the CV system were also impacted. Real‐time RT‐PCR and/or Western blotting analysis were employed to confirm the expression patterns of selected genes such as 25‐hydroxyvitamin D‐24‐hydroxylase, Wilms' tumor gene 1, transforming growth factorβ3, plasminogen activator inhibitor‐1, thrombospondin‐1 (THBS1), and thrombomodulin (TM). This study provides insight into understanding the role of VDR in regulating gene expression in resting smooth muscle cells. J. Cell. Biochem. 100: 1395–1405, 2007. © 2006 Wiley‐Liss, Inc.
Comprehensive analysis of chemical bonding in boron clusters
Authors: Zubarev Dmitry Yu. , Boldyrev Alexander I. 
Published: November 2006

AbstractWe present a comprehensive analysis of chemical bonding in pure boron clusters. It is now established in joint experimental and theoretical studies that pure boron clusters are planar or quasi‐planar at least up to twenty atoms. Their planarity or quasi‐planarity was usually discussed in terms of π‐delocalization or π‐aromaticity. In the current article, we demonstrated that one cannot ignore σ‐electrons and that the presence of two‐center two‐electron (2c2e) peripheral BB bonds together with the globally delocalized σ‐electrons must be taken into consideration when the shape of pure boron cluster is discussed. The global aromaticity (or global antiaromaticity) can be assigned on the basis of the 4n + 2 (or 4n) electron counting rule for either π‐ or σ‐electrons in the planar structures. We showed that pure boron clusters could have double (σ‐ and π‐) aromaticity (B, B4, B, B, B, B, B8, B, B, B10, B, B12, and B), double (σ‐ and π‐) antiaromaticity (B, B15), or conflicting aromaticity (B5−,σ‐antiaromatic and π‐aromatic and B14, σ‐aromatic and π‐antiaromatic). Appropriate geometric fit is also an essential factor, which determines the shape of the most stable structures. In all the boron clusters considered here, the peripheral atoms form planar cycles. Peripheral 2c2e BB bonds are built up from s to p hybrid atomic orbitals and this enforces the planarity of the cycle. If the given number of central atoms (1, 2, 3, or 4) can perfectly fit the central cavity then the overall structure is planar. Otherwise, central atoms come out of the plane of the cycle and the overall structure is quasi‐planar. © 2006 Wiley Periodicals, Inc. J Comput Chem, 2007
σ and π contributions to the induced magnetic field: Indicators for the mobility of electrons in molecules
Authors: Heine Thomas , Islas Rafael , Merino Gabriel 
Published: November 2006

AbstractThe authors discuss the role of the σ and π contributions to the induced magnetic field for simple hydrocarbons containing a double or a triple bond, as well as for benzene and cyclobutadiene. While the magnetic field induced by the σ electrons is short‐ranged, the π system is responsible for the formation of long‐range cones. These cones influence the chemical shift of atoms by additional shielding (for aromatic) or deshielding (for antiaromatic molecules) contributions. While the hydrogen atoms of benzene are found to lie within the deshielded region of the magnetic field induced by the π electrons, they are shielded by the total induced magnetic field. The induced magnetic field of the π electrons support Pople's model on the basis of first‐principles calculations. © 2006 Wiley Periodicals, Inc. J Comput Chem 2007
HIV‐1 negatively affects the survival/maturation of cord blood CD34+ hematopoietic progenitor cells differentiated towards megakaryocytic lineage by HIV‐1 gp120/CD4 membrane interaction
Authors: Gibellini Davide , Vitone Francesca , Buzzi Marina , Schiavone Pasqua , De Crignis Elisa , Cicola Ronny , Conte Roberto , Ponti Cristina , Re Maria Carla 
Published: November 2006

AbstractTo investigate the mechanisms involved in the human immunodeficiency virus type 1 (HIV‐1)‐related thrombocytopenia (TP), human umbilical cord blood (UCB) CD34+ hematopoietic progenitor cells (HPCs) were challenged with HIV‐1IIIb and then differentiated by thrombopoietin (TPO) towards megakaryocytic lineage. This study showed that HIV‐1, heat‐inactivated HIV‐1, and HIV‐1 recombinant gp120 (rgp120) activated apoptotic process of megakaryocyte (MK) progenitors/precursors and decreased higher ploidy MK cell fraction. All these inhibitory effects on MK survival/maturation and platelets formation were elicited by the interaction between gp120 and CD4 receptor on the cell membrane in the absence of HIV‐1 productive infection. In fact, in our experimental conditions, HPCs were resistant to HIV‐1 infection and no detectable productive infection was observed. We also evaluated whether the expression of specific cytokines, such as TGF‐β1 and APRIL, involved in the regulation of HPCs and MKs proliferation, was modulated by HIV‐1. The specific protein and mRNA detection analysis, during TPO‐induced differentiation, demonstrated that HIV‐1 upregulates TGF‐β1 and downregulates APRIL expression through the CD4 engagement by gp120. Altogether, these data suggest that survival/differentiation of HPCs committed to MK lineage is negatively affected by HIV‐1 gp120/CD4 interaction. This long‐term inhibitory effect is also correlated to specific cytokines regulation and it may represent an additional mechanism to explain the TP occurring in HIV‐1 patients. J. Cell. Physiol. 210: 315–324, 2007. © 2006 Wiley‐Liss, Inc.
Identification of differentially expressed microRNAs by microarray: A possible role for microRNA genes in pituitary adenomas
Authors: Bottoni Arianna , Zatelli Maria Chiara , Ferracin Manuela , Tagliati Federico , Piccin Daniela , Vignali Cristina , Calin George A. , Negrini Massimo , Croce Carlo M. , degli Uberti Ettore C. 
Published: November 2006

AbstractMicroRNAs (miRNAs) are small non‐coding RNAs that control gene expression by targeting mRNA. It has been demonstrated that miRNA expression is altered in many human cancers, suggesting that they may play a role in human neoplasia. To determine whether miRNA expression is altered in pituitary adenomas, we analyzed the entire miRNAome in 32 pituitary adenomas and in 6 normal pituitary samples by microarray and by Real‐Time PCR. Here, we show that 30 miRNAs are differentially expressed between normal pituitary and pituitary adenomas. Moreover, 24 miRNAs were identified as a predictive signature of pituitary adenoma and 29 miRNAs were able to predict pituitary adenoma histotype. miRNA expression could differentiate micro‐ from macro‐adenomas and treated from non‐treated patient samples. Several of the identified miRNAs are involved in cell proliferation and apoptosis, suggesting that their deregulated expression may be involved in pituitary tumorigenesis. Predictive miRNAs could be potentially useful diagnostic markers, improving the classification of pituitary adenomas. J. Cell. Physiol. 210: 370–377, 2007. © 2006 Wiley‐Liss, Inc.
Connective tissue growth factor (CTGF) acts as a downstream mediator of TGF‐β1 to induce mesenchymal cell condensation
Authors: Song Jason J. , Aswad Rulla , Kanaan Reem A. , Rico Mario C. , Owen Thomas A. , Barbe Mary F. , Safadi Fayez F. , Popoff Steven N. 
Published: November 2006

AbstractMesenchymal cell (MC) condensation or the aggregation of MCs precedes chondrocyte differentiation and is required for subsequent cartilage formation during endochondral ossification. In this study, we used micromass cultures of C3H10T1/2 cells as an in vitro model system for studying MC condensation and the events important for this process. Transforming growth factor β1 (TGF‐β1) served as the initiator of MC condensation in our model system and we were interested in determining whether CTGF functions as a downstream mediator of TGF‐β1. CTGF is a matricellular protein that has been found to be expressed in MC condensations and in the perichondrium. Micromass cultures of C3H10T1/2 cells condensed under TGF‐β1 stimulation concomitant with dramatic up‐regulation of CTGF mRNA and protein levels. CTGF silencing by either CTGF siRNA or CTGF antisense oligonucleotide approaches showed that TGF‐β1‐induced condensation was CTGF dependent. Furthermore, silencing of CTGF expression resulted in significant reductions in cell proliferation and migration, events that are crucial during MC condensation. In addition, up‐regulation of Fibronectin (FN) and suppression of Sox9 expression by TGF‐β1 was also found to be mediated by CTGF. Immunofluorescence of developing mouse vertebrae showed that CTGF, TGF‐β1 and FN were co‐expressed in condensations of MCs, while Sox9 expression was low at this stage. During subsequent chondrogenesis, Sox9 expression was high in chondrocytes while CTGF expression was limited to the perichondrium. Thus, CTGF is an essential downstream mediator of TGF‐β1‐induced MC condensation through its effects on cell proliferation and migration. CTGF is also involved in up‐regulating FN and suppressing Sox9 expression during TGF‐β1 induced MC condensation. J. Cell. Physiol. 210: 398–410, 2007. © 2006 Wiley‐Liss, Inc.
Combinatorial treatment of non‐small‐cell lung cancers with gefitinib and Ad.mda‐7 enhances apoptosis‐induction and reverses resistance to a single therapy
Authors: Emdad Luni , Lebedeva Irina V. , Su Zao‐Zhong , Gupta Pankaj , Sarkar Devanand , Settleman Jeffrey , Fisher Paul B. 
Published: November 2006

AbstractActivation of the epidermal growth factor receptor (EGFR) contributes to the pathogenesis of non‐small‐cell lung carcinomas (NSCLC) and gefitinib, a selective reversible EGFR inhibitor, is effective in treating patients with NSCLC. However, clinical resistance to gefitinib is a frequent occurrence highlighting the need for improved therapeutic strategies. Melanoma differentiation associated gene‐7 (mda‐7)/Interleukin‐24 (IL‐24) (mda‐7/IL‐24) displays cancer‐selective apoptosis induction when delivered via a replication‐incompetent adenovirus (Ad.mda‐7). In this study, the effect of Ad.mda‐7 infection, either alone or in combination with gefitinib, was analyzed in a panel of NSCLC cell lines carrying wild‐type EGFR (H‐460 and H‐2030) or mutant EGFR (H‐1650 and H‐1975). While H‐2030 and H‐1650 cells were sensitive, H‐460 and H‐1975 cells were resistance to growth inhibition by Ad.mda‐7, which was reversed by the combination of Ad.mda‐7 and gefitinib. This combination increased MDA‐7/IL‐24 and downstream effector double‐stranded RNA‐activated protein kinase (PKR) protein expression, promoting apoptosis induction of NSCLC cells. Inhibition of PKR significantly inhibited apoptosis induction by Ad.mda‐7 when administered alone but not when used in combination with gefitinib. The combination treatment also augmented inhibition of EGFR signaling. Our findings indicate that a combinatorial treatment with Ad.mda‐7 and gefitinib may provide benefit in the treatment of NSCLC, especially in patients displaying resistance to clinically used EGFR inhibitors. J. Cell. Physiol. 210: 549–559, 2007. © 2006 Wiley‐Liss, Inc.
PECAM‐1 modulates thrombin‐induced tissue factor expression on endothelial cells
Authors: Zhang Jenny J. , Kelm Robert J. , Biswas Purba , Kashgarian Michael , Madri Joseph A. 
Published: November 2006

AbstractPlatelet endothelial cell adhesion molecule‐1 (PECAM‐1) (CD31) is known to inhibit platelet function and thrombus formation. The mechanisms involved in PECAM‐1's roles as a modulator of hemostasis are still not completely understood. We examined the role of PECAM‐1 as a regulator of tissue factor (TF) expression, a known important inducer of thrombosis. Wildtype and CD31KO mice underwent transient (30 min) renal ischemia followed by 24 h re‐perfusion and their kidneys assessed for apoptosis, fibrin formation, and tissue factor expression. CD31KO mice exhibited increased tubular epithelial and endothelial apoptosis, increased fibrin deposition, and tissue factor expression. Human umbilical vein endothelial cells (HUVEC) transfected with antisense (AS) PECAM‐1 oligonucleotides to downregulate PECAM‐1 expression, exhibited greater induction of TF mRNA and protein expression as well as increased expression and nuclear localization of the transcription factor Egr‐1 compared to scrambled AS PECAM‐1 (Scr)‐treated HUVEC following thrombin stimulation. TF induction was found to be mediated through thrombin receptor PAR‐1 and the Gαi/o subunit of G‐protein, confirmed by PAR‐1 antagonist and pertussis toxin inhibition respectively. Thrombin‐mediated TF induction was dependent on Rho Kinase activity, phosphorylation of p38MAPK and p85 & Akt dephosphorylation. The inverse correlation of PI3K–Akt phosphorylation with p38 MAPK phosphorylation was confirmed by pharmacological inhibition. These studies suggest that PECAM‐1 is involved in regulating a signaling pathway, affecting PI3K and Akt activation, p38 MAPK phosphorylation, which in turn, affects Egr‐1 expression and nuclear translocation, ultimately affecting TF expression. These findings provide new insights into the action of PECAM‐1 as a modulator of thrombosis. J. Cell. Physiol. 210: 527–537, 2007. © 2006 Wiley‐Liss, Inc.
Cell cycle‐dependent activity of the volume‐ and Ca2+‐activated anion currents in Ehrlich lettre ascites cells
Authors: Klausen Thomas Kjær , Bergdahl Andreas , Hougaard Charlotte , Christophersen Palle , Pedersen Stine F. , Hoffmann Else K. 
Published: November 2006

AbstractRecent evidence implicates the volume‐regulated anion current (VRAC) and other anion currents in control or modulation of cell cycle progression; however, the precise involvement of anion channels in this process is unclear. Here, Cl− currents in Ehrlich Lettre Ascites (ELA) cells were monitored during cell cycle progression, under three conditions: (i) after osmotic swelling (i.e., VRAC), (ii) after an increase in the free intracellular Ca2+ concentration (i.e., the Ca2+‐activated Cl− current, CaCC), and (iii) under steady‐state isotonic conditions. The maximal swelling‐activated VRAC current decreased in G1 and increased in early S phase, compared to that in G0. The isotonic steady‐state current, which seems to be predominantly VRAC, also decreased in G1, and increased again in early S phase, to a level similar to that in G0. In contrast, the maximal CaCC current (500 nM free Ca2+ in the pipette), was unaltered from G0 to G1, but decreased in early S phase. A novel high‐affinity anion channel inhibitor, the acidic di‐aryl‐urea NS3728, which inhibited both VRAC and CaCC, attenuated ELA cell growth, suggesting a possible mechanistic link between cell cycle progression and cell cycle‐dependent changes in the capacity for conductive Cl− transport. It is suggested that in ELA cells, entrance into the S phase requires an increase in VRAC activity and/or an increased potential for regulatory volume decrease (RVD), and at the same time a decrease in CaCC magnitude. J. Cell. Physiol. 210: 831–842, 2007. © 2006 Wiley‐Liss, Inc.
Solitary gastric melanotic schwannoma: Sonographic findings
Authors: Chen Yang‐Yuan , Yen Hsu‐Heng , Soon Maw‐Soan 
Published: November 2006

AbstractSolitary gastric schwannoma is rare, and solitary melanotic schwannoma is even rarer, posing a dilemma in diagnosis and treatment. We report the case of a 69‐year‐old woman with gastric melanotic schwannoma who presented with nausea, vomiting, and abdominal pain. Abdominal sonographic examination revealed a 5‐cm hypoechoic mass in the epigastric area that was confirmed to be a gastric submucosal tumor on endoscopic examination. The diagnosis of melanotic schwannoma was confirmed via sonographically guided percutaneous core biopsy. The tumor was resected, and no recurrence has occurred in a 3‐year follow‐up. © 2006 Wiley Periodicals, Inc. J Clin Ultrasound, 2006