bluuebunny/crossref_metadata_2025_split huggingface dataset:
Accurate and fast algorithm of the molecular incomplete gamma function with a complex argument
Authors: Ishida Kazuhiro 
Published: February 2004

AbstractSeveral efficient algorithms for the accurate and fast calculation of the molecular incomplete gamma function Fm(z) with a complex argument z are developed. The complex incomplete gamma function is arising in molecular integrals over the gauge‐including atomic orbitals. Two kinds of algorithms are recommended: (1) a high‐precision version and (2) a fast version. The high‐precision version is able to guarantee 15 significant figures (10−15 in the relative error) and the fast version is able to guarantee 12 significant figures (10−12 in the relative error), at worst, within the double‐precision arithmetic. The fast version is about 5–20 times faster than the high‐precision version. For most molecular calculations, the fast version will give a satisfied precision. © 2004 Wiley Periodicals, Inc. J Comput Chem 25: 739–748, 2004
Nature of bonding in the sulfuryl group
Authors: Chesnut D. B. , Quin L. D. 
Published: February 2004

AbstractThe SO sulfuryl bond in a number of representative sulfoxides and sulfones has been studied at the B3LYP/6‐311+G(d,p) level in the atoms‐in‐molecules (AIM) approach involving the AIM delocalization index and the Cioslowski–Mixon localized orbitals and associated covalent bond order. The sulfuroxygen covalent bond is strongly polarized toward oxygen and the oxygen lone pairs provide significant backbonding to create short and strong SO bonds, similar in nature to those found in the analogous phosphoryl (PO) bond. Although the sulfoxides in general have larger delocalization indices than the sulfones, there is no correlation between these quantities and the bond dissociation energies. © 2004 Wiley Periodicals, Inc. J Comput Chem 25: 734–738, 2004
Intramolecular CH…Ccarbene hydrogen bonds and competing interactions in monoprotonated tripodal carbenes
Authors: Howard Siân T. , Abernethy Colin D. 
Published: February 2004

AbstractThe anionic tripodal N‐heterocyclic carbene (C3N2H3)3BH− first prepared by Fehlhammer, together with three neutral variants, (C3N2H3)3CH, (C3N2H3)3P, and (C3N2H3)3SiH, have been studied using quantum chemical methods. Isodesmic reactions are used to deduce that the phosphine‐bridgehead species in particular has a large‐resonance stabilization energy. All the podands undergo substantial conformational change on excitation to the lowest triplet electronic state, with effective localization of the excitation on one of the heterocyclic rings, dearomatizing it. On monoprotonation of the ground states, three of these species display intramolecular C‐H…Ccarbene hydrogen bonding: The nature and strength of these interactions is explored using model (intermolecularly hydrogen‐bonded) complexes, isodesmic reactions, and GIAO calculations of chemical shifts. One surprising result is that C‐H…Ccarbene hydrogen bonds involving ethenic hydrogens can be almost as strong as those involving the imidazolium proton (first identified by Arduengo). The case of the monoprotonated carbon bridgehead species is in particular intriguing. It is stabilized by a competitive Ccarbene…N interaction of sufficient strength to override the C‐H…Ccarbene bonding motif observed in the other structures. © 2004 Wiley Periodicals, Inc. J Comput Chem 25: 649–659, 2004
TDDFT investigation on nucleic acid bases: Comparison with experiments and standard approach
Authors: Shukla M.K. , Leszczynski Jerzy 
Published: February 2004

AbstractA comprehensive theoretical study of electronic transitions of canonical nucleic acid bases, namely guanine, adenine, cytosine, uracil, and thymine, was performed. Ground state geometries were optimized at the MP2/6‐311G(d,p) level. The nature of respective potential energy surfaces was determined using the harmonic vibrational frequency analysis. The MP2 optimized geometries were used to compute electronic vertical singlet transition energies at the time‐dependent density functional theory (TDDFT) level using the B3LYP functional. The 6‐311++G(d,p), 6‐311(2+,2+)G(d,p), 6‐311(3+,3+)G(df,pd), and 6‐311(5+,5+)G(df,pd) basis sets were used for the transition energy calculations. Computed transition energies were found in good agreement with the corresponding experimental data. However, in higher transitions, the Rydberg contaminations were also obtained. The existence of πσ* type Rydberg transition was found near the lowest singlet ππ* state of all bases, which may be responsible for the ultrafast deactivation process in nucleic acid bases. © 2004 Wiley Periodicals, Inc. J Comput Chem 25: 768–778, 2004
Changes in macrophage function and morphology due to biomedical polyurethane surfaces undergoing biodegradation
Authors: Matheson Loren A. , Santerre J. Paul , Labow Rosalind S. 
Published: February 2004

AbstractMonocytes are recruited to the material surface of an implanted biomedical device recognizing it as a foreign body. Differentiation into macrophages subsequently occurs followed by fusion to form foreign body giant cells (FBGCs). Consequently, implants can become degraded, cause chronic inflammation or become isolated by fibrous encapsulation. In this study, a relationship between material surface chemistry and the FBGC response was demonstrated by seeding mature monocyte‐derived macrophages (MDMs) on polycarbonate‐based polyurethanes that differed in their chemical structures (synthesized with poly(1,6‐hexyl 1,2‐ethyl carbonate) diol, and either 14C‐hexane diisocyanate and butanediol (BD) (referred to as HDI) or 4,4′‐methylene bisphenyl diisocyanate and 14C‐BD (referred to as MDI)) and material degradation assessed. At 48 h of cell‐material interaction, the FBGC attached to HDI were more multinucleated (73%) compared to MDI or the polystyrene (PS) control (21 and 36%, respectively). There was a fivefold increase in the synthesis and secretion of a protein with an approximate molecular weight of 48 kDa and a pI of 6.1 (determined by two‐dimensional gel electrophoresis) only from cells seeded on HDI. Immunoprecipitation confirmed that MSE and CE were synthesized and secreted de novo. Immunoblotting also showed an increase in secreted monocyte‐specific esterase (MSE) and cholesterol esterase (CE) from cells seeded on HDI relative to PS and MDI. Significantly more radiolabel (14C) release and esterase activity were elicited by MDMs on HDI than MDI (P < 0.05). The material that was more degradable (HDI), elicited greater protein synthesis and esterase secretion as well as more multinucleated MDMs than MDI, suggesting that the material surface chemistry modulates the function of MDM at the site of an inflammatory response to an implanted device. J. Cell. Physiol. 199: 8–19, 2004© 2003 Wiley‐Liss, Inc.
Utilizing endocrine secretory pathways in salivary glands for systemic gene therapeutics
Authors: Voutetakis Antonis , Wang Jianghua , Baum Bruce J. 
Published: February 2004

AbstractMammalian salivary glands are commonly used models of exocrine secretion. However, there is substantial experimental evidence showing the physiological existence of endocrine secretory pathways in these tissues. The use of gene transfer technology in vivo has allowed the unambiguous demonstration of these endocrine pathways. We and others have exploited such findings and evaluated salivary glands as possible target tissues for systemic applications of gene therapeutics. Salivary glands present numerous advantages for this purpose, including being well encapsulated, which limits extra‐glandular vector dissemination, and having the luminal membranes of almost all parenchymal cells accessible via intraoral delivery of vectors through the main excretory ducts. Existing studies suggest that clinical benefits will result from salivary gland targeted systemic gene therapeutics. J. Cell. Physiol. 199: 1–7, 2004. Published 2003 Wiley‐Liss, Inc.
Inosine stimulates chemotaxis, Ca2+‐transients and actin polymerization in immature human dendritic cells via a pertussis toxin‐sensitive mechanism independent of adenosine receptors
Authors: Idzko Marco , Panther Elisabeth , Bremer Hinrich C. , Windisch Wolfram , Sorichter Stephan , Herouy Yared , Elsner Peter , Mockenhaupt Maja , Girolomoni Giampiero , Norgauer Johannes 
Published: February 2004

AbstractInosine is an endogenous purine nucleoside, which is formed by adenosine deaminidase during adenosine breakdown and is released into the extracellular space from the sympathetic nervous system or injured cells. Here, we studied the biological activity of inosine on human dendritic cells (DC), which are specialized antigen presenting cells characterized by their ability to migrate from the blood to peripheral tissues, and then to secondary lymphoid organs where they initiate adaptive immune responses. In immature DC, inosine concentration‐dependently stimulated Ca2+‐transients, actin polymerization, and chemotaxis. Experiments with adenosine receptor antagonists and pertussis toxin (PTX) as well as desensitization studies suggested that the activity of inosine was mediated by a G protein‐coupled receptor pathway independent of adenosine receptors. DC, induced to mature by lipopolysaccharide, lost their ability to respond towards inosine with these activities. Moreover, inosine did neither influence membrane expression of CD54, CD80, CD83, CD86, HLA‐DR, and MHC class I molecules nor modulated secretion of interleukin (IL)‐12, IL‐10, and tumor necrosis factor alpha in immature and lipopolysaccharide‐matured DC. In aggregate, our study indicates that inosine may be involved in the trafficking control system of immature DC, and mediates its chemotactic activity by a PTX‐sensitive mechanism independent of adenosine receptors. J. Cell. Physiol. 199: 149–156, 2004© 2003 Wiley‐Liss, Inc.
Down‐regulation of MEK/ERK signaling by E‐cadherin‐dependent PI3K/Akt pathway in differentiating intestinal epithelial cells
Authors: Laprise Patrick , Langlois Marie‐Josée , Boucher Marie‐Josée , Jobin Christian , Rivard Nathalie 
Published: February 2004

AbstractIn vitro experiments have shown that the establishment of cell–cell contacts in intestinal epithelial cell cultures is a critical step in initiating ERK inhibition, cell cycle arrest, and induction of the differentiation process. Herein, we determined the mechanisms through which E‐cadherin‐mediated cell–cell contacts modulate the ERK pathway in intestinal epithelial cells. We report that: (1) removal of calcium from the culture medium of newly confluent Caco‐2/15 cells (30 min, 4 mM EGTA) results in the disruption of both adherens and tight junctions and clearly decreases Akt phosphorylation while increasing MEK and ERK activities. Akt, MEK, and ERK activation levels return to control levels 60 min after calcium restoration; (2) the use of E‐cadherin blocking antibodies efficiently prevents Akt phosphorylation and MEK–ERK inhibition after 70 min of calcium restoration; (3) using the PI3K inhibitor LY294002 (15 μM) in calcium switch experiments, we demonstrate that the assembly of adherens junctions activates Akt activity and triggers the inhibition of ERK1/2 activities in a PI3K‐dependent manner; (4) adenoviral infection of confluent Caco‐2/15 cells with a constitutively active mutant of Akt1 strongly represses ERK1/2 activities; (5) inhibition of PI3K abolishes Akt activity but leads to a rapid and sustained activation of the MEK–ERK1/2 in confluent differentiating Caco‐2/15 cells, but not in undifferentiated growing Caco‐2/15 cells. Our data suggest that E‐cadherin engagement leads to MEK/ERK inhibition in a PI3K/Akt‐dependent pathway. This mechanism may account for the role of E‐cadherin in proliferation/differentiation transition along the crypt‐villus axis of the human intestinal epithelium. J. Cell. Physiol. 199: 32–39, 2004© 2003 Wiley‐Liss, Inc.
Intrinsic hematopoietic stem cell/progenitor plasticity: Inversions
Authors: Colvin Gerald A. , Lambert Jean‐François , Moore Brian E. , Carlson Jane E. , Dooner Mark S. , Abedi Mehrdad , Cerny Jan , Quesenberry Peter J. 
Published: February 2004

AbstractTraditional concepts indicate that stem cells give rise to progenitor cells in a hierarchical system. We studied murine engraftable stem cells (ESCs) and progenitors in in vitro and found that ESC and progenitors exist in a reversible continuum, rather then a hierarchy. B6.SJL and BALB/c marrow cells were serially cultured with thrombopoietin (TPO), FLT‐3 ligand (FLT‐3L), and steel factor through cell cycle. Progenitors (high‐proliferative potential colony‐forming cells (HPP‐CFC) and colony‐forming unit culture (CFU‐c)) and ESC capacity was determined. The cell cycle status of purified lineagenegativerhodaminelowHoechstlow stem cells was determined under the same conditions using tritiated thymidine incorporation and cell counts. We found an inverse relationship between progenitors and ESC, which occurred during the first cell cycle transit and was reversible. We have termed these progenitor/stem cell inversions and found that these inversions were consistently seen at 28–32 h of culture, representing early S‐phase. We observed 13 major reversible increases in progenitor numbers from one time‐point to another during the first cell cycle transit; this was coupled with 11 major ESC decreases and in 2 instances ESC were at baseline. These studies indicate that primitive marrow cells reversibly shift from ESC to progenitors without differentiation occurring. They exist as a fluctuating continuum. J. Cell. Physiol. 199: 20–31, 2004© 2003 Wiley‐Liss, Inc.
RACK1 is a functional target of the E1A oncoprotein
Authors: Severino Anna , Baldi Alfonso , Cottone Giuliano , Han Mei , Sang Nianli , Giordano Antonio , Maria Mileo Anna , Paggi Marco G. , De Luca Antonio 
Published: February 2004

AbstractThe adenoviral E1A proteins have been implicated in promotion of proliferation and transformation, inhibition of differentiation, induction of apoptosis, regulation of transcription, and suppression of tumor growth. The ability of E1A to override the fundamental controls of host cells is based on its ability to physically interact with several cellular proteins. We recently characterized RACK1 as a new E1A‐interacting protein. In this report, we show that the extreme N‐terminal region of E1A, spanning from aminoacids 1–36, and the conserved WD regions of RACK1 are responsible for this interaction. We also demonstrate that E1A and RACK1 colocalize at the perinuclear membrane in the cells. Furthermore, we provide evidence that E1A is able to antagonize the inhibitory effects of RACK1 on Src activity. These results suggest that RACK1 signaling pathway may be a functional target of E1A, contributing to E1A oncogenic effect in the host cells. J. Cell. Physiol. 199: 134–139, 2004© 2003 Wiley‐Liss, Inc.
Inhibition of ShcA isoforms p46/p52Shc enhances HIV‐1 replication in CD4+ T‐lymphocytes
Authors: Benetti Luca , Calistri Arianna , Ulivieri Cristina , Cabrelle Anna , Baldari Cosima T. , Palù Giorgio , Parolin Cristina 
Published: February 2004

AbstractHIV‐1 infection decreases the number of CD4+ T‐cells, and apoptosis has been suggested among the mechanisms. Proteins of the Shc family are involved in a complex network of signal transduction, differentiation, and apoptotic response to stress in many different cell types. Out of three homologous gene products (ShcA, ShcB, and ShcC), only two splicing variants of ShA are expressed in T‐lymphocytes, namely p46Shc and p52Shc. In the present study, we report that inhibition of p46Shc and p52Shc by a dominant negative mutant enhances the yield of HIV‐1 particles production without affecting efficiency of viral gene expression in CD4+‐infected cells. The increase in HIV‐1 replication in cells expressing the dominant negative mutant isoform ultimately correlates with a decrease in the percentage of cells entering apoptosis. The data presented suggest that ShcA proteins can play a role in committing CD4+ T‐cells to apoptosis, as a response to HIV‐1 infection. J. Cell. Physiol. 199: 40–46, 2004© 2003 Wiley‐Liss, Inc.
Activity of the matrix metalloproteinase‐9 promoter in human normal and tumor cells
Authors: Morelli Cristina , Campioni Katia , Parolin Cristina , Palù Giorgio , Tognon Mauro 
Published: February 2004

AbstractMatrix metalloproteinases (MMPs) belong to a family of proteins essential for those processes involving extracellular matrix degradation, such as embryonic development, morphogenesis, and tissue resorption and remodeling. Some members of this family play a crucial role also in tumor invasion. Most notably, MMP‐9 is expressed in invasive tumors, and represents a key protein in brain tumor progression, whereas it is not expressed in adult normal tissues. The expression of the MMP‐9, like other members of the family, is transcriptionally regulated. We, therefore, postulated that the MMP‐9 promoter could be useful in driving selective expression of exogenous genes in tumor cells. This represents a key feature for gene therapy applications, since currently employed viral promoters induce severe organ toxicity, limiting the clinical benefits. In this study, we investigated the activity of the MMP‐9 promoter in driving exogenous gene expression in human cell lines. High levels of reporter gene expression were detected in tumor derived cell lines, whereas the MMP‐9 promoter activity in non‐tumor cells was negligible. Furthermore, we show that tumor necrosis factor alpha (TNFα) is able to enhance considerably the MMP‐9 promoter activity only in tumor cells. Since recent studies have indicated that MMP‐9 enzymatic activity is detectable in the blood, it would be possible to screen potential responsive patients for a tumor gene therapy approach based on the MMP‐9 promoter. Taken together these data suggest that MMP‐9 promoter has the characteristics for transcritpionally targeted and inducible gene therapy applications. J. Cell. Physiol. 199: 126–133, 2004© 2003 Wiley‐Liss, Inc.
Actin re‐distribution in response to hydrogen peroxide in airway epithelial cells
Authors: Boardman Kendrick C. , Aryal Ashish M. , Miller William M. , Waters Christopher M. 
Published: February 2004

AbstractReactive oxygen species (ROS) disrupt the barrier function of airway epithelial cells through a mechanism that appears to involve remodeling of the actin cytoskeleton. Similarly, keratinocyte growth factor (KGF) has been shown to protect against ROS‐induced loss of barrier function through a mechanism that may also involve the actin cytoskeleton. To further determine the role of the actin cytoskeleton in ROS‐induced barrier injury, we quantified the relative amount of total actin associated with the cytoskeleton following exposure to hydrogen peroxide (H2O2) and pretreatment with KGF. We also determined the role of the actin–myosin contractile mechanism in the process by quantifying the relative amount of myosin heavy chain (MHC) associated with the cytoskeleton. While the transepithelial resistance (TER) of a monolayer of airway epithelial cells (Calu‐3) decreased after 2 h of continuous exposure to 0.5 mM H2O2, actin and MHC, both dissociated from the cytoskeleton within 15 min of H2O2 exposure. The TER of the monolayers remained depressed although both actin and myosin returned to the cytoskeleton by 4 h after the initiation of H2O2 exposure. Filamentous actin (f‐actin) staining suggested that the re‐associating actin took the form of short fibers associated with cortical actin rather than long stress fibers. Furthermore, pretreatment with KGF prevented the loss of actin and MHC from the actin cytoskeleton but did not prevent the decrease in TER. These studies suggest that actin disassembly from the cytoskeleton is important in the loss of barrier function, but that it is not the overall amount of actin that is associated with the cytoskeleton that is important, rather it is the contribution this actin makes to the architectural cohesiveness of the cell that contributes to the barrier function. J. Cell. Physiol. 199: 57–66, 2004© 2003 Wiley‐Liss, Inc.
Crosstalk of hypoxia‐mediated signaling pathways in upregulating plasminogen activator inhibitor‐1 expression in keloid fibroblasts
Authors: Zhang Qunzhou , Wu Yidi , Chau Cindy H. , Ann David K. , Bertolami Charles N. , Le Anh D. 
Published: February 2004

AbstractKeloids are skin fibrotic conditions characterized by an excess accumulation of extracellular matrix (ECM) components secondary to trauma or surgical injuries. Previous studies have shown that plasminogen activator inhibitor‐1 (PAI‐1) can be upregulated by hypoxia and may contribute to keloid pathogenesis. In this study we investigate the signaling mechanisms involved in hypoxia‐mediated PAI‐1 expression in keloid fibroblasts. Using Northern and Western blot analysis, transient transfections, and pharmacological agents, we demonstrate that hypoxia‐induced upregulation of PAI‐1 expression is mainly controlled by hypoxia inducible factors‐1α (HIF‐1α) and that hypoxia leads to a rapid and transient activation of phosphatidylinositol‐3‐kinase/Akt (PI3‐K/Akt) and extracellular signal‐regulated kinases 1/2 (ERK1/2). Treatment of cells with PI‐3K/Akt inhibitor (LY294002) and tyrosine protein kinase inhibitor (genistein) significantly attenuated hypoxia‐induced PAI‐1 mRNA and protein expression as well as promoter activation, apparently via an inhibition of the hypoxia‐induced stabilization of HIF‐1α protein, attenuation of the steady‐state level of HIF‐1α mRNA, and its DNA‐binding activity. Even though disruption of ERK1/2 signaling pathway by PD98059 abolished hypoxia‐induced PAI‐1 promoter activation and mRNA/protein expression in keloid fibroblasts, it did not inhibit the hypoxia‐mediated stabilization of HIF‐1α protein and the steady‐state level of HIF‐1α mRNA nor its DNA binding activity. Our findings suggest that a combination of several signaling pathways, including ERK1/2, PI3‐K/Akt, and protein tyrosine kinases (PTKs), may contribute to the hypoxia‐mediated induction of PAI‐1 expression via activation of HIF‐1α in keloid fibroblasts. J. Cell. Physiol. 199: 89–97, 2004© 2003 Wiley‐Liss, Inc.
Ceramide induces caspase‐dependent and ‐independent apoptosis in A‐431 cells
Authors: Zhao Sheng , Yang Ya‐Nan , Song Jian‐Guo 
Published: February 2004

AbstractWe investigated the ceramide‐induced apoptosis and potential mechanism in A‐431 cells. Ceramide treatment causes the round up and the death of A‐431 cells that is associated with p38 activation and can be observed in 10 h. Short‐time ceramide treatment‐induced cell death is not associated with the typical apoptotic phenotypes, such as the translocation of phosphatidylserine (PS) from inner layer to outer layer of the plasma membrane, loss of mitochondrial membrane potential, DNA fragmentation, caspase activation, and PARP or PKC‐δ degradation. SB202190, a specific inhibitor of p38 mitogen‐activated protein (MAP) kinase, but not caspase inhibitor, blocks the cell death induced by short‐time ceramide treatment (within 12 h). Whereas neither inhibition of p38 MAP kinase nor inhibition of caspases blocks cell death induced by prolonged ceramide treatment. Moreover, incubation of cells with ceramide for a long time (over 12 h) results in the reduction of proportion of S phase accompanied with typical apoptotic cell death phenotypes that are different from the cell death induced by short‐time ceramide treatment. Our data demonstrated that ceramide‐induced apoptotic cell death involves both caspase‐dependent and caspase‐independent signaling pathways. The caspase‐independent cell death that occurred in relatively early stage of ceramide treatment is mediated via p38 MAP kinase, which can progress into a stage that is associated with changes of cell cycle events and involves both caspase‐dependent and ‐independent mechanisms. J. Cell. Physiol. 199: 47–56, 2004© 2003 Wiley‐Liss, Inc.