bluuebunny/crossref_metadata_2025_split huggingface dataset:
Motif Reconstruction in Clusters and Layers: Benchmarks for the Kawska–Zahn Approach to Model Crystal Formation
Authors: Milek Theodor , Duchstein Patrick , Seifert Gotthard , Zahn Dirk 
Published: January 2010

AbstractA recently developed atomistic simulation scheme for investigating ion aggregation from solution is transferred to the morphogenesis of metal clusters grown from the vapor and layers deposited on a substrate surface. Both systems are chosen as benchmark models for intense motif reorganization during aggregate/layer growth. The applied simulation method does not necessarily involve global energy minimization after each growth event, but instead describes crystal growth as a series of structurally related configurations which may also include local energy minima. Apart from the particularly favorable high‐symmetry configurations known from experiments and global energy minimization, we also demonstrate the investigation of transient structures. In the spirit of Ostwald’s step rule, a continuous evolution of the aggregate/layer structure during crystal growth is observed.
c‐Rel but not NF‐κB1 is important for T regulatory cell development
Authors: Deenick Elissa K. , Elford Alisha R. , Pellegrini Marc , Hall Håkan , Mak Tak W. , Ohashi Pamela S. 
Published: January 2010

AbstractRegulatory T (Treg) cells are crucial for maintaining peripheral tolerance and controlling T‐cell responses. The generation of Treg in the thymus requires TCR triggering and CD28 costimulation. Engagement of these receptors induces a number of signalling pathways, including the activation of NF‐κB via PKCθ and the Bcl‐10/CARMA1/MALT complex. Previous studies have shown that PKCθ, Bcl‐10 and CARMA1 are important for Treg development. It is unclear, however, whether different members of the NF‐κB family contribute to Treg development or homeostasis. In this study, we show that Treg numbers are reduced in the absence of c‐Rel but not NF‐κB1 (p50). Furthermore, using mixed bone marrow chimeras from WT and KO animals, we demonstrate that the requirement for PKCθ, Bcl‐10 and c‐Rel is T‐cell intrinsic, and cannot be rescued by the presence of WT cells. Therefore, c‐Rel and NF‐κB1 have differential roles in Treg development.
Determination of the Nature of Exchange Interactions in the 3d–4f Magnetic Chain {[Cu(salen)Pr(hfac)3]2(L)}n (L = 4,4′‐Bipyridine, Pyrazine)
Authors: Pointillart Fabrice , Bernot Kevin 
Published: January 2010

AbstractThe reaction of copper(II)–praseodymium(III) 3d–4f precursors with nitrogenated ligands yields to a 3d–4f–4f–3d pseudo‐1D compound with the formula {[{Cu(salen)}{Pr(hfac)3}2(pyz)](H2O)3} (pyz = pyrazole). A “comparative method” was used to determine the nature of the magnetic interactions in this magnetic chain, by analysing the magnetic behaviour of diamagnetic or building‐block analogues. This method allows the estimation of the nature of all the magnetic interactions in the compound even in the presence of the orbitally degenerate PrIII ion. Two intramolecular exchange interactions [3d(CuII)–4f(PrIII) and 4f(PrIII)–4f(PrIII)] and one intermolecular exchange interaction [3d(CuII)–3d(CuII)] have been identified, and they have been found to be antiferromagnetic. The buildings blocks were obtained by reaction of Cu(salen) complexes with Pr(hfac)3·3H2O, and the dinuclear [Cu(salen)Pr(hfac)3(H2O)n] {hfac– = 1,1,1,5,5,5‐hexafluoroacetylacetonate, H2salen = N,N′‐ethane‐1,2‐diylbis(salicylidenamine), n = 0 or 1} or the heterotetranuclear {[{Cu(salen)}{Pr(hfac)3}2(bpy)](CHCl3)2} compounds were formed. The diamagnetic analogues were obtained by substituting copper(II) by nickel(II). Evidence of a change of the crystal field around the PrIII ion as a result of the presence of a nitrogenated ligand in its coordination sphere is provided. The change in the crystal field leads to a different energy distribution of the Stark sublevels and allows the determination of the CuII–PrIII interaction.
Does age at onset have clinical significance in older adults with bipolar disorder?
Authors: Chu David , Gildengers Ariel G. , Houck Patricia R. , Anderson Stewart J. , Mulsant Benoit H. , Reynolds Charles F. , Kupfer David J. 
Published: January 2010

AbstractObjectiveWhile age at onset may be useful in explaining some of the heterogeneity of bipolar disorder (BD) in large, mixed age groups, investigations to date have found few meaningful clinical differences between early versus late age at onset in older adults with BD.MethodsData were collected from sixty‐one subjects aged 60 years and older, mean (SD) age 67.6 (7.0), with BD I (75%) and II (25%). Subjects were grouped by early (<40 years; n = 43) versus late (≥40 years; n = 18) age at onset. Early versus late onset groups were compared on psychiatric comorbidity, medical burden, and percentage of days well during study participation.ResultsExcept for family history of major psychiatric illnesses, there were no differences between the groups on demographic or clinical variables. Patients with early and late onset experienced similar percentages of days well; however, those with early onset had slightly more percentage of days depressed than those with late onset (22% versus 13%)ConclusionDistinguishing older adults with BD by early or late age at onset has limited clinical usefulness. Copyright © 2010 John Wiley & Sons, Ltd.
Borders, extent, and topography of human perirhinal cortex as revealed using multiple modern neuroanatomical and pathological markers
Authors: Ding Song‐Lin , Van Hoesen Gary W. 
Published: January 2010

AbstractDespite rapidly increasing interests in specific contributions of different components of human medial temporal lobe (MTL) to memory and memory impairments in normal aging and in many abnormal conditions such as Alzheimer's disease and Pick's disease, few modern neuroanatomical studies are available about the borders, extent, and topography of human perirhinal areas 35 and 36, which are important components of the MTL memory system. By a combined use of several cellular, neurochemical, and pathological markers, which mainly include neuronal nuclear antigen, calcium‐binding proteins (parvalbumin and calbindin‐D28k), nonphosphorylated neurofilament protein (SMI‐32), Wisteria floribunda agglutinin, and abnormally phosphorylated tau (AT8), this study has revealed that the borders of human perirhinal areas 35 and 36 are significantly different from those defined with conventional Nissl staining. In general, areas 35 and 36 occupy the ventromedial temporopolar and rhinal sulcal regions, the collateral sulcal region, and the anterior two‐thirds of fusiform gyrus or occipitotemporal gyrus. Furthermore, the precise borders, extent, and topography of human areas 35 and 36 and adjoining entorhinal cortex were marked at different anteroposterior levels of the MTL with reference to variations of rhinal and collateral sulci and other useful landmarks. These findings would provide reliable neuroanatomical base for the great and yet rapidly increasing number of neuroimaging studies of the human MTL structures in healthy and many abnormal conditions. Hum Brain Mapp, 2010. © 2010 Wiley‐Liss, Inc.
Ventral tegmental area disruption selectively affects CA1/CA2 but not CA3 place fields during a differential reward working memory task
Authors: Martig Adria K. , Mizumori Sheri J.Y. 
Published: January 2010

AbstractHippocampus (HPC) receives dopaminergic (DA) projections from the ventral tegmental area (VTA) and substantia nigra. These inputs appear to provide a modulatory signal that influences HPC dependent behaviors and place fields. We examined how efferent projections from VTA to HPC influence spatial working memory and place fields when the reward context changes. CA1 and CA3 process environmental context changes differently and VTA preferentially innervates CA1. Given these anatomical data and electrophysiological evidence that implicate DA in reward processing, we predicted that CA1 place fields would respond more strongly to both VTA disruption and changes in the reward context than CA3 place fields. Rats (N = 9) were implanted with infusion cannula targeting VTA and recording tetrodes aimed at HPC. Then they were tested on a differential reward, win‐shift working memory task. One recording session consisted of 5 baseline and 5 manipulation trials during which place cells in CA1/CA2 (N = 167) and CA3 (N = 94) were recorded. Prior to manipulation trials rats were infused with either baclofen or saline and then subjected to control or reward conditions during which the learned locations of large and small reward quantities were reversed. VTA disruption resulted in an increase in errors, and in CA1/CA2 place field reorganization. There were no changes in any measures of CA3 place field stability during VTA disruption. Reward manipulations did not affect performance or place field stability in CA1/CA2 or CA3; however, changes in the reward locations “rescued” performance and place field stability in CA1/CA2 when VTA activity was compromised, perhaps by trigging compensatory mechanisms. These data support the hypothesis that VTA contributes to spatial working memory performance perhaps by maintaining place field stability selectively in CA1/CA2. © 2010 Wiley‐Liss, Inc.
CXCL10/CXCR3 signaling in glia cells differentially affects NMDA‐induced cell death in CA and DG neurons of the mouse hippocampus
Authors: van Weering Hilmar R.J. , Boddeke Hendrikus W.G.M. , Vinet Jonathan , Brouwer Nieske , de Haas Alexander H. , van Rooijen Nico , Thomsen Allan R. , Biber Knut P.H. 
Published: January 2010

AbstractThe chemokine CXCL10 and its receptor CXCR3 are implicated in various CNS pathologies since interference with CXCL10/CXCR3 signaling alters the onset and progression in various CNS disease models. However, the mechanism and cell‐types involved in CXCL10/CXCR3 signaling under pathological conditions are far from understood. Here, we investigated the potential role for CXCL10/CXCR3 signaling in neuronal cell death and glia activation in response to N‐methyl‐D‐aspartic acid (NMDA)‐induced excitotoxicity in mouse organotypic hippocampal slice cultures (OHSCs). Our findings demonstrate that astrocytes express CXCL10 in response to excitotoxicity. Experiments in OHSCs derived from CXCL10‐deficient (CXCL10−/−) and CXCR3‐deficient (CXCR3−/−) revealed that in the absence of CXCL10 or CXCR3, neuronal cell death in the CA1 and CA3 regions was diminished after NMDA‐treatment when compared to wild type OHSCs. In contrast, neuronal cell death in the DG region was enhanced in both CXCL10−/− and CXCR3−/− OHSCs in response to a high (50 μM) NMDA‐concentration. Moreover, we show that in the absence of microglia the differential changes in neuronal vulnerability between CXCR3−/− and wild type OHSCs are fully abrogated and therefore a prominent role for microglia in this process is suggested. Taken together, our results identify a region‐specific role for CXCL10/CXCR3 signaling in neuron‐glia and glia‐glia interactions under pathological conditions. © 2010 Wiley‐Liss, Inc.
Lesions affecting the right hippocampal formation differentially impair short‐term memory of spatial and nonspatial associations
Authors: Braun Mischa , Weinrich Christiane , Finke Carsten , Ostendorf Florian , Lehmann Thomas‐Nicolas , Ploner Christoph J. 
Published: January 2010

AbstractConverging evidence from behavioral and imaging studies suggests that within the human medial temporal lobe (MTL) the hippocampal formation may be particularly involved in recognition memory of associative information. However, it is unclear whether the hippocampal formation processes all types of associations or whether there is a specialization for processing of associations involving spatial information. Here, we investigated this issue in six patients with postsurgical lesions of the right MTL affecting the hippocampal formation and in ten healthy controls. Subjects performed a battery of delayed match‐to‐sample tasks with two delays (900/5,000 ms) and three set sizes. Subjects were requested to remember either single features (colors, locations, shapes, letters) or feature associations (color‐location, color‐shape, color‐letter). In the single‐feature conditions, performance of patients did not differ from controls. In the association conditions, a significant delay‐dependent deficit in memory of color‐location associations was found. This deficit was largely independent of set size. By contrast, performance in the color‐shape and color‐letter conditions was normal. These findings support the hypothesis that a region within the right MTL, presumably the hippocampal formation, does not equally support all kinds of visual memory but rather has a bias for processing of associations involving spatial information. Recruitment of this region during memory tasks appears to depend both on processing type (associative/nonassociative) and to‐be‐remembered material (spatial/nonspatial). © 2010 Wiley‐Liss, Inc.
Association of endothelial nitric oxide synthase and mitochondrial dysfunction in the hippocampus of scrapie‐infected mice
Authors: Park Jeong‐Ho , Kim Boe‐Hyun , Park Seok‐Joo , Jin Jae‐Kwang , Jeon Yong‐Chul , Wen Guang Y. , Shin Hae‐Young , Carp Richard I. , Kim Yong‐Sun 
Published: January 2010

AbstractThe elevation of nitric oxide (NO) within the central nervous system (CNS) is known to be associated with the pathogenesis of neurodegenerative diseases such as HIV‐associated dementia (HAD), brain ischemia, Parkinson's disease, and Alzheimer's disease. NO is enzymatically formed by the enzyme nitric oxide synthase (NOS). There are two forms of NOS, the constitutive and the inducible form. The constitutive form is present in endothelial cells (eNOS) and neurons (nNOS). The inducible form (iNOS) is expressed in various cell types including astroglia and microglia of the CNS. Using an animal model, we investigated the involvement of eNOS in the pathology of prion disease. We showed dramatic upregulation of eNOS immunoreactivity in reactive astroglial cells in the hippocampus in the prion disease animal model, scrapie in mice. Expression of eNOS was upregulated in cytosolic and mitochondrial fractions of whole brain. In the hippocampal region, eNOS was widely overexpressed in various components of the cell. We found that eNOS dramatically accumulated in hippocampal mitochondria and was particularly prevalent in structurally dysfunctional mitochondria. In association with the accumulation of eNOS in mitochondria, we showed that mitochondrial superoxide dismutase (Mn‐SOD or SOD2), cytochrome c, and ATP activity were downregulated both in whole brain and in the hippocampal region. These results indicate that eNOS plays a role in the development of dysfunctional mitochondria and this, in turn, could induce some of the histopathological changes seen in prion diseases. © 2010 Wiley‐Liss, Inc.
2‐methoxyestradiol‐mediated anti‐tumor effect increases osteoprotegrin expression in osteosarcoma cells
Authors: Benedikt Michaela B. , Mahlum Eric W. , Shogren Kristen L. , Subramaniam Malayannan , Spelsberg Thomas C. , Yaszemski Michael J. , Maran Avudaiappan 
Published: January 2010

AbstractOsteosarcoma is a bone tumor that frequently develops during adolescence. 2‐Methoxyestradiol (2‐ME), a naturally occurring metabolite of 17β‐estradiol, induces cell cycle arrest and cell death in human osteosarcoma cells. To investigate whether the osteoprotegrin (OPG) protein plays a role in 2‐ME actions, we studied the effect of 2‐ME treatment on OPG gene expression in human osteosarcoma cells. 2‐ME treatment induced OPG gene promoter activity and mRNA levels. Also, Western blot analysis showed that 2‐ME treatment increased OPG protein levels in MG63, KHOS, 143B and LM7 osteosarcoma cells by 3‐, 1.9‐, 2.8‐, and 2.5‐fold, respectively, but did not affect OPG expression in normal bone cells. In addition, increases in OPG protein levels were observed in osteosarcoma cell culture media after 3 days of 2‐ME treatment. The effect of 2‐ME on osteosarcoma cells was ligand‐specific as parent estrogen, 17β‐estradiol and a tumorigenic estrogen metabolite, 16α‐hydroxyestradiol, which do not affect osteosarcoma cell cycle and cell death, had no effect on OPG protein expression. Furthermore, co‐treating osteosarcoma cells with OPG protein did not further enhance 2‐ME‐mediated anti‐tumor effects. OPG‐released in 2‐ME‐treated cultures led to an increase in osteoblastic activity and a decrease in osteoclast number, respectively. These findings suggest that OPG is not directly involved in 2‐ME‐mediated anti‐proliferative effects in osteosarcoma cells, but rather participates in anti‐resorptive functions of 2‐ME in bone tumor environment. J. Cell. Biochem. 109: 950–956, 2010. © 2010 Wiley‐Liss, Inc.
Extracellular‐regulated kinase—mitogen‐activated protein kinase cascade: Unsolved issues
Authors: Bodart Jean‐François L. 
Published: January 2010

AbstractThis review point out several aspects regarding the mitogen‐activated protein kinase (MAPK)/extracellular‐regulated kinase (Erk) network, which are still pending issues in the understanding how this pathway integrate information to drive cell fates. Focusing on the role of Erk during cell cycle, it has to be underlined that Erk downstream effectors, which are required for mitosis progression and contribute to aneuploidy during tumorigenesis, remain to be determined. In addition to the identity of the terminal enzymes or effectors of Erk, it has to be stressed that the dynamic nature of the Erk signal is itself a key factor in cell phenotype decisions. Development of biophotonics strategies for monitoring the Erk network at the spatiotemporal level in living cells, as well as computational and hypothesis‐driven approaches, are called to unravel the principles by which signaling networks create biochemical and biological specificities. Finally, Erk dynamics might also be impacted by other post‐translational modification than phosphorylation, such as O‐GlcNAcylation. J. Cell. Biochem. 109: 850–857, 2010. © 2010 Wiley‐Liss, Inc.
Expression of phosphoinositide‐specific phospholipase C isoenzymes in cultured astrocytes activated after stimulation with lipopolysaccharide
Authors: Lo Vasco Vincenza Rita , Fabrizi Cinzia , Fumagalli Lorenzo , Cocco L. 
Published: January 2010

AbstractSignal transduction pathways, involved in cell cycle and activities, depend on various components including lipid signalling molecules, such as phosphoinositides and related enzymes. Many evidences support the hypothesis that inositol lipid cycle is involved in astrocytes activation during neurodegeneration. Previous studies investigated the pattern of expression of phosphoinositide‐specific phospholipase C (PI‐PLC) family isoforms in astrocytes, individuating in cultured neonatal rat astrocytes, supposed to be quiescent cells, the absence of some isoforms, accordingly to their well known tissue specificity. The same study was conducted in cultured rat astrocytoma C6 cells and designed a different pattern of expression of PI‐PLCs in the neoplastic counterpart, accordingly to literature suggesting a PI signalling involvement in tumour progression. It is not clear the role of PI‐PLC isoforms in inflammation; recent data demonstrate they are involved in cytokines production, with special regard to IL‐6. PI‐PLCs expression in LPS treated neonatal rat astrocytes performed by using RT‐PCR, observed at 3, 6, 18 and 24 h intervals, expressed: PI‐PLC beta1, beta4 and gamma1 in all intervals analysed; PI‐PLC delta1 at 6, 18 and 24 h; PI‐PLC delta3 at 6 h after treatment. PI‐PLC beta3, delta4 and epsilon, present in untreated astrocytes, were not detected after LPS treatment. Immunocytochemical analysis, performed to visualize the sub‐cellular distribution of the expressed isoforms, demonstrated different patterns of localisation at different times of exposure. These observations suggest that PI‐PLCs expression and distribution may play a role in ongoing inflammation process of CNS. J. Cell. Biochem. 109: 1006–1012, 2010. © 2010 Wiley‐Liss, Inc.
CtBP levels control intergenic transcripts, PHO/YY1 DNA binding, and PcG recruitment to DNA
Authors: Basu Arindam , Atchison Michael L. 
Published: January 2010

AbstractCarboxy‐terminal binding protein (CtBP) is a well‐known corepressor of several DNA binding transcription factors in Drosophila as well as in mammals. CtBP is implicated in Polycomb Group (PcG) complex‐mediated transcriptional repression because it can bind to some PcG proteins, and mutation of the ctbp gene in flies results in lost PcG protein recruitment to Polycomb Response Elements (PREs) and lost PcG repression. However, the mechanism of reduced PcG DNA binding in CtBP mutant backgrounds is unknown. We show here that in a Drosophila CtBP mutant background, intergenic transcripts are induced across several PRE sequences and this corresponds to reduced DNA binding by PcG proteins Pleiohomeotic (PHO) and Polycomb (Pc), and reduced trimethylation of histone H3 on lysine 27, a hallmark of PcG repression. Restoration of CtBP levels by expression of a CtBP transgene results in repression of intergenic transcripts, restored PcG binding, and elevated trimethylation of H3 on lysine 27. Our results support a model in which CtBP regulates expression of intergenic transcripts that controls DNA binding by PcG proteins and subsequent histone modifications and transcriptional activity. J. Cell. Biochem. 110: 62–69, 2010. © 2010 Wiley‐Liss, Inc.
Symmetrization of the AMBER and CHARMM force fields
Authors: Małolepsza Edyta , Strodel Birgit , Khalili Mey , Trygubenko Semen , Fejer Szilard N. , Wales David J. 
Published: January 2010

AbstractThe AMBER and CHARMM force fields are analyzed from the viewpoint of the permutational symmetry of the potential for feasible exchanges of identical atoms and chemical groups in amino and nucleic acids. In each case, we propose schemes for symmetrizing the potentials, which greatly facilitate the bookkeeping associated with constructing kinetic transition networks via geometry optimization. © 2010 Wiley Periodicals, Inc. J Comput Chem, 2010
Nonclassical fullerenes with a heptagon violating the pentagon adjacency penalty rule
Authors: Gan Li‐Hua , Zhao Jian‐Qiang , Hui Qun 
Published: January 2010

AbstractNonclassical fullerenes with heptagon(s) and their derivatives have attracted increasing attention, and the studies on them are performing to enrich the chemistry of carbon. Density functional theory calculations are performed on nonclassical fullerenes Cn (n = 46, 48, 50, and 52) to give insight into their structures and stability. The calculated results demonstrate that the classical isomers generally satisfy the pentagon adjacency penalty rule. However, the nonclassical isomers with a heptagon are more energetically favorable than the classical ones with the same number of pentagon–pentagon bonds (B55 bonds), and many of them are even more stable than some classical isomers with fewer B55 bonds. The nonclassical isomers with the lowest energy are higher in energy than the classical ones with the lowest energy, because they have more B55 bonds. Generally, the HOMO–LUMO gaps of the former are larger than those of the latter. The sphericity and asphericity are unable to rationalize the unique stability of the nonclassical fullerenes with a heptagon. The pyramidization angles of the vertices shared by two pentagons and one heptagon are smaller than those of the vertices shared by two pentagons and one hexagon. It is concluded that the strain in the fused pentagons can be released by the adjacent heptagons partly, and consequently, it is a common phenomenon for nonclassical fullerenes to violate the pentagon adjacent penalty rule. These findings are heuristic and conducive to search energetically favorable isomers of Cn, especially as n is 62, 64, 66, and 68, respectively. © 2010 Wiley Periodicals, Inc. J Comput Chem, 2010