bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increasing the time step with mass scaling in Born‐Oppenheimer ab initio QM/MM molecular dynamics simulations
Authors: Zheng Han , Wang Shenglong , Zhang Yingkai 
Published: April 2009

AbstractBorn‐Oppenheimer ab initio QM/MM molecular dynamics simulation with umbrella sampling is a state‐of‐the‐art approach to calculate free energy profiles of chemical reactions in complex systems. To further improve its computational efficiency, a mass‐scaling method with the increased time step in MD simulations has been explored and tested. It is found that by increasing the hydrogen mass to 10 amu, a time step of 3 fs can be employed in ab initio QM/MM MD simulations. In all our three test cases, including two solution reactions and one enzyme reaction, the resulted reaction free energy profiles with 3 fs time step and mass scaling are found to be in excellent agreement with the corresponding simulation results using 1 fs time step and the normal mass. These results indicate that for Born‐Oppenheimer ab initio QM/MM molecular dynamics simulations with umbrella sampling, the mass‐scaling method can significantly reduce its computational cost while has little effect on the calculated free energy profiles. © 2009 Wiley Periodicals, Inc. J Comput Chem, 2009
Differences amid bone marrow and cord blood hematopoietic stem/progenitor cell division kinetics
Authors: da Silva Cláudia Lobato , Gonçalves Raquel , Porada Christopher D. , Ascensão João L. , Zanjani Esmail D. , Cabral Joaquim M.S. , Almeida‐Porada Graça 
Published: April 2009

AbstractHuman hematopoietic stem/progenitor cells (HSC) isolated based upon specific patterns of CD34 and CD38 expression, despite phenotypically identical, were found to be functionally heterogeneous, raising the possibility that reversible expression of these antigens may occur during cellular activation and/or proliferation. In these studies, we combined PKH67 tracking with CD34/CD38 immunostaining to compare cell division kinetics between human bone marrow (BM) and cord blood (CB)‐derived HSC expanded in a serum‐free/stromal‐based system for 14 days (d), and correlated CD34 and CD38 expression with the cell divisional history. CB cells began dividing 24 h earlier than BM cells, and significantly higher numbers underwent mitosis during the time in culture. By d10, over 55% of the CB‐cells reached the ninth generation, whereas BM‐cells were mostly distributed between the fifth and seventh generation. By d14, all CB cells had undergone multiple cell divisions, while 0.7–3.8% of BM CD34+ cells remained quiescent. Furthermore, the percentage of BM cells expressing CD34 decreased from 60.8 ± 6.3% to 30.6 ± 6.7% prior to initiating division, suggesting that downmodulation of this antigen occurred before commencement of proliferation. Moreover, with BM, all primitive CD34+CD38− cells present at the end of culture arose from proliferating CD34+CD38+ cells that downregulated CD38 expression, while in CB, a CD34+CD38− population was maintained throughout culture. These studies show that BM and CB cells differ significantly in cell division kinetics and expression of CD34 and CD38, and that the inherent modulation of these antigens during ex vivo expansion may lead to erroneous quantification of the stem cell content of the expanded graft. J. Cell. Physiol. 220: 102–111, 2009. © 2009 Wiley‐Liss, Inc.
Elevated Golgi pH impairs terminal N‐glycosylation by inducing mislocalization of Golgi glycosyltransferases
Authors: Rivinoja Antti , Hassinen Antti , Kokkonen Nina , Kauppila Annika , Kellokumpu Sakari 
Published: April 2009

AbstractAcidic pH of the Golgi lumen is known to be crucial for correct glycosylation, transport and sorting of proteins and lipids during their transit through the organelle. To better understand why Golgi acidity is important for these processes, we have examined here the most pH sensitive events in N‐glycosylation by sequentially raising Golgi luminal pH with chloroquine (CQ), a weak base. We show that only a 0.2 pH unit increase (20 µM CQ) is sufficient to markedly impair terminal α(2,3)‐sialylation of an N‐glycosylated reporter protein (CEA), and to induce selective mislocalization of the corresponding α(2,3)‐sialyltransferase (ST3) into the endosomal compartments. Much higher pH increase was required to impair α(2,6)‐sialylation, or the proximal glycosylation steps such as β(1,4)‐galactosylation or acquisition of Endo H resistance, and the steady‐state localization of the key enzymes responsible for these modifications (ST6, GalT I, MANII). The overall Golgi morphology also remained unaltered, except when Golgi pH was raised close to neutral. By using transmembrane domain chimeras between the ST6 and ST3, we also show that the luminal domain of the ST6 is mainly responsible for its less pH sensitive localization in the Golgi. Collectively, these results emphasize that moderate Golgi pH alterations such as those detected in cancer cells can impair N‐glycosylation by inducing selective mislocalization of only certain Golgi glycosyltransferases. J. Cell. Physiol. 220: 144–154, 2009. © 2009 Wiley‐Liss, Inc.
Enhanced transgene expression in the mouse skeletal muscle infected by the adeno‐associated viral vector with the human elongation factor 1α promoter and a human chromatin insulator
Authors: Mori‐Uchino Mayuyo , Takeuchi Takamasa , Murakami Isao , Yano Tetsu , Yasugi Toshiharu , Taketani Yuji , Nakagawa Keiichi , Kanda Tadahito 
Published: April 2009

AbstractBackgroundEfficient and continuous expression of a therapeutic transgene is a key factor for improving the efficacy of gene therapy. Some insulators are known to contribute to continuous high‐level expression of a therapeutic transgene.MethodsUsing the human AAVS1 insulator (DHS) found in the AAVS1 DNase I hypersensitive site, chicken β‐globin insulator (cHS4) and sea urchin arylsufatase insulator (Ars), we newly constructed three recombinant adeno‐associated virus vectors (rAAV) and examined their capability of transducing the mouse quadriceps muscle.ResultsDHS increased transgene expression from the human elongation factor 1α promoter (EF) by 1000‐fold, up to the high level achieved by the human cytomegalovirus immediate early promoter/enhancer (CMV), which comprises an extremely strong promoter for driving a transgene. cHS4 enhanced the expression by 100‐fold, whereas Ars did not. The enhanced expression was maintained for at least 24 weeks. Vector copy numbers were similar with and without DHS or cHS4; thus, the enhancement is most likely due to up‐regulated transcription. Neither DHS, nor cHS4 affected transgene expression from CMV. DHS enhanced expression from the human muscle creatine kinase promoter/enhancer by 100‐fold in mice, as did DHS from EF.ConclusionsAlthough DHS was unable to further enhance high expression from the strong viral enhancer/promoter, it enhanced low expression from the human promoters by 100‐ to 1000‐fold. Thus, DHS may be useful for constructing rAAVs that express a therapeutic transgene from less efficient, tissue specific promoters. Copyright © 2009 John Wiley & Sons, Ltd.
Families of pairs of graphs with a large number of common cards
Authors: Bowler Andrew , Brown Paul , Fenner Trevor 
Published: April 2009

AbstractThe vertex‐deleted subgraph G−v, obtained from the graph G by deleting the vertex v and all edges incident to v, is called a card of G. The deck of G is the multiset of its unlabelled vertex‐deleted subgraphs. The number of common cards of G and H (or between G and H) is the cardinality of the multiset intersection of the decks of G and H. In this article, we present infinite families of pairs of graphs of order n ≥ 4 that have at least \documentclass{article}\footskip=0pc\pagestyle{empty}\begin{document}\begin{eqnarray*}2\lfloor\frac{1}{3}(n-1)\rfloor\end{eqnarray*}\end{document} common cards; we conjecture that these, along with a small number of other families constructed from them, are the only pairs of graphs having this many common cards, for sufficiently large n. This leads us to propose a new stronger version of the Reconstruction Conjecture. In addition, we present an infinite family of pairs of graphs with the same degree sequence that have \documentclass{article}\footskip=0pc\pagestyle{empty}\begin{document}\begin{eqnarray*}\frac{2}{3}(n+5-2\sqrt{3n+6})\end{eqnarray*}\end{document} common cards, for appropriate values of n, from which we can construct pairs having slightly fewer common cards for all other values of n≥10. We also present infinite families of pairs of forests and pairs of trees with \documentclass{article}\footskip=0pc\pagestyle{empty}\begin{document}\begin{eqnarray*}2\lfloor\frac{1}{3}(n-4)\rfloor\end{eqnarray*}\end{document} and \documentclass{article}\footskip=0pc\pagestyle{empty}\begin{document}\begin{eqnarray*}2\lfloor\frac{1}{3}(n-5)\rfloor\end{eqnarray*}\end{document} common cards, respectively. We then present new families that have the maximum number of common cards when one graph is connected and the other disconnected. Finally, we present a family with a large number of common cards, where one graph is a tree and the other unicyclic, and discuss how many cards are required to determine whether a graph is a tree. © 2009 Wiley Periodicals, Inc. J Graph Theory 63: 146–163, 2010
Finite fields and the 1‐chromatic number of orientable surfaces
Authors: Korzhik Vladimir P. 
Published: April 2009

AbstractThe 1‐chromatic number χ1(Sp) of the orientable surface Sp of genus p is the maximum chromatic number of all graphs which can be drawn on the surface so that each edge is crossed by no more than one other edge. We show that if there exists a finite field of order 4m+1, m≥3, then 8m+2≤χ1(S)≤8m+3, where 8m+3 is Ringel's upper bound on χ1(S). © 2009 Wiley Periodicals, Inc. J Graph Theory 63: 179–184, 2010
Balanced judicious bipartitions of graphs
Authors: Xu Baogang , Yan Juan , Yu Xingxing 
Published: April 2009

AbstractA bipartition of the vertex set of a graph is called balanced if the sizes of the sets in the bipartition differ by at most one. B. Bollobás and A. D. Scott, Random Struct Alg 21 (2002), 414–430 conjectured that if G is a graph with minimum degree of at least 2 then V(G) admits a balanced bipartition V1, V2 such that for each i, G has at most |E(G)|/3 edges with both ends in Vi. The minimum degree condition is necessary, and a result of B. Bollobás and A. D. Scott, J. Graph Theory 46 (2004), 131–143 shows that this conjecture holds for regular graphs G(i.e., when Δ(G)=δ(G)). We prove this conjecture for graphs G with \documentclass{article}\footskip=0pc\pagestyle{empty}\begin{document}\begin{eqnarray*}\Delta(G)\le\frac{7}{5}\delta(G)\end{eqnarray*}\end{document}; hence, it holds for graphs ]ensuremathG with \documentclass{article}\footskip=0pc\pagestyle{empty}\begin{document}\begin{eqnarray*}\delta(G)\ge\frac{5}{7}|V(G)|\end{eqnarray*}\end{document}. © 2009 Wiley Periodicals, Inc. J Graph Theory 63: 210–225, 2010
Towards a comprehensive model of feather regeneration
Authors: Maderson Paul F.A. , Hillenius Willem J. , Hiller Uwe , Dove Carla C. 
Published: April 2009

AbstractUnderstanding of the regeneration of feathers, despite a 140 year tradition of study, has remained substantially incomplete. Moreover, accumulated errors and mis‐statements in the literature have confounded the intrinsic difficulties in describing feather regeneration. Lack of allusion to Rudall's (Rudall [1947] Biochem Biophys Acta 1:549–562) seminal X‐ray diffraction study that revealed two distinct keratins, β‐ and α‐, in a mature feather, is one of the several examples where lack of citation long inhibited progress in understanding. This article reviews and reevaluates the available literature and provides a synthetic, comprehensive, morphological model for the regeneration of a generalized, adult contour feather. Particular attention is paid to several features that have previously been largely ignored. Some of these, such as the β‐keratogenic sheath and the α‐keratogenic, supra‐umbilical, pulp caps, are missing from mature, functional feathers sensu stricto because they are lost through preening, but these structures nevertheless play a critical role in development. A new developmental role for a tissue unique to feathers, the medullary pith of the rachis and barb rami, and especially its importance in the genesis of the superior umbilical region (SUR) that forms the transition from the spathe (rachis and vanes) to the calamus, is described. It is postulated that feathers form through an intricate interplay between cyto‐ and histodifferentiative processes, determined by patterning signals that emanate from the dermal core, and a suite of interacting biomechanical forces. Precisely regulated patterns of loss of intercellular adhesivity appear to be the most fundamental aspect of feather morphogenesis and regeneration: rather than a hierarchically branched structure, it appears more appropriate to conceive of feathers as a sheet of mature keratinocytes that is “full of holes. J. Morphol. 2009. © 2009 Wiley‐Liss, Inc.
Effects of temperature elevation on neuronal inhibition in hippocampal neurons of immature and mature rats
Authors: Qu Lintao , Leung L. Stan 
Published: April 2009

AbstractFebrile seizures are the most common seizure type in children, and hyperthermia may contribute to seizure generation during fever. We have previously demonstrated that hyperthermia suppressed γ‐aminobutyric acid (GABA)‐ergic synaptic transmission in CA1 neurons of immature rats. However, whether this suppression is age‐dependent is unknown. Moreover, it is unclear whether hyperthermia has differential effects on neuronal inhibition in CA1 pyramidal cells (PCs) and dentate gyrus granule cells (GCs). In this study, we investigated the effects of hyperthermia on GABAA and GABAB receptor‐mediated inhibitory postsynaptic currents (IPSCs) in CA1 and DG neurons from immature (11–17 days old) and mature (6–8 weeks old) rats using whole‐cell recordings in vitro. In immature rats, hyperthermia decreased the peak amplitude of GABAA receptor‐mediated IPSCs (GABAA IPSCs) in PCs but not in GCs. However, hyperthermia decreased the decay time constant of GABAA IPSCs to a similar extent in both PCs and GCs. In mature rats, hyperthermia decreased the peak amplitude but not the decay time constant of GABAA IPSCs in both PCs and GCs. Hyperthermia decreased charge transfer (area) of the GABAA IPSC of PCs more in immature than in mature rats. In contrast, hyperthermia decreased the GABAB receptor‐mediated IPSCs to the same degree in immature and mature rats, for either CA1 or DG neurons. Because the hippocampus has been found to be involved in hyperthermia‐induced behavioral seizures in immature rats, we suggest that the higher sensitivity of CA1 inhibitory synaptic function to hyperthermia in immature compared with mature rats might partially explain the higher susceptibility for febrile seizures in immature animals. © 2009 Wiley‐Liss, Inc.
Interleukin‐6 increases intracellular Ca2+ concentration and induces catecholamine secretion in rat carotid body glomus cells
Authors: Fan Juan , Zhang Bo , Shu Hai‐Feng , Zhang Xiao‐Yu , Wang Xi , Kuang Fang , Liu Ling , Peng Zheng‐Wu , Wu Rui , Zhou Zhuan , Wang Bai‐Ren 
Published: April 2009

AbstractAlthough abundant evidence indicates mutual regulation between the immune and the central nervous systems, how the immune signals are transmitted to the brain is still an unresolved question. In a previous study we found strong expression of proinflammatory cytokine receptors, including interleukin (IL)‐1 receptor I and IL‐6 receptor α in the rat carotid body (CB), a well‐known arterial chemoreceptor that senses a variety of chemostimuli in the arterial blood. We demonstrated that IL‐1 stimulation increases intracellular calcium ([Ca2+]i) in CB glomus cells, releases ATP, and increases the discharge rate in carotid sinus nerve. To explore the effect of IL‐6 on CB, here we examine the effect of IL‐6 on [Ca2+]i and catecholamine (CA) secretion in rat CB glomus cells. Calcium imaging showed that extracellular application of IL‐6 induced a rise in [Ca2+]i in cultured glomus cells. Amperometry showed that local application of IL‐6 evoked CA release from glomus cells. Furthermore, the CA secretory response to IL‐6 was blocked by 200 μM Cd2+, a well‐known Ca2+ channel blocker. Our experiments provide further evidence for the responsiveness of the CB to proinflammatory cytokines and indicate that the CB might play a role in inflammation sensing and transmission of such information to the brain. © 2009 Wiley‐Liss, Inc.
Role of P2Y1 receptor in astroglia‐to‐neuron signaling at dorsal spinal cord
Authors: Zeng Jun‐Wei , Liu Xiao‐Hong , Zhao Yan‐Dong , Xiao Zhi , He Wen‐Juan , Hu Zhi‐An , Ruan Huai‐Zhen 
Published: April 2009

AbstractSeveral studies have shown that astrocytes release neurotransmitters into the extracellular space that may then activate receptors on nearby neurons. In the present study, the actions of adenosine 5′‐O‐(2‐thiodiphosphate) (ADPbetaS)‐activated astrocyte conditioned medium (ADPbetaS‐ACM) on cultured dorsal spinal cord neurons were evaluated by using confocal laser scanning microscopy and whole‐cell patch‐clamp recording. ADPbetaS caused astrocytic glutamate efflux (43 μM), which in turn induced inward currents in dorsal horn neurons with short time in culture. The inward currents were abolished by 2‐amino‐5‐phosphonlanoicacid (AP‐5; NMDAR antagonist) plus 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX; non‐NMDAR antagonist) but were unaffected by MRS2179 (selective P2Y1 receptor antagonist). Furthermore, N6‐methyl‐2′‐deoxyadenosine‐3′,5′‐bisphosphate (MRS2179) was used to block glutamate release from astrocytes. As a result, ADPbetaS‐ ACM‐induced inward currents in neurons were significantly blocked. On the other hand, both NMDAR and non‐NMDAR were involved in ADPbetaS‐ACM (concentration was diluted to one‐tenth)‐evoked small [Ca2+]i transients in neurons. Under this condition, the values of glutamate concentrations in the medium are close to values for extracellular glutamate concentrations under physiological conditions. For this reason, it is possible that astrocyte‐derived glutamate is important for distant neuron under physiological conditions at dorsal spinal cord. These observations indicate that astrocytic P2Y1 receptor activation triggered glutamate efflux, which acts on distant neurons to elevate calcium levels or acts on nearby neurons to evoke inward current. Finally, our results support the conclusion that the astrocytic P2Y1 receptor plays an important role in bidirectional communication between astrocytes and neurons. © 2009 Wiley‐Liss, Inc.
Poststroke subgranular and rostral subventricular zone proliferation in a mouse model of neonatal stroke
Authors: Kadam S.D. , Mulholland J.D. , McDonald J.W. , Comi A.M. 
Published: April 2009

AbstractStroke in the neonatal brain is an understudied cause of neurologic morbidity. Recently we have characterized a new immature mouse model of stroke utilizing unilateral carotid ligation alone to produce infarcts and acute seizures in postnatal day 12 (P12) CD‐1 mice. In this study, the amount of poststroke neural progenitor proliferation was examined in the subgranular (SGZ) of the dentate gyrus and the subventricular zone (SVZ) 7, 14, and 21days after ischemia (DAI). A single IP injection (50 mg/kg) of bromodeoxyuridine (BrdU) given 2 hr before perfusion fixation labeled newborn cells. Early cell phenotypes were quantified by colabeling with GFAP, nestin, and DCX. Control mice revealed an age‐dependent decrease in neural proliferation, with an ∼50% drop in BrdU‐labeled cell counts at P33 compared with P19 both in the SGZ and in the SVZ. Significant reduction in the amount of neural proliferation in the ipsilateral injured SGZ of ligated mice correlated with both the severity of the stroke‐injury and the acute seizure scores. Similar correlations were not detected contralaterally. Contralateral SGZ neural proliferation was initially lowered at 7 DAI but normalized by 21 DAI. In both injured and control brains, ∼90% of newborn SGZ cells colabeled with nestin, ∼30% colabeled with GFAP, and a few colabeled with DCX. In contrast, poststroke SVZ cell proliferation was enhanced ipsi‐ more than contralaterally at 7 DAI. In the SVZ, the enhanced neural proliferation normalized to control levels by P33. In conclusion, the neural cell proliferation was differentially altered in the SGZ vs. SVZ after neonatal stroke. © 2009 Wiley‐Liss, Inc.
Evaluation of predicted knee‐joint muscle forces during gait using an instrumented knee implant
Authors: Kim Hyung J. , Fernandez Justin W. , Akbarshahi Massoud , Walter Jonathan P. , Fregly Benjamin J. , Pandy Marcus G. 
Published: April 2009

AbstractMusculoskeletal modeling and optimization theory are often used to determine muscle forces in vivo. However, convincing quantitative evaluation of these predictions has been limited to date. The present study evaluated model predictions of knee muscle forces during walking using in vivo measurements of joint contact loading acquired from an instrumented implant. Joint motion, ground reaction force, and tibial contact force data were recorded simultaneously from a single subject walking at slow, normal, and fast speeds. The body was modeled as an 8‐segment, 21‐degree‐of‐freedom articulated linkage, actuated by 58 muscles. Joint moments obtained from inverse dynamics were decomposed into leg‐muscle forces by solving an optimization problem that minimized the sum of the squares of the muscle activations. The predicted knee muscle forces were input into a 3D knee implant contact model to calculate tibial contact forces. Calculated and measured tibial contact forces were in good agreement for all three walking speeds. The average RMS errors for the medial, lateral, and total contact forces over the entire gait cycle and across all trials were 140 ± 40 N, 115 ± 32 N, and 183 ± 45 N, respectively. Muscle coordination predicted by the model was also consistent with EMG measurements reported for normal walking. The combined experimental and modeling approach used in this study provides a quantitative framework for evaluating model predictions of muscle forces in human movement. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 27:1326–1331, 2009
Quantifying the motion of Kager's fat pad
Authors: Ghazzawi Ahmad , Theobald Peter , Pugh Neil , Byrne Carl , Nokes Len 
Published: April 2009

AbstractKager's fat pad is located in Kager's triangle between the Achilles tendon, the superior cortex of the calcaneus, and flexor hallucis longus (FHL) muscle and tendon. Its biomechanical functions are not yet established, but recent studies suggest it performs important biomechanical roles as it is lined by a synovial membrane and its retrocalcaneal protruding wedge can be observed moving into the bursal space during ankle plantarflexion. Such features have prompted hypotheses that the protruding wedge assists in the lubrication of the Achilles tendon subtendinous area, distributes stress at the Achilles enthesis, and removes debris from within the retrocalcaneal bursa. This study examined the influence of FHL activity and Achilles tendon load on the protruding wedge sliding distance, using both dynamic ultrasound imaging and surface electromyogram. Intervolunteer results showed sliding distance was independent of FHL activity. This study has shown the protruding wedge to slide on average 60% further into the retrocalcaneal bursa when comparing the Achilles tendon loaded versus unloaded, consistently reaching the distal extremity. Sliding distance was dependant on a change in the Achilles tendon insertion angle. Our results support a number of hypothesized biomechanical functions of the protruding wedge including: lubrication of the subtendinous region; reduction of pressure change within the Achilles tendon enthesis organ; and removal of debris from within the retrocalcaneal bursa. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 27:1457–1460, 2009