bluuebunny/crossref_metadata_2025_split huggingface dataset:
Improving the accuracy of predicting disulfide connectivity by feature selection
Authors: Zhu Lin , Yang Jie , Song Jiang‐Ning , Chou Kuo‐Chen , Shen Hong‐Bin 
Published: February 2010

AbstractDisulfide bonds are primary covalent cross‐links formed between two cysteine residues in the same or different protein polypeptide chains, which play important roles in the folding and stability of proteins. However, computational prediction of disulfide connectivity directly from protein primary sequences is challenging due to the nonlocal nature of disulfide bonds in the context of sequences, and the number of possible disulfide patterns grows exponentially when the number of cysteine residues increases. In the previous studies, disulfide connectivity prediction was usually performed in high‐dimensional feature space, which can cause a variety of problems in statistical learning, such as the dimension disaster, overfitting, and feature redundancy. In this study, we propose an efficient feature selection technique for analyzing the importance of each feature component. On the basis of this approach, we selected the most important features for predicting the connectivity pattern of intra‐chain disulfide bonds. Our results have shown that the high‐dimensional features contain redundant information, and the prediction performance can be further improved when these high‐dimensional features are reduced to a lower but more compact dimensional space. Our results also indicate that the global protein features contribute little to the formation and prediction of disulfide bonds, while the local sequential and structural information play important roles. All these findings provide important insights for structural studies of disulfide‐rich proteins. © 2010 Wiley Periodicals, Inc. J Comput Chem, 2010
Investigation of excited‐state properties of fluorene–thiophene oligomers by the SAC‐CI theoretical approach
Authors: Poolmee Potjaman , Hannongbua Supa 
Published: February 2010

AbstractExcited states of fluorene‐ethylenedioxythiophene (FEDOT) and fluorene‐S,S‐dioxide‐thiophene (FTSO2) monomers and dimers were studied by the symmetry‐adapted cluster (SAC)‐configuration interaction (CI) method. The absorption and emission peaks observed in the experimental spectra were theoretically assigned. The first three excited states of the optimized conformers, and the conformers of several torsional angles, were computed by SAC‐CI/D95(d). Accurate absorption spectra were simulated by taking the thermal average for the conformers of torsional angles from 0° to 90°. The conformers of torsional angles 0°, 15°, and 30° mainly contributed to the absorption spectra. The full width at half‐maximum of the FEDOT absorption band is 0.60 eV (4839 cm−1), which agrees very well with the experimental value of 0.61 eV (4900 cm−1). The maximum absorption wavelength is located at 303 nm, which is close to those of the experimental band (327 nm). The calculated absorption spectrum of FTSO2 showed two bands in the range of 225–450 nm. This agrees very well with the available experimental spectrum of a polymer of FTSO2, where two bands are detected. The excited‐state geometries were investigated by CIS/6‐31G(d). These showed a quinoid‐type structure which exhibited a shortening of the inter‐ring distance (0.06 Å for FEDOT and 0.04 Å for FTSO2). The calculated emission energy of FEDOT is 3.43 eV, which agrees very well with the available experimental data (3.46 eV). The fwhmE is about 0.49 eV (3952 cm−1), while the experimental fwhm is 0.43 eV (3500 cm−1). For FTSO2, two bands were also found in the emission spectrum. © 2010 Wiley Periodicals, Inc. J Comput Chem, 2010
Time‐dependent density functional theory study on the hydrogen bonding‐induced twisted intramolecular charge‐transfer excited states of 2‐(4′‐N,N‐dimethylaminophenyl)imidazo[4,5‐b]pyridine
Authors: Yin Shu‐Hui , Liu Yufang , Zhang Wei , Guo Ming‐Xing , Song Peng 
Published: February 2010

AbstractIn this work, the time‐dependent density functional theory (TDDFT) method was carried out to investigate the hydrogen‐bonded intramolecular charge‐transfer excited state of 2‐(4′‐N,N‐dimethylaminophenyl)imidazo[4,5‐b]pyridine (DMAPIP) in methanol (MeOH) solvent. All the geometric conformations of the ground state and locally excited (LE) state and the twisted intramolecular charge‐transfer (TICT) state for isolated DMAPIP and its hydrogen‐bonded complexes have been optimized. At the same time, the absorption and fluorescence spectra of DMAPIP and the hydrogen‐bonded complexes in different electronic states are also calculated. We theoretically demonstrated for the first time that the intermolecular hydrogen bond formed between DMAPIP and MeOH can induce the formation of the TICT state for DMAPIP in MeOH solvent. Therefore, the two components at 414 and 506 nm observed in the fluorescence spectra of DMAPIP in MeOH solvent were reassigned in this work. The fluorescence peak at 414 nm is confirmed to be the LE state. Furthermore, the red‐shifted shoulder at 506 nm should be originated from the hydrogen‐bonded TICT excited state. © 2010 Wiley Periodicals, Inc. J Comput Chem, 2010
27 ps DFT molecular dynamics simulation of α‐maltose: A reduced basis set study
Authors: Schnupf Udo , Willett J. L. , Momany Frank A. 
Published: February 2010

AbstractDFT molecular dynamics simulations are time intensive when carried out on carbohydrates such as α‐maltose. In a recent publication (Momany et al., J. Mol. Struct. THEOCHEM, submitted) forces for dynamics were generated from B3LYP/6‐31+G* electronic structure calculations. The implicit solvent method COSMO was applied to simulate the solution environment. Here we present a modification of the DFT method that keeps the critical aspects of the larger basis set (B3LYP/6‐31+G*) while allowing the less‐essential atom interactions to be calculated using a smaller basis set, thus allowing for faster completion without sacrificing the interactions dictating the hydrogen bonding networks in α‐maltose. In previous studies, the gg′‐gg‐c solvated form quickly converged to the “r” form during a 5 ps dynamics run. This important conformational transition is tested by carrying out a long 27 ps simulation. The trend for the “r” conformer to be most stable during dynamics when fully solvated, is confirmed, resulting in ∼20/80% c/r population. Further, the study shows that considerable molecular end effects are important, the reducing end being fairly stable, the O6H pointing at the O5, while the nonreducing end moves freely to take on different conformations. Some “kink” and transition state forms are populated during the simulation. The average H1′···H4 distance of 2.28 Å confirms that the syn form is the primary glycosidic conformation, while the average C1′O1′C4 bond angle was 118.8°, in excellent agreement with experimental values. The length of this simulation allowed the evaluation of vibrational frequencies by Fourier transform of the velocity correlation function, taken from different time segments along the simulation path. © 2010 Wiley Periodicals, Inc. J Comput Chem, 2010
Convergent and divergent validity of the relationship profile test: investigating the relationship with attachment, interpersonal distress and psychological health
Authors: Haggerty Greg , Blake Margaret , Siefert Caleb J. 
Published: February 2010

AbstractThe present study looked to illustrate the convergent and divergent validity of the Relationship Profile Test (RPT), which is a 30‐item self‐report measuring destructive overdependence, dysfunctional detachment, and healthy dependence. The RPT items are written to draw upon Bornstein's (1992, 1993) 4‐component model as well as other essential components of the dimension in question (Bornstein et al., 2003). The results reveal that the subscales of the RPT are related in predictable ways to scores on measures of adult attachment, interpersonal distress, and psychological health and well‐being. The clinical implications of the results and the assessment of dependency in the clinical setting are discussed. © 2010 Wiley Periodicals, Inc. J Clin Psychol 66: 1–14, 2010.
Epigenetically regulated clonal heritability of CTA expression profiles in human melanoma
Authors: Fratta Elisabetta , Sigalotti Luca , Colizzi Francesca , Covre Alessia , Nicolay Hugues JMG , Danielli Riccardo , Fonsatti Ester , Altomonte Maresa , Calabrò Luana , Coral Sandra , Maio Michele 
Published: February 2010

AbstractThe intratumoral heterogeneity of cancer testis antigens (CTA) expression, which is driven by promoter methylation status, may hamper the effectiveness of CTA‐directed vaccination of melanoma patients. Thus, we investigated whether the intratumoral heterogeneity of CTA expression is inherited at cellular level, or evolves throughout cellular replication, leading to a phenotypically unstable tumor cell population with reduced immunogenicity and/or able to escape immune control. Utilizing a previously characterized ex vivo clonal model of intratumoral heterogeneity of CTA expression in melanoma, Mel 313 MAGE‐A3‐low clone 5 (clone 5M3‐low) and MAGE‐A3‐high clone 14 (clone 14M3‐high) were sub‐cloned and analyzed for CTA profile. Molecular assays demonstrated that levels of MAGE‐A3 expression were highly conserved among generated sub‐clones, as compared to parental clones. A similar behavior was identified for an extensive panel of other CTA investigated. Inherited levels of MAGE‐A3 expression correlated with the extent of promoter methylation among clone 5M3‐low and clone 14M3‐high sub‐clones analyzed. Treatment of clone 5M3‐low with a DNA hypomethylating agent (DHA) resulted in an up‐regulated expression of MAGE‐A3, which was inherited at single cell level, being still detectable at day 60 in its sub‐clones. Bisulfite sequencing demonstrated that also MAGE‐A3 promoter methylation status was inherited among sub‐clones generated from DHA‐treated clone 5M3‐low and strictly correlated with MAGE‐A3 expression levels in investigated sub‐clones. Similar results were obtained for additional CTA studied. Altogether our findings demonstrate that constitutive and DHA‐modified CTA profiles of melanoma cells are clonally inherited throughout cellular replications, thus providing relevant insights to improve the effectiveness of CTA‐based immunotherapy. J. Cell. Physiol. 223: 352–358, 2010. © 2010 Wiley‐Liss, Inc.
Decreased levels of Cx43 gap junctions result in ameloblast dysregulation and enamel hypoplasia inGja1Jrt/+mice
Authors: Toth K. , Shao Q. , Lorentz R. , Laird D.W. 
Published: February 2010

AbstractCoordinated differentiation of the ameloblast cell layer is essential to enamel matrix protein deposition and subsequent mineralization. It has been hypothesized that this process is governed by Cx43‐based gap junctional intercellular communication as oculodentodigital dysplasia (ODDD) patients harboring autosomal‐dominant mutations in Cx43 exhibit enamel defects typically resulting in early adulthood tooth loss. To assess the role of Cx43 in tooth development we employ a mouse model of ODDD that harbors a G60S Cx43 mutant,Gja1Jrt/+, and appears to exhibit tooth abnormalities that mimic the human disease. We found that total Cx43 plaques at all stages of ameloblast differentiation, as well as within the supporting cell layers, were greatly reduced inGja1Jrt/+incisors compared to wild‐type littermate controls. To characterize theGja1Jrt/+mouse tooth phenotype, mice were sacrificed prior to tooth eruption (postnatal day 7), weaning (postnatal day 21), and adulthood (2 months postnatal). A severely disorganizedGja1Jrt/+mouse ameloblast layer and abnormal accumulation of amelogenin were observed at stages when the cells were active in secretion and mineralization. Differences in enamel thickness became more apparent after tooth eruption and incisor exposure to the oral cavity suggesting that enamel integrity is compromised, leading to rapid erosion. Additional analysis of incisors from mutant mice revealed that they were longer with a thicker dentin layer than their wild‐type littermates, which may reflect a mechanical stress response to the depleted enamel layer. Together, these data show that reduced levels of Cx43 gap junctions result in ameloblast dysregulation, enamel hypoplasia, and secondary tissue responses. J. Cell. Physiol. 223:601–609, 2010. © 2010 Wiley‐Liss, Inc.
Electric power in nanoscale devices with full Coulomb interaction
Authors: Albareda G. , Alarcón A. , Oriols X. 
Published: February 2010

AbstractAn accurate reformulation of the electric power in quasi‐ballistic (classical or quantum) scenarios is deduced within an explicit many‐particle treatment of the Coulomb interaction. The traditional definition of the electric power is compared with the new formulation presented here for classical bulk, quantum well and quantum wire double‐gate MOSFETs by means of 3D many‐electron Monte Carlo simulations. The accurate results with the many‐electron approach show not‐negligible discrepancies when compared with the conventional definition. Such small discrepancies become very important when the single‐transistor power is multiplied by the huge number of transistors present in the state‐of‐the‐art integrated circuits. Copyright © 2010 John Wiley & Sons, Ltd.
Functional central nervous system myelin repair in an adult mouse model of demyelination caused by proteolipid protein overexpression
Authors: Espinosa‐Jeffrey A. , Hitoshi S. , Zhao P. , Awosika O. , Agbo C. , Olaniyan E. , Garcia J. , Valera R. , Thomassian A. , Chang‐Wei R. , Yamaguchi M. , de Vellis J. , Ikenaka K. 
Published: February 2010

AbstractTwo types of interventions to remyelinate the adult demyelinated central nervous system were investigated in heterozygous transgenic mice overexpressing the proteolipid protein gene. 1) A cocktail of trophic factors, “TS1,” was directed toward the activation of the endogenous pool of neural progenitors to increase the number of myelinating oligodendrocytes (OL) in the brain. 2) A combinatorial approach in which OL progenitors were coinjected with TS1 into the corpus callosum of wild‐type and He4e transgenic mice that displayed hindlimb paralysis. The levels of locomotor ability in these mice were evaluated after a single treatment. The data showed that a single administration of either one of the interventions had similar therapeutic effects, alleviating the symptoms of demyelination and leading to the recovery of hindlimb function. Histological and immunofluorescent examination of brain sections showed extensive remyelination that was sufficient to reverse hindlimb paralysis in transgenic mice. When the interventions were administered prior to hindlimb paralysis, He4e mice were able to walk up to 1 year of age without paralysis. © 2010 Wiley‐Liss, Inc.
NRAGE is a negative regulator of nerve growth factor‐stimulated neurite outgrowth in PC12 cells mediated through TrkA‐ERK signaling
Authors: Feng Zhenhua , Li Kaizhen , Liu Mei , Wen Chuanjun 
Published: February 2010

AbstractNRAGE, also denominated as MAGE‐D1 or Dlxin‐1, is firstly identified as a molecule interacting with NGF low affinity receptor p75NTR. It facilitates cell cycle arrest and NGF‐dependent neuronal apoptosis. Here we report that NRAGE is downregulated while p75NTR is upregulated during the process of NGF‐induced neuronal differentiation of PC12 cells. Knockdown of NRAGE by RNA interference accelerates NGF‐mediated neurite outgrowth. In addition, in the NRAGE‐suppressed cells, NGF‐induced ERK activation is increased and this activation is MEK‐dependent. Conversely, NRAGE overexpression significantly represses NGF‐induced ERK activation. Further studies revealed that NRAGE downregulates TrkA expression through a post‐transcriptional manner and thereby blocks NGF‐induced TrkA phosphrylation at tyrosine‐490. Altogether, these data indicate for the first time that NRAGE is an endogenous inhibitor for NGF‐induced neuronal differentiation of PC12 cells by regulating TrkA‐ERK signaling. © 2010 Wiley‐Liss, Inc.
Induction of parkinsonism‐related proteins in the spinal motor neurons of transgenic mouse carrying a mutant SOD1 gene
Authors: Morimoto Nobutoshi , Nagai Makiko , Miyazaki Kazunori , Ohta Yasuyuki , Kurata Tomoko , Takehisa Yasushi , Ikeda Yoshio , Matsuura Tohru , Asanuma Masato , Abe Koji 
Published: February 2010

AbstractAmyotrophic lateral sclerosis is a progressive and fatal disease caused by selective death of motor neurons, and a number of these patients carry mutations in the superoxide dismutase 1 (SOD1) gene involved in ameliorating oxidative stress. Recent studies indicate that oxidative stress and disruption of mitochondrial homeostasis is a common mechanism for motor neuron degeneration in amyotrophic lateral sclerosis and the loss of midbrain dopamine neurons in Parkinson's disease. Therefore, the present study investigated the presence and alterations of familial Parkinson's disease‐related proteins, PINK1 and DJ‐1, in spinal motor neurons of G93ASOD1 transgenic mouse model of amyotrophic lateral sclerosis. Following onset of disease, PINK1 and DJ‐1 protein expression increased in the spinal motor neurons. The activated form of p53 also increased and translocated to the nuclei of spinal motor neurons, followed by increased expression of p53‐activated gene 608 (PAG608). This is the first report demonstrating that increased expression of PAG608 correlates with activation of phosphorylated p53 in spinal motor neurons of an amyotrophic lateral sclerosis model. These results provide further evidence of the profound correlations between spinal motor neurons of amyotrophic lateral sclerosis and parkinsonism‐related proteins. © 2010 Wiley‐Liss, Inc.
The comparison of mouse full metallothionein‐1 versus α and β domains and metallothionein‐1‐to‐3 mutation following traumatic brain injury reveals different biological motifs
Authors: Manso Yasmina , Serra Montserrat , Comes Gemma , Giralt Mercedes , Carrasco Javier , Cols Neus , Vašák Milan , González‐Duarte Pilar , Hidalgo Juan 
Published: February 2010

AbstractTraumatic injury to the brain is one of the leading causes of injury‐related death or disability, but current therapies are limited. Previously it has been shown that the antioxidant proteins metallothioneins (MTs) are potent neuroprotective factors in animal models of brain injury. The exogenous administration of MTs causes effects consistent with the roles proposed from studies in knock‐out mice. We herewith report the results comparing full mouse MT‐1 with the independent α and β domains, alone or together, in a cryoinjury model. The lesion of the cortex caused the mice to perform worse in the horizontal ladder beam and the rota‐rod tests; all the proteins showed a modest effect in the former test, while only full MT‐1 improved the performance of animals in the rota‐rod, and the α domain showed a rather detrimental effect. Gene expression analysis by RNA protection assay demonstrated that all proteins may alter the expression of host‐response genes such as GFAP, Mac1 and ICAM, in some cases being the β domain more effective than the α domain or even the full MT‐1. A MT‐1‐to‐MT‐3 mutation blunted some but not all the effects caused by the normal MT‐1, and in some cases increased its potency. Thus, splitting the two MT‐1 domains do not seem to eliminate all MT functions but certainly modifies them, and different motifs seem to be present in the protein underlying such functions. © 2010 Wiley‐Liss, Inc.
Inflammasome signaling at the heart of central nervous system pathology
Authors: Chakraborty Swarupa , Kaushik Deepak Kumar , Gupta Malvika , Basu Anirban 
Published: February 2010

AbstractNeuroinflammation is a complex innate response of neural tissue against harmful effects of diverse stimuli viz., pathogens, damaged cells and irritants within the Central Nervous System (CNS). Studies show that multiple inflammatory mediators including cytokines, chemokines and prostaglandins are elevated in the Cerebrospinal Fluid (CSF) and in post‐mortem brain tissues of patients with history of neuroinflammatory conditions as well as neurodegenerative disorders like Alzheimer's disease, Parkinson's disease and Multiple Sclerosis. The innate immunity mediators in the brain, namely microglia and astrocytes, express certain Pattern Recognition Receptors (PRRs), which are always on ‘high‐alert’ for pathogens or other inflammatory triggers and participate in the assembly and activation of the inflammasome. The inflammasome orchestrates the activation of the precursors of proinflammatory caspases, which in turn, cleave the precursor forms of interleukin‐1β, IL‐18 and IL‐33 into their active forms; the secretion of which leads to a potent inflammatory response, and/or influences the release of toxins from glial and endothelial cells. Altered expression of inflammasome mediators can either promote or inhibit neurodegenerative processes. Therefore, modulating the inflammasome machinery seems a better combat strategy than summarily suppressing all inflammation in most neuroinflammatory conditions. In the current review we have surveyed the identified triggers and pathways of inflammasome activation and the following events which ultimately accomplish the innate inflammatory response in the CNS, with a goal to provide an analytical insight into disease pathogenesis that might provide cues for devising novel therapeutic strategies. © 2010 Wiley‐Liss, Inc.
Thyroid hormone enhances transected axonal regeneration and muscle reinnervation following rat sciatic nerve injury
Authors: Panaite Petrica‐Adrian , Barakat‐Walter Ibtissam 
Published: February 2010

AbstractImprovement of nerve regeneration and functional recovery following nerve injury is a challenging problem in clinical research. We have already shown that following rat sciatic nerve transection, the local administration of triiodothyronine (T3) significantly increased the number and the myelination of regenerated axons. Functional recovery is a sum of the number of regenerated axons and reinnervation of denervated peripheral targets. In the present study, we investigated whether the increased number of regenerated axons by T3‐treatment is linked to improved reinnervation of hind limb muscles. After transection of rat sciatic nerves, silicone or biodegradable nerve guides were implanted and filled with either T3 or phosphate buffer solution (PBS). Neuromuscular junctions (NMJs) were analyzed on gastrocnemius and plantar muscle sections stained with rhodamine α‐bungarotoxin and neurofilament antibody. Four weeks after surgery, most end‐plates (EPs) of operated limbs were still denervated and no effect of T3 on muscle reinnervation was detected at this stage of nerve repair. In contrast, after 14 weeks of nerve regeneration, T3 clearly enhanced the reinnervation of gastrocnemius and plantar EPs, demonstrated by significantly higher recovery of size and shape complexity of reinnervated EPs and also by increased acetylcholine receptor (AChRs) density on post synaptic membranes compared to PBS‐treated EPs. The stimulating effect of T3 on EP reinnervation is confirmed by a higher index of compound muscle action potentials recorded in gastrocnemius muscles. In conclusion, our results provide for the first time strong evidence that T3 enhances the restoration of NMJ structure and improves synaptic transmission. © 2010 Wiley‐Liss, Inc.