bluuebunny/crossref_metadata_2025_split huggingface dataset:
Tensile tests of polypropylene monitored by SAXS. Comparing the stretch‐hold technique to the dynamic technique
Authors: Stribeck Norbert , Nöchel Ulrich , Funari Sérgio S. , Schubert Tom 
Published: February 2008

AbstractAdvanced instrumentation at synchrotron beamlines facilitates considerable reduction of the exposure required for the recording of low‐noise small‐angle X‐ray scattering (SAXS) patterns. Concerning the monitoring of tensile tests on polymer materials by SAXS means that change‐over from the stretch‐hold technique to more practical dynamic straining is possible, although the strain rate is still by a factor of 100 lower than that relevant in industry and service. As hard‐elastic polypropylene (PP) is tested, considerably different scattering patterns are recorded after switching to the dynamic technique. Even though during exposure the elongation is no longer constant when applying the dynamic technique, the images collected in stretch‐hold technique appear much more blurred. The observed immediate relaxation of nanostructure induced by stopping the extensometer is analyzed by means of the multidimensional chord distribution function (CDF): The extension of the crystalline lamellae is increasing. Their thicknesses are becoming non‐uniform. The range of order is shortening. Cross‐hatched lamellae are formed. © 2008 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 46: 721–726, 2008
Infrared absorption spectroscopy of polycarbonate at high pressure
Authors: Kraus R. G. , Emmons E. D. , Thompson J. S. , Covington A. M. 
Published: February 2008

AbstractHigh‐pressure Fourier‐transform infrared absorption spectroscopy has been performed on polycarbonate, using a diamond anvil cell to produce pressures up to ∼6 GPa. The frequencies of the vibrational modes have been measured as a function of pressure. Individual mode Grüneisen parameters have been determined for six vibrational modes. The data were fit to models that included both volume‐dependent and ‐independent Grüneisen parameters. The vibrational frequency shifts as a function of pressure have been found to be consistent with those measured for similar types of bonds in other molecules. © 2008 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 46: 734–742, 2008
Irradiation enhances the metastatic potential of prostatic small cell carcinoma xenografts
Authors: Agemy Lilach , Harmelin Alon , Waks Tova , Leibovitch Ilan , Rabin Tatyana , Pfeffer M. Raphael , Eshhar Zelig 
Published: February 2008

AbstractBACKGROUNDSmall cell carcinoma of the prostate (SCCP) is a rare subset of prostate cancer (0.5–2% of all prostatic carcinomas), predominantly composed of neuroendocrine (NE) cells, with a very poor prognosis. Irradiation is one of the mainstay options for SCCP local treatment, yet, little is known about the clinical response of these aggressive tumors to radiotherapy.METHODSUsing SCID mice, the response to fractionated ionizing radiation (IR) of two unique human NE xenografts of SCCP (WISH‐PC2 and WM‐4A) was investigated.RESULTSFractionated irradiation of WISH‐PC2 xenografts using total doses of >24 Gy induced a delay in tumor growth, while total doses of >36 Gy led to local tumor eradication. However, most of the irradiated mice suffered from disseminated metastases. Similarly, in the WM‐4A xenograft, a total dose of 20 Gy led to tumor growth delay and some of the mice also developed metastases. Non‐irradiated local xenografts failed to disseminate, even following surgical excision of the main tumor mass; however, tumor cells administered intravenously did form metastases. Metastases of both xenografts were located in the adrenal/kidney and inter‐scapular regions, areas rich in brown adipose tissue. A correlation was found between the appearance of irradiation‐induced metastases and activation of the gelatinase activity of matrix metalloproteinase‐9.CONCLUSIONSClinically, this study raises the possibility that radiation to SCCP may promote metastatic disease. For patients in whom prostate biopsy shows a predominance of small cell cancer, it may be necessary to deliver systemic therapy together with the radiotherapy in order to prevent the development of metastases. Prostate 68: 530–539, 2008. © 2008 Wiley‐Liss, Inc.
Dysregulation of Dkk‐3 expression in benign and malignant prostatic tissue
Authors: Zenzmaier Christoph , Untergasser Gerold , Hermann Martin , Dirnhofer Stephan , Sampson Natalie , Berger Peter 
Published: February 2008

AbstractBACKGROUNDThe Dickkopf (Dkk) family comprises four members Dkk‐1, ‐2, ‐3, and ‐4. Dkk‐3, the most divergent family member, unlike the others does not modulate Wnt signaling. Dkk‐3 is proposed to function as a secreted tumor suppressor since it is downregulated in a number of cancer cells and prostate cancer tissue and thus may be a promising candidate molecule for therapeutic interference.METHODSThe in situ tissue localization of Dkk‐3 protein in normal prostate (NP), benign prostatic hyperplasia (BPH), and prostate carcinoma (PCa) was investigated by immunohistochemistry (IHC)/immunofluorescence. In addition, biological function of Dkk‐3 in terms of proliferation and viability was evaluated in primary prostate basal epithelial cells (PrEC), stromal cells (PrSC), and established human PCa cell lines by treatment with recombinant protein or by overexpression.RESULTSStimulation with purified recombinant protein and overexpression of Dkk‐3 did not significantly alter in vitro cell proliferation in any primary or tumor cell line evaluated. Dkk‐3 was expressed in both the basal and secretory epithelium of NP. In BPH expression was restricted to defined basal cells and was absent in tumor cells of high grade PCa. In contrast to normal prostatic tissue, Dkk‐3 was upregulated in subglandular blood vessels of BPH and in the reactive stroma of PCa tissue.CONCLUSIONSOur results indicate that Dkk‐3 expression in the normal epithelium of the prostate is lost during benign and malignant transformation and differentiation processes. The loss of expression seems to be counterbalanced by upregulation of Dkk‐3 expression in the blood vessels of the remodeled tissue. Prostate 68: 540–547, 2008. © 2008 Wiley‐Liss, Inc.
1α,25‐Dihydroxyvitamin D3 down‐regulates expression of prostate specific membrane antigen in prostate cancer cells
Authors: Serda Rita E. , Bisoffi Marco , Thompson Todd A. , Ji Ming , Omdahl John L. , Sillerud Laurel O. 
Published: February 2008

AbstractBACKGROUNDProstate specific membrane antigen (PSMA) expression correlates with prostate cancer grade and is increased in hormone‐refractory prostate cancer. The increased expression of PSMA following androgen deprivation therapy may be a consequence of the down‐regulation of PSMA expression by androgen. Moreover, 1α,25‐dihydroxyvitamin D3 (1,25‐VD) has been shown to suppress prostate cancer progression as well as cell motility and invasion. Since PSMA is positively correlated with both of these characteristics, we hypothesized that 1,25‐VD would regulate PSMA expression.METHODSLNCaP prostate cancer cells were treated with 1,25‐VD, followed by analysis of cell surface PSMA expression. The PSMA enhancer, located within the third intron of the PSMA gene, was cloned into a reporter vector and regulation by 1,25‐VD was investigated. The role of the androgen receptor (AR) in 1,25‐VD mediated suppression of PSMA expression was examined using Casodex and AR specific siRNA.RESULTSSurface expression of PSMA was significantly decreased in a dose‐dependent manner by 10 nM 1,25‐VD or greater. Regulation by 1,25‐VD occurred at the level of the PSMA enhancer. Over‐expression of the vitamin D receptor (VDR) also decreased expression of PSMA. Additionally, suppression of AR translation using siRNA technology blocked the suppressive effect of 1,25‐VD on PSMA expression, however inhibition of PSMA expression by 1,25‐VD occurred in the absence of androgens.CONCLUSIONSSuppression of PSMA by 1,25‐VD occurs at the level of the PSMA enhancer and is elevated by over‐expression of the VDR. This regulation involves the AR, but is not dependent on the presence of androgens. Prostate 68: 773–783, 2008. © 2008 Wiley‐Liss, Inc.
An iterative knowledge‐based scoring function for protein–protein recognition
Authors: Huang Sheng‐You , Zou Xiaoqin 
Published: February 2008

AbstractUsing an efficient iterative method, we have developed a distance‐dependent knowledge‐based scoring function to predict protein–protein interactions. The function, referred to as ITScore‐PP, was derived using the crystal structures of a training set of 851 protein–protein dimeric complexes containing true biological interfaces. The key idea of the iterative method for deriving ITScore‐PP is to improve the interatomic pair potentials by iteration, until the pair potentials can distinguish true binding modes from decoy modes for the protein–protein complexes in the training set. The iterative method circumvents the challenging reference state problem in deriving knowledge‐based potentials. The derived scoring function was used to evaluate the ligand orientations generated by ZDOCK 2.1 and the native ligand structures on a diverse set of 91 protein–protein complexes. For theboundtest cases, ITScore‐PP yielded a success rate of 98.9% if the top 10 ranked orientations were considered. For the more realisticunboundtest cases, the corresponding success rate was 40.7%. Furthermore, for faster orientational sampling purpose, several residue‐level knowledge‐based scoring functions were also derived following the similar iterative procedure. Among them, the scoring function that uses the side‐chain center of mass (SCM) to represent a residue, referred to as ITScore‐PP(SCM), showed the best performance and yielded success rates of 71.4% and 30.8% for the bound and unbound cases, respectively, when the top 10 orientations were considered. ITScore‐PP was further tested using two other published protein–protein docking decoy sets, the ZDOCK decoy set and the RosettaDock decoy set. In addition to binding mode prediction, the binding scores predicted by ITScore‐PP also correlated well with the experimentally determined binding affinities, yielding a correlation coefficient ofR= 0.71 on a test set of 74 protein–protein complexes with known affinities. ITScore‐PP is computationally efficient. The average run time for ITScore‐PP was about 0.03 second per orientation (including optimization) on a personal computer with 3.2 GHz Pentium IV CPU and 3.0 GB RAM. The computational speed of ITScore‐PP(SCM) is about an order of magnitude faster than that of ITScore‐PP. ITScore‐PP and/or ITScore‐PP(SCM) can be combined with efficient protein docking software to study protein–protein recognition. Proteins 2008. © 2008 Wiley‐Liss, Inc.
Biological roles of specific peptides in enzymes
Authors: Meroz Yasmine , Horn David 
Published: February 2008

AbstractIt has recently been shown (Kunik et al., PLOS Comput Biol 2007;3(8):e167) that the occurrence of specific peptides (SPs) on sequences of enzymes allows for accurate EC classification of enzymes. We inquire whether these SPs play important roles in bringing about the enzymatic function. This is assessed by cross‐checking the occurrence of SPs on enzymes with Swiss‐Prot annotations and PDB spatial structures of enzymes. Analyzing the coverage of functional annotations of enzymes, we demonstrate that SPs contain major fractions of all annotated features. This result is statistically highly significant and associates over 10% of all SPs with important biological markers. Concentrating on DNA binding regions, relevant to LexA repressor enzymes, we find interesting coverage patterns. Moreover, for the same data, we demonstrate that SPs allow for subclassification of the relevant bacteria into phylogenetic classes. An analysis of mutagen annotations on SPs appearing on all enzymes leads to the conclusion that mutations on SPs tend to damage the enzymatic function much more than expected from a background model, hence SPs are of high importance to enzymatic functions. SPs that lie in 3D pockets that are shared by active and binding sites, are shown to be significantly enriched by glycine, leading to the hypothesis that they are responsible for conformational plasticity. Finally we show that SPs can partially resolve outstanding difficult problems of convergent evolution by representing correctly enzyme functions in spite of remote homologies in sequence and in structure. Proteins 2008. © 2008 Wiley‐Liss, Inc.
On the relationship between the protein structure and protein dynamics
Authors: Lu Chih‐Hao , Huang Shao‐Wei , Lai Yan‐Long , Lin Chih‐Peng , Shih Chien‐Hua , Huang Cuen‐Chao , Hsu Wei‐Lun , Hwang Jenn‐Kang 
Published: February 2008

AbstractRecently, we have developed a method (Shih et al., Proteins: Structure, Function, and Bioinformatics 2007;68: 34–38) to compute correlation of fluctuations of proteins. This method, referred to as the protein fixed‐point (PFP) model, is based on the positional vectors of atoms issuing from the fixed point, which is the point of the least fluctuations in proteins. One corollary from this model is that atoms lying on the same shell centered at the fixed point will have the same thermal fluctuations. In practice, this model provides a convenient way to compute the average dynamical properties of proteins directly from the geometrical shapes of proteins without the need of any mechanical models, and hence no trajectory integration or sophisticated matrix operations are needed. As a result, it is more efficient than molecular dynamics simulation or normal mode analysis. Though in the previous study the PFP model has been successfully applied to a number of proteins of various folds, it is not clear to what extent this model will be applied. In this article, we have carried out the comprehensive analysis of the PFP model for a dataset comprising 972 high‐resolution X‐ray structures with pairwise sequence identity ≤25%. We found that in most cases the PFP model works well. However, in case of proteins comprising multiple domains, each domain should be treated separately as an independent dynamical module with its own fixed point; and in case of the protein complex comprising a number of subunits, if functioning as a biological unit, the whole complex should be considered as one single dynamical module with one fixed point. Under such considerations, the resultant correlation coefficient between the computed and the X‐ray structural B‐factors for the data set is 0.59 and 75% (727/972) of proteins with a correlation coefficient ≥0.5. Our result shows that the fixed‐point model is indeed quite general and will be a useful tool for high throughput analysis of dynamical properties of proteins. Proteins 2008. © 2008 Wiley‐Liss, Inc.
Insights into the interactions between HIV‐1 integrase and human LEDGF/p75 by molecular dynamics simulation and free energy calculation
Authors: Zhao Yaxue , Li Weihua , Zeng Juan , Liu Guixia , Tang Yun 
Published: February 2008

AbstractHuman cellular protein LEDGF/p75 (lens epithelium‐derived growth factor) is an important binding partner of human immunodeficiency virus type 1 (HIV‐1) integrase (IN). Without LEDGF/p75, HIV‐1 can not complete its life cycle. To study the detailed interactions between LEDGF/p75 and HIV‐1 IN, and then obtain the hotspots at the binding interface, 13 ns molecular dynamics simulations were carried out here. One‐hundred snapshots extracted from the last 4 ns trajectories were used for calculation of binding free energy and decomposition of the energy by residue. First, the structural changes and their dynamic interactions were investigated focused on the production stage. And then, the free energy was discussed. On the basis of the above results, it could be suggested that residues Gln168, Glu170, and Thr174 in chain A of IN, Thr125, and Trp131 in chain B of IN as well as Ile365, Asp366, Phe406, and Val408 in LEDGF/p75 were responsible for their binding. These results might be helpful for discovery and design of small molecules to interrupt the interaction between HIV‐1 IN and LEDGF/p75. Proteins 2008. © 2008 Wiley‐Liss, Inc.
Relationship between energy distribution and fold stability: Insights from molecular dynamics simulations of native and mutant proteins
Authors: Morra Giulia , Colombo Giorgio 
Published: February 2008

AbstractMost proteins must fold to a well‐defined structure with a minimal stability to perform their function. Here we use a simple, molecular dynamics‐based, energy decomposition approach to map the principal energetic interactions in a set of proteins representative of different folds. This work involves the all‐atom simulation and analysis of the native structures and mutants of five different proteins representative of an all‐alpha (yACPB, Protein A), all‐beta (SH3), and a mixed α/β fold (Proteins G and L). Given a certain structure, a native sequence and a set of mutants, we show that our model discriminates the ability of a mutation to yield a more or less stable protein, in agreement with experimental data, catching the principal energetic determinants of protein stabilization. Our approach identifies the interaction determinants responsible to define a fold and shows that mutations can either modulate the strength of pair‐wise coupling between residues important for folding, or modify the profile of the principal interactions. Furthermore, we address the question of how to evaluate the fitness of a sequence to a given structure by comparing the information contained in the energy map, which recapitulates the chemistry of the sequence, to that contained in the contact map, which recapitulates the fold topology. The results show that the better fit between the energetic properties of the sequence and the fold topology corresponds to a higher stabilization of the protein. We discuss the relevance of these observations to the analysis of protein designability and to the rational evolution of new sequences. Proteins 2008. © 2008 Wiley‐Liss, Inc.
Crystal structure of Natratoxin, a novel snake secreted phospholipaseA2 neurotoxin from Naja atra venom inhibiting A‐type K+ currents
Authors: Hu Pu , Sun Lei , Zhu Zhi‐Qiang , Hou Xiao‐Wei , Wang Shu , Yu Shan‐Shan , Wang Hui‐Li , Zhang Ping , Wang Ming , Niu Li‐Wen , Teng Mai‐Kun , Ruan Di‐Yun 
Published: February 2008

AbstractSnake secreted phospholipasesA2 (sPLA2s) are widely used as pharmacological tools to investigate their role in diverse pathophysiological processes. Some members of snake venom sPLA2s have been found to block voltage‐activated K+ channels (Kv channels). However, most studies involved in their effects on ion channels were indirectly performed on motor nerve terminals while few studies were directly done on native neurons. Here, a novel snake sPLA2 peptide neurotoxin, Natratoxin, composed of 119 amino acid residues and purified from Naja atra venom was reported. It was characterized using whole‐cell patch‐clamp in acutely dissociated rat dorsal root ganglion (DRG) neurons. It was found to effectively inhibit A‐type K+ currents and cause alterations of channel gating characters, such as the shifts of steady‐state activation and inactivation curves to hyperpolarization direction and changes of V1/2 and slope factor. Therefore, Natratoxin was suggested to be a gating modifier of Kv channel. In addition, this inhibitory effect was found to be independent of its enzymatic activity. These results suggested that the toxin enacted its inhibitory effect by binding to Kv channel. To further elucidate the structural basis for this electrophysiological phenomenon, we determined the crystal structure of Natratoxin at 2.2 Å resolution by molecular replacement method and refined to an R‐factor of 0.190. The observed overall fold has a different structural organization from other K+ channel inhibitors in animal toxins. Compared with other Kv channel inhibitors, a similar putative functional surface in its C‐terminal was revealed to contribute to protein–protein interaction in such a blocking effect. Our results demonstrated that the spatial distribution of key amino acid residues matters most in the recognition of this toxin towards its channel target rather than its type of fold. Proteins 2008. © 2008 Wiley‐Liss, Inc.
US grower perceptions and experiences with glyphosate‐resistant weeds
Authors: Foresman Chuck , Glasgow Les 
Published: February 2008

AbstractBACKGROUND: A survey of 400 growers of maize, soybeans and cotton was made in the United States to determine perceptions, experiences and management practices with glyphosate‐resistant weeds. The survey included growers in the north (corn belt) and south (cotton belt) of the USA in spring 2006.RESULTS: Interestingly, 24 and 39% of northern and southern growers, respectively, assumed they had glyphosate weed resistance on their farm. Of the 200 southern growers interviewed, 67% had planted continuous glyphosate‐resistant (GR) crops for a period of 3–5 years. According to the survey respondents, the key method for managing glyphosate‐resistant weeds was to rotate to other herbicides.CONCLUSION: Growers do value GR crop technology but are adopting measures to manage resistance only as needed. Copyright © 2008 Society of Chemical Industry
Field resistance to QoI fungicides in Podosphaera fusca is not supported by typical mutations in the mitochondrial cytochrome b gene
Authors: Fernández‐Ortuño Dolores , Torés Juan A , de Vicente Antonio , Pérez‐García Alejandro 
Published: February 2008

AbstractBACKGROUND: A single nucleotide polymorphism in the mitochondrial cytochrome b gene confers resistance to strobilurin (QoI) fungicides in phytopathogenic fungi. Recent studies have revealed worrying levels of resistance to strobilurins in Podosphaera fusca (Fr.) U Braun & N Shishkoff comb. nov. [ = Sphaerothecafusca (Fr.) S Blumer], the main causal agent of cucurbit powdery mildew in Spain. In the present study the underlying resistance mechanism to QoI fungicides in the Spanish populations of P. fusca was investigated.RESULTS: Analysis of the Qo domains of cytochrome b in a collection of isolates revealed that none of the typical mutations conferring resistance to QoI, including the G143A and F129L substitutions, was present in the QoI‐resistant isolates. Moreover, although different amino acid polymorphisms were observed in the two regions spanning the Qo site, none of them consistently distinguished QoI‐resistant from QoI‐sensitive strains. Exposure to salicylhydroxamic acid (SHAM), a specific inhibitor of alternative oxidase, in the presence of trifloxystrobin did not have any effect on QoI resistance, ruling out alternative respiration as the mechanism of resistance. Sensitivity tests to a battery of respiration inhibitors revealed high levels of cross‐resistance to all Qo‐inhibitors tested but not to Qi‐inhibitors, these features resembling those of a target‐site‐based resistance.CONCLUSIONS: The results indicate that the mechanism responsible for QoI resistance in P. fusca is not linked to typical mutations in cytochrome b gene and that the absence of the G143A substitution cannot be explained by an intron following codon 143. These are important observations, especially in relation to the possible molecular diagnosis of resistance. Copyright © 2008 Society of Chemical Industry