bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effective elimination of nucleic acids from bacterial protein samples for optimized blue native polyacrylamide gel electrophoresis
Authors: Liang Jingdan , Niu Qiule , Xu Xinping , Luo Yuanming , Zhou Xiufen , Deng Zixin , Wang Zhijun 
Published: July 2009

AbstractNucleic acids remaining within bacterial protein samples from Streptomyces lividans and Escherichia coli were found to interfere significantly with blue native polyacrylamide gel electrophoresis (BN‐PAGE), a technique used frequently for analyzing bacterial protein complexes in proteomics studies. We have used ultracentrifugation and/or precipitation of cell lysates with streptomycin sulfate to eliminate nucleic acids from total and/or membrane protein samples. Nucleic acid‐binding proteins were first enriched by precipitation with streptomycin sulfate, and contaminating nucleic acids were then eliminated by precipitation by adding polyethyleneimine. The performance of BN‐PAGE was found to be dramatically improved by these sample preparation steps.
Multi‐user diversity and multiplexing with orthogonal multiple beams in packet‐based wireless systems
Authors: Oh Dong‐Chan , Lee Yong‐Hwan 
Published: July 2009

AbstractMultiple beams are generated in parallel to achieve multiplexing gain with the use of packet scheduling in wireless systems. However, the use of orthogonal random multiple beams might deteriorate system performance due to inter‐user interference. To alleviate this interference problem, we adjust the number of orthogonal random multiple beams according to the operating condition. To reduce the search complexity for finding optimum orthogonal multi‐beam combination, we further consider the use of a sequential search scheme. Finally, the performance of the proposed schemes is analysed and verified by computer simulation. Numerical results show that the proposed schemes are quite applicable to real environments where the channel information is not perfectly available. Copyright © 2009 John Wiley & Sons, Ltd.
Non‐pecuniary returns to higher education: the effect on smoking intensity in the UK
Authors: Bratti Massimiliano , Miranda Alfonso 
Published: July 2009

AbstractThis paper investigates whether higher education (HE) produces non‐pecuniary returns via a reduction in the intensity of consumption of health‐damaging substances. In particular, it focuses on current smoking intensity of the British individuals sampled in the 29‐year follow‐up survey of the 1970 British Cohort Study. We estimate endogenous dummy ordinal response models for cigarette consumption and show that HE is endogenous with respect to smoking intensity and that even when endogeneity is accounted for, HE is found to have a strong negative effect on smoking intensity. Moreover, pecuniary channels, such as occupation and income, mediate only a minor part of the effect of HE. Our results are robust to modelling individual self‐selection into current smoking participation (at age 29) and to estimating a dynamic model in which past smoking levels affect current smoking levels. Copyright © 2009 John Wiley & Sons, Ltd.
Pan-caspase inhibitor VX-166 reduces fibrosis in an animal model of nonalcoholic steatohepatitis #
Authors: Witek Rafal P. , Stone Carl W. , Karaca Gamze F. , Syn Wing-Kin , Pereira Thiago A. , Agboola Kolade M. , Omenetti Alessia , Jung Youngmi , Teaberry Vanessa , Choi Steve S. , Guy Cynthia D. , Pollard John , Charlton Peter , Diehl Anna Mae 
Published: July 2009

Abstract
Nonalcoholic fatty liver disease (NAFLD) is a potentially progressive liver disease that culminates in cirrhosis. Cirrhosis occurs more often in individuals with nonalcoholic steatohepatitis (NASH) than in those with steatosis (nonalcoholic fatty liver [NAFL]). The difference between NAFL and NASH is the extent of hepatocyte apoptosis, which is more extensive in NASH. Because phagocytosis of apoptotic cells activates hepatic stellate cells (HSCs), we examined the hypothesis that a pan-caspase inhibitor, VX-166, would reduce progression of fibrosis in a mouse model of NASH. Male db/db mice were fed methionine/choline-deficient (MCD) diets to induce NASH and liver fibrosis. Mice were gavaged once daily with either the pan-caspase inhibitor VX-166 (6 mg/kg/d; Vertex, Abingdon, UK) or vehicle only and sacrificed at 4 or 8 weeks. Treatment with an MCD diet increased alanine aminotransferase (ALT), caspase-3 activity, terminal deoxynucleotidyl transferase–mediated dUTP nick-end labeling (TUNEL)-positive cells, NASH, and fibrosis. Treatment of MCD-fed mice with VX-166 decreased active caspase-3, TUNEL-positive cells, and triglyceride content (P < 0.05). However, ALT levels were similar in VX-166–treated mice and vehicle-treated controls. Histological findings also confirmed that both groups had comparable liver injury (NAFLD activity score ≥6). Nevertheless, VX-166–treated MCD-fed mice demonstrated decreased α-smooth muscle actin expression (4 weeks, P < 0.05; 8 weeks, P < 0.005) and had reduced hepatic levels of collagen 1α1 messenger RNA (8 weeks, P < 0.05). Hydroxyproline content and Sirius red staining of VX-166–treated livers confirmed decreases in fibrosis. Conclusion: Inhibiting hepatic apoptosis suppresses the development of fibrosis in mice with NASH. Beneficial effects on liver fibrosis were associated with reductions in hepatic steatosis, but occurred without obvious improvement in liver injury. These findings are consistent with evidence that apoptosis triggers HSC activation and liver fibrosis and suggest that caspase inhibitors may be useful as an antifibrotic NASH therapy. (Hepatology 2009.)
Ectopic growth of hippocampal mossy fibers in a mutated GAP‐43 transgenic mouse with impaired spatial memory retention
Authors: Holahan Matthew R. , Honegger Kyle S. , Routtenberg Aryeh 
Published: July 2009

AbstractIn a previous study, it was shown that transgenic mice, designated G‐NonP, forget the location of a water maze hidden platform when tested 7 days after the last training day (Holahan and Routtenberg (2008) Hippocampus 18:1099–1102). The memory loss in G‐NonP mice might be related to altered hippocampal architecture suggested by the fact that in the rat, 7 days after water maze training, there is discernible mossy fiber (MF) growth (Holahan et al. (2006) Hippocampus 16:560–570; Rekart et al. (2007) Learn Mem 14:416–421). In the present report, we studied the distribution of the MF system within the hippocampus of naïve, untrained, G‐NonP mouse. In WT mice, the MF projection was restricted to the stratum lucidum of CA3 with no detectable MF innervation in distal stratum oriens (dSO). In G‐NonP mice, in contrast, there was an ectopic projection terminating in the CA3 dSO. Unexpectedly, there was nearly a complete loss of immunostaining for the axonal marker Tau1 in the G‐NonP transgenic mice in the MF terminal fields indicating that transgenesis itself leads to off‐target consequences (Routtenberg (1996) Trends Neurosci 19:471–472). Because transgenic mice overexpressing nonmutated, wild type GAP‐43 do not show this ectopic growth (Rekart et al., in press) and the G‐NonP mice overexpress a mutated form of GAP‐43 precluding its phosphorylation by protein kinase C (PKC), the possibility exists that permanently dephosphorylated GAP‐43 disrupts normal axonal fasciculation which gives rise to the ectopic growth into dSO. © 2009 Wiley‐Liss, Inc.
Methoxylated isoflavones, cajanin and isoformononetin, have non‐estrogenic bone forming effect via differential mitogen activated protein kinase (MAPK) signaling
Authors: Bhargavan Biju , Gautam Abnish Kumar , Singh Divya , Kumar Amit , Chaurasia Sumit , Tyagi Abdul Malik , Yadav Dinesh Kumar , Mishra Jay Sharan , Singh Amar Bahadur , Sanyal Sabyasachi , Goel Atul , Maurya Rakesh , Chattopadhyay Naibedya 
Published: July 2009

AbstractFollowing a lead obtained from stem‐bark extract of Butea monosperma, two structurally related methoxyisoflavones; cajanin and isoformononetin were studied for their effects in osteoblasts. Cajanin had strong mitogenic as well as differentiation‐promoting effects on osteoblasts that involved subsequent activation of MEK‐Erk and Akt pathways. On the other hand, isoformononetin exhibited potent anti‐apoptotic effect in addition to promoting osteoblast differentiation that involved parallel activation of MEK‐Erk and Akt pathways. Unlike genistein or daidzein, none of these two compounds appear to act via estrogen receptors in osteoblast. Once daily oral (by gavage) treatment for 30 consecutive days was given to recently weaned female Sprague–Dawley rats with each of these compounds at 10.0 mg kg−1 day−1 dose. Cajanin increased bone mineral density (BMD) at all skeletal sites studied, bone biomechanical strength, mineral apposition rate (MAR) and bone formation rate (BFR), compared with control. BMD levels at various anatomic positions were also increased with isoformononetin compared with control however, its effect was less potent than cajanin. Isoformononetin had no effect on the parameters of bone biomechanical strength although it enhanced MAR and BFR compared with control. Isoformononetin had very mild uterotrophic effect, whereas cajanin was devoid of any such effect. Our data suggest that cajanin is more potent than isoformononetin in accelerating peak bone mass achievement. To the best of our knowledge, this work represents the first attempt to elucidate structure‐activity relationship between the two methoxylated isoflavones regarding their effects in osteoblasts and bone formation. J. Cell. Biochem. 108: 388–399, 2009. © 2009 Wiley‐Liss, Inc.
How to obtain statistically converged MM/GBSA results
Authors: Genheden Samuel , Ryde Ulf 
Published: July 2009

AbstractThe molecular mechanics/generalized Born surface area (MM/GBSA) method has been investigated with the aim of achieving a statistical precision of 1 kJ/mol for the results. We studied the binding of seven biotin analogues to avidin, taking advantage of the fact that the protein is a tetramer with four independent binding sites, which should give the same estimated binding affinities. We show that it is not enough to use a single long simulation (10 ns), because the standard error of such a calculation underestimates the difference between the four binding sites. Instead, it is better to run several independent simulations and average the results. With such an approach, we obtain the same results for the four binding sites, and any desired precision can be obtained by running a proper number of simulations. We discuss how the simulations should be performed to optimize the use of computer time. The correlation time between the MM/GBSA energies is ∼5 ps and an equilibration time of 100 ps is needed. For MM/GBSA, we recommend a sampling time of 20–200 ps for each separate simulation, depending on the protein. With 200 ps production time, 5–50 separate simulations are required to reach a statistical precision of 1 kJ/mol (800–8000 energy calculations or 1.5–15 ns total simulation time per ligand) for the seven avidin ligands. This is an order of magnitude more than what is normally used, but such a number of simulations is needed to obtain statistically valid results for the MM/GBSA method. © 2009 Wiley Periodicals, Inc. J Comput Chem 2010
Absorption and fluorescence emission spectroscopic characters of naphtho‐homologated yy‐DNA bases and effect of methanol solution and base pairing
Authors: Zhang Laibin , Li Huifang , Li Jilai , Chen Xiaohua , Bu Yuxiang 
Published: July 2009

AbstractA comprehensive theoretical study of electronic transitions of naphtho‐homologated base analogs, namely, yy‐T, yy‐C, yy‐A, and yy‐G, was performed. The nature of the low‐lying excited states is discussed, and the results are compared with those from experiment and also with those of y‐bases. Geometrical characteristics of the lowest excited singlet ππ* and nπ* states were explored using the CIS method, and the effects of methanol solution and paring with their complementary natural bases on the relevant absorption and emission spectra of these modified bases were examined. The calculated excitation and emission energies agree well with the measured data, where experimental results are available. In methanol solution, the fluorescence from yy‐A and yy‐G would be expected to occur around 539 and 562 nm, respectively, suggesting that yy‐A is a green‐colored fluorophore, whereas yy‐G is a yellow‐colored fluorophore. The methanol solution was found to red‐shift both the absorption and emission maxima of yy‐A, yy‐T, and yy‐C, but blue‐shift those for yy‐G. Generally, though base pairing has no significant effects on the absorption and fluorescence maxima of yy‐A, yy‐C, and yy‐T, it blue‐shifts those for yy‐G. © 2009 Wiley Periodicals, Inc. J Comput Chem 2010
New one‐step synthesis of pyrazolo[1,5‐a]pyrimidine and pyrazolo[1,5‐a]quinazoline derivatives via multicomponent reactions
Authors: Ghotekar Bhausaheb K. , Jachak Madhukar N. , Toche Raghunath B. 
Published: July 2009

Abstract
magnified imageA series of pyrazolopyrimidine and pyrazoloquinozoline derivatives has been synthesized in one step by multicomponent reactions using, 5‐aminopyrazole, p‐substitutedbenzoylacetonitrile/dimedone and triethylorthoesters. pyrazolopyrimidine derivatives were also studied for their absorption and fluorescence maxima. J. Heterocyclic Chem., (2009).
Self termination of ring opening reaction of p‐substituted phenol‐based benzoxazines: An obstructive effect via intramolecular hydrogen bond
Authors: Chirachanchai Suwabun , Laobuthee Apirat , Phongtamrug Suttinun 
Published: July 2009

Abstract
magnified imageThe ring opening polymerizations of p‐substituted phenol‐based benzoxazines are self‐terminated as soon as dimers form. The polymerization of benzoxazine monomers does not proceed according to the theoretical mechanism even though the conditions, temperature, molar ratio, solvent polarity, and reactant ratio are varied. The speculated mechanism, involving the unique structure of a dimer with inter‐ and intramolecular hydrogen bonds, is applied to explain an obstructive effect on ring opening polymerization. In this article, we clarify an important case which the stereo structure of the compound controls the reaction and prevents the polymerization expected from the theoretical mechanism. J. Heterocyclic Chem., (2009).
Synthesis of 2,4,5‐triaryl‐5H‐chromeno[4,3‐b]pyridines under microwave radiation
Authors: Wu Hui , Wan Yu , Chen Xiu‐Mei , Chen Cai‐Fa , Lu Lei‐Lei , Xin Hai‐Qiang , Xu Hua‐Hong , Pang Li‐Ling , Ma Rui , Yue Cai‐Hui 
Published: July 2009

Abstract
magnified image2,4,5‐Triaryl‐5H‐chromeno[4,3‐b]pyridines were synthesized from a three‐component cascade reaction of 2′‐hydroxyacetophenone, aromatic aldehyde, and ammonium acetate catalyzed by 2‐1′‐methylimidazolium‐3‐yl‐1‐ethyl sulfate under microwave irradiation. Nine new bonds and two new rings were formed in one‐pot. J. Heterocyclic Chem., (2009).
Tissue kallikrein alleviates glutamate‐induced neurotoxicity by activating ERK1
Authors: Liu Ling , Zhang Renliang , Liu Kui , Zhou Houguang , Tang Yuping , Su Jinjin , Yu Xiaoyan , Yang Xuelian , Tang Min , Dong Qiang 
Published: July 2009

AbstractGlutamate‐induced neurotoxicity consequent to N‐methyl‐D‐aspartic acid (NMDA) and 2‐amino‐3‐(3‐hydroxy‐5‐methyl‐isoxazol‐4‐yl) propionic acid (AMPA) receptor activation underlies the pathogenesis of a wide range of central nervous system disorders, including brain ischemia. Prevention of ischemia/reperfusion (I/R)‐induced neuronal injury has long been regarded as an effective therapeutic strategy for ischemia. Human tissue kallikrein (TK) gene transfer has been shown to protect neurons against cerebral I/R‐induced apoptosis and oxidative stress, via activation of the brandykinin B2 receptor (B2R). However, little is known about the role of TK on glutamate‐induced neurotoxicity. Here we report that pretreatment of cultured cortical neurons with TK largely prevented glutamate‐induced morphological changes and cell death. We found that TK pretreatment alleviated glutamate‐induced oxidative stress by inhibiting neuronal nitric oxide synthase (nNOS) activity, thereby reducing the generation of nitric oxide (NO) and reactive oxygen species (ROS). Blockage of NMDA and AMPA receptors by their specific antagonists MK801 and CNQX had effects similar to those of TK administration. Furthermore, we found that the extracellular signal‐regulated kinase 1/2 cascade (ERK1/2), particularly ERK1, and nuclear factor‐κB (NF‐κB) were involved in TK neuroprotection against glutamate‐induced neurotoxicity. TK pretreatment activated ERK1 and NF‐κB, leading to enhanced expression of brain‐derived neurotrophic factor (BDNF) mRNA and antiapoptotic gene Bcl‐2 protein. Collectively, these findings demonstrate that TK attenuates glutamate‐induced apoptosis through an intracellular signaling pathway including activation of B2R, ERK1/2, and NF‐κB and up‐regulation of BDNF and Bcl‐2 expression. Thus, TK represents a promising therapeutic strategy for ischemic stroke. © 2009 Wiley‐Liss, Inc.
Notch‐Hes1 pathway contributes to the cochlear prosensory formation potentially through the transcriptional down‐regulation of p27Kip1
Authors: Murata Junko , Ohtsuka Toshiyuki , Tokunaga Akinori , Nishiike Suetaka , Inohara Hidenori , Okano Hideyuki , Kageyama Ryoichiro 
Published: July 2009

AbstractThe Notch signaling pathway has a crucial role in the differentiation of hair cells and supporting cells by mediating “lateral inhibition” via the ligands Delta‐like1 (Dll1) and Jagged2 (Jag2) and the effectors Hes1 and Hes5 during mammalian inner ear development. Recently, another Notch ligand, Jagged1 (Jag1)‐dependent Notch activation, has been revealed to be important for the determination of the prosensory region in the earlier stage before cell differentiation. However, little is known about the effectors of the Notch pathway in this context. P27Kip1, a cyclin‐dependent kinase inhibitor, is also known to demarcate the prosensory region in the cochlear primordium, which consists of the sensory progenitors that have completed their terminal mitoses. Hes1 reportedly promotes precursor cell proliferation through the transcriptional down‐regulation of p27Kip1 in the thymus, liver, and brain. In this study, we observed Hes1 as a mediator between the Notch signaling pathway and the regulation of proliferation of sensory precursor cells by p27Kip1 in the developing cochlea. We showed that Hes1, but not Hes5, was weakly expressed at the time of onset of p27Kip1. The expression pattern of Hes1 prior to cell differentiation was similar to that of activated Notch1. P27Kip1 was up‐regulated and BrdU‐positive S‐phase cells were reduced in the developing cochlear epithelium of Hes1 null mice. These results suggest that the Notch‐Hes1 pathway may contribute to the adequate proliferation of sensory precursor cells via the potential transcriptional down‐regulation of p27Kip1 expression and play a pivotal role in the correct prosensory determination. © 2009 Wiley‐Liss, Inc.
O‐linked β‐N‐acetylglucosaminylation in mouse embryonic neural precursor cells
Authors: Yanagisawa Makoto , Yu Robert K. 
Published: July 2009

AbstractIn neural stem cells (NSCs), glycoconjugates and carbohydrate antigens are known not only to serve as excellent cell surface biomarkers for cellular differentiation and development but also to play important functional roles in determining cell fate. O‐linked β‐N‐acetylglucosamine (O‐GlcNAc), which modifies nuclear and cytoplasmic proteins on the serine and threonine residues, is also expected to play an important regulatory role. It is not known, however, whether O‐GlcNAc is expressed in NSCs or what the function of this expression is. In this study, we evaluated the patterns and possible functions of O‐GlcNAcylation in mouse embryonic neuroepithelial cells (NECs), which are known to be rich in NSCs. We confirmed the expression of O‐GlcNAc transferase, O‐GlcNAcase, and several O‐GlcNAcylated proteins in NECs. Treatment of NECs with O‐GlcNAcase inhibitors, PUGNAc and streptozotocin, induced robust accumulation of O‐GlcNAc in NECs and reduction of number of NECs. In O‐GlcNAcase inhibitor‐treated NECs, the Ras‐mitogen‐activated protein kinase pathway and the phosphatidylinositol 3‐kinase‐Akt pathway, important for proliferation and survival, respectively, were intact, but caspase‐3, an executioner for cell death, was activated. These results suggest the possibility that O‐GlcNAc is involved in cell death signaling in NECs. Furthermore, in NECs, we identified an O‐GlcNAc‐modified protein, Sp1 transcription factor. Our study is the first to evaluate expression and functions of O‐GlcNAc in NECs. © 2009 Wiley‐Liss, Inc.
Leukemia inhibitory factor regulates the timing of oligodendrocyte development and myelination in the postnatal optic nerve
Authors: Ishibashi Tomoko , Lee Philip R. , Baba Hiroko , Fields R. Douglas 
Published: July 2009

AbstractLeukemia inhibitory factor (LIF) promotes the survival of oligodendrocytes both in vitro and in an animal model of multiple sclerosis, but the possible role of LIF signaling in myelination during normal development has not been investigated. We find that LIF−/− mice have a pronounced myelination defect in optic nerve at postnatal day 10. Myelin basic protein (MBP)‐ and proteolipid protein (PLP)‐positive myelin was evident throughout the optic nerve in the wild‐type mice, but staining was present only at the chiasmal region in LIF−/− mice of the same age. Further experiments suggest that the myelination defect was a consequence of a delay in maturation of oligodendrocyte precursor cell (OPC) population. The number of Olig2‐positive cells was dramatically decreased in optic nerve of LIF−/− mice, and the distribution of Olig2‐positive cells was restricted to the chiasmal region of the nerve in a steep gradient toward the retina. Gene expression profiling and cell culture experiments revealed that OPCs from P10 optic nerve of LIF−/− mice remained in a highly proliferative immature stage compared with littermate controls. Interestingly, by postnatal day 14, MBP immunostaining in the LIF−/− optic nerve was comparable to that of LIF+/+ mice. These results suggest that, during normal development of mouse optic nerve, there is a defined developmental time window when LIF is required for correct myelination. Myelination seems to recover by postnatal day 14, so LIF is not necessary for the completion of myelination during postnatal development. © 2009 Wiley‐Liss, Inc.