bluuebunny/crossref_metadata_2025_split huggingface dataset:
On the performance of sudden‐expansion pipe without/with cross‐flow injection: experimental and numerical studies
Authors: El‐Askary W. A. , El‐Mayet M. , Balabel A. 
Published: April 2011

SUMMARYThe paper explores the possibilities that different turbulence closures offer, for in‐depth analysis of a complex flow. The case under investigation is steady, turbulent flow in a pipe with sudden expansion without/with normal‐to‐wall injection through jets. This is a typical geometry where generation of turbulence energy takes place, due to sudden change in boundary conditions. This study is aimed at investigating the capability of a developed computational program by the present authors with three different turbulence models to calculate the mean flow variables. Three two‐equation models are implemented, namely the standard linear k − ε model, the low Reynolds number k − ε model and the cubic nonlinear eddy viscosity (NLEV) k − ε model. The performance of the chosen turbulence models is investigated with regard to the available data in the literature including velocity profiles, turbulent kinetic energy and reattachment position in a pipe expansion. In order to further assess the reliability of the turbulence models, an experimental program was conducted by the present authors also at the fluid mechanics laboratory of Menoufiya University. Preliminary measurements, including the surface pressure along the two walls of the expansion pipe and the pressure drop without and with the presence of different arrangements of wall jets produced by symmetrical or asymmetrical fluid cross‐flow injection, are introduced.The results of the present studies demonstrate the superiority of the cubic NLEV k − ε model in predicting the flow characteristics over the entire domain. The simple low Reynolds number k − ε model also gives good prediction, especially when the reattachment point is concerned.The evaluation of the reattachment point and the pressure‐loss coefficient is numerically addressed in the paper using the cubic NLEV k − ε model. The results show that the injection location can control the performance of the pipe‐expansion system. It is concluded that the introduction of flow injection can increase the energy loss in the pipe expansion. The near‐field turbulence structure is also considered in the present study and it is noticed that the turbulence level is strongly affected by the cross‐flow injection and the jet location. Copyright © 2011 John Wiley & Sons, Ltd.
Synthesis, characterization, and crystal structure of cis‐[Pt(Me)2{PPh2(OMe)}2] and the conversion into cis‐[Pt(OH2)2{PPh2(OMe)}2][OTf]2
Authors: Itazaki Masumi , Shigesato Yuka , Nakazawa Hiroshi 
Published: April 2011

AbstractThe reaction of Pt(Me)2 (cod) (cod = η2:η2‐1,5‐cyclooctadiene) with 2 equivalents of PPh2(OMe) afforded a bis(phosphinite)platinum complex cis‐[Pt(Me)2{PPh2(OMe)}2] (1). The reaction of 1 with trifluoromethanesulfonic acid HOTf (OTf‐ = CF3O2 SO‐) and then H2O produced a di(aqua)platinum complex cis‐[Pt(OH2)2{PPh2(OMe)}2][OTf]2 (2). New complexes 1 and 2 were fully characterized using NMR measurements and elemental analyses. Furthermore, structures of 1 and 2 were determined by single crystal X‐ray diffraction studies. © 2011 Wiley Periodicals, Inc. Heteroatom Chem 22:371–376, 2011; View this article online at wileyonlinelibrary.com. DOI 10.1002/hc.20692
Differential cycling rates of Kv4.2 channels in proximal and distal dendrites of hippocampal CA1 pyramidal neurons
Authors: Nestor Michael W. , Hoffman Dax A. 
Published: April 2011

AbstractThe heterogeneous expression of voltage‐gated channels in dendrites suggests that neurons perform local microdomain computations at different regions. It has been shown that A‐type K+ channels have a nonuniform distribution along the primary apical dendrite in CA1 pyramidal neurons, increasing with distance from the soma. Kv4.2 channels, which are responsible for the somatodendritic A‐type K+ current in CA1 pyramidal neurons, shape local synaptic input, and regulate the back‐propagation of APs into dendrites. Experiments were performed to test the hypothesis that Kv4.2 channels are differentially trafficked at different regions along the apical dendrite during basal activity and upon stimulation in CA1 neurons. Proximal (50–150 μm from the soma, primary and oblique) and distal (>200 μm) apical dendrites were selected. The fluorescence recovery after photobleaching (FRAP) technique was used to measure basal cycling rates of EGFP‐tagged Kv4.2 (Kv4.2g). We found that the cycling rate of Kv4.2 channels was one order of magnitude slower at both primary and oblique dendrites between 50 and 150 μm from the soma. Kv4.2 channel cycling increased significantly at 200 to 250 μm from the soma. Expression of a Kv4.2 mutant lacking a phosphorylation site for protein kinase‐A (Kv4.2gS552A) abolished this distance‐dependent change in channel cycling; demonstrating that phosphorylation by PKA underlies the increased mobility in distal dendrites. Neuronal stimulation by α‐amino‐3‐hydroxyl‐5‐methyl‐4‐isoxazole‐propionate (AMPA) treatment increased cycling of Kv4.2 channels significantly at distal sites only. This activity‐dependent increase in Kv4.2 cycling at distal dendrites was blocked by expression of Kv4.2gS552A. These results indicate that distance‐dependent Kv4.2 mobility is regulated by activity‐dependent phosphorylation of Kv4.2 by PKA. © 2011 Wiley Periodicals, Inc.
The WWP1 ubiquitin E3 ligase increases TRAIL resistance in breast cancer
Authors: Zhou Zhongmei , Liu Rong , Chen Ceshi 
Published: April 2011

AbstractWW domain containing E3 ubiquitin protein ligase 1 (WWP1) is an HECT domain‐containing E3 ligase regulating apoptosis. The WWP1 gene is frequently amplified and overexpressed in estrogen receptor α (ERα)‐positive breast cancer. Inhibition of WWP1 by siRNA induced apoptosis in MCF7 and HCC1500. In our study, we demonstrate that WWP1 depletion by siRNA activated the extrinsic apoptotic pathway. WWP1 depletion‐induced apoptosis was rescued by the overexpression of the wild‐type WWP1 but not the E3 ligase inactive WWP1‐C890A mutant in MCF7 cells. In contrast, WWP1‐C890A enhanced apoptosis, suggesting that the E3 ligase activity is required for WWP1 to promote cell survival. The expression levels of WWP1 in four breast cancer cell lines were specifically correlated with the tumor necrosis factor (TNF)‐related apoptosis‐inducing ligand (TRAIL) resistance, but not TNFα and doxorubicin resistance. Both WWP1 depletion and dominant negative WWP1 overexpression increased the TRAIL‐induced caspase‐8 recruitment and apoptosis although WWP1 did not regulate FLIP and death receptor levels. Depletion of the initial caspase‐8 blocked WWP1 inhibition‐induced apoptosis in MCF7. These findings suggest that inhibition of WWP1 may be combined with TRAIL to suppress ERα‐positive breast cancer cell survival.
An RNAi screen identifies USP2 as a factor required for TNF‐α‐induced NF‐κB signaling
Authors: Metzig Marie , Nickles Dorothee , Falschlehner Christina , Lehmann‐Koch Judith , Straub Beate K. , Roth Wilfried , Boutros Michael 
Published: April 2011

AbstractTumor necrosis factor α (TNF‐α) signaling pathways play important roles during tumorigenesis and inflammation. Ubiquitin‐dependent processes are central to the regulation of TNF‐α and nuclear factor κB (NF‐κB) signaling. We performed a targeted siRNA screen for ubiquitin‐specific proteases (USPs) and identified USP2 as a modulator of TNF‐α‐induced NF‐κB signaling. We showed that USP2 is required for the phosphorylation of IκB, nuclear translocation of NF‐κB and expression of NF‐κB‐dependent target genes and IL‐8 secretion. Our study also provides evidence for isoform‐specific functions of USP2. The immunohistochemical analysis of breast carcinomas revealed that USP2 expression is frequently downregulated. Together, our results implicate USP2 as a novel positive regulator of TNF‐α‐induced NF‐κB signaling and show that its expression is altered in tumor cells.
Molecular Selective Binding and Nanofabrication of Cucurbituril/Cyclodextrin Pairs
Authors: Chen Yong , Zhang Ying‐Ming , Liu Yu 
Published: April 2011

AbstractCucurbiturils (CBs) and cyclodextrins (CDs) are two important classes of macrocyclic molecules, both of which have the capability of forming stable complexes with various molecular or ionic substrates. These capabilities consequently make them attractive as both receptors for molecular recognition and building blocks for the construction of nano‐scaled supramolecular systems. This review mainly deals with representative contributions in comparative studies of selective binding and molecular assembly behaviors of cucurbiturils and cyclodextrins possessing different types of hydrophobic cavities. It also gives a description of the construction of nanometer‐scaled supramolecular architectures through the cooperative assembly employing cucurbiturils and cyclodextrins, as well as their functions. This review will be addressed to students and researchers interested in the supramolecular chemistry of cucurbiturils and cyclodextrins, especially that involving these two classes of macrocyclic receptors in a single system.
The Mechanism of Cucurbituril Formation
Authors: Isaacs Lyle 
Published: April 2011

AbstractThis article begins by describing the synthesis and recognition properties of the cucurbit[n]uril homologues CB[5], CB[6], CB[7], CB[8], and CB[10]. Subsequently, we describe the state‐of‐the‐art in understanding the mechanism of CB[n] formation. We describe the experiments that establish that glycoluril (1 H) undergoes condensation with formaldehyde by a combination of chain‐growth and step‐growth polymerization processes. Chain‐growth processes deliver methylene bridged glycoluril oligomers 2 C–8 C as intermediates that may undergo macrocyclization to nor‐seco‐CB[n] when the oligomer is long enough (5 C–8 C) and subsequently form CB[n]. Step‐growth processes allow oligomers to condense to give longer oligomers connected by a single CH2‐bridge that undergo macrocyclization to deliver (±)‐bis‐nor‐seco‐CB[6] and bis‐nor‐seco‐CB[10]. Lastly, we describe some of the exciting new recognition processes of the newly formed members of the CB[n] family. For example, bis‐nor‐seco‐CB[10] undergoes homotropic allostery during ternary complex formation, (±)‐bis‐nor‐seco‐CB[6] exhibits moderately diastereoselective recognition processes (d.r. up to 88 : 12) with chiral ammonium ions in water, and nor‐seco‐CB[6] functions as an aldehyde reactive CB[n] synthon that can control the folding of alkanediammonium ions into a backfolded conformation in water.
Supramolecular Assemblies Constructed by Cucurbituril‐Catalyzed Click Reaction
Authors: Tuncel Dönüs , Ünal Özlem , Artar Müge 
Published: April 2011

AbstractCucurbituril homologues are multi‐functional macrocycles that can find applications in many areas and have numerous interesting features setting them apart from the other macrocycles. Among them, the ability of one of the cucurbituril homologues, cucurbit[6]uril (CB6), to catalyze 1,3‐dipolar cycloaddition in a regiospecific fashion is truly exceptional. Using this feature, small molecules can be clicked together to form complex structures in a very efficient way. Accordingly, in this article we review recent research involving the use of CB6‐catalyzed 1,3‐dipolar cycloaddition or the click reaction of CB6 in the construction of supramolecular assemblies including rotaxanes, pseudorotaxanes, polyrotaxanes, polypseudorotaxanes, molecular switches, machines, and nanovalves.
Transcriptional and post‐transcriptional down‐regulation of cyclin D1 contributes to C6 glioma cell differentiation induced by forskolin
Authors: He Songmin , Zhu Wenbo , Zhou Yuxi , Huang Yijun , Ou Yanqiu , Li Yan , Yan Guangmei 
Published: April 2011

AbstractMalignant gliomas are the most common and lethal intracranial tumors, and differentiation therapy shows great potential to be a promising candidate for their treatment. Here, we have elaborated that a PKA activator, forskolin, represses cell growth via cell cycle arrest in the G0/G1 phase and induces cell differentiation characteristic with elongated processes and restoration of GFAP expression. In mechanisms, we verified that forskolin significantly diminishes the mRNA and protein level of a key cell cycle regulator cyclin D1, and maintenance of low cyclin D1 expression level was required for forskolin‐induced proliferation inhibition and differentiation by gain and loss of function approaches. In addition, that forskolin down‐regulated the cyclin D1 by proteolytic (post‐transcriptional) mechanisms was dependent on GSK‐3β activation at Ser9. The pro‐differentiation activity of forskolin and related molecular mechanisms imply that forskolin can be developed into a candidate for the future in differentiation therapy of glioma, and cyclin D1 is a promising target for pro‐differentiation strategy. J. Cell. Biochem. 112: 2241–2249, 2011. © 2011 Wiley‐Liss, Inc.
ER‐resident Gi2 protein controls sar1 translocation onto the ER during budding of transport vesicles
Authors: Nakagawa Hiroshi , Umadome Haruka , Miyazaki Shuichi , Tanaka Katsuhiro , Nishimura Kazuhiko , Komori Masayuki , Matsuo Saburo 
Published: April 2011

AbstractIn our previous study, fluoride ([AlF4]−) disturbed ER‐to‐Golgi transport through the activation of ER‐resident heterotrimeric G protein (ER‐G protein). Therefore, ER‐G protein may be implicated in ER‐to‐Golgi transport at the early stage prior to coat protein assembly. Sar1 translocation onto the endoplasmic reticulum (ER) membrane is suppressed by non‐selective protein kinase inhibitor H89, suggesting the participation of H89‐sensitive kinase in this process. To investigate the involvement of ER‐G protein in ER‐to‐Golgi transport, the effect of Gi protein activator (mastoparan 7) was examined on Sar1 translocation onto the ER in a cell‐free system consisting of microsome membrane and cytosol. Sar1 translocation onto the microsome membrane was induced by addition of GTPγS in the cell‐free system. Translocation of Sar1 by GTPγS was suppressed significantly by both H89 and mastoparan 7. Mastoparan 7 suppressed the translocation of Sar1 onto the microsome membrane with dosage dependency, but mastoparan 17, the inactive analog of mastoparan 7, had no effect on Sar1 translocation. The suppressive effect of mastoparan 7 was recovered by treatment with pertussis toxin (IAP). Moreover, Gi2 protein was detected on the microsome membrane by western blotting for heterotrimeric Gi proteins. These results indicate that ER‐Gi2 protein modulated Sar1 translocation onto the ER, suggesting that ER‐resident Gi2 protein is an important negative regulator of vesicular transport at the early stage of vesicle formation before coat protein assembly on the ER. J. Cell. Biochem. 112: 2250–2256, 2011. © 2011 Wiley‐Liss, Inc.
Synthesis of 3H‐labeled Tetrabenazine (TBZ)
Authors: Rhee Sung‐Whi , Ryan Kenneth J. , Tanga Mary J. 
Published: April 2011

AbstractTetrabenazine (TBZ) (1,3,4,6,7,11b‐hexahydro‐9,10‐dimethoxy‐3‐(2‐methylpropyl)‐2H‐benzo[a]quinolin‐2‐one), a vesicular monamine transporter 2 inhibitor, was prepared as a tritium‐labeled compound with high specific activity and radiochemical purity. Catalytic hydrogenation of a precursor with the terminal double bond was used to introduce the tritium. This method provides tritium‐labeled TBZ with high specific activity and radiochemical purity, which allow the further investigation of a TBZ in the neurological field. Copyright © 2011 John Wiley & Sons, Ltd.
Neutron structure of type‐III antifreeze protein allows the reconstruction of AFP–ice interface
Authors: Howard Eduardo I. , Blakeley Matthew P. , Haertlein Michael , Haertlein Isabelle Petit‐ , Mitschler Andre , Fisher Stuart J. , Siah Alexandra Cousido‐ , Salvay Andrés G. , Popov Alexandre , Dieckmann Christoph Muller‐ , Petrova Tatiana , Podjarny Alberto 
Published: April 2011

AbstractAntifreeze proteins (AFPs) inhibit ice growth at sub‐zero temperatures. The prototypical type‐III AFPs have been extensively studied, notably by X‐ray crystallography, solid‐state and solution NMR, and mutagenesis, leading to the identification of a compound ice‐binding surface (IBS) composed of two adjacent ice‐binding sections, each which binds to particular lattice planes of ice crystals, poisoning their growth. This surface, including many hydrophobic and some hydrophilic residues, has been extensively used to model the interaction of AFP with ice. Experimentally observed water molecules facing the IBS have been used in an attempt to validate these models. However, these trials have been hindered by the limited capability of X‐ray crystallography to reliably identify all water molecules of the hydration layer. Due to the strong diffraction signal from both the oxygen and deuterium atoms, neutron diffraction provides a more effective way to determine the water molecule positions (as D2O). Here we report the successful structure determination at 293 K of fully perdeuterated type‐III AFP by joint X‐ray and neutron diffraction providing a very detailed description of the protein and its solvent structure. X‐ray data were collected to a resolution of 1.05 Å, and neutron Laue data to a resolution of 1.85 Å with a “radically small” crystal volume of 0.13 mm3. The identification of a tetrahedral water cluster in nuclear scattering density maps has allowed the reconstruction of the IBS‐bound ice crystal primary prismatic face. Analysis of the interactions between the IBS and the bound ice crystal primary prismatic face indicates the role of the hydrophobic residues, which are found to bind inside the holes of the ice surface, thus explaining the specificity of AFPs for ice versus water. Copyright © 2011 John Wiley & Sons, Ltd.
Ischemia‐induced changes in glucagon‐like peptide‐1 receptor and neuroprotective effect of its agonist, exendin‐4, in experimental transient cerebral ischemia
Authors: Hyun Lee Choong , Yan Bingchun , Yoo Ki‐Yeon , Choi Jung Hoon , Kwon Seung‐Hae , Her Song , Sohn Youdong , Hwang In Koo , Cho Jun Hwi , Kim Young‐Myeong , Won Moo‐Ho 
Published: April 2011

AbstractGlucagon‐like peptide‐1 receptor (GLP‐1R) protects against neuronal damages in the brain. In the present study, ischemia‐induced changes in GLP‐1R immunoreactivity in the gerbil hippocampal CA1 region were evaluated after transient cerebral ischemia; in addition, the neuroprotective effect of the GLP‐1R agonist exendin‐4 (EX‐4) against ischemic damage was studied. GLP‐1R immunoreactivity and its protein levels in the ischemic CA1 region were highest at 1 day after ischemia/reperfusion (I/R). At 4 days after I/R, GLP‐1R immunoreactivity was hardly detected in CA1 pyramidal neurons, and its protein level was lowest. GLP‐1R protein level was increased again at 10 days after I/R, and GLP‐1R immunoreactivity was found in astrocytes and GABAergic interneurons. In addition, EX‐4 treatment attenuated ischemia‐induced hyperactivity, neuronal damage, and microglial activation in the ischemic CA1 region in a dose‐dependent manner. EX‐4 treatment also induced the elevation of GLP‐1R immunoreactivity and protein levels in the ischemic CA1 region. These results indicate that GLP‐1R is altered in the ischemic region after an ischemic insult and that EX‐4 protects against ischemia‐induced neuronal death possibly by increasing GLP‐1R expression and attenuating microglial activation against transient cerebral ischemic damage. © 2011 Wiley‐Liss, Inc.
Surgical implications of mesenteric lymph node metastasis from advanced ovarian cancer after bowel resection
Authors: Baiocchi Glauco , Cestari Lourival Augusto , Macedo Mariana Petaccia , Oliveira Renato Almeida Rosa , Fukazawa Elza Mieko , Faloppa Carlos Chaves , Kumagai Lillian Yuri , Badiglian‐Filho Levon , Menezes Ademir Narciso Oliveira , Cunha Isabela Werneck , Soares Fernando Augusto 
Published: April 2011

AbstractBackgroundStudies addressing mesenteric and mesocolic lymph node metastasis in patients with advanced ovarian cancer that have undergone bowel resection are lacking.MethodsA retrospective analysis was performed in a series of 50 individuals who underwent surgical cytoreduction for epithelial ovarian cancer that included bowel resection from April 2004 to September 2010.ResultsForty‐one patients had bowel resection with mesenteric lymph nodes that were suitable for analysis. Twenty‐four (58.5%) patients underwent retosigmoidectomies, 14 (34.1%) received other types of colectomies, and three (7.3%) underwent small bowel resection. There was serosal involvement in 14 cases (34.1%), muscularis propria invasion in 13 cases (31.7%), submucosa invasion in six cases (14.6%), and mucosa in eight cases (19.5%). Lymphatic invasion was observed in 24 patients (58.5%). A median of 14 mesenteric lymph nodes were analyzed. Metastatic lymph nodes were observed in 29 (70.7%) cases. Invasion into the muscularis propria (P = 0.036), lymphatic invasion (P = 0.045), and retroperitoneal lymph node metastasis (P = 0.002) correlated significantly with mesenteric lymph node involvement.ConclusionsResection of regional lymph nodes of affected organs that is similar to surgical procedures that are performed for colorectal carcinoma is an appropriate, optimal debulking surgery for patients with ovarian carcinoma. J. Surg. Oncol. 2011; 104:250–254. © 2011 Wiley‐Liss, Inc.
Trends in surgical oncology research in Australia during the period 1998–2009—a bibliometric review
Authors: Chua Terence C. , Crowe Philip J. , Morris David L. 
Published: April 2011

AbstractObjectiveTo evaluate the distribution and scope of surgical research in Australia relating to malignant diseases in the field of surgery.MethodSurgical publications relating to adult malignant diseases originating from Australia were identified from a systematic literature examination using PubMed during a 12‐year period between 1998 and 2009. The origin of the article, journal impact factor (IF), type of research and its subspecialty discipline were recorded.ResultsOver a 12‐year period, 1,132 papers were published in various journals at a median annual rate of 98 papers. Four hundred eighty‐five (43%) papers arose from institutions in New South Wales, 225 (20%) papers from Victoria, 150 (13%) papers from South Australia, 106 (9%) papers from Western Australia, and 77 (7%) papers from Queensland. The mean IF was 3.22 (SD = 2.5). Papers were most commonly published in journals including the ANZ Journal of Surgery (n = 237, 21%), Annals of Surgical Oncology (n = 50, 4%), British Journal of Surgery (n = 38, 3%), and Diseases of the Colon and Rectum (n = 36, 3%). The mean IF of papers published per year ranged from 2.55 to 3.87. The most number of papers were published in the fields of urological oncology (n = 103, 9%), hepatopancreaticobiliary oncology (n = 144, 13%), breast oncology (n = 174, 15%), and colorectal oncology (n = 222, 20%).ConclusionBibliometric findings of this review suggest that there is a growth in high scientific research publications in the field of surgical oncology in Australia, indicating an interest in this discipline. This research trend may impact on the national research strategy for clinical cancer control. J. Surg. Oncol. 2011;104:216–219. © 2011 Wiley‐Liss, Inc.