bluuebunny/crossref_metadata_2025_split huggingface dataset:
Physico‐Chemical Characterization of Nanofiltration Membranes
Authors: Boussu Katleen , De Baerdemaeker Jérémie , Dauwe Charles , Weber Marc , Lynn Kelvin G. , Depla Diederik , Aldea Steliana , Vankelecom Ivo F. J. , Vandecasteele Carlo , Van der Bruggen Bart 
Published: January 2007

AbstractThis study presents a methodology for an in‐depth characterization of six representative commercial nanofiltration membranes. Laboratory‐made polyethersulfone membranes are included for reference. Besides the physical characterization [molecular weight cut‐off (MWCO), surface charge, roughness and hydrophobicity], the membranes are also studied for their chemical composition [attenuated total reflectance Fourier spectroscopy (ATR‐FTIR) and X‐ray photoelectron spectroscopy (XPS)] and porosity [positron annihilation spectroscopy (PAS)]. The chemical characterization indicates that all membranes are composed of at least two different layers. The presence of an additional third layer is proved and studied for membranes with a polyamide top layer. PAS experiments, in combination with FIB (focused ion beam) images, show that these membranes also have a thinner and a less porous skin layer (upper part of the top layer). In the skin layer, two different pore sizes are observed for all commercial membranes: a pore size of 1.25–1.55 Å as well as a pore size of 3.20–3.95 Å (both depending on the membrane type). Thus, the pore size distribution in nanofiltration membranes is bimodal, in contrast to the generally accepted log‐normal distribution. Although the pore sizes are rather similar for all commercial membranes, their pore volume fraction and hence their porosity differ significantly.
Toward routine billion‐variable optimization using genetic algorithms
Authors: Goldberg David E. , Sastry Kumara , Llorà Xavier 
Published: January 2007

AbstractThe push for better understanding and design of complex systems requires the solution of challenging optimization problems with large numbers of decision variables. This note presents principled results demonstrating the scalable solution of a difficult test function on instances over a billion variables using a parallel implementation of a genetic algorithm (GA). The problem addressed is a noisy, blind problem over a vector of binary decision variables. Noise is added equaling a tenth of the deterministic objective function variance of the problem, thereby making it difficult for simple hillclimbers to find the optimal solution. The genetic algorithm used—the compact GA—is able to find the optimum in the presence of noise quickly, reliably, and accurately, and the solution scalability follows known convergence theories. These results on noisy problem together with other results on problems involving varying modularity, hierarchy, and overlap foreshadow routine solution of billion‐variable problems across the landscape of complexity science. © 2007 Wiley Periodicals, Inc. Complexity 12: 27–29, 2007
Antimicrobial peptides human β‐defensin (hBD)‐3 and hBD‐4 activate mast cells and increase skin vascular permeability
Authors: Chen Xuejun , Niyonsaba François , Ushio Hiroko , Hara Mutsuko , Yokoi Hidenori , Matsumoto Kenji , Saito Hirohisa , Nagaoka Isao , Ikeda Shigaku , Okumura Ko , Ogawa Hideoki 
Published: January 2007

AbstractAntimicrobial peptides human β‐defensins (hBD) are mainly produced by epithelia of several organs including skin, and participate in innate immunity by killing invading pathogens. Besides their microbicidal activities, hBD activate several inflammatory and immune cells. Since hBD are generated by tissues where mast cells are present, we hypothesized that these peptides could activate mast cells. In this study, we demonstrated that both hBD‐3 and hBD‐4 induced mast cell degranulation, prostaglandin D2 production, intracellular Ca2+ mobilization and chemotaxis. Furthermore, hBD‐3‐ and hBD‐4‐induced activation of mast cells was suppressed by pertussis toxin and U‐73122, inhibitors for G protein and phospholipase C, respectively. We further revealed that hBD‐3 and hBD‐4 increased vascular permeability in the skin, which was dependent on the presence of mast cells, because hBD‐3 and hBD‐4 failed to enhance vascular permeability in mast cell‐deficient Ws/Ws rats. We also demonstrated that hBD‐3 and hBD‐4 induced phosphorylation of MAPK p38 and ERK1/2, which were further required for hBD‐mediated mast cell activation, as evidenced by the inhibitory effects of p38 and ERK1/2 inhibitors on mast cell degranulation. Together, these findings suggest the key role of hBD in inflammatory responses by recruiting and activating mast cells, and increasing vascular permeability.
TREM‐1 promotes survival during septic shock in mice
Authors: Gibot Sébastien , Massin Frederic , Marcou Markella , Taylor Valerie , Stidwill Ray , Wilson Peter , Singer Mervyn , Bellingan Geoff 
Published: January 2007

AbstractTriggering receptor expressed on myeloid (TREM)‐1 is integral to the inflammatory response occurring during septic shock, although its precise function has yet to be determined. Here we show that in vivo silencing of TREM‐1 using siRNA duplexes in a fecal peritonitis mouse model resulted in a blunted inflammatory response and increased mortality. This was associated with impaired bacterial clearance related to marked inhibition of the neutrophil oxidative burst. By contrast, TREM‐1‐silenced mice were highly resistant to a lethal endotoxin challenge, while partial silencing of TREM‐1 in the bacterial peritonitis model produced a significant survival benefit. These data highlight the crucial role of the TREM‐1 pathway in mounting an adequate inflammatory and cytotoxic response to polymicrobial sepsis, and both the therapeutic promise and potential risks of its modulation.
Dectin‐1 promotes fungicidal activity of human neutrophils
Authors: Kennedy Adam D. , Willment Janet A. , Dorward David W. , Williams David L. , Brown Gordon D. , DeLeo Frank R. 
Published: January 2007

AbstractHuman polymorphonuclear leukocytes (PMN) are a first line of defense against fungal infections. PMN express numerous pattern recognition receptors (PRR) that facilitate identification of invading microorganisms and ultimately promote resolution of disease. Dectin‐1 (β‐glucan receptor) is a PRR expressed on several cell types and has been studied on monocytes and macrophages. However, the role played by dectin‐1 in the recognition and killing of fungi by PMN is unknown. We investigated the ability of dectin‐1 to mediate human PMN phagocytosis and fungicidal activity. Dectin‐1 was expressed on the surface of PMN from all subjects tested (n=29) and in an intracellular compartment that co‐sedimented with azurophilic granules in Percoll density gradients. Soluble β‐glucan and mAb GE2 (anti‐dectin‐1) inhibited binding and phagocytosis of zymosan by human PMN (e.g., ingestion was inhibited 40.1% by 30 min, p<0.001), and blocked reactive oxygen species production. Notably, soluble β‐glucan and GE2 inhibited phagocytosis and killing of Candida albicans by PMN (inhibition of killing was 54.8% for β‐glucan and 36.2% for GE2, p<0.01). Our results reveal a mechanism whereby PMN dectin‐1 plays a key role in the recognition and killing of fungal pathogens by the innate immune system.
N‐Functionalization of Azoles through Coupling Reactions with Alkoxydienyl and Alkoxystyryl Boronic Esters
Authors: Deagostino Annamaria , Prandi Cristina , Zavattaro Chiara , Venturello Paolo 
Published: January 2007

AbstractAlkoxydienyl boronates 1a and 1b and alkoxystyryl boronate 2 have been used in various copper mediated cross‐coupling reactions with azoles. A variety of N‐alkoxydienyl‐ and N‐styrylazoles have been synthesized under mild conditions. The process utilizes Cu(OAc)2 in the presence of CsF in CH2Cl2 at room temperature. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007)
Removal of boron dissolved in water
Authors: Kluczka Joanna , Ciba Jerzy , Trojanowska Jolanta , Zolotajkin Maria , Turek Marian , Dydo Piotr 
Published: January 2007

AbstractThe study aimed to investigate boron adsorption on activated carbon, activated carbon impregnated with different substances, activated alumina, zirconium dioxide and silica‐aerosil. The removal of boron from water was carried out in static and dynamic systems. Isotherms for boron adsorption from model aqueous solutions on various adsorbents were applied and Langmuir constants were calculated. The results indicate that the application of the impregnants increases the ability of activated carbon to adsorb boron. The first removal of boron using activated carbon impregnated with mannitol compared favorably with other impregnants. © 2007 American Institute of Chemical Engineers Environ Prog 26:71–77, 2007.
Hydrodistillation of caraway by direct induction heating assisted by a magnetic field process
Authors: Rivera L. Lagunez , Vilarem G. 
Published: January 2007

AbstractThis paper presents the development of a new method of hydrodistillation of the essential oil of caraway (Carum carvi L.) by direct induction heating assisted by magnetic field (DIHMF) and the development of the required apparatus. Water and food salt (99.8% sodium chloride) were used as electrolyte solutions and at the same time as an extractant solution. The method was tested on caraway fruits as a source of carvone and limonene as the main components. The essential oil of this fruit was also isolated by conventional hydrodistillation as a standard method on both laboratory and pilot scale. The isolated volatile products obtained by the two methods were analysed using gas chromatography (GC). The obtained results were then compared. Even though DIHMF hydrodistillation ensures the isolation of the essential oils as well as conventional hydrodistillation, the time required to obtain the isolated products is remarkably shorter. Copyright © 2007 John Wiley & Sons, Ltd.
An examination of momentum strategies in commodity futures markets
Authors: Shen Qian , Szakmary Andrew C. , Sharma Subhash C. 
Published: January 2007

AbstractCommodity futures and equity markets differ in several important respects. Nevertheless, it was found that momentum profits in commodities are highly significant for holding periods as long as 9 months, and returns to momentum strategies are roughly equal in magnitude to those that have been reported in stocks. The profits documented are too large to be subsumed by transactions costs. Although the momentum strategies appear to be quite risky, their profitability cannot be fully accounted for in the context of a market factor model. Further, it is shown that momentum profits eventually reverse if positions are maintained long enough after portfolio formation. © 2007 Wiley Periodicals, Inc. Jrl Fut Mark 27:227–256, 2007
Anatomical subsite discrepancy in relation to the impact of the consumption of alcohol, tobacco and betel quid on esophageal cancer
Authors: Lee Chien‐Hung , Wu Deng‐Chyang , Lee Jang‐Ming , Wu I‐Chen , Goan Yih‐Gang , Kao Ein‐Long , Huang Hsiao‐Ling , Chan Te‐Fu , Chou Shah‐Hwa , Chou Yi‐Pin , Ho Chi‐Kung , Wu Ming‐Tsang 
Published: January 2007

AbstractThe carcinogenetic impact of risk factors on esophageal cancer (EC) may differ according to the portion of the esophagus where the tumor occurs. It is unclear why more esophageal squamous cell carcinomas (SCC) developed in the middle location. We carried out a multicenter case–control study in Taiwan to assess anatomical subsite risk discrepancy for this neoplasm in regard to the consumption of alcohol, tobacco and betel quid. Four hundred forty seven incident patients with pathology‐proven SCC of the esophagus (107 were upper‐third [U/3‐EC], 199 middle‐third [M/3‐EC] and 141 lower‐third [L/3‐EC] cases), as well as 1,022 gender, age and study hospital matched controls were analyzed by unordered polytomous logistic regression. All consumption of the three substances was related to the development of each subsite of EC, with a heterogeneously higher risk for current smokers (adjusted odds ratio (AOR) = 6.2) found in M/3‐EC and for current chewers, in U/3‐EC (AOR = 4.9). The joint risk of contracting lower two‐third EC for drinking and smoking appeared to significantly surpass those estimated by a multiplicative interaction model. Concomitant exposure to these two agents brought the risks of EC at all three subsites up to 10‐ to 23.9‐fold and additional tobacco‐free betel quid to a 30.3‐ to 75.0‐fold. In conclusion, tumor subsite discrepancy risk is related to prolonged exposure to tobacco and betel quid with inflorescence. Alcohol interacts with tobacco in a stronger supra‐multiplicative way in the middle portion of the esophagus, probably explaining why esophageal SCC occurs more commonly at this anatomical location. © 2007 Wiley‐Liss, Inc.
Retracted: Inhibition of heat shock protein‐90 modulates multiple functions required for survival of human T‐cell leukemia virus type I‐infected T‐cell lines and adult T‐cell leukemia cells
Authors: Kawakami Hirochika , Tomita Mariko , Okudaira Taeko , Ishikawa Chie , Matsuda Takehiro , Tanaka Yuetsu , Nakazato Tetsuro , Taira Naoya , Ohshiro Kazuiku , Mori Naoki 
Published: January 2007

Abstract Retraction: The following article has been retracted through agreement between the first author and several coauthors, the journal Editor‐in‐Chief, Peter Lichter, and John Wiley & Sons, Ltd.: Kawakami H, Tomita M, Okudaira T, Ishikawa C, Matsuda T, Tanaka Y, Nakazato T, Taira N, Ohshiro K, Mori N. (2007). Inhibition of heat shock protein‐90 modulates multiple functions required for survival of human T‐cell leukemia virus type I‐infected T‐cell lines and adult T‐cell leukemia cells. Int J Cancer; 120 (April (8)): 1811‐1820, published online on 17 JAN 2007 in Wiley Online Library (www.onlinelibrary.wiley.com). After an investigation the retraction has been agreed due to inappropriate duplication of images and overlap with other published work.
DNA demethylation of vascular endothelial growth factor‐C is associated with gene expression and its possible involvement of lymphangiogenesis in gastric cancer
Authors: Matsumura Shunji , Oue Naohide , Mitani Yoshitsugu , Kitadai Yasuhiko , Yasui Wataru 
Published: January 2007

AbstractPrevious studies have indicated that lymphangiogenesis in solid tumors is associated with lymphatic metastasis. Overexpression of Vascular endothelial growth factor (VEGF)‐C plays a major role in lymphangiogenesis in cancers. In the present study, DNA methylation and expression of the VEGF‐C gene was investigated in gastric cancer (GC). Four GC cell lines (MKN‐45, MKN‐74, HSC‐39 and HSC‐43) showed no expression of VEGF‐C, and the VEGF‐C gene was found to be methylated in these cells. In contrast, 7 GC cell lines (MKN‐1, MKN‐7, MKN‐28, TMK‐1, KATO‐III, SH101‐P4 and HSC‐44PE) expressed VEGF‐C, and the VEGF‐C gene was found to be unmethylated in these cell lines. In addition, expression of VEGF‐C mRNA was retrieved by treatment with a demethylating agent, Aza‐2′‐deoxycytidine. In GC tissue samples, bisulfite DNA sequencing analysis revealed that VEGF‐C was not methylated in 9 (29.0%) of 31 GC samples, whereas demethylation was not observed in corresponding non‐neoplastic mucosa samples. Overexpression of VEGF‐C mRNA was observed in 16 (51.6%) of 31 GC samples by quantitative reverse transcription‐polymerase chain reaction. Of the 9 GC cases with VEGF‐C demethylation, 8 (88.9%) overexpressed VEGF‐C. In contrast, of the 22 GC cases without VEGF‐C demethylation, 8 (36.4%) overexpressed VEGF‐C (p = 0.0155). Furthermore, lymphatic vessel density determined by immunostaining of podoplanin in GC tissues was associated with overexpression of VEGF‐C (p < 0.0001). These results suggest that demethylation and activation of the VEGF‐C gene is likely involved in lymphangiogenesis in GC. © 2007 Wiley‐Liss, Inc.
Mammalian target of rapamycin is activated in human gastric cancer and serves as a target for therapy in an experimental model
Authors: Lang Sven A. , Gaumann Andreas , Koehl Gudrun E. , Seidel Ulrike , Bataille Frauke , Klein Dagmar , Ellis Lee M. , Bolder Ulrich , Hofstaedter Ferdinand , Schlitt Hans‐Jürgen , Geissler Edward K. , Stoeltzing Oliver 
Published: January 2007

AbstractThe mammalian target of rapamycin (mTOR) has become an interesting target for cancer therapy through its influence on oncogenic signals, which involve phosphatidylinositol‐3‐kinase and hypoxia‐inducible factor‐1α (HIF‐1α). Since mTOR is an upstream regulator of HIF‐1α, a key mediator of gastric cancer growth and angiogenesis, we investigated mTOR activation in human gastric adenocarcinoma specimens and determined whether rapamycin could inhibit gastric cancer growth in mice. Expression of phospho‐mTOR was assessed by immunohistochemical analyses of human tissues. For in vitro studies, human gastric cancer cell lines were used to determine S6K1, 4E‐BP‐1 and HIF‐1α activation and cancer cell motility upon rapamycin treatment. Effects of rapamycin on tumor growth and angiogenesis in vivo were assessed in both a subcutaneous tumor model and in an experimental model with orthotopically grown tumors. Mice received either rapamycin (0.5 mg/kg/day or 1.5 mg/kg/day) or diluent per intra‐peritoneal injections. In addition, antiangiogenic effects were monitored in vivo using a dorsal‐skin‐fold chamber model. Immunohistochemical analyses showed strong expression of phospho‐mTOR in 60% of intestinal‐ and 64% of diffuse‐type human gastric adenocarcinomas. In vitro, rapamycin‐treatment effectively blocked S6K1, 4E‐BP‐1 and HIF‐1α activation, and significantly impaired tumor cell migration. In vivo, rapamycin‐treatment led to significant inhibition of subcutaneous tumor growth, decreased CD31‐positive vessel area and reduced tumor cell proliferation. Similar significant results were obtained in an orthotopic model of gastric cancer. In the dorsal‐skin‐fold chamber model, rapamycin‐treatment significantly inhibited tumor vascularization in vivo. In conclusion, mTOR is frequently activated in human gastric cancer and represents a promising new molecular target for therapy. © 2007 Wiley‐Liss, Inc.
Silibinin synergizes with mitoxantrone to inhibit cell growth and induce apoptosis in human prostate cancer cells
Authors: Flaig Thomas W. , Su Lih‐Jen , Harrison Gail , Agarwal Rajesh , Glodé Leonard Michael 
Published: January 2007

AbstractThe purpose of these experiments was to assess the synergistic activity of silibinin with chemotherapy agents in clinical use against prostate cancer. Silybin‐phytosome, a commercially available formulation containing silibinin, has recently been studied in a phase I clinical trial. The silibinin doses used in the present study are clinically achievable based on the preliminary phase I data. DU145, PC‐3 and LNCaP prostate cancer cells were seeded in 96‐well plates in triplicate. Twenty‐four hours later, silibinin (10, 20 and 40 μM) and either mitoxantrone or docetaxel were added to the designated wells. Seventy‐two hours post‐treatment, cell viability was determined with a tetrazolium‐based assay. The combination index (CI) for determination of a synergistic effect was calculated, with values of <0.9 indicating synergy and values >1.1 antagonism. Apoptosis was also assessed using a luminescent assay after 72 hr of treatment with media alone, silibinin, mitoxantrone, or silibinin plus mitoxantrone. Silibinin showed a synergistic effect with mitoxantrone, as measured by reduction in cell viability. The CI values ranged from 0.413 to 2.650 for the combination of silibinin and mitoxantrone; in contrast, treatment with docetaxel and silibinin showed little or no synergy, with CI values of 0.898–4.469. In concordance with these findings, the addition of silibinin increased the level of apoptosis compared to mitoxantrone alone, particularly in the PC‐3 cells. The combination of silibinin and mitoxantrone exhibits a pattern of synergy in reducing cell viability with increased apoptosis. These data are important in the planning of future clinical applications of silibinin. © 2007 Wiley‐Liss, Inc.
Simultaneous blockade of VEGFR‐1 and VEGFR‐2 activation is necessary to efficiently inhibit experimental melanoma growth and metastasis formation
Authors: Gille Jens , Heidenreich Regina , Pinter Andreas , Schmitz Judith , Boehme Beatrice , Hicklin Daniel J. , Henschler Reinhard , Breier Georg 
Published: January 2007

AbstractMetastasis continues to be the major cause of morbidity and mortality in malignant melanoma. In our study, we explored whether inhibition of VEGFR‐1 or VEGFR‐2 signaling conveys distinct suppressive effects on B16 melanoma subcutaneous growth and metastasis formation. The inhibition of VEGFR‐1 or ‐2 alone had no significant influence on both melanoma growth and metastasis formation. In contrast, simultaneous blockade of VEGFR‐1 and ‐2 signaling strongly suppressed progression in both B16 tumor models. There was no expression of VEGFR‐1 or ‐2 detectable on the B16 cells used, excluding the melanoma cells as direct therapeutic targets. Analyzing the contribution of progenitor‐like cells during melanoma metastasis formation, we observed an enhanced proliferation and mobilization of VEGFR‐1+ myeloid and VEGFR‐2+ endothelial cells with progenitor potential by the induction of melanoma lung metastasis, which was not influenced by interference with VEGFR signaling. These results indicate that the antimetastatic effects exerted by combined inhibition of VEGFR‐1 and ‐2 signaling were mediated via targeting cell populations other than progenitors only. Sole inhibition of VEGFR‐1 signaling led to a strong reduction of the CD45‐positive inflammatory infiltrate in the tumor tissue. However, the formation of lung metastasis was not affected, indicating that inhibition of the inflammatory response was not sufficient to efficiently block B16 melanoma metastasis development. Taken together, our data suggest that in the utilized B16 tumor models the blockade of both the inflammatory and the VEGFR‐2‐dependent angiogenic response are necessary to effectively inhibit solid tumor growth and formation of lung metastasis by B16 melanoma cells. © 2007 Wiley‐Liss, Inc.
Theoretical density functional theory studies on interactions of small biologically active molecules with isolated heme group
Authors: Rutkowska‐Zbik Dorota , Witko Malgorzata , Stochel Grazyna 
Published: January 2007

AbstractWe present ab‐initio density functional theory studies on the interactions of small biologically active molecules, namely NO, CO, O2, H2O, and NO with the full‐size heme group. Our results show that the small molecule–iron bond is the strongest in carbonyl and the weakest in nitrite system. Trans influence induced by NO binding to the five‐coordinate heme complex is shown. Nitric oxide in the resulting complex might be described as NO−. The differences among the small ligands of XO type (CO, NO, O2), and their distant chemical behavior from H2O and NO ligands in binding to the Fe(II) ion, are shown. Moreover, the role of the heme ring as a reservoir of electrons in the studied complexes is invoked. The analysis of the parameters defining the iron–histidine bond indicates that this bond is longer and weaker in nitrosyl and carbonyl complexes than in the other systems. Our findings support the proposed mechanism of soluble guanylate cyclase (sGC) activation and suggest that the first step of sGC activation by CO may be the same as during the activation by NO. Obtained results are then compared with the data concerning smaller model of the heme, the porphyrin complexes, available in the literature. © 2007 Wiley Periodicals, Inc. J Comput Chem 28: 825–831, 2007