bluuebunny/crossref_metadata_2025_split huggingface dataset:
Soil compaction associated with cut-to-length and whole-tree harvesting of a coniferous forest
Authors: Han Sang-Kyun , Han Han-Sup , Page-Dumroese Deborah S. , Johnson Leonard R. 
Published: July 2009

The degree and extent of soil compaction, which may reduce productivity of forest soils, is believed to vary by the type of harvesting system, and a field-based study was conducted to compare soil compaction from cut-to-length (CTL) and whole-tree (WT) harvesting operations. The CTL harvesting system used less area to transport logs to the landings than did the WT harvesting system (19%–20% vs. 24%–25%). At high soil moisture levels (25%–30%), both CTL and WT harvestings caused a significant increase of soil resistance to penetration (SRP) and bulk density (BD) in the track compared with the undisturbed area (p < 0.05). In the center of trails, however, only WT harvesting resulted in a significant increase of SRP and BD compared with the undisturbed area (p < 0.05). Slash covered 69% of the forwarding trail area in the CTL harvesting units; 37% was covered by heavy slash (40 kg·m–2) while 32% was covered by light slash (7.3 kg·m–2). Heavy slash was more effective in reducing soil compaction in the CTL units (p < 0.05). Prediction models were developed that can be used to estimate percent increases in SRP and BD over undisturbed areas for both CTL and WT harvesting systems.
Chapter 9 Meson Spectroscopy
Authors: Bian Jian-Ming , Bytev Vladimir , Chen Ying , Jin Hong-Ying , Jin Shan , Qin Hu , Shen Xiao-Yan , Wu Ning , Xu Guo-Fa , Zhang Zhen-Xia , Zhao Qiang , Zhemchugov Alexey , Zheng Han-Qing , Zhu Shi-Lin , Zou Bing-Song 
Published: July 2009

The following sections are included: Introduction Conventional Meson Spectrum Glueball Spectrum Hybrid Mesons Multiquarks Molecular States
Chapter 22 Leptonic, Semileptonic D(DS) Decays and CKM Matrix Elements
Authors: Yang Ya-Dong , Li Hai-Bo , Zou Jia-Heng , Chen Jiang-Chuan , Liu Jian , Rong Gang , Yang Mao-Zhi , Liu Hui-Hui , Ma Hai-Long , Charles J. , Descotes-Genon S. , Lacker H. , Li H. B. , Roos L. , T'Jampens S. , Xing Z. Z. 
Published: July 2009

The following sections are included: Leptonic Decays Semileptonic Decays Impact on CKM Measurements
DISCRETE CHOICES UNDER SOCIAL INFLUENCE: GENERIC PROPERTIES
Authors: GORDON MIRTA B. , NADAL JEAN-PIERRE , PHAN DENIS , SEMESHENKO VIKTORIYA 
Published: July 2009

We consider a model of socially interacting individuals that make a binary choice in a context of positive additive endogenous externalities. It encompasses as particular cases several models from the sociology and economics literature. We extend previous results to the case of a general distribution of idiosyncratic preferences, called here Idiosyncratic Willingnesses to Pay (IWP). When j, the ratio of the social influence strength to the standard deviation of the IWP distribution, is small enough, the inverse demand is a classical monotonic (decreasing) function of the adoption rate. However, even if the IWP distribution is mono-modal, there is a critical value of j above which the inverse demand is non-monotonic. Thus, depending on the price, there are either one or several equilibria.Beyond this first result, we exhibit the generic properties of the boundaries limiting the regions where the system presents different types of equilibria (unique or multiple). These properties are shown to depend only on qualitative features of the IWP distribution: modality (number of maxima), smoothness and type of support (compact or infinite). The main results are summarized as phase diagrams in the space of the model parameters, on which the regions of multiple equilibria are precisely delimited. We also discuss the links between the model and the random field Ising model studied in the physics literature.
DECAYS OF η AND η' MESONS–AN INTRODUCTION
Authors: KUPSC ANDRZEJ 
Published: July 2009

Decays of η and η' mesons are a laboratory for low energy strong interactions. The rate of isospin breaking decays into three pions constrain ratios of the light quark masses. Particle distributions from hadronic decays allow to study the elementary processes of the low energy Quantum Chromodynamics: π - π and π - η interactions. Radiative and conversion decays of the η and η' mesons provide information about internal structure of the mesons and the decay mechanism is strongly influenced by vector meson resonances. The lecture gives an introduction to the common decays of η and η' mesons. The main theme of the lecture are three body decays: hadronic decays, radiative decays into π+π-γ, π0γγ and Dalitz decays into ℓ+ℓ-γ.
Complex open-system design by quasi-agents
Authors: Bastani Behzad , Greaves David 
Published: July 2009

Drastically increasing involvement of Computer Science in different aspects of human life and sciences and the reciprocal dependency these sciences have developed on Computer Science and technology have deployed extremely challenging grounds for software architecture and design as a discipline. The requirements related to the management of complexity which is in the essence of these new domains combined with sizes which are orders of magnitude larger than the conventional business applications necessitate development of new paradigms. Since we are in fact beyond the age of writing one program by one group which takes care of one type of issue for one class of users, the new paradigms should guarantee some type of technical pluralism which allows indefinite number of people addressing indefinite aspects of complex clusters of issues in an ongoing effort over indefinite amount of time. The technical basis should provide for easy and ideally automated integration of all such efforts. This means the capability of random program design and integration based on a supporting and unifying conceptual framework. In contributing to these principles, Nuclear-Process Oriented Analysis and Modeling (NPOAM) [3] presented the capability of random modeling and design while establishing itself on the supporting framework of Abstraction-oriented Frames [4]. In an ongoing research to further modularize and streamline this methodology, this paper presents the idea and method of application of NPOAM to agent-base systems. The accomplishment of this goal is substantiated through a double implementation effort, one in an agent simulation environment and the other through the use of industrial strength modeling and application development tools.
This paper also extends the agent-oriented framework to propose a new concept named "quasi-agents" which is essentially related to mostly deterministic environments and offers examples of quasi-agents in implementation.
An Extragradient Method and Proximal Point Algorithm for Inverse Strongly Monotone Operators and Maximal Monotone Operators in Banach Spaces
Authors: Plubtieng Somyot , Sriprad Wanna 
Published: July 2009

AbstractWe introduce an iterative scheme for finding a common element of the solution set of a maximal monotone operator and the solution set of the variational inequality problem for an inverse strongly-monotone operator in a uniformly smooth and uniformly convex Banach space, and then we prove weak and strong convergence theorems by using the notion of generalized projection. The result presented in this paper extend and improve the corresponding results of Kamimura et al. (2004), and Iiduka and Takahashi (2008). Finally, we apply our convergence theorem to the convex minimization problem, the problem of finding a zero point of a maximal monotone operator and the complementary problem.
Bone Morphogenetic Proteins 2 and 5 Are Down-regulated in Adrenocortical Carcinoma and Modulate Adrenal Cell Proliferation and Steroidogenesis
Authors: Johnsen Inga K. , Kappler Roland , Auernhammer Christoph J. , Beuschlein Felix 
Published: July 2009

Abstract
Bone morphogenetic proteins (BMP) have been shown to affect tumorigenesis in a variety of tumors. Quantitative PCR analysis revealed down-regulation of BMP2 and BMP5 in tissue samples from adrenocortical carcinoma and adrenocortical tumor cell lines compared with normal adrenal glands. Integrity of BMP-dependent pathways in these cell lines could be shown by activation of the Smad1/5/8 pathway with subsequent increase of ID protein expression upon incubation with BMP2 or BMP5. On a functional level, BMP treatment resulted in inhibition of cell proliferation and viability in a dose- and time-dependent manner. This growth inhibitory effect was associated with BMP-dependent reduction of AKT phosphorylation under baseline conditions and under insulin-like growth factor costimulation. Furthermore, steroidogenic function, including melanocortin-2 receptor and steroidogenic enzyme expressions, was profoundly reduced. In vitro demethylation treatment and overexpression of GATA6 resulted in reactivation of BMP-dependent pathways with concomitant modulation of steroidogenesis. Taken together, we show that loss of expression of members of the BMP family of ligands is a common finding in adrenocortical tumors and we provide evidence that BMP-dependent pathways are likely to be involved in the modulation of the malignant and functional phenotype of adrenocortical cancer cells. [Cancer Res 2009;69(14):5784–92]
MicroRNA miR-29 Modulates Expression of Immunoinhibitory Molecule B7-H3: Potential Implications for Immune Based Therapy of Human Solid Tumors
Authors: Xu Hong , Cheung Irene Y. , Guo Hong-Fen , Cheung Nai-Kong V. 
Published: July 2009

Abstract
B7-H3, a surface immunomodulatory glycoprotein, inhibits natural killer cells and T cells. The monoclonal antibody (mAb) 8H9 is specific for 4Ig-B7-H3, the long and principal form of B7-H3. Early results from radioimmunotherapy using 8H9 have shown promise in patients with metastatic solid tumors to the central nervous system. Whereas B7-H3 transcript was ubiquitously expressed in a wide spectrum of human solid tumors as well as human normal tissues, B7-H3 protein was preferentially expressed only in tumor tissues. By quantitative reverse transcription-PCR, all three isoforms of microRNA miR-29 (a, b, and c) were highly expressed in normal tissues. However, they were down-regulated in a broad spectrum of solid tumors, including neuroblastoma, sarcomas, brain tumors, and tumor cell lines. B7-H3 protein expression was inversely correlated with miR-29 levels in both cell lines and tumor tissues tested. Using luciferase reporter assay, miR-29a was shown to directly target B7-H3 3′ untranslated region, and knock-in and knockdown of miR-29a led to down-regulation and up-regulation, respectively, of B7-H3 protein expression. The ability of miR-29 to control B7-H3 protein expression has implications in immune escape by solid tumors. Differential modulation of this key immunoinhibitory molecule in tumor versus normal tissues may advance both cell-mediated immunotherapy and antibody-based targeted strategies using the B7-H3–specific mAb 8H9. [Cancer Res 2009;69(15):6275–81]
The Serine Protease Inhibitor Protease Nexin-1 Controls Mammary Cancer Metastasis through LRP-1–Mediated MMP-9 Expression
Authors: Fayard Bérengère , Bianchi Fabrizio , Dey Julien , Moreno Eliza , Djaffer Sabrina , Hynes Nancy E. , Monard Denis 
Published: July 2009

Abstract
Through their ability to degrade the extracellular matrix, proteases mediate cancer cell invasion and metastasis. Paradoxically, some serine protease inhibitors (serpins) are often overexpressed in human tumors. Using computational analysis, we found that the RNA level of protease nexin-1 (PN-1), a serpin that blocks numerous proteases activity, is significantly elevated in estrogen receptor-α-negative and in high-grade breast cancer. The in silico approach was complemented by mechanistic studies on two mammary cancer cell lines, the PN-1-negative 168FARN cells and the PN-1-positive 4T1 cells, both of which form primary mammary tumors, but only 4T1 tumors are able to metastasize to the lungs. We show that treatment of 168FARN cells with PN-1 stimulates extracellular signal-regulated kinase activation via low-density lipoprotein receptor-related protein-1 (LRP-1) binding, resulting in increased matrix metalloproteinase (MMP)-9 RNA, protein, and secreted activity. PN-1–silenced 4T1 cells express low MMP-9 levels. Moreover, injection of PN-1–silenced cells into mice did not affect 4T1 primary mammary tumor outgrowth; however, the tumors had impaired metastatic potential, which could be restored by reexpressing soluble MMP-9 in the PN-1–silenced 4T1 cells. Thus, using mammary tumor models, we describe a novel pathway whereby the serpin PN-1 by binding LRP-1 stimulates extracellular signal-regulated kinase signaling, MMP-9 expression, and metastatic spread of mammary tumors. Importantly, an analysis of 126 breast cancer patients revealed that those whose breast tumors had elevated PN-1 levels had a significantly higher probability to develop lung metastasis, but not metastasis to other sites, on relapse. These results suggest that PN-1 might become a prognostic marker in breast cancer. [Cancer Res 2009;69(14):5690–8]
Transcriptional Output of the Salvador/Warts/Hippo Pathway Is Controlled in Distinct Fashions in Drosophila melanogaster and Mammalian Cell Lines
Authors: Zhang Xiaomeng , Milton Claire C. , Humbert Patrick O. , Harvey Kieran F. 
Published: July 2009

Abstract
The Salvador/Warts/Hippo (SWH) pathway is an important modulator of organ size, and deregulation of pathway activity can lead to cancer. Several SWH pathway components are mutated or expressed at altered levels in different human tumors including NF2, LATS1, LATS2, SAV1, and YAP. The SWH pathway regulates tissue growth by restricting the activity of the transcriptional coactivator protein known as Yorkie (Yki) in Drosophila melanogaster and Yes-associated protein (YAP) in mammals. Yki/YAP drives tissue growth in partnership with the Scalloped (Sd)/TEAD1-4 transcription factors. Yki/YAP also possesses two WW domains, which contact several proteins that have been suggested to either promote or inhibit the ability of Yki to induce transcription. To investigate the regulatory role of the Yki/YAP WW domains, we analyzed the functional consequence of mutating these domains. WW domain mutant YAP promoted transformation and migration of breast epithelial cells with increased potency, suggesting that WW domains mediate the inhibitory regulation of YAP in these cells. By contrast, the WW domains were required for YAP to promote NIH-3T3 cell transformation and for the ability of Yki to drive tissue growth in D. melanogaster and optimally activate Sd. This shows that Yki/YAP WW domains have distinct regulatory roles in different cell types and implies the existence of proteins that promote tissue growth in collaboration with Yki and Sd. [Cancer Res 2009;69(15):6033–41]
Progressive Tumor Formation in Mice with Conditional Deletion of TGF-β Signaling in Head and Neck Epithelia Is Associated with Activation of the PI3K/Akt Pathway
Authors: Bian Yansong , Terse Anita , Du Juan , Hall Bradford , Molinolo Alfredo , Zhang Pin , Chen Wanjun , Flanders Kathleen C. , Gutkind J. Silvio , Wakefield Lalage M. , Kulkarni Ashok B. 
Published: July 2009

Abstract
The precise role of transforming growth factor (TGF)-β signaling in head and neck squamous cell carcinoma (SCC) is not yet fully understood. Here, we report generation of an inducible head- and neck-specific knockout mouse model by crossing TGF-β receptor I (Tgfbr1) floxed mice with K14-CreERtam mice. By applying tamoxifen to oral cavity of the mouse to induce Cre expression, we were able to conditionally delete Tgfbr1 in the mouse head and neck epithelia. On tumor induction with 7,12-dimethylbenz(a)anthracene (DMBA), 45% of Tgfbr1 conditional knockout (cKO) mice (n = 42) developed SCCs in the head and neck area starting from 16 weeks after treatment. However, no tumors were observed in the control littermates. A molecular analysis revealed an enhanced proliferation and loss of apoptosis in the basal layer of the head and neck epithelia of Tgfbr1 cKO mice 4 weeks after tamoxifen and DMBA treatment. The most notable finding of our study is that the phosphoinositide 3-kinase (PI3K)/Akt pathway was activated in SCCs that developed in the Tgfbr1 cKO mice on inactivation of TGF-β signaling through Smad2/3 and DMBA treatment. These observations suggest that activation of Smad-independent pathways may contribute cooperatively with inactivation of Smad-dependent pathways to promote head and neck carcinogenesis in these mice. Our results revealed the critical role of the TGF-β signaling pathway and its cross-talk with the PI3K/Akt pathway in suppressing head and neck carcinogenesis. [Cancer Res 2009;69(14):5918–26]
High Efficacy of a Listeria-Based Vaccine against Metastatic Breast Cancer Reveals a Dual Mode of Action
Authors: Kim Sun Hee , Castro Francisco , Paterson Yvonne , Gravekamp Claudia 
Published: July 2009

Abstract
Most cancer vaccines induce CTL responses to tumor-associated antigens (TAA). Killing of tumor cells occurs through TAA-specific CTL-mediated cytolysis. Here, we show that one preventive followed by two therapeutic immunizations with an attenuated Listeria monocytogenes (LM)–based vaccine eradicates all metastases and almost the entire primary tumor in the syngeneic, aggressive mouse breast tumor model 4T1. We provide strong evidence that this is due to the combined result of direct kill by Listeria infecting the tumor cells and by CTL responses against Listeria antigens. We showed by electron microscopy that LM expressing truncated listeriolysin O (LLO) and amino acid fragments 311 to 660 of TAA Mage-b (LM-LLO-Mage-b311-660) and the control strain LM-LLO infect tumor cells in vitro and in vivo. In vitro data indicate that tumor cell death occurs through activation of NADP+ oxidase and increased intracellular Ca2+ levels, both resulting in the production of high ROS levels. Because both LM-LLO and LM-LLO-Mage-b311-660 showed equally strong efficacies in vivo, we concluded that LM-LLO was crucial and Mage-b was of less importance. We found strong CTL responses to LM-LLO in the spleen, and depletion of CD8 T cells in vivo resulted in significant tumor regrowth (52%) in LM-LLO–vaccinated mice, indicating that LM-LLO–specific CTL indeed partially contributed to tumor cell kill in vivo. This dual mode of action of a Listeria-based vaccine has not been described before and may provide new directions in the development of more effective vaccines against metastatic breast cancer. [Cancer Res 2009;69(14):5860–6]
Biochemical, Cellular, and In vivo Activity of Novel ATP-Competitive and Selective Inhibitors of the Mammalian Target of Rapamycin
Authors: Yu Ker , Toral-Barza Lourdes , Shi Celine , Zhang Wei-Guo , Lucas Judy , Shor Boris , Kim Jamie , Verheijen Jeroen , Curran Kevin , Malwitz David J. , Cole Derek C. , Ellingboe John , Ayral-Kaloustian Semiramis , Mansour Tarek S. , Gibbons James J. , Abraham Robert T. , Nowak Pawel , Zask Arie 
Published: July 2009

Abstract
The mammalian target of rapamycin (mTOR) is centrally involved in cell growth, metabolism, and angiogenesis. While showing clinical efficacy in a subset of tumors, rapamycin and rapalogs are specific and allosteric inhibitors of mTOR complex 1 (mTORC1), but they do not directly inhibit mTOR complex 2 (mTORC2), an emerging player in cancer. Here, we report chemical structure and biological characterization of three pyrazolopyrimidine ATP-competitive mTOR inhibitors, WAY-600, WYE-687, and WYE-354 (IC50, 5–9 nmol/L), with significant selectivity over phosphatidylinositol 3-kinase (PI3K) isofoms (&gt;100-fold). Unlike the rapalogs, these inhibitors acutely blocked substrate phosphorylation by mTORC1 and mTORC2 in vitro and in cells in response to growth factor, amino acids, and hyperactive PI3K/AKT. Unlike the inhibitors of PI3K or dual-pan PI3K/mTOR, cellular inhibition of P-S6K1(T389) and P-AKT(S473) by the pyrazolopyrimidines occurred at significantly lower inhibitor concentrations than those of P-AKT(T308) (PI3K-PDK1 readout), showing mTOR selectivity in cellular setting. mTOR kinase inhibitors reduced AKT downstream function and inhibited proliferation of diverse cancer cell lines. These effects correlated with a strong G1 cell cycle arrest in both the rapamycin-sensitive and rapamycin-resistant cells, selective induction of apoptosis, repression of global protein synthesis, and down-regulation of angiogenic factors. When injected into tumor-bearing mice, WYE-354 inhibited mTORC1 and mTORC2 and displayed robust antitumor activity in PTEN-null tumors. Together, our results highlight mechanistic differentiation between rapalogs and mTOR kinase inhibitors in targeting cancer cell growth and survival and provide support for clinical development of mTOR kinase inhibitors as new cancer therapy. [Cancer Res 2009;69(15):OF6232–9]
Reactivation of Androgen Receptor–Regulated TMPRSS2:ERG Gene Expression in Castration-Resistant Prostate Cancer
Authors: Cai Changmeng , Wang Hongyun , Xu Youyuan , Chen Shaoyong , Balk Steven P. 
Published: July 2009

Abstract
It seems clear that androgen receptor (AR)–regulated expression of the TMPRSS2:ERG fusion gene plays an early role in prostate cancer (PC) development or progression, but the extent to which TMPRSS2:ERG is down-regulated in response to androgen deprivation therapy (ADT) and whether AR reactivates TMPRSS2:ERG expression in castration-resistant PC (CRPC) have not been determined. We show that ERG message levels in TMPRSS2:ERG fusion-positive CRPC are comparable with the levels in fusion gene–positive primary PC, consistent with the conclusion that the TMPRSS2:ERG expression is reactivated by AR in CRPC. To further assess whether TMPRSS2:ERG expression is initially down-regulated in response to ADT, we examined VCaP cells, which express the TMPRSS2:ERG fusion gene, and xenografts. ERG message and protein rapidly declined in response to removal of androgen in vitro and castration in vivo. Moreover, as observed in the clinical samples, ERG expression was fully restored in the VCaP xenografts that relapsed after castration, coincident with AR reactivation. AR reactivation in the relapsed xenografts was also associated with marked increases in mRNA encoding AR and androgen synthetic enzymes. These results show that expression of TMPRSS2:ERG, similarly to other AR-regulated genes, is restored in CRPC and may contribute to tumor progression. [Cancer Res 2009;69(15):6027–32]
Fibulin-5 Suppresses Lung Cancer Invasion by Inhibiting Matrix Metalloproteinase-7 Expression
Authors: Yue Wen , Sun Quanhong , Landreneau Rodney , Wu Chuanyue , Siegfried Jill M. , Yu Jian , Zhang Lin 
Published: July 2009

Abstract
The high mortality rate of lung cancer is largely due to the spread of disease to other organs. However, the molecular changes driving lung cancer invasion and metastasis remain unclear. In this study, we identified fibulin-5, a vascular ligand for integrin receptors, as a suppressor of lung cancer invasion and metastasis. Fibulin-5 was silenced by promoter hypermethylation in a majority of lung cancer cell lines and primary tumors. It inhibited lung cancer cell invasion and down-regulated matrix metalloproteinase-7 (MMP-7), which promoted lung cancer cell invasion. Knockdown of fibulin-5 was sufficient to stimulate cell invasion and MMP-7 expression. The expression levels of fibulin-5 and MMP-7 were inversely correlated in lung tumors. Suppression of MMP-7 expression by fibulin-5 was mediated by an integrin-binding RGD motif via the extracellular signal-regulated kinase (ERK) pathway. Furthermore, overexpression of fibulin-5 in H460 lung cancer cells inhibited metastasis in mice. Collectively, these results suggest that epigenetic silencing of fibulin-5 promotes lung cancer invasion and metastasis by activating MMP-7 expression through the ERK pathway. [Cancer Res 2009;69(15):6339–46]