bluuebunny/crossref_metadata_2025_split huggingface dataset:
MAIN FACTORS CONTROLLING THE COMPOSITIONAL VARIABILITY OF SEEPAGE OILS FROM TRUJILLO STATE, WESTERN VENEZUELA
Authors: Galarraga F. , Urbani F. , Escobar M. , Márquez G. , Martínez M. , Tocco R. 
Published: June 2010

The organic geochemistry of eighteen samples of seepage oils from Trujillo State, Western Venezuela, was investigated. These oils are probably derived from the predominantly marine Cretaceous La Luna Formation which is near peak maturity for oil generation. A range of biomarkers (n‐alkanes, acyclic isoprenoids, phenanthrene and alkyl‐phenanthrenes, as well as dibenzothiophene and alkyl‐dibenzothiophenes) were analysed by gas chromatography ‐ mass spectrometry (GC‐MS).The seepage oils have been modified as a result of water washing and biodegradation. A first group of samples were slightly biodegraded with the partial loss of n‐ and iso‐alkanes. Other samples fall into two groups: those that are moderately degraded, with partial depletion of acyclic isoprenoids; and those that are severely altered, as indicated by the partial or total absence of hopanes.One objective of this work was to evaluate the factors influencing the compositional differences of the three samples sets. In‐situ measurements, together with the interpretation of the geochemical data, suggest that diverse factors were responsible for these variations. These included different degrees of alteration due to biodegradation and water washing, as well as differences in flow rate towards the surface.
Creating and maintaining oral health for dependent people in institutional settings
Authors: Glassman Paul , Subar Paul 
Published: June 2010

AbstractThe absolute number and percentage of the population of dependent individuals in institutional settings are growing dramatically in the United States. The current dominant office‐based oral health delivery system is not adequately addressing the oral health needs of these populations and is unlikely to do so in the future.There are multiple challenges in providing oral health services for dependent people in institutional settings. To achieve improvements in the oral health of these populations, we must change the education of oral health professionals, educate staff in institutional settings about oral health, integrate oral health activities into general health and social service systems, use existing oral health professionals in new ways in community settings, develop new categories of oral health professionals, and reform oral health delivery and reimbursement systems.Developing new models of oral health services for dependent individuals in institutional settings may provide an opportunity to create a new paradigm of care based on integration of oral health services with general health and social services with an emphasis on prevention and health promotion activities.
Envisioning success: the future of the oral health care delivery system in the United States
Authors: Garcia Raul I. , Inge Ronald E. , Niessen Linda , DePaola Dominick P. 
Published: June 2010

AbstractThe elimination of oral health disparities in the US will require enhancing access to oral health care services. The workshop convened in 2009 by the Institute of Medicine on the “US Oral Health Workforce in the Coming Decade” highlighted both the current workforce's failure to meet the nation's needs as well as the promising opportunities presented by various workforce strategies to significantly enhance access and improve oral health outcomes. In this article, we have briefly reviewed and expanded on the contributions in this special issue of the Journal of Public Health Dentistry, with the goal of identifying common themes and providing a framework for evaluation. There are several key areas where change is critically needed in order to ensure successful implementation of any new workforce models. These areas include a) the public and private financing of dental care, b) the dental educational system, and c) state and federal policies.
Trend analysis of diabetic prevalence and incidence in a rural area of South Korea between 2003–2008
Authors: Jeong Ji Yun , Kim Jung‐Guk , Kim Bo‐Wan , Moon Seong Su , Kim Hye‐Soon , Park Keun‐Gyu , Won Kyu Chang , Lee Hyoung Woo , Yoon Ji Sung , Shon Ho‐Sang , Lee Ji Hyun , Jung Eui‐Dal , Park Mi Young , Chun Byung‐Yeol , Kim Keon‐Yeop , Hwang Tae‐Yoon , Lee Mi‐Young , Lee In‐Kyu 
Published: June 2010

AbstractAims/Introduction:  This study determined the change in prevalence of diabetes and prediabetes over a period of 5 years in South Korea. The incidence of diabetes and prediabetes and risk factors associated with the development of diabetes were also investigated.Materials and Methods:  The Dalseong population‐based cohort survey recruited 1806 subjects who were over 20‐years‐old in 2003. Five years later, 1287 of the original subjects were re‐evaluated and 187 new subjects were added to the study. All participants completed a questionnaire, were given a physical examination, and provided blood samples for analysis including 2 h oral glucose tolerances.Results:  Age‐adjusted prevalence of diabetes rose from 6.7% in 2003 to 9.1% in 2008. The prevalence of prediabetes also increased from 18.5% in 2003 to 28.4% in 2008. The incidence rates of diabetes and prediabetes were 18.3 per 1000 person‐years and 55.4 per 1000 person‐years, respectively. The development of diabetes was associated with impaired fasting glucose (IFG) (odds ratio [OR] 5.661), impaired glucose tolerance (IGT) (OR: 6.013), age (OR 1.013), and waist‐to‐hip ratio (OR 1.513). After excluding the IFG and IGT, systolic blood pressure (OR 1.023), high‐sensitivity C‐reactive protein (hsCRP; OR 1.097), triglyceride (OR 1.002) and waist‐to‐hip ratio (OR 1.696) were statistically significant risk factors in a multivariate logistic regression analysis.Conclusions:  A significant rise in the prevalence of diabetes and prediabetes was observed between 2003 and 2008. In addition, this study newly demonstrated that waist‐to‐hip ratio and hsCRP were associated with the development of diabetes after adjusting for several confounding factors. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2010.00045.x, 2010)
A Hybrid Proximal Point Three-Step Algorithm for Nonlinear Set-Valued Quasi-Variational Inclusions System Involving "Equation missing" -Accretive Mappings
Authors: Li Hong-Gang , Xu AnJian , Jin MaoMing 
Published: June 2010

AbstractThe main purpose of this paper is to introduce and study a new class of generalized nonlinear set-valued quasi-variational inclusions system involving "Equation missing"-accretive mappings in Banach spaces. By using the resolvent operator due to Lan-Cho-Verma associated with "Equation missing"-accretive mappings and the matrix analysis method, we prove the convergence of a new hybrid proximal point three-step iterative algorithm for this system of set-valued variational inclusions and an existence theorem of solutions for this kind of the variational inclusions system. The results presented in this paper generalize, improve, and unify some recent results in this field.
Tetraspanin CD151 Regulates Transforming Growth Factor β Signaling: Implication in Tumor Metastasis
Authors: Sadej Rafał , Romanska Hanna , Kavanagh Dean , Baldwin Gouri , Takahashi Takashi , Kalia Neena , Berditchevski Fedor 
Published: June 2010

AbstractTetraspanin CD151 is associated with laminin-binding integrins and controls tumor cell migration and invasion. By analyzing responses of breast cancer cells to various growth factors, we showed that depletion of CD151 specifically attenuates transforming growth factor β1 (TGFβ1)–induced scattering and proliferation of breast cancer cells in three-dimensional Matrigel. CD151-dependent cell scattering requires its association with either α3β1 or α6 integrins, but it is independent of the recruitment of CD151 to tetraspanin-enriched microdomains. We also found that CD151 regulates the compartmentalization of TGF-β type I receptor (TβRI/ALK-5) and specifically controls the TGFβ1-induced activation of p38. In contrast, signaling leading to activation of Smad2/3, c-Akt, and Erk1/2 proteins was comparable in CD151(+) and CD151(−) cells. Attenuation of TGFβ1-induced responses correlated with reduced retention in the lung vascular bed, inhibition of pneumocyte-induced scattering of breast cancer cells in three-dimensional Matrigel, and decrease in experimental metastasis to the lungs. These results identify CD151 as a positive regulator of TGFβ1-initiated signaling and highlight the important role played by this tetraspanin in TGFβ1-induced breast cancer metastasis. Cancer Res; 70(14); 6059–70. ©2010 AACR.
Compensatory Upregulation of Tyrosine Kinase Etk/BMX in Response to Androgen Deprivation Promotes Castration-Resistant Growth of Prostate Cancer Cells
Authors: Dai Bojie , Chen Hege , Guo Shengjie , Yang Xi , Linn Douglas E. , Sun Feng , Li Wei , Guo Zhiyong , Xu Kexin , Kim Oekyung , Kong Xiangtian , Melamed Jonathan , Qiu Shaopeng , Chen Hegang , Qiu Yun 
Published: June 2010

Abstract
We previously showed that targeted expression of non–receptor tyrosine kinase Etk/BMX in mouse prostate induces prostate intraepithelial neoplasia, implying a possible causal role of Etk in prostate cancer development and progression. Here, we report that Etk is upregulated in both human and mouse prostates in response to androgen ablation. Etk expression seems to be differentially regulated by androgen and interleukin 6 (IL-6), which is possibly mediated by the androgen receptor (AR) in prostate cancer cells. Our immunohistochemical analysis of tissue microarrays containing 112 human prostate tumor samples revealed that Etk expression is elevated in hormone-resistant prostate cancer and positively correlated with tyrosine phosphorylation of AR (Pearson correlation coefficient ρ = 0.71, P &lt; 0.0001). AR tyrosine phosphorylation is increased in Etk-overexpressing cells, suggesting that Etk may be another tyrosine kinase, in addition to Src and Ack-1, which can phosphorylate AR. We also showed that Etk can directly interact with AR through its Src homology 2 domain, and such interaction may prevent the association of AR with Mdm2, leading to stabilization of AR under androgen-depleted conditions. Overexpression of Etk in androgen-sensitive LNCaP cells promotes tumor growth while knocking down Etk expression in hormone-insensitive prostate cancer cells by a specific shRNA that inhibits tumor growth under androgen-depleted conditions. Taken together, our data suggest that Etk may be a component of the adaptive compensatory mechanism activated by androgen ablation in prostate and may play a role in hormone resistance, at least in part, through direct modulation of the AR signaling pathway. Cancer Res; 70(13); 5587–96. ©2010 AACR.
Characterization of a Novel Mechanism of Genomic Instability Involving the SEI1/SET/NM23H1 Pathway in Esophageal Cancers
Authors: Li Yan , Nie Chang-Jun , Hu Liang , Qin Yanru , Liu Hai-bo , Zeng Ting-Ting , Chen Leilei , Fu Li , Deng Wen , Chen Shu-Peng , Jia Wei-Hua , Zhang Chunyu , Xie Dan , Guan Xin-Yuan 
Published: June 2010

Abstract
Amplification of 19q is a frequent genetic alteration in many solid tumors, and SEI1 is a candidate oncogene within the amplified region. Our previous study found that the oncogenic function of SEI1 was associated with chromosome instability. In this study, we report a novel mechanism of genomic instability involving the SEI1-SET-NM23H1 pathway. Overexpression of SEI1 was observed in 57 of 100 of esophageal squamous cell carcinoma cases. Functional study showed that SEI1 had strong tumorigenic ability, and overexpression of SEI1 could induce the genomic instability by increasing micronuclei formation and reducing the number of chromosomes. Further study found that SEI1 was able to upregulate SET expression and subsequently promote the translocation of a small amount of NM23H1 from the cytoplasm to the nucleus. Nuclear NM23H1 can induce DNA damage through its DNA nick activity. Unlike CTL attack, only a small amount of NM23H1 translocated into the nucleus (&lt;10%) induced by the overexpression of SEI1. Further study found that the small amount of NM23H1 only induced minor DNA damage and subsequently increased genomic instability, rather than inducing irreparable DNA damage and initiating apoptosis by CTL attack. Sister chromatid exchange experiment found that the translocation of small amount of NM23H1 into the nucleus induced by the overexpressions of SEI1/SET could increase the frequency of sister chromatid exchange. In addition, overexpression of SEI1 was associated with poor prognosis of esophageal squamous cell carcinoma. Taken together, these findings define a novel mechanism of genomic instability and malignant progression in esophageal cancers, a deadly disease of increasing incidence in developed countries. Cancer Res; 70(14); 5695–705. ©2010 AACR.
Alternatively Spliced RAGEv1 Inhibits Tumorigenesis through Suppression of JNK Signaling
Authors: Kalea Anastasia Z. , See Fiona , Harja Evis , Arriero Maria , Schmidt Ann Marie , Hudson Barry I. 
Published: June 2010

Abstract
Receptor for advanced glycation end products (RAGE) and its ligands are overexpressed in multiple cancers. RAGE has been implicated in tumorigenesis and metastasis, but little is known of the mechanisms involved. In this study, we define a specific functional role for an alternate splice variant termed RAGE splice variant 1 (RAGEv1), which encodes a soluble endogenous form of the receptor that inhibits tumorigenesis. RAGEv1 was downregulated in lung, prostate, and brain tumors relative to control matched tissues. Overexpressing RAGEv1 in tumor cells altered RAGE ligand stimulation of several novel classes of genes that are critical in tumorigenesis and metastasis. Additionally, RAGEv1 inhibited tumor formation, cell invasion, and angiogenesis induced by RAGE ligand signaling. Analysis of signal transduction pathways underlying these effects revealed marked suppression of c-jun-NH2-kinase (JNK) pathway signaling, and JNK inhibition suppressed signaling through the RAGE pathway. Tumors expressing RAGEv1 were significantly smaller than wild-type tumors and displayed prominently reduced activation of JNK. Our results identify RAGEv1 as a novel suppressor, the study of which may offer new cancer therapeutic directions. Cancer Res; 70(13); 5628–38. ©2010 AACR.
The Vascular Endothelial Growth Factor Receptor Tyrosine Kinase Inhibitors Vatalanib and Pazopanib Potently Induce Apoptosis in Chronic Lymphocytic Leukemia Cells In vitro and In vivo
Authors: Paesler Julian , Gehrke Iris , Gandhirajan Rajesh Kumar , Filipovich Alexandra , Hertweck Magdalena , Erdfelder Felix , Uhrmacher Sabrina , Poll-Wolbeck Simon Jonas , Hallek Michael , Kreuzer Karl-Anton 
Published: June 2010

Abstract
Purpose: There is evidence that vascular endothelial growth factor (VEGF) is a critical microenvironmental factor that exerts angiogenesis-independent effects on the survival of chronic lymphocytic leukemia (CLL) cells. Vatalanib and pazopanib are potent orally available VEGF receptor tyrosine kinase inhibitors. We investigated the efficacy and selectivity of both compounds in CLL cells, simulated potential combination with conventional cytostatics, and tested the effect of both substances on CLL-like tumor xenografts.
Experimental Design: Primary CLL and normal peripheral blood cells were tested for viability after incubation with varying concentrations of both inhibitors. Further, phosphorylation status of VEGF receptor on treatment, caspase activation, and poly(ADP-ribose) polymerase cleavage were assessed. Combinations of each inhibitor with fludarabine, vincristine, and doxorubicin were analyzed for possible synergistic effects in vitro. For in vivo testing, mice grafted with the CLL-like cell line JVM-3 were treated orally with each inhibitor.
Results: Vatalanib and pazopanib decreased phosphorylation of the VEGF receptor, along with induction of apoptosis in CLL cells in clinically achievable concentrations. Healthy B cells were only mildly affected. Immunoblots showed downregulation of the antiapoptotic proteins XIAP and MCL1, whereas poly(ADP-ribose) polymerase cleavage was increased. Combinations with conventional cytostatic agents resulted in synergistic effects. Treatment of xenografted mice with 100 mg/kg of body weight for 21 days resulted in tumor inhibition rates of 76% (vatalanib) and 77% (pazopanib). In two mice, a total tumor eradication could be observed. No gross systemic toxicity occurred.
Conclusion: We conclude that VEGF inhibition is a promising new therapeutic approach in CLL. Vatalanib and pazopanib seem to be effective and safe candidates to be further evaluated for this purpose. Clin Cancer Res; 16(13); 3390–8. ©2010 AACR.
ADAM-17: A Target to Increase Chemotherapeutic Efficacy in Colorectal Cancer?
Authors: Lee Adam M. , Diasio Robert B. 
Published: June 2010

Abstract
Chemotherapy-induced activation of ADAM-17 results in increased growth factor shedding and activation of growth factor receptor-mediated pro-survival response. Enhanced ADAM-17 activity and HER ligand shedding results in resistance to chemotherapy in CRC. Therapies that decrease ADAM-17 activity in conjunction with current treatments may enhance response rates in advanced CRC patients. Clin Cancer Res; 16(13); 3319–21. ©2010 AACR.
Telomerase as an Important Target of Androgen Signaling Blockade for Prostate Cancer Treatment
Authors: Liu Shuang , Qi Yanfeng , Ge Yubin , Duplessis Tamika , Rowan Brian G. , Ip Clement , Cheng Helen , Rennie Paul S. , Horikawa Izumi , Lustig Arthur J. , Yu Qun , Zhang Haitao , Dong Yan 
Published: June 2010

AbstractAs the mainstay treatment for advanced prostate cancer, androgen deprivation therapy (ADT) targets the action of androgen receptor (AR) by reducing androgen level and/or by using anti-androgen to compete with androgens for binding to AR. Albeit effective in extending survival, ADT is associated with dose-limiting toxicity and the development of castration-resistant prostate cancer (CRPC) after prolonged use. Because CRPC is lethal and incurable, developing effective strategies to enhance the efficacy of ADT and circumvent resistance becomes an urgent task. Continuous AR signaling constitutes one major mechanism underlying the development of CRPC. The present study showed that methylseleninic acid (MSA), an agent that effectively reduces AR abundance, could enhance the cancer-killing efficacy of the anti-androgen bicalutamide in androgen-dependent and CRPC cells. We found that the combination of MSA and bicalutamide produced a robust downregulation of prostate-specific antigen and a recently identified AR target, telomerase, and its catalytic subunit, human telomerase reverse transcriptase. The downregulation of hTERT occurs mainly at the transcriptional level, and reduced AR occupancy of the promoter contributes to downregulation. Furthermore, apoptosis induction by the two agents is significantly mitigated by the restoration of hTERT. Our findings thus indicate that MSA in combination with anti-androgen could represent a viable approach to improve the therapeutic outcome of ADT. Given the critical role of hTERT/telomerase downregulation in mediating the combination effect and the fact that hTERT/telomerase could be measured in blood and urine, hTERT/telomerase could serve as an ideal tumor-specific biomarker to monitor the efficacy of the combination therapy noninvasively. Mol Cancer Ther; 9(7); 2016–25. ©2010 AACR.
Targeted Therapies for Non–Small Cell Lung Cancer: An Evolving Landscape
Authors: Pal Sumanta Kumar , Figlin Robert A. , Reckamp Karen 
Published: June 2010

Abstract
Over the past decade, a multitude of targeted agents have been explored in the treatment of advanced non–small cell lung cancer (NSCLC). Thus far, two broad classes of agents have been implemented in clinical practice: (a) vascular endothelial growth factor (VEGF)-directed therapies and (b) antagonists of the epidermal growth factor receptor (EGFR). In the former category, the agent bevacizumab (a monoclonal antibody) has shown landmark improvements in survival when added to cytotoxic therapy. Small molecule tyrosine kinase inhibitors (TKI) targeting the VEGF receptor (i.e., sunitinib, sorafenib, and vandetanib) show activity in phase II clinical studies. With respect to EGFR-directed therapies, the TKIs gefitinib and erlotinib have shown significant benefit, and have uncovered valuable information about the biology of lung cancer. Outside of therapies directed specifically at VEGF- and EGFR-mediated signaling, trials evaluating insulin-like growth factor-1 receptor (IGF-IR)-targeting agents, cyclooxygenase-2 (COX-2) inhibitors, c-met inhibitors, irreversible pan-HER inhibitors, mammalian target of rapamycin (mTOR) inhibitors, and histone deacetylase (HDAC) inhibitors are ongoing. Inhibitors of ALK show great promise in patients with the relevant gene translocation. Herein, the clinical development of novel therapies for NSCLC is described, including some discussion of relevant biomarkers and determination of synergy with both cytotoxic therapy and other targeted agents. Mol Cancer Ther; 9(7); 1931–44. ©2010 AACR.
Profiling Lipoxygenase Metabolism in Specific Steps of Colorectal Tumorigenesis
Authors: Shureiqi Imad , Chen Dongning , Day R. Sue , Zuo Xiangsheng , Hochman Fredric Lyone , Ross William A. , Cole Rhonda A. , Moy Ofie , Morris Jeffrey S. , Xiao Lianchun , Newman Robert A. , Yang Peiying , Lippman Scott M. 
Published: June 2010

Abstract
Lipoxygenases (LOX) are key enzymes for the oxidative metabolism of polyunsaturated fatty acids into biologically active products. Clinical data on comparative levels of various LOX products in tumorigenesis are lacking. Therefore, we examined the profiles of several LOX products (5-LOX, 12-LOX, 15-LOX-1, and 15-LOX-2) by liquid chromatography/tandem mass spectrometry in the major steps of colorectal tumorigenesis (normal, polyp, and cancer) in a clinical study of 125 subjects (49 with normal colon, 36 with colorectal polyps, and 40 with colorectal cancer) who underwent prospective colorectal biopsies to control for various potential confounding factors (e.g., diet, medications). Mean 13-hydroxyoctadecadienoic acid (13-HODE) levels were significantly higher in normal colon [mean, 36.11 ng/mg protein; 95% confidence interval (95% CI), 31.56-40.67] than in paired colorectal cancer mucosa (mean, 27.01 ng/mg protein; 95% CI, 22.00-32.02; P = 0.0002), and in normal colon (mean, 37.15 ng/mg protein; 95% CI, 31.95-42.34) than in paired colorectal polyp mucosa (mean, 28.07 ng/mg protein; 95% CI, 23.66-32.48; P &lt; 0.001). Mean 13-HODE levels, however, were similar between the left (mean, 37.15 ng/mg protein; 95% CI, 31.95-42.35) and the right normal colon (mean, 32.46 ng/mg protein; 95% CI, 27.95-36.98; P = 0.09). No significant differences with regard to 12- or 15-hydroxyeicosatetraenoic acid or leukotriene B4 levels were detected between normal, polyp, and cancer mucosae. 15-LOX-1 inhibited interleukin-1β expression. This study establishes that reduced 13-HODE levels are a specific alteration in the LOX product profile associated with human colorectal tumorigenesis. Cancer Prev Res; 3(7); 829–38. ©2010 AACR.