bluuebunny/crossref_metadata_2025_split huggingface dataset:
Walking and the Perception of Neighborhood Attributes Among U.S. Adults—2012
Authors: Paul Prabasaj , Carlson Susan A. , Fulton Janet E. 
Published: October 2016

Background:The association between walking and environmental attributes depends on walking purpose. This study, based on a large survey of U.S. adults, examined the association between perceived neighborhood safety and built environment attributes, and walking for transportation and leisure.Methods:Data were obtained on transportation and leisure-time walking, perceived neighborhood safety and built environment attributes, and demographic characteristics from the summer wave of the 2012 ConsumerStyles survey of 3951 U.S. adults. Associations were examined by demographic characteristics.Results:Seventy-five percent of respondents reported walking for either transportation (54%) or leisure (56%) in the past week, 59% reported no safety concern, and 36% reported absence of any built environment attribute of walkability nearby. Respondents with more education, and those who lived in metropolitan areas were more likely to report built environment attributes supportive of walking. All built environment attributes examined, as well as safety concern due to speeding vehicles, were associated with walking after adjustment for demographic characteristics.Conclusion:Walking, particularly for transportation, is associated with many built environment attributes among U.S. adults. These attributes may be important to consider when designing and modifying the built environment of communities, especially those which are less walkable.
Evaluation of a Shelter-Based Diet and Physical Activity Intervention for Homeless Adults
Authors: Kendzor Darla E. , Allicock Marlyn , Businelle Michael S. , Sandon Lona F. , Gabriel Kelley Pettee , Frank Summer G. 
Published: October 2016

Background:The current study evaluated the feasibility and effectiveness of a diet and physical activity intervention for homeless adults.Methods:Shelter residents (N = 32) were randomly assigned to a 4-week diet and physical activity intervention (n = 17) or an assessment-only control group (n = 15). Intervention participants received tailored educational newsletters, pedometers with step goals, and twice daily fruit/vegetable snacks. Key measures included 24-hour dietary recall interviews and accelerometer-measured moderate-to-vigorous intensity physical activity (MVPA).Results:At baseline, 68.8% of participants were overweight or obese, 93.8% reported food insecurity, and 43.8% reported activity levels below physical activity guidelines. Baseline dietary recall interviews indicated low fruit/vegetable consumption, and elevated intake of added sugar, saturated fat, and sodium relative to current dietary recommendations. During the 4-week study period, intervention participants engaged in significantly greater accelerometer-measured daily MVPA (P < .001) than controls (median = 60 daily minutes p vs. 41 daily minutes). Between groups differences in fruit/vegetable consumption at the end of treatment did not reach statistical significance. Most participants reported that the intervention was helpful for increasing fruit/vegetable intake and physical activity.Conclusions:Findings highlight the potential to improve dietary quality and increase physical activity among sheltered homeless adults.
Genomic Evolution of Two Acinetobacter baumannii Clinical Strains from ST-2 Clones Isolated in 2000 and 2010 (ST-2_clon_2000 and ST-2_clon_2010)
Authors: López M. , Rueda A. , Florido J. P. , Blasco L. , Gato E. , Fernández-García L. , Martínez-Martínez L. , Fernández-Cuenca F. , Pachón J. , Cisneros J. M. , Garnacho-Montero J. , Vila J. , Rodríguez-Baño J. , Pascual A. , Bou G. , Tomás M. 
Published: October 2016

ABSTRACT

Acinetobacter baumannii
is a successful nosocomial pathogen due to its ability to persist in hospital environments by acquiring mobile elements such as transposons, plasmids, and phages. In this study, we compared two genomes of
A. baumannii
clinical strains isolated in 2000 (ST-2_clon_2000) and 2010 (ST-2_clon_2010) from GenBank project PRJNA308422.
Paleo-Asian oceanic slab under the North China craton revealed by carbonatites derived from subducted limestones
Authors: Chen Chunfei , Liu Yongsheng , Foley Stephen F. , Ducea Mihai N. , He Detao , Hu Zhaochu , Chen Wei , Zong Keqing 
Published: October 2016

Abstract
It is widely accepted that the lithospheric mantle under the North China craton (NCC) has undergone comprehensive refertilization due to input from surrounding subducted slabs. However, the possible contribution from the Paleo-Asian oceanic slab to the north is poorly constrained, largely because of the lack of convincing evidence for the existence of this slab under the NCC. We report here carbonatite intruding Neogene alkali basalts in the Hannuoba region, close to the northern margin of the NCC. Trace element patterns with positive Sr and U anomalies, negative high field strength elements (Nb, Ta, Zr, Hf, and Ti) and Ce anomalies, high 87Sr/86Sr ratios (0.70522-0.70796), and high δ18OSMOW (standard mean ocean water) values (22.2‰–23‰) indicate that this carbonatite had a limestone precursor. However, the presence of coarse-grained mantle-derived clinopyroxene, orthopyroxene, and olivine, and chemical features of the carbonates suggest that the carbonate melts were derived from the mantle. The carbonates have high 143Nd/144Nd ratios (0.51282-0.51298) and show negative correlation between CaO and Ni contents, resulting from reaction between carbonate melt and peridotite. Considering the regional tectonic setting, the carbonatite probably formed by melting of subducted sedimentary carbonate rocks that formed part of the Paleo-Asian oceanic slab, and thus could provide the first direct evidence for the presence of the Paleo-Asian oceanic slab beneath the NCC.
Hamstring injuries in elite Gaelic football: an 8-year investigation to identify injury rates, time-loss patterns and players at increased risk
Authors: Roe Mark , Murphy John C , Gissane Conor , Blake Catherine 
Published: October 2016

BackgroundHamstring injuries occur frequently in field sports, yet longitudinal information to guide prevention programmes is missing.AimInvestigate longitudinal hamstring injury rates and associated time loss in elite Gaelic football, while identifying subgroups of players at increased risk.Methods38 data sets from 15 elite male Gaelic football teams were received by the National Gaelic Athletic Association (GAA) Injury Surveillance Database between 2008 and 2015. Injury and exposure data were provided by the team's medical staff via an online platform.Results391 hamstring injuries were sustained accounting for 21% (95% CI 20.0% to 21.7%) of all injuries. Prevalence was 21% (95% CI 19.2% to 23.4%). Incidences were 2.2 (95% CI 1.9 to 2.4) per 1000 exposure hours, and 7.0 (95% CI 6.5 to 7.1) times greater in match play than in training. Typically each team sustained 9.0 (95% CI 7.0 to 11.0) hamstring injuries per season affecting the: bicep femoris belly (44%; 95% CI 39.4% to 48.7%); proximal musculotendinous junction (13%; 95% CI 9.8% to 16.3%); distal musculotendinous junction (12%; 95% CI 8.6% to 14.9%) and semimembranosis/semitendinosis belly (9%; 95% CI 6.3% to 11.7%). ∼36% (95% CI 31.5% to 41.0%) were recurrent injuries. Mean time loss was 26.0 (95% CI 21.1 to 33.0) days, which varied with age, injury type and seasonal cycle. Hamstring injuries accounted for 31% (95% CI 25.8% to 38.2%) of injury-related time loss. Previously injured players (rate ratio (RR)=3.3), players aged 18–20 years (IRR=2.3) or >30 years (RR=2.3), as well as defensive (IRR=2.0) and midfield players (RR=1.5), were most at risk of sustaining a hamstring injury. Comparisons of 2008–2011 with 2012–2015 seasons revealed a 2-fold increase in hamstring injury incidences. Between 2008 and 2015 training incidence increased 2.3-fold and match-play incidences increased 1.3-fold.ConclusionsHamstring injuries are the most frequent injury in elite Gaelic football, with incidences increasing from 2008–2011 to 2012–2015. Tailoring risk management strategies to injury history, age and playing position may reduce the burden of hamstring injuries.
National complicated acute diverticulitis (CADS) study: a protocol for a prospective observational scoping study for acute diverticulitis
Authors: Shaikh Shafaque 
Published: October 2016

BackgroundDiverticular disease is a widely prevalent disease in western society, and acute diverticulitis is a common acute surgical presentation. However, there is a lack of level 1 evidence addressing the multifaceted presentations associated with acute diverticulitis. There is also a lack of robust epidemiological data that could be used to meaningfully inform randomised controlled trials. The National CADS project aims to generate baseline data for a cohort of patients managed for clinically suspected acute diverticulitis and evaluate the impact of variability in the management approach on patient outcomes in the short (3 months) and long (2 years) term.MethodA Unit policy questionnaire will be completed by the principal investigator from all participating centres prior to study initiation. All patients aged above 18 years admitted with clinical suspicion of acute diverticulitis will be included from UK hospitals providing acute surgical care. Demographic, clinical, inpatient stay and outpatient follow-up data will be collected for index admissions between July and September 2014, 3 months follow-up and finally a 2-year follow-up.ResultsThe study attracted participation from 108 centres nationally and has so far generated data on 2500 patients admitted between 1 July 2014 and 30 September 2014. Short-term follow-up data have been obtained for this cohort.ConclusionsThe National CADS study is currently ongoing with the long-term outcomes data anticipated to be submitted in autumn of 2016.
Surface Expression of TGFβ Docking Receptor GARP Promotes Oncogenesis and Immune Tolerance in Breast Cancer
Authors: Metelli Alessandra , Wu Bill X. , Fugle Caroline W. , Rachidi Saleh , Sun Shaoli , Zhang Yongliang , Wu Jennifer , Tomlinson Stephen , Howe Philip H. , Yang Yi , Garrett-Mayer Elizabeth , Liu Bei , Li Zihai 
Published: October 2016

Abstract
GARP encoded by the Lrrc32 gene is the cell surface docking receptor for latent TGFβ, which is expressed naturally by platelets and regulatory T cells (Treg). Although Lrrc32 is amplified frequently in breast cancer, the expression and relevant functions of GARP in cancer have not been explored. Here, we report that GARP exerts oncogenic effects, promoting immune tolerance by enriching and activating latent TGFβ in the tumor microenvironment. We found that human breast, lung, and colon cancers expressed GARP aberrantly. In genetic studies in normal mammary gland epithelial and carcinoma cells, GARP expression increased TGFβ bioactivity and promoted malignant transformation in immunodeficient mice. In breast carcinoma–bearing mice that were immunocompetent, GARP overexpression promoted Foxp3+ Treg activity, which in turn contributed to enhancing cancer progression and metastasis. Notably, administration of a GARP-specific mAb limited metastasis in an orthotopic model of human breast cancer. Overall, these results define the oncogenic effects of the GARP–TGFβ axis in the tumor microenvironment and suggest mechanisms that might be exploited for diagnostic and therapeutic purposes. Cancer Res; 76(24); 7106–17. ©2016 AACR.
Abstract A16: Expression of PD-L1 and BCG immunotherapy in non-muscle invasive bladder cancer
Authors: Heo Jun Hyeok , Jin Hyun A. , Kang You Hyun , Kim Ki Hong , Hong Sung Joon , Han Kyung Seok 
Published: October 2016

Abstract
Background: Immunotherapy based on BCG has been a standard therapy to prevent recurrence and progression in bladder cancer. Activation of immune checkpoints by binding PD-1 to its ligands, PD-L1, is vital for physiologic regulation of immune system.
Tumor cells can co-opt the PD-1 pathway to escape from immunosurveillance mechanism. We investigated expression of immune checkpoints and their effects on T cells in bladder cancer.
Methods: A panel of transitional cell carcinoma cell lines (UC-3,T24,KU1919 and 253J) and normal human bladder urothelial cells (SVHUC1) were used to evaluate expression of immune checkpoints. Western blot analysis was used for protein expressions from cell lines and qPCR for RNA expression from human bladder tissues. Human bladder cancer/normal paired tissues were obtained at two time points; surgical resection and then after BCG immunotherapy. Immunohistochemical staining was performed to assess infiltration and distribution of CD4+ and CD8+ T cells in bladder tumor tissues and normal bladder tissues. Immune cells were isolated and T cells were isolated by FACS sorting after immune cell isolation from tumor/normal tissues.
Results: PD-L1 proteins were highly expressed in bladder cancer cell lines compared to normal bladder epithelial cell line (SVHUC1). In paired human samples (cancer and normal tissues), PD-L1 were also highly expressed in bladder cancer tissues compared with paired normal tissues. Real time RT-PCR confirmed the high expression of PD-L1 in bladder cancer tissues. Interestingly, normal epithelial tissues regenerated after surgical resection of the tumor and BCG immunotherapy had low PD- after surgical resection and BCG immunotherapy while recurred tumor showed high expression of PD-L1. Isolation of TIL and immunohistochemical staining with CD4/CD8 showed that T cells were more infiltrated in bladder cancer tissues compared to paired normal tissues. Mouse bladder tumor model expressing PD-L1 showed increased CD3+CD4+ T cells and Treg cells.
Conclusion: PD-L1 are highly expressed in bladder cancer. CD3+CD4+ T cells and Treg cells are highly infiltrated in human and mouse bladder cancer tissues. Our data suggest that PD-L1 might be involved in tumor recurrence after BCG immunotherapy and might be a novel targets in bladder cancer.
Citation Format: Jun Hyeok Heo, Hyun A. Jin, You Hyun Kang, Ki Hong Kim, Sung Joon Hong, Kyung Seok Han. Expression of PD-L1 and BCG immunotherapy in non-muscle invasive bladder cancer. [abstract]. In: Proceedings of the AACR Special Conference: Function of Tumor Microenvironment in Cancer Progression; 2016 Jan 7–10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2016;76(15 Suppl):Abstract nr A16.
Abstract A17: An integrin agonist suppresses breast cancer by reducing CD11b+ leukocytes, promoting anti-tumor immunity
Authors: Khan Samia Q. , Faridi Mohd H. , Ruffell Brian , Lopez Ana M. S. , Jehangir Shehryar , Barbosa Antonio J. , Torroella-Kouri Marta , Coussens Lisa M. , Varner Judith , Gupta Vineet 
Published: October 2016

Abstract
Breast cancer remains the second highest cancer-related cause of death in women today. Neoadjuvant therapies reduce tumor size in patients but long-term survival remains poor. Tumor microenvironment shows a significant infiltration of CD11b+ tumor associated macrophages (TAMs) that promote tumor growth and metastases, while suppressing T-cell mediated anti-tumor immunity, suggesting that reducing infiltration of CD11b+ TAMs could have a therapeutic benefit. We recently developed a novel small molecule that targets CD11b+ cells and reduces their migration and tissue recruitment. Unlike previously described strategies, our methodology involves allosteric activation of CD11b, which induces transient increase in adhesion of CD11b+ cells to the vascular endothelium, thereby reducing the ability of the myeloid cells to transmigrate out of circulation and suppressing their recruitment into tumor and inflamed tissues. However, it is currently not known as to whether small molecule mediated CD11b activation can reduce TAM infiltration in tumors and whether that will have a therapeutic benefit. Here, we present results from studies with our lead compound leukadherin1 (LA1) in murine models of breast cancer. Our studies show that treatment of established syngeneic Cl66 orthotopic breast tumors in Balb/c mice with LA1 significantly reduces tumor growth and increases survival. LA1 treatment significantly reduced infiltration of CD11b+ cells into the tumor stroma, without affecting the levels of cells in circulation. LA1 treatment also significantly reduced expression of molecules that promote angiogenesis and tumor growth including MMP9, S100A8 and ARG1 that coincided with decreased CD31 and α-SMA, suggesting tumor vasculature disruption. Immune cell profiling revealed that LA1 treatment further promotes anti-tumor immunity by increasing the influx of cytotoxic CD8+ T cells into tumors. These data provide a rationale for using allosteric CD11b agonists to target TAM recruitment as a novel therapeutic approach for breast cancer.
Citation Format: Samia Q. Khan, Mohd H. Faridi, Brian Ruffell, Ana M. S. Lopez, Shehryar Jehangir, Antonio J. Barbosa, Marta Torroella-Kouri, Lisa M. Coussens, Judith Varner, Vineet Gupta. An integrin agonist suppresses breast cancer by reducing CD11b+ leukocytes, promoting anti-tumor immunity. [abstract]. In: Proceedings of the AACR Special Conference: Function of Tumor Microenvironment in Cancer Progression; 2016 Jan 7–10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2016;76(15 Suppl):Abstract nr A17.
Abstract A26: The RON tyrosine kinase accelerates pancreatic duct neoplasia and activates a positive autocrine/paracrine signaling loop that promotes alternative macrophage activation
Authors: Babicky Michele L. , Harper Megan M. , Mose Evangeline S. , Jaquish Dawn J. , French Randall P. , Waltz Susan E. 
Published: October 2016

Abstract
Introduction: The RON (receptor d'origine nantais) tyrosine kinase is overexpressed in &gt;80% of human pancreatic cancers, but its effect on pancreatic carcinogenesis is largely unknown.
Methods: We developed a transgenic mouse that overexpresses RON specifically in the pancreas (Pdx-1-RON). Additionally, we utilized an existing transgenic mouse with a functionally inactive RON tyrosine kinase domain (Pdx-1-RTK-/-). These strains were crossed with the established CK murine model of pancreatic cancer yielding compound strains, RCK and CK/TK-/-. We performed immunofluorescent staining, flow cytometry, and western blot analysis on the tissues from these animals to study the effects of RON overexpression and the loss of RON signaling in the setting of oncogenic Kras.
Results: RON overexpression results in increased acinar-ductal metaplasia, accelerates PanIN progression to invasive cancer, and results in an accumulation of alternatively-activated (MRC1+) macrophages in the tumor microenvironment. We found that RON overexpression results in upregulation of its own ligand, macrophage-stimulating protein (MSP), activating a positive autocrine/paracrine signaling loop that effects tumor growth and the differentiation of tumor-associated macrophages. Knockdown of RON expression and/or MSP expression results in decreased tumor growth in vivo. Additionally, loss of RON signaling in CK/TK-/- mice leads to a profound decrease in alternatively-activated (MRC1+) macrophages in the tumor microenvironment. In contrast, these animals demonstrate an accumulation of classically activated (CD11c+) macrophages. RON signaling is also associated with downregulation of the chemokine, monocyte chemoattractant protein-1 (MCP-1), a known driver of CD11c+ macrophage activation. The correlation of RON and MSP and the inverse correlation with MCP-1 expression were validated in a database analysis of human pancreatic tumor specimens.
Conclusion: Our studies demonstrate that murine RON overexpression accelerates the development of invasive pancreatic cancer in the setting of oncogenic Kras. Active RON signaling results in upregulation of its own ligand, MSP, initiating a positive autocrine/paracrine feedback loop that promotes tumor growth and alters the differentiation of macrophages in the tumor microenvironment.
Citation Format: Michele L. Babicky, Megan M. Harper, Evangeline S. Mose, Dawn J. Jaquish, Randall P. French, Susan E. Waltz. The RON tyrosine kinase accelerates pancreatic duct neoplasia and activates a positive autocrine/paracrine signaling loop that promotes alternative macrophage activation. [abstract]. In: Proceedings of the AACR Special Conference: Function of Tumor Microenvironment in Cancer Progression; 2016 Jan 7–10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2016;76(15 Suppl):Abstract nr A26.
Abstract A29: Effects of obesity on regulation of macrophage population in the prostate tumor microenvironment
Authors: Galvan Gloria C. , Apte Shruti , deGraffenried Linda A. 
Published: October 2016

Abstract
Background: Obesity is associated with a greater risk of prostate cancer mortality, but the mechanisms driving this progression are still unclear. A high concentration of macrophages within the tumor microenvironment, especially tumor-associated macrophages (TAMs), has been linked to progression and metastasis in numerous cancer types, including prostate. Obesity increases circulating levels of monocyte chemotactic protein-1 (MCP-1), a chemokine involved in monocyte migration. In addition, prostaglandin E2 (PGE2), a molecule closely associated with obesity, appears to be involved in macrophage polarization. Our preliminary in vitro data suggest that obese conditions promote both macrophage recruitment and TAM polarization.
Hypothesis: Based upon these preliminary results, we hypothesize that obesity-induced prostate cancer progression is due, in part, to increased TAM concentrations in the prostate tumor micro-environment, promoting pro-metastatic signaling.
Methods: In order to mimic the prostate tumor microenvironment, an in vitro model composed of adipose stromal cells, macrophages, prostate cancer epithelial cells and sera from obese and non-obese men was used to assess the impact of obesity on the paracrine signaling network. Matrigel invasion chambers were used to assess macrophage recruitment. qPCR was used to measure mRNA levels of proteins associated with a TAM phenotype as well as mRNA levels of MCP-1 and cyclooxygenase-2 (COX-2), an enzyme involved in PGE2 production.
Results: Obese conditions resulted in increased macrophage recruitment and increased mRNA levels of TAM markers in macrophages. Furthermore, MCP-1 mRNA levels in adipose stromal cells and prostate cancer cells were higher under obese conditions compared to non-obese conditions. Similarly, obese conditions increased COX-2 mRNA levels in prostate cancer cells.
Conclusions: Data from our in vitro study suggest that obesity may promote macrophage infiltration into the prostate tumor microenvironment and play a role in macrophage polarization towards a tumor-associated phenotype. This study will potentially serve to determine the value of macrophage and TAM concentration as biomarkers in this patient population, and lay the foundation for future studies investigating whether this phenomenon might be an effective therapeutic target.
Citation Format: Gloria C. Galvan, Shruti Apte, Linda A. deGraffenried. Effects of obesity on regulation of macrophage population in the prostate tumor microenvironment. [abstract]. In: Proceedings of the AACR Special Conference: Function of Tumor Microenvironment in Cancer Progression; 2016 Jan 7–10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2016;76(15 Suppl):Abstract nr A29.