bluuebunny/crossref_metadata_2025_split huggingface dataset:
Association between bariatric surgery and rate of hospitalisations for stable angina pectoris in obese adults
Authors: Shimada Yuichi J , Tsugawa Yusuke , Iso Hiroyasu , Brown David FM , Hasegawa Kohei 
Published: February 2017

ObjectiveObesity and stable angina pectoris (SAP) are important public health problems in the USA. However, little is known about whether weight reduction affects the rate of SAP-related morbidities. This study was designed to test the hypothesis that bariatric surgery is associated with a lower rate of hospitalisations for SAP in obese adults.MethodsWe performed a self-controlled case series study of obese adults with SAP who underwent bariatric surgery using a population-based inpatient database in three states (California, Florida and Nebraska) from 2005 to 2011. The primary outcome was hospitalisation for SAP. We used conditional logistic regression to compare the rate of the outcome event during sequential 12-month periods, using presurgery months 13–24 as a reference period.ResultsOur sample consisted of 953 patients with SAP who underwent bariatric surgery. The median age was 57 years, 51% were women, and 78% were non-Hispanic white. During the reference period, 25.3% (95%CI, 22.5% to 28.1%) had a hospitalisation for SAP. The rate remained stable in the subsequent 12-month presurgery period (adjusted OR (aOR) 0.84 (95% CI, 0.69 to 1.02); p=0.07). In the first 12-month period after bariatric surgery, we observed a significantly lower rate (9.1% (95% CI, 7.3% to 11.0%); aOR 0.33 (95% CI, 0.26 to 0.43); p<0.0001). Similarly, the rate remained significantly lower in the subsequent 13–24 months after bariatric surgery (8.7% (95% CI, 6.9% to 10.5%); aOR 0.31 (95% CI, 0.24 to 0.41); p<0.0001).ConclusionIn this population-based study of obese adults with SAP, we found that the rate of hospitalisations for SAP was lower by two-thirds after bariatric surgery.
The impact of between analytical platform variability on the classification of pleural effusions into exudate or transudate using Light's criteria
Authors: Cornes Michael P , Chadburn Andrew J , Thomas Claire , Darby Catherine , Webster Rachel , Ford Clare , Gama Rousseau 
Published: February 2017

BackgroundLight's criteria are ratios of pleural fluid to serum total protein (TP), pleural fluid to serum lactate dehydrogenase (LDH) and pleural fluid LDH to the upper reference limit for serum LDH. They are used to classify pleural effusions into an exudate or transudate when pleural fluid protein is 25–35 g/L. We evaluated the impact of between analytical platforms on the classification of pleural effusions using Light's criteria.MethodsLight's criteria were used to classify pleural effusions with fluid TP between 25 and 35 g/L into exudate and transudate. LDH and TP were analysed using an Abbott ARCHITECT c16000 analyser using a lactate to pyruvate method for LDH and two Roche Cobas 800 c702 analysers, one using a lactate to pyruvate method (laboratory B) and one a lactate to pyruvate method (laboratory C).ResultsEighty-three paired serum and pleural fluid samples were analysed. Of these, 44 samples had a pleural fluid TP between 25 and 35 g/L and were classified according to Light's criteria. Classification of pleural fluid into transudate or exudate using different analytical platforms was 82% concordant. The LDH ratio and TP ratio were similar in laboratory B and laboratory C, but these were respectively lower (p<0.001) and higher (p<0.001) than those at laboratory A.ConclusionsAlthough Light's criteria are ratios, which should minimise interassay variability, we report 18% discordance between different analytical platforms. The discordance was largely due to the performance of LDH and to a lesser extent protein assays in pleural fluid. Laboratories should be aware that assays may perform differently in serum and pleural fluid.
Exploring and Enabling DevOps for Data Analytical System with Essential Demands Elicitation
Authors: Zheng Jiabin , Liu Yan , Lin Jin 
Published: February 2017

DevOps is an emerging concept and methodology for bridging the gap in the process of software development. At present, applying DevOps to data analytical system (DAS) is increasingly embraced. But the characteristics of this system, such as data protection, always leads to a series of constrains. It results in more difficulty of conducting DevOps on DAS. Moreover, there are no DevOps solutions for reference. Therefore, exploring DevOps for DAS is valuable. In this paper, we illustrate DevOps demands of DAS from different perspectives, and constantly emphasize the importance of automation toolchain. Based on them, a process model for DAS DevOps (D2Ops) is proposed to clarify participants activities. In order to improve the efficiency, we attempt to integrate the automation toolchain. With the consideration of stability, six generic process components are designed to support this model. They can be the selection criteria for specific automation tools. We also present a reference facility based on these generic process components, and illustrate its implementation combining with a practical case. Furthermore, for a better D2Ops practice, the cross-cutting concerns are considered from the perspective of its data intensive trait.
A novel murine model of esophageal nonerosive reflux disease: from inflammation to impairment in mucosal integrity
Authors: Silva Renan O. , Oliveira Francisco Fábio B. , Bingana Rudy D. , Arruda Mailton O. , Woodland Philip , Lee Chung , Souza Miguel A. N. , Soares Pedro M. G. , Santos Armênio A. , Sifrim Daniel , Souza Marcellus H. L. P. 
Published: February 2017

Nonerosive reflux disease (NERD) is a highly prevalent phenotype of the gastroesophageal reflux disease. In this study, we developed a novel murine model of NERD in mice with microscopic inflammation and impairment in the epithelial esophageal barrier. Female Swiss mice were subjected to the following surgical procedure: the transitional region between the forestomach and the glandular portion of the stomach was ligated, and a nontoxic ring was placed around the duodenum near the pylorus. The control group underwent sham surgery. The animals were euthanized at 1, 3, 7, and 14 days after surgery. Survival and body weight were monitored daily. Esophageal wet weight, macroscopic lesion, histopathological alterations, myeloperoxidase (MPO) activity, cytokine levels, transepithelial electrical resistance (TEER), and mucosal permeability were evaluated. The survival rate was 78% at 14 days, with mild loss in body weight. Surgery did not induce erosive esophagitis but instead induced microscopic inflammation and increased esophageal wet weight, IL-6, keratinocyte-derived cytokine (KC) levels, and MPO activity with maximal peak between 3 and 7 days and resolution at 14 days postsurgery. Epithelial esophageal barrier was evaluated in operated mice at 7 and 14 days postsurgery; a decrease in TEER and increase in the esophageal epithelial permeability were observed compared with the sham-operated group. In addition, the inhibition of acid secretion with omeprazole significantly prevented the esophageal inflammation and impairment of barrier function at 7 days postsurgery. Thus we established a novel experimental model of NERD in mice, which can contribute to understanding the pathophysiological events associated with NERD.NEW & NOTEWORTHY In this study, we standardized an experimental model of nonerosive reflux disease (NERD) in mice. This model involves an acute inflammatory response followed by impaired esophageal mucosal integrity, even in the absence of inflammation. Thus this model can serve for evaluation of pathophysiological aspects of NERD and open new perspectives for therapeutic strategies for patients with this disorder.
Myocardial ischemic tolerance in rats subjected to endurance exercise training during adaptation to chronic hypoxia
Authors: Alánová Petra , Chytilová Anna , Neckář Jan , Hrdlička Jaroslav , Míčová Petra , Holzerová Kristýna , Hlaváčková Markéta , Macháčková Kristýna , Papoušek František , Vašinová Jana , Benák Daniel , Nováková Olga , Kolář František 
Published: February 2017

Chronic hypoxia and exercise are natural stimuli that confer sustainable cardioprotection against ischemia-reperfusion (I/R) injury, but it is unknown whether they can act in synergy to enhance ischemic resistance. Inflammatory response mediated by tumor necrosis factor-α (TNF-α) plays a role in the infarct size limitation by continuous normobaric hypoxia (CNH), whereas exercise is associated with anti-inflammatory effects. This study was conducted to determine if exercise training performed under conditions of CNH (12% O2) affects myocardial ischemic resistance with respect to inflammatory and redox status. Adult male Wistar rats were assigned to one of the following groups: normoxic sedentary, normoxic trained, hypoxic sedentary, and hypoxic trained. ELISA and Western blot analysis, respectively, were used to quantify myocardial cytokines and the expression of TNF-α receptors, nuclear factor-κB (NF-κB), and selected components of related signaling pathways. Infarct size and arrhythmias were assessed in open-chest rats subjected to I/R. CNH increased TNF-α and interleukin-6 levels and the expression of TNF-α type 2 receptor, NF-κB, inducible nitric oxide synthase (iNOS), cytosolic phospholipase A2α, cyclooxygenase-2, manganese superoxide dismutase (MnSOD), and catalase. None of these effects occurred in the normoxic trained group, whereas exercise in hypoxia abolished or significantly attenuated CNH-induced responses, except for NF-κB, iNOS, and MnSOD. Both CNH and exercise reduced infarct size, but their combination provided the same degree of protection as CNH alone. In conclusion, exercise training does not amplify the cardioprotection conferred by CNH. High ischemic tolerance of the CNH hearts persists after exercise, possibly by maintaining the increased antioxidant capacity despite attenuating TNF-α-dependent protective signaling.NEW & NOTEWORTHY Chronic hypoxia and regular exercise are natural stimuli that confer sustainable myocardial protection against acute ischemia-reperfusion injury. Signaling mediated by TNF-α via its type 2 receptor plays a role in the cardioprotective mechanism of chronic hypoxia. In the present study, we found that exercise training of rats during adaptation to hypoxia does not amplify the infarct size-limiting effect. Ischemia-resistant phenotype is maintained in the combined hypoxia-exercise setting despite exercise-induced attenuation of TNF-α-dependent protective signaling.
Skeletal muscle bioenergetics during all-out exercise: mechanistic insight into the oxygen uptake slow component and neuromuscular fatigue
Authors: Broxterman Ryan M. , Layec Gwenael , Hureau Thomas J. , Amann Markus , Richardson Russell S. 
Published: February 2017

Although all-out exercise protocols are commonly used, the physiological mechanisms underlying all-out exercise performance are still unclear, and an in-depth assessment of skeletal muscle bioenergetics is lacking. Therefore, phosphorus magnetic resonance spectroscopy (31P-MRS) was utilized to assess skeletal muscle bioenergetics during a 5-min all-out intermittent isometric knee-extensor protocol in eight healthy men. Metabolic perturbation, adenosine triphosphate (ATP) synthesis rates, ATP cost of contraction, and mitochondrial capacity were determined from intramuscular concentrations of phosphocreatine (PCr), inorganic phosphate (Pi), diprotonated phosphate ([Formula: see text]), and pH. Peripheral fatigue was determined by exercise-induced alterations in potentiated quadriceps twitch force (Qtw) evoked by supramaximal electrical femoral nerve stimulation. The oxidative ATP synthesis rate (ATPOX) attained and then maintained peak values throughout the protocol, despite an ~63% decrease in quadriceps maximal force production. ThusATPOXnormalized to force production (ATPOXgain) significantly increased throughout the exercise (1st min: 0.02 ± 0.01, 5th min: 0.04 ± 0.01 mM·min−1·N−1), as did the ATP cost of contraction (1st min: 0.048 ± 0.019, 5th min: 0.052 ± 0.015 mM·min−1·N−1). Additionally, the pre- to postexercise change in Qtw(−52 ± 26%) was significantly correlated with the exercise-induced change in intramuscular pH ( r = 0.75) and [Formula: see text] concentration ( r = 0.77). In conclusion, the all-out exercise protocol utilized in the present study elicited a “slow component-like” increase in intramuscular ATPOXgain as well as a progressive increase in the phosphate cost of contraction. Furthermore, the development of peripheral fatigue was closely related to the perturbation of specific fatigue-inducing intramuscular factors (i.e., pH and [Formula: see text] concentration).NEW & NOTEWORTHY The physiological mechanisms and skeletal muscle bioenergetics underlying all-out exercise performance are unclear. This study revealed an increase in oxidative ATP synthesis rate gain and the ATP cost of contraction during all-out exercise. Furthermore, peripheral fatigue was related to the perturbation in pH and deprotonated phosphate ion. These findings support the concept that the oxygen uptake slow component arises from within active skeletal muscle and that skeletal muscle force generating capacity is linked to the intramuscular metabolic milieu.
Pancreatic Cancer: Progress and Challenges in a Rapidly Moving Field
Authors: Collisson Eric A. , Olive Kenneth P. 
Published: February 2017

Abstract
“Pancreatic Cancer: Advances in Science and Clinical Care,” a Special Conference of the American Association for Cancer Research, was held in Orlando, FL, on May 12 to 15, bringing together more than 450 basic, translational, clinical, and epidemiologic pancreatic cancer researchers as well as pancreatic cancer patients, survivors, and advocates. Pancreatic cancer remains one of the great challenges in medicine, but the accelerating pace of research and early hints of clinical successes to come were palpable throughout the meeting. Prominent meeting themes included immunology and the tumor microenvironment, heterogeneity of both the epithelial and stromal compartments, personalized medicine efforts to integrate molecular information into clinical practice, new approaches to early detection, and clinical trials using a host of novel targeted therapies. Adding to the vibrant atmosphere of the meeting, a coalition of pancreatic cancer research and support foundations participated, with several innovative initiatives announced by individual organizations. We present here a summary of meeting highlights, a series of “success factors” that will benchmark the progress of the field over the next 2 years, and three challenges to the pancreatic cancer research community as it moves toward to the goal of extending patient survival. Cancer Res; 77(5); 1060–2. ©2017 AACR.
Prediagnosis Leukocyte Telomere Length and Risk of Ovarian Cancer
Authors: Yang Meng , Prescott Jennifer , Poole Elizabeth M. , Rice Megan S. , Kubzansky Laura D. , Idahl Annika , Lundin Eva , De Vivo Immaculata , Tworoger Shelley S. 
Published: February 2017

Abstract
Background: The associations between telomere length and cancer risk are equivocal, and none have examined the association between prediagnosis leukocyte telomere length (LTL) and the risk of developing ovarian cancer.
Methods: We prospectively measured LTL collected from 442 ovarian cancer cases and 727 controls in the Nurses' Health Studies and the Northern Sweden Health and Disease Study. Cases were matched to one or two controls on age, menopausal status, and date of blood collection. Odds ratios (OR) and 95% confidence intervals (CI) were estimated using conditional logistic regression.
Results: LTL was measured a median of 9.5 years before ovarian cancer diagnosis among cases. We observed a decreased risk of ovarian cancer with longer LTL. In multivariable models, women in the top quartile of LTL had an OR for ovarian cancer of 0.67 (95% CI, 0.46–0.97) compared with those in the bottom quartile. Inverse associations were stronger for nonserous cases (ORquartile 4 vs. quartile 1 of LTL = 0.55, 95% CI, 0.33–0.94) and rapidly fatal cases (i.e., cases who died within 3 years of diagnosis; ORquartile 4 vs. quartile 1 of LTL = 0.55, 95% CI, 0.32–0.95).
Conclusions: Our prospective findings suggest that longer circulating LTL may be associated with a lower ovarian cancer risk, especially for nonserous and rapidly fatal cases. The evaluation of LTL in relation to ovarian cancer risk by tumor subtypes is warranted in larger prospective studies.
Impact: Prediagnosis LTL may reflect an early event in the ovarian cancer development and could serve as a biomarker to predict future risk. Cancer Epidemiol Biomarkers Prev; 26(3); 339–45. ©2017 AACR.
Adolescents and Young Adults with Acute Lymphoblastic Leukemia and Acute Myeloid Leukemia: Impact of Care at Specialized Cancer Centers on Survival Outcome
Authors: Wolfson Julie , Sun Can-Lan , Wyatt Laura , Stock Wendy , Bhatia Smita 
Published: February 2017

Abstract
Background: Adolescents and young adults (AYA; 15–39 years) with acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) experience inferior survival when compared with children. Impact of care at NCI-designated Comprehensive Cancer Centers (CCC) or Children's Oncology Group sites (COG) on survival disparities remains unstudied.
Methods: Using the Los Angeles cancer registry, we identified 1,870 ALL or AML patients between 1 and 39 years at diagnosis. Cox regression analyses assessed risk of mortality; younger age + CCC/COG served as the referent group. Logistic regression was used to determine odds of care at CCC/COG, adjusting for variables above.
Results: ALL outcome: AYAs at non-CCC/COG experienced inferior survival (15–21 years: HR = 1.9, P = 0.005; 22–29 years: HR = 2.6, P &lt; 0.001; 30–39 years: HR = 3.0, P &lt; 0.001). Outcome at CCC/COG was comparable between children and young AYAs (15–21 years: HR = 1.3, P = 0.3; 22–29 years: HR = 1.2, P = 0.2) but was inferior for 30- to 39-year-olds (HR = 3.4, P &lt; 0.001). AML outcome: AYAs at non-CCC/COG experienced inferior outcome (15–21 years: HR = 1.8, P = 0.02; 22–39 years: HR = 1.4, P = 0.06). Outcome at CCC/COG was comparable between children and 15- to 21-year-olds (HR = 1.3, P = 0.4) but was inferior for 22- to 39-year-olds (HR = 1.7, P = 0.05). Access: 15- to 21-year-olds were less likely to use CCC/COG than children (P &lt; 0.001). In 22- to 39-year-olds, public/uninsured (ALL: P = 0.004; AML&lt;0.001), African American/Hispanics (ALL: P = 0.03), and 30- to 39-year-olds (ALL: P = 0.03) were less likely to use CCC/COG.
Conclusions: Poor survival in AYAs with ALL and AML is mitigated by care at CCC/COG. Barriers to CCC/COG care include public/uninsured, and African American/Hispanic race/ethnicity.
Impact: Care at CCC/COG explains, in part, inferior outcomes in AYAs with ALL and AML. Key sociodemographic factors serve as barriers to care at specialized centers. Cancer Epidemiol Biomarkers Prev; 26(3); 312–20. ©2017 AACR.
Atorvastatin Decreases HBx-Induced Phospho-Akt in Hepatocytes via P2X Receptors
Authors: Ghalali Aram , Martin-Renedo Javier , Högberg Johan , Stenius Ulla 
Published: February 2017

Abstract
Hepatocellular carcinoma (HCC) is rated as the fifth most common malignancy and third in cancer-related deaths worldwide. Statins, HMG-CoA reductase inhibitors, are potent cholesterol-lowering drugs, and recent epidemiologic evidence suggests that statins prevent aggressive HCC development. Previous experiments revealed that statins downregulate phosphorylated Akt (pAkt). Here, it is demonstrated that atorvastatin decreases nuclear pAkt levels in pancreatic and lung cancer cell lines within minutes, and this rapid effect is mediated by the purinergic P2X receptors. Akt is upregulated by hepatitis viruses and has oncogenic activity in HCC; therefore, we tested the possibility that the P2X–Akt pathway is important for the anticipated anticancer effects of statins in hepatocytes. Atorvastatin decreased hepatitis B virus X protein- and insulin-induced pAkt and pGsk3β (Ser9) levels. Furthermore, Akt-induced lipogenesis was counteracted by atorvastatin, and these statin-induced effects were dependent on P2X receptors. Statin also decreased proliferation and invasiveness of hepatocytes. These data provide mechanistic evidence for a P2X receptor–dependent signaling pathway by which statins decrease pAkt, its downstream phosphorylation target pGsk3β, and lipogenesis in hepatocytes.
Implications: The Akt pathway is deregulated and may act as a driver in HCC development; the P2X–Akt signaling pathway may have a role in anticancer effects of statins. Mol Cancer Res; 15(6); 714–22. ©2017 AACR.
Revisiting Seed and Soil: Examining the Primary Tumor and Cancer Cell Foraging in Metastasis
Authors: de Groot Amber E. , Roy Sounak , Brown Joel S. , Pienta Kenneth J. , Amend Sarah R. 
Published: February 2017

Abstract
Metastasis is the consequence of a cancer cell that disperses from the primary tumor, travels throughout the body, and invades and colonizes a distant site. On the basis of Paget's 1889 hypothesis, the majority of modern metastasis research focuses on the properties of the metastatic "seed and soil," but the implications of the primary tumor "soil" have been largely neglected. The rare lethal metastatic "seed" arises as a result of the selective pressures in the primary tumor. Optimal foraging theory describes how cancer cells adopt a mobile foraging strategy to balance predation risk and resource reward. Further selection in the dispersal corridors leading out of the primary tumor enhances the adaptive profile of the potentially metastatic cell. This review focuses on the selective pressures of the primary tumor "soil" that generate lethal metastatic "seeds" which is essential to understanding this critical component of prostate cancer metastasis.
Implication: Elucidating the selective pressures of the primary tumor “soil” that generate lethal metastatic “seeds” is essential to understand how and why metastasis occurs in prostate cancer. Mol Cancer Res; 15(4); 361–70. ©2017 AACR.