bluuebunny/crossref_metadata_2025_split huggingface dataset:
Rapid sequence induction of anaesthesia via the intraosseous route: a prospective observational study
Authors: Barnard E B G , Moy R J , Kehoe A D , Bebarta V S , Smith J E 
Published: June 2014

BackgroundIntraosseous (IO) drug infusion has been reported to have similar pharmacokinetics to intravenous (IV) infusion. In military and civilian trauma, the IO route is often used to obtain rapid and reliable parenteral access for drug administration. Only a few case reports have described the use of IO infusion to administer drugs for rapid sequence induction of anaesthesia (RSI).ObjectiveWe aimed to assess the feasibility of the administration of RSI drugs via an IO catheter in a prospective observational study.MethodsA prospective observational study was undertaken at a combat hospital in Afghanistan. A validated data form was used to record the use of IO drugs for RSI by the prehospital, physician-led Medical Emergency Response Team (MERT), and by inhospital physicians. Data were captured between January and May 2012 by interview with MERT physicians and inhospital physicians directly after RSI. The primary outcome measure was the success rate of first-pass intubation with direct laryngoscopy.Results34 trauma patients (29 MERT and 5 inhospital) underwent RSI with IO drug administration. The median age was 24 years and median injury severity score 25; all were male. The predominant mechanism of injury was blast (n=24), followed by penetrating (n=6), blunt (n=3) and burn (n=1). First-pass intubation success rate was 97% (95% CI 91% to 100%). A Cormack-Lehane grade 1 view, by direct laryngoscopy, was obtained at first look in 91% (95% CI 81% to 100%) of patients.ConclusionsIn this prospective, observational study, IO drug administration was successfully used for trauma RSI, with a comparable first pass intubation success than published studies describing the IV route.Trial registration numberRCDM/Res/Audit/1036/12/0162.
Microstructure and magnetostrictive properties of epoxy-bonded Tb1-xNdx(Fe0.8Co0.2)1.93 (0.20 ≤ x ≤ 0.75) composites
Authors: Pan Z. B. , Liu J. J. , Liu X. Y. , Wang R. , Wang J. , Si P. Z. 
Published: June 2014

An epoxy-resin bonding route was used to produce composite rods of the highly magnetostrictive alloys Tb 1-x Nd x( Fe 0.8 Co 0.2)1.93 (0.20 ≤ x ≤ 0.75). The structure, spin configuration, magnetostriction and particle size are investigated by means of X-ray diffraction (XRD), a standard strain technique and scanning electron microscope (SEM). The epoxy-bonded 0–3 type and pseudo 1–3 type composites are successfully fabricated, respectively. XRD analysis shows that the easy magnetization direction (EMD) for the alloy of x = 0.20 lies along 〈111〉 axis. The magnetic curing field makes the particles align as a particulate chain and also causes the particles rotating along its EMD direction. The pseudo 1–3 type epoxy-bonded composite has a larger magnetostriction than that of the 0–3 type composite, which can be attributed to the larger magnetostriction coefficient λ111, EMD lying along 〈111〉 direction, the 〈111〉-textured orientation and the chain structure. A large saturation magnetostriction (λ0S ~ 570 ppm) is achieved for the 1–3 type epoxy/ Tb 0.35 Nd 0.65( Fe 0.8 Co 0.2)1.93 composite (about 150–250 μm, 10 kOe), which approaches 70% of its monolithic alloy. Furthermore, it only contains 27 vol.% alloy particles in the insulating epoxy matrix and performs a low magnetic anisotropy, which could make it technologically interesting for the field of Nd -containing magnetostrictive materials.
Allen–Cahn approximation of mean curvature flow in Riemannian manifolds, II: Brakke's flows
Authors: Pisante Adriano , Punzo Fabio 
Published: June 2014

We prove convergence of solutions to the parabolic Allen–Cahn equation to Brakke's motion by mean curvature in Riemannian manifolds with Ricci curvature bounded from below. Our results hold for a general class of initial conditions and extend previous results from [T. Ilmanen, Convergence of the Allen–Cahn equation to the Brakke's motion by mean curvature, J. Differential Geom. 31 (1993) 417–461] even in Euclidean space. We show that a sequence of measures, associated to energy density of solutions of the parabolic Allen–Cahn equation, converges in the limit to a family of rectifiable Radon measures, which evolves by mean curvature flow in the sense of Brakke. A key role is played by nonpositivity of the limiting energy discrepancy and a local almost monotonicity formula (a weak counterpart of Huisken's monotonicity formula) proved in [Allen–Cahn approximation of mean curvature flow in Riemannian manifolds, I, uniform estimates, to appear in Ann. Sc. Norm. Super. Pisa Cl. Sci.; arXiv:1308.0569], to get various density bounds for the limiting measures.
Optimizing the value of reservoir simulation through quality-assured initialization
Authors: Worthington Paul F. , Hattingh Shane K. F. 
Published: June 2014

The initialization of a reservoir simulator calls for the populating of a three-dimensional dynamic grid-cell model using subsurface data and interrelational algorithms that have been synthesized to be fit for purpose. These prerequisites are rarely fully satisfied in practice. This paper sets out to strengthen initialization through four key thrusts, all of which seek to optimize the bridgehead between reservoir geoscience and reservoir engineering, and thereby maximize value from reservoir simulation. The first addresses representative data acquisition, which includes the key-well concept as a framework for the cost-effective incorporation of free-fluid porosity and permeability within an initialization database. The second concerns the preparation of these data and their products for populating the static and dynamic models. Important elements are dynamically conditioned net-reservoir cut-offs, recognition of primary flow units, and establishing interpretative algorithms at the simulator grid-cell scale for application over net-reservoir zones. The third thrust is directed at the internal consistency of capillary character, relative permeability properties and petrophysically-derived hydrocarbon saturations over net reservoir. This exercise is central to the simulation function and it is an integral component of hydraulic data partitioning. The fourth concerns the handling of formation heterogeneity and anisotropy, especially from the standpoint of directional parametric averaging and interpretative algorithms. These matters have been synthesized into a workflow for optimizing the initialization of reservoir simulators. In so doing, a further important consideration is the selection of the appropriate procedures that are available within and specific to different software packages.
It is the authors’ experience that implementation of these thrusts has demonstrably enhanced the authentication of reservoir simulators through more readily attainable history matches with less required tuning. This outcome is attributed to a more systematic initialization process with a lower risk of artefacts. Of course, these benefits feed through to more assured estimates of ultimate recovery and, thence, hydrocarbon reserves.
Joint Management of Energy Harvesting, Storage, and Usage for Green Wireless Sensor Networks
Authors: Jin Xi , Kong Fanxin , Zeng Peng , Deng Qingxu , Xu Huiting 
Published: June 2014

Recently, energy harvesting has been emerging as a promising technique to prolong the lifetime for wireless sensor nodes. Most existing efforts address the design of energy harvesting and sensor node subsystem separately or ignore some real-world constraints. In this paper, we study how to codesign the two subsystems and how to jointly manage energy harvesting, storage, and usage. We first propose a novel system architecture for energy harvesting which employs several supercapacitors to eliminate the conflicts on charging and discharging among different system components. Then, we present a method to schedule their charging and discharging, which is proved to be able to guarantee zero waste of the harvested energy if the battery is not full. Third, we propose an optimal algorithm to minimize different components’ capacity and two heuristic algorithms to maximize the system reward. We conduct extensive experiments based on real-life data traces. Results show that the proposed system architecture can harvest more energy compared to the state of the art, and the capacity optimization algorithm can choose the most suitable size for each system component.
Crosstalk between Glioma-Initiating Cells and Endothelial Cells Drives Tumor Progression
Authors: Jeon Hye-Min , Kim Sung-Hak , Jin Xun , Park Jong Bae , Kim Se Hoon , Joshi Kaushal , Nakano Ichiro , Kim Hyunggee 
Published: June 2014

Abstract
Glioma-initiating cells (GIC), which reside within the perivascular microenvironment to maintain self-renewal capacity, are responsible for glioblastoma initiation, progression, and recurrence. However, the molecular mechanisms controlling crosstalk between GICs and endothelial cells are poorly understood. Here, we report that, in both GICs and endothelial cells, platelet-derived growth factor (PDGF)–driven activation of nitric oxide (NO) synthase increases NO-dependent inhibitor of differentiation 4 (ID4) expression, which in turn promotes JAGGED1–NOTCH activity through suppression of miR129 that specifically represses JAGGED1 suppression. This signaling axis promotes tumor progression along with increased GIC self-renewal and growth of tumor vasculature in the xenograft tumors, which is dramatically suppressed by NOTCH inhibitor. ID4 levels correlate positively with NOS2 (NO synthase-2), HES1, and HEY1 and negatively with miR129 in primary GICs. Thus, targeting the PDGF–NOS–ID4–miR129 axis and NOTCH activity in the perivascular microenvironment might serve as an efficacious therapeutic modality for glioblastoma. Cancer Res; 74(16); 4482–92. ©2014 AACR.
Allergic Diseases and Risk of Hematopoietic Malignancies in a Cohort of Postmenopausal Women: A Report from the Iowa Women's Health Study
Authors: Linabery Amy M. , Prizment Anna E. , Anderson Kristin E. , Cerhan James R. , Poynter Jenny N. , Ross Julie A. 
Published: June 2014

AbstractBackground: Allergic diseases signify immune dysregulation attributable to underlying genetics and environmental exposures. Associations between various allergies and hematopoietic cancers have been observed, albeit inconsistently; however, few prospective studies have examined the risk, and even fewer among older adults.Methods: We examined risk of incident hematopoietic cancers in those reporting allergic diseases in a population-based cohort of 22,601 older women (Iowa Women's Health Study). Self-reported allergic status, including asthma, hay fever, eczema, and/or other allergies, was determined via questionnaire in 1997 (mean age, 72 years; range, 63–81 years). Incident cancers were ascertained by linkage with the Iowa Cancer Registry from 1997 to 2011. Cox proportional hazards regression was performed to estimate multivariate-adjusted HR and 95% confidence intervals (CI) for myeloid (N = 177) and lymphoid (N = 437) malignancies, respectively.Results: Allergic diseases were not associated with risk of myeloid (HR, 1.00; 95% CI, 0.72–1.37) or lymphoid (HR, 0.99; 95% CI, 0.81–1.22) malignancies overall, or for most allergic and malignant subtypes examined. Self-reported asthma was positively associated with development of myelodysplastic syndrome (MDS; HR, 2.00; 95% CI, 0.93–4.32). In addition, there was a 30% to 40% decrease in risk of both lymphoid and myeloid cancers in those reporting rural residences but no association in those reporting urban residences; the interaction between residence and allergy was statistically significant for lymphoid malignancies (Pinteraction = 0.05).Conclusions and Impact: These results suggest that asthma may contribute to the pathogenesis of MDS, a finding consistent with the chronic antigen stimulation hypothesis. Susceptibility differences by location of residence are concordant with the hygiene hypothesis and merit additional exploration. Cancer Epidemiol Biomarkers Prev; 23(9); 1903–12. ©2014 AACR.
Functional Ex Vivo Assay to Select Homologous Recombination–Deficient Breast Tumors for PARP Inhibitor Treatment
Authors: Naipal Kishan A.T. , Verkaik Nicole S. , Ameziane Najim , van Deurzen Carolien H.M. , ter Brugge Petra , Meijers Matty , Sieuwerts Anieta M. , Martens John W. , O'Connor Mark J. , Vrieling Harry , Hoeijmakers Jan H.J. , Jonkers Jos , Kanaar Roland , de Winter Johan P. , Vreeswijk Maaike P. , Jager Agnes , van Gent Dik C. 
Published: June 2014

Abstract
Purpose: Poly(ADP-ribose) polymerase (PARP) inhibitors are promising targeted treatment options for hereditary breast tumors with a homologous recombination (HR) deficiency caused by BRCA1 or BRCA2 mutations. However, the functional consequence of BRCA gene mutations is not always known and tumors can be HR deficient for other reasons than BRCA gene mutations. Therefore, we aimed to develop a functional test to determine HR activity in tumor samples to facilitate selection of patients eligible for PARP inhibitor treatment.
Experimental design: We obtained 54 fresh primary breast tumor samples from patients undergoing surgery. We determined their HR capacity by studying the formation of ionizing radiation induced foci (IRIF) of the HR protein RAD51 after ex vivo irradiation of these organotypic breast tumor samples. Tumors showing impaired RAD51 IRIF formation were subjected to genetic and epigenetic analysis.
Results: Five of 45 primary breast tumors with sufficient numbers of proliferating tumor cells were RAD51 IRIF formation deficient (11%, 95% CI, 5%–24%). This HR defect was significantly associated with triple-negative breast cancer (OR, 57; 95% CI, 3.9–825; P = 0.003). Two of five HR-deficient tumors were not caused by mutations in the BRCA genes, but by BRCA1 promoter hypermethylation.
Conclusion: The functional RAD51 IRIF assay faithfully identifies HR-deficient tumors and has clear advantages over gene sequencing. It is a relatively easy assay that can be performed on biopsy material, making it a powerful tool to select patients with an HR-deficient cancer for PARP inhibitor treatment in the clinic. Clin Cancer Res; 20(18); 4816–26. ©2014 AACR.
Demethylating Drugs as Novel Analgesics for Cancer Pain
Authors: Viet Chi T. , Dang Dongmin , Ye Yi , Ono Kentaro , Campbell Ronald R. , Schmidt Brian L. 
Published: June 2014

Abstract
Purpose: In this study, we evaluated the analgesic potential of demethylating drugs on oral cancer pain. Although demethylating drugs could affect expression of many genes, we focused on the mu-opioid receptor (OPRM1) gene pathway, because of its role in pain processing. We determined the antinociceptive effect of OPRM1 re-expression in a mouse oral cancer model.
Experimental Design: Using a mouse oral cancer model, we determined whether demethylating drugs produced antinociception through re-expression of OPRM1. We then re-expressed OPRM1 with adenoviral transduction and determined if, and by what mechanism, OPRM1 re-expression produced antinociception. To determine the clinical significance of OPRM1 on cancer pain, we quantified OPRM1 methylation in painful cancer tissues and nonpainful contralateral normal tissues of patients with oral cancer, and nonpainful dysplastic tissues of patients with oral dysplasia.
Results: We demonstrated that OPRM1 was methylated in cancer tissue, but not normal tissue, of patients with oral cancer, and not in dysplastic tissues from patients with oral dysplasia. Treatment with demethylating drugs resulted in mechanical and thermal antinociception in the mouse cancer model. This behavioral change correlated with OPRM1 re-expression in the cancer and associated neurons. Similarly, adenoviral-mediated OPRM1 re-expression on cancer cells resulted in naloxone-reversible antinociception. OPRM1 re-expression on oral cancer cells in vitro increased β-endorphin secretion from the cancer, and decreased activation of neurons that were treated with cancer supernatant.
Conclusion: Our study establishes the regulatory role of methylation in cancer pain. OPRM1 re-expression in cancer cells produces antinociception through cancer-mediated endogenous opioid secretion. Demethylating drugs have an analgesic effect that involves OPRM1. Clin Cancer Res; 20(18); 4882–93. ©2014 AACR.
The Lipid Kinase PI4KIIIβ Is Highly Expressed in Breast Tumors and Activates Akt in Cooperation with Rab11a
Authors: Morrow Anne A. , Alipour Mohsen Amir , Bridges Dave , Yao Zemin , Saltiel Alan R. , Lee Jonathan M. 
Published: June 2014

Abstract
Emerging evidence now implicates phosphatidylinositol 4-kinases (PI4K), enzymes that generate PI(4)P from phosphatidylinositol (PtdIns), in cancer. In this study, we investigate the role of PI4KIIIβ, one of four mammalian PI4Ks, in breast cancer. Although PI4KIIIβ protein levels are low in normal breast tissue, we find that approximately 20% of primary human breast tumors overexpress it. Expression of PI4KIIIβ in breast carcinoma cells leads to increased Akt activation, dependent on increased PI(3,4,5)P3 production. However, a kinase-inactive version of PI4KIIIβ also led to increased Akt activation, and no changes in PI(4)P or PI(4,5)P2 lipid abundance were detected in the PI4KIIIβ-overexpressing cells. This implies that PI4KIIIβ regulates PI(3,4,5)P3 and Akt independent of PI(4)P production. We find that the PI4KIIIβ-binding protein, Rab11a, a small GTPase that regulates endosomal recycling, is involved in PI4KIIIβ-mediated activation of Akt, as RNAi depletion of Rab11a impairs Akt activation. Furthermore, ectopic PI4KIIIβ expression alters cellular Rab11a distribution and enhances recruitment of PI4KIIIβ and Rab11a to recycling endosomes. This work suggests that PI4KIIIβ affects PI3K/Akt signaling through Rab11a and endosomal trafficking, independent of its lipid kinase activity. Thus, PI4KIIIβ likely plays a role in breast oncogenesis and that cooperation between Rab11a and PI4KIIIβ represents a novel Akt activation pathway. Mol Cancer Res; 12(10); 1492–508. ©2014 AACR.
CD44-Mediated Adhesion to Hyaluronic Acid Contributes to Mechanosensing and Invasive Motility
Authors: Kim Yushan , Kumar Sanjay 
Published: June 2014

Abstract
The high-molecular-weight glycosaminoglycan, hyaluronic acid (HA), makes up a significant portion of the brain extracellular matrix. Glioblastoma multiforme (GBM), a highly invasive brain tumor, is associated with aberrant HA secretion, tissue stiffening, and overexpression of the HA receptor CD44. Here, transcriptomic analysis, engineered materials, and measurements of adhesion, migration, and invasion were used to investigate how HA/CD44 ligation contributes to the mechanosensing and invasive motility of GBM tumor cells, both intrinsically and in the context of Arg-Gly-Asp (RGD) peptide/integrin adhesion. Analysis of transcriptomic data from The Cancer Genome Atlas reveals upregulation of transcripts associated with HA/CD44 adhesion. CD44 suppression in culture reduces cell adhesion to HA on short time scales (0.5-hour postincubation) even if RGD is present, whereas maximal adhesion on longer time scales (3 hours) requires both CD44 and integrins. Moreover, time-lapse imaging demonstrates that cell adhesive structures formed during migration on bare HA matrices are more short lived than cellular protrusions formed on surfaces containing RGD. Interestingly, adhesion and migration speed were dependent on HA hydrogel stiffness, implying that CD44-based signaling is intrinsically mechanosensitive. Finally, CD44 expression paired with an HA-rich microenvironment maximized three-dimensional invasion, whereas CD44 suppression or abundant integrin-based adhesion limited it. These findings demonstrate that CD44 transduces HA-based stiffness cues, temporally precedes integrin-based adhesion maturation, and facilitates invasion.
Implications: This study reveals that the CD44 receptor, which is commonly overexpressed in GBM tumors, is critical for cell adhesion, invasion, and mechanosensing of an HA-based matrix. Mol Cancer Res; 12(10); 1416–29. ©2014 AACR.
Plasma Tocopherols and Risk of Prostate Cancer in the Selenium and Vitamin E Cancer Prevention Trial (SELECT)
Authors: Albanes Demetrius , Till Cathee , Klein Eric A. , Goodman Phyllis J. , Mondul Alison M. , Weinstein Stephanie J. , Taylor Philip R. , Parnes Howard L. , Gaziano J. Michael , Song Xiaoling , Fleshner Neil E. , Brown Powel H. , Meyskens Frank L. , Thompson Ian M. 
Published: June 2014

Abstract
The Selenium and Vitamin E Cancer Prevention Trial (SELECT) showed higher prostate cancer incidence in men supplemented with high-dose α-tocopherol. We, therefore, examined whether presupplementation plasma α-tocopherol or γ-tocopherol was associated with overall or high-grade prostate cancer. A stratified case–cohort sample that included 1,746 incident prostate cancer cases diagnosed through June 2009 and a subcohort of 3,211 men was derived from the SELECT trial of 35,533 men. Plasma was collected at entry from 2001 to 2004, and median follow-up was 5.5 years (range, 0–7.9 years). Incidence of prostate cancer as a function of plasma α-tocopherol, γ-tocopherol, and supplementation with α-tocopherol or selenomethionine was estimated by the hazard ratio (HR). Plasma γ-tocopherol was not associated with prostate cancer. Men with higher α-tocopherol concentrations seemed to have risk similar to that of men with lower concentrations [overall HR for fifth (Q5) vs. first quintile (Q1), 1.21; 95 % confidence interval (CI), 0.88–1.66; P-trend = 0.24; in the trial placebo arm, Q5 HR, 0.85; 95% CI, 0.44–1.62; P-trend = 0.66]. We found a strong positive plasma α-tocopherol association among men receiving the trial selenomethionine supplement [Q5 HR, 2.04; 95% CI, 1.29–3.22; P-trend = 0.005]. A positive plasma α-tocopherol–prostate cancer association also seemed limited to high-grade disease (Gleason grade, 7–10; overall Q5 HR, 1.59; 95% CI, 1.13–2.24; P-trend = 0.001; among men receiving selenomethionine, Q5 HR, 2.12; 95% CI, 1.32–3.40; P-trend = 0.0002). Our findings indicate that higher plasma α-tocopherol concentrations may interact with selenomethionine supplements to increase high-grade prostate cancer risk, suggesting a biologic interaction between α-tocopherol and selenium itself or selenomethionine. Cancer Prev Res; 7(9); 886–95. ©2014 AACR.