bluuebunny/crossref_metadata_2025_split huggingface dataset:
Barriers to Mask Wearing for Influenza‐like Illnesses Among Urban Hispanic Households
Authors: Ferng Yu‐hui , Wong‐McLoughlin Jennifer , Barrett Angela , Currie Leanne , Larson Elaine 
Published: December 2010

ABSTRACT Objectives:To identify barriers to mask wearing and to examine the factors associated with the willingness to wear masks among households.Design and Sample:We used data sources from a study assessing the impact of 3 nonpharmaceutical interventions on the rates of influenza: exit interviews; home visits with a subset of the mask group; and a focus group.Measures:Risk perception score, univariate analysis, and logistic regression were conducted to identify the characteristics and predictors of mask use. Thematic barriers to mask wearing were identified from qualitative data obtained at home visits and focus group.Results:Respondents from the mask group, when compared with the nonmask group, demonstrated higher risk perception scores concerning influenza (maximum score: 60, means: 37.6 and 30.2,p<.001) and increased perception of effectiveness of mask wearing (maximum score: 10, means: 7.8 and 7.3,p=.043). There was no significant association between demographic, attitudinal, or knowledge variables and adherence to wearing masks. Thematic barriers were identified such as social acceptability of mask use, comfort and fit, and perception of the risk/need for masks.Conclusions:Face masks may not be an effective intervention for seasonal or pandemic influenza unless the risk perception of influenza is high. Dissemination of culturally appropriate mask use information by health authorities and providers must be emphasized when educating the public.
Perturbations of dendritic excitability in epilepsy
Authors: Tang Cha‐Min , Thompson Scott M. 
Published: December 2010

SummaryThe dendritic arbor is the site of complex interactions between synaptic excitation and intrinsic excitability. This interaction is determined by the ion channels expressed on the dendritic arbor. The expression and gating properties of these channels can be perturbed in conditions associated with epilepsy that lead to hyperexcitability. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
PASSaGE: Pattern Analysis, Spatial Statistics and Geographic Exegesis. Version 2
Authors: Rosenberg Michael S. , Anderson Corey Devin 
Published: December 2010

Summary 1. Spatial analysis has become increasingly popular in the biological sciences, particularly in disciplines such as landscape ecology and landscape genetics. However, many statistical functions for performing spatial analysis are not readily available (except in the most limited manner) in common, easy‐to‐use statistical packages or geographic information systems (GIS) software. 2. Over the last decade, the software package Pattern Analysis, Spatial Statistics and Geographic Exegesis (PASSaGE) has been popular tool for conducting spatial statistics. PASSaGE is completely free and has a user‐friendly graphical user interface. A new version of PASSaGE, rewritten from the ground up, has now been released and is available for download. 3. PASSaGE 2 is significantly more user friendly than the original release and provides an excellent platform for both scientific analysis and classroom training. PASSaGE 2 includes a broad array of spatial statistical analyses not commonly found in other software packages or GIS software, all in an easy‐to‐use framework. It includes support for one‐, two‐ and three‐dimensional spatial analysis, including a number of unique and newly developed approaches.
Vectorial Form of Ekeland-Type Variational Principle in Locally Convex Spaces and Its Applications
Authors: Eshghinezhad S , Fakhar M 
Published: December 2010

AbstractBy using a Dane"Equation missing"' drop theorem in locally convex spaces we obtain a vectorial form of Ekeland-type variational principle in locally convex spaces. From this theorem, we derive some versions of vectorial Caristi-Kirk's fixed-point theorem, Takahashi's nonconvex minimization theorem, and Oettli-Théra's theorem. Furthermore, we show that these results are equivalent to each other. Also, the existence of solution of vector equilibrium problem is given.
Iterative Algorithms for Finding Common Solutions to Variational Inclusion Equilibrium and Fixed Point Problems
Authors: Tan JF , Chang SS 
Published: December 2010

AbstractThe main purpose of this paper is to introduce an explicit iterative algorithm to study the existence problem and the approximation problem of solution to the quadratic minimization problem. Under suitable conditions, some strong convergence theorems for a family of nonexpansive mappings are proved. The results presented in the paper improve and extend the corresponding results announced by some authors.
Delivery of NKG2D Ligand Using an Anti-HER2 Antibody-NKG2D Ligand Fusion Protein Results in an Enhanced Innate and Adaptive Antitumor Response
Authors: Cho Hyun-Mi , Rosenblatt Joseph D. , Tolba Khaled , Shin Sarah J. , Shin Daniel S. , Calfa Carmen , Zhang Yu , Shin Seung-Uon 
Published: December 2010

AbstractNKG2D ligands link the innate and adapative immune response by activating the receptors expressed on effector cells of both the innate (NK) and adaptive immune systems (CD8+ T cells). In this study, we explored the potential therapeutic utility of this intersection by fusing the murine NKG2D ligand Rae-1β to the 3′ end of an anti-HER2 IgG3 antibody containing an intact Fc domain (anti-HER2 IgG3-Rae-1β), thereby targeting an NK cell activation signal to HER2+ breast tumor cells. The antitumor efficacy of this anti-HER2-Rae-1β fusion protein was examined in a mouse mammary tumor model engineered to express HER2 (EMT6-HER2 cells). We observed an enhanced cytotoxic response of NK effectors against EMT-HER2 cells in vitro. Mice implanted on one flank with EMT6-HER2 cells and contralaterally with control EMT6 cells exhibited rapid regression of EMT6-HER2 tumors but delayed regression of contralateral EMT6 tumors. IFNγ was implicated, given a lack of antitumor efficacy in IFNγ−/− mice. Depletion of either NK cells or CD8+ T cells abrogated tumor growth inhibition, suggesting essential roles for each in the observed antitumor activity. Mice rejecting EMT6-HER2 tumors after anti-HER2-Rae-1β treatment showed markedly decreased tumor growth when rechallenged with EMT6-HER2 or EMT6 cells, whereas both EMT6 and EMT6-HER2 cells grew in control mice, indicating the development of an adaptive memory response. Our findings demonstrate that administration of an antibody-NKG2D ligand fusion protein can enhance innate and adaptive immune antitumor responses, also evoking additional nontargeted antigens to enhance the potential clinical utility of this approach. Cancer Res; 70(24); 10121–30. ©2010 AACR.
The Inflammasome Component Nlrp3 Impairs Antitumor Vaccine by Enhancing the Accumulation of Tumor-Associated Myeloid-Derived Suppressor Cells
Authors: van Deventer Hendrik W. , Burgents Joseph E. , Wu Qing Ping , Woodford Rita-Marie T. , Brickey W. June , Allen Irving C. , McElvania-Tekippe Erin , Serody Jonathan S. , Ting Jenny P.-Y. 
Published: December 2010

Abstract
The inflammasome is a proteolysis complex that generates the active forms of the proinflammatory cytokines interleukin (IL)-1β and IL-18. Inflammasome activation is mediated by NLR proteins that respond to microbial and nonmicrobial stimuli. Among NLRs, NLRP3 senses the widest array of stimuli and enhances adaptive immunity. However, its role in antitumor immunity is unknown. Therefore, we evaluated the function of the NLRP3 inflammasome in the immune response using dendritic cell vaccination against the poorly immunogenic melanoma cell line B16-F10. Vaccination of Nlrp3−/− mice led to a relative 4-fold improvement in survival relative to control animals. Immunity depended on CD8+ T cells and exhibited immune specificity and memory. Increased vaccine efficacy in Nlrp3−/− hosts did not reflect differences in dendritic cells but rather differences in myeloid-derived suppressor cells (MDSC). Although Nlrp3 was expressed in MDSCs, the absence of Nlrp3 did not alter either their functional capacity to inhibit T cells or their presence in peripheral lymphoid tissues. Instead, the absence of Nlrp3 caused a 5-fold reduction in the number of tumor-associated MDSCs found in host mice. Adoptive transfer experiments also showed that Nlrp3−/− MDSCs were less efficient in reaching the tumor site. Depleting MDSCs with an anti–Gr-1 antibody increased the survival of tumor-bearing wild-type mice but not Nlrp3−/− mice. We concluded that Nlrp3 was critical for accumulation of MDSCs in tumors and for inhibition of antitumor T-cell immunity after dendritic cell vaccination. Our findings establish an unexpected role for Nlrp3 in impeding antitumor immune responses, suggesting novel approaches to improve the response to antitumor vaccines by limiting Nlrp3 signaling. Cancer Res; 70(24); 10161–9. ©2010 AACR.
A Unique Metastasis Gene Signature Enables Prediction of Tumor Relapse in Early-Stage Hepatocellular Carcinoma Patients
Authors: Roessler Stephanie , Jia Hu-Liang , Budhu Anuradha , Forgues Marshonna , Ye Qing-Hai , Lee Ju-Seog , Thorgeirsson Snorri S. , Sun Zhongtang , Tang Zhao-You , Qin Lun-Xiu , Wang Xin Wei 
Published: December 2010

Abstract
Metastasis-related recurrence often occurs in hepatocellular carcinoma (HCC) patients who receive curative therapies. At present, it is challenging to identify patients with high risk of recurrence, which would warrant additional therapies. In this study, we sought to analyze a recently developed metastasis-related gene signature for its utility in predicting HCC survival, using 2 independent cohorts consisting of a total of 386 patients who received radical resection. Cohort 1 contained 247 predominantly HBV-positive cases analyzed with an Affymetrix platform, whereas cohort 2 contained 139 cases with mixed etiology analyzed with the NCI Oligo Set microarray platform. We employed a survival risk prediction algorithm with training, test, and independent cross-validation strategies and found that the gene signature is predictive of overall and disease-free survival. Importantly, risk was significantly predicted independently of clinical characteristics and microarray platform. In addition, survival prediction was successful in patients with early disease, such as small (&lt;5 cm in diameter) and solitary tumors, and the signature predicted particularly well for early recurrence risk (&lt;2 years), especially when combined with serum alpha fetoprotein or tumor staging. In conclusion, we have shown in 2 independent cohorts with mixed etiologies and ethnicity that the metastasis gene signature is a useful tool to predict HCC outcome, suggesting the general utility of this classifier. We recommend the use of this classifier as a molecular diagnostic test to assess the risk that an HCC patient will develop tumor relapse within 2 years after surgical resection, particularly for those with early-stage tumors and solitary presentation. Cancer Res; 70(24); 10202–12. ©2010 AACR.
Targeting γδ T Lymphocytes for Cancer Immunotherapy: From Novel Mechanistic Insight to Clinical Application
Authors: Gomes Anita Q. , Martins Duarte S. , Silva-Santos Bruno 
Published: December 2010

Abstract
Abundant interferon-γ secretion, potent cytotoxicity, and major histocompatibility complex–independent targeting of a large spectrum of tumors make γδ T cells attractive mediators of cancer immunotherapy. However, a better understanding of the molecular mechanisms involved in tumor cell recognition and γδ T-cell activation is required to improve the limited success of γδ T-cell–mediated treatments. Here, we review key advances in basic knowledge made over the past 3 years, and summarize the results of γδ T-cell–based clinical trials concluded to date. We also highlight new research directions on the basis of the modulation of receptors that control the function of γδ T cells. Cancer Res; 70(24); 10024–7. ©2010 AACR.
AZ960, a Novel Jak2 Inhibitor, Induces Growth Arrest and Apoptosis in Adult T-Cell Leukemia Cells
Authors: Yang Jing , Ikezoe Takayuki , Nishioka Chie , Furihata Mutsuo , Yokoyama Akihito 
Published: December 2010

Abstract
Adult T-cell leukemia/lymphoma (ATL) is a highly aggressive disease in which the Jak2/Stat5 pathway is constitutively activated. This study found that AZ960, a novel inhibitor of Jak2 kinase, effectively induced growth arrest and apoptosis of human T-cell lymphotropic virus type 1, HTLV-1–infected T cells (MT-1 and MT-2) in parallel with downregulation of the phosphorylated forms of Jak2 and Bcl-2 family proteins including Bcl-2 and Mcl-1. Interestingly, AZ960 increased levels of Bcl-xL in MT-1 and MT-2 cells in association with accumulation of cAMP response element-binding protein bound to the Bcl-xL promoter as measured by chromatin immunoprecipitation assay. Importantly, genetic inhibition of Bcl-xL by a small interfering RNA potentiated antiproliferative effects of AZ960 in MT-1 cells. Taken together, Jak2 is an attractive molecular target for treatment of ATL. Concomitant blockade of Jak2 and Bcl-xL may be a promising treatment strategy for this lethal disease. Mol Cancer Ther; 9(12); 3386–95. ©2010 AACR.
Contrasting Effects of Nutlin-3 on TRAIL- and Docetaxel-Induced Apoptosis Due to Upregulation of TRAIL-R2 and Mcl-1 in Human Melanoma Cells
Authors: Tseng Hsin-Yi , Jiang Chen Chen , Croft Amanda , Tay Kwang Hong , Thorne Rick Francis , Yang Fan , Liu Hao , Hersey Peter , Zhang Xu Dong 
Published: December 2010

Abstract
Wild-type p53 is commonly expressed in melanoma but does not appear to be effective in the induction of apoptosis. One explanation is that p53 is targeted for degradation by the E3 ligase MDM2. However, we found in this study that blockade of the interaction of p53 and MDM2 by the MDM2 antagonist nutlin-3 in melanoma cells did not induce apoptosis, even though it upregulated p53 and its proapoptotic targets. Nevertheless, nutlin-3 enhanced TRAIL-induced apoptosis as a result of p53-mediated upregulation of TRAIL-R2. Unexpectedly, nutlin-3 upregulated Mcl-1, which attenuated apoptotic signaling triggered by TRAIL, and inhibited apoptosis induced by the microtubule-targeting drug docetaxel. The increase in Mcl-1 was related to a p53-independent transcriptional mechanism, but stabilization of the Mcl-1 protein played a dominant role, as nutlin-3 upregulated the Mcl-1 protein to a much greater extent than the Mcl-1 mRNA, and this was associated with prolonged half-life time and reduced ubiquitination of the protein. Knockdown of p53 blocked the upregulation of the Mcl-1 protein, indicating that p53 plays a critical role in the stabilization of Mcl-1. The contrasting effects of nutlin-3 on TRAIL- and docetaxel-induced apoptosis were confirmed in fresh melanoma isolates. Collectively, these results show that nutlin-3 may be a useful agent in combination with TRAIL and, importantly, uncover a novel regulatory effect of p53 on the expression of Mcl-1 in melanoma cells on treatment with nutlin-3, which may antagonize the therapeutic efficacy of other chemotherapeutic drugs in addition to docetaxel in melanoma. Mol Cancer Ther; 9(12); 3363–74. ©2010 AACR.
Chemoprevention of Chemically Induced Skin Tumorigenesis by Ligand Activation of Peroxisome Proliferator–Activated Receptor-β/δ and Inhibition of Cyclooxygenase 2
Authors: Zhu Bokai , Bai Robert , Kennett Mary J. , Kang Boo-Hyon , Gonzalez Frank J. , Peters Jeffrey M. 
Published: December 2010

Abstract
Ligand activation of peroxisome proliferator–activated receptor-β/δ (PPARβ/δ) and inhibition of cyclooxygenase-2 (COX2) activity by nonsteroidal anti-inflammatory drugs (NSAID) can both attenuate skin tumorigenesis. The present study examined the hypothesis that combining ligand activation of PPARβ/δ with inhibition of COX2 activity will increase the efficacy of chemoprevention of chemically induced skin tumorigenesis over that observed with either approach alone. To test this hypothesis, wild-type and Pparβ/δ-null mice were initiated with 7,12-dimethylbenz[a]anthracene (DMBA), topically treated with 12-O-tetradecanoylphorbol-13-acetate to promote tumorigenesis, and then immediately treated with topical application of the PPARβ/δ ligand GW0742, dietary administration of the COX2 inhibitor nimesulide, or both GW0742 and nimesulide. Ligand activation of PPARβ/δ with GW0742 caused a PPARβ/δ-dependent delay in the onset of tumor formation. Nimesulide also delayed the onset of tumor formation and caused inhibition of tumor multiplicity (46%) in wild-type mice but not in Pparβ/δ-null mice. Combining ligand activation of PPARβ/δ with dietary nimesulide resulted in a further decrease of tumor multiplicity (58%) in wild-type mice but not in Pparβ/δ-null mice. Biochemical and molecular analysis of skin and tumor samples show that these effects were due to the modulation of terminal differentiation, attenuation of inflammatory signaling, and induction of apoptosis through both PPARβ/δ-dependent and PPARβ/δ-independent mechanisms. Increased levels and activity of PPARβ/δ by nimesulide were also observed. These studies support the hypothesis that combining ligand activation of PPARβ/δ with inhibition of COX2 activity increases the efficacy of preventing chemically induced skin tumorigenesis as compared with either approach alone. Mol Cancer Ther; 9(12); 3267–77. ©2010 AACR.
Comparison of a Novel, Single-Lead Atrial Sensing System With a Dual-Chamber Implantable Cardioverter-Defibrillator System in Patients Without Antibradycardia Pacing Indications
Authors: Sticherling Christian , Zabel Markus , Spencker Sebastian , Meyerfeldt Udo , Eckardt Lars , Behrens Steffen , Niehaus Michael ,   for the ADRIA Investigators
Published: December 2010

Background—
Supraventricular tachyarrhythmias are the main cause for inappropriate therapy by implantable cardioverter-defibrillators (ICDs). For better rhythm discrimination, an atrial electrogram is helpful and usually obtained from an additional atrial lead, even in the absence of sinus node or atrioventricular nodal disease. An A+-ICD system with integrated atrial sensing rings mounted 15 to 18 cm from the tip of an ICD lead may obviate the need to implant a separate atrial lead. The aim of the study was to compare the novel A+-ICD and a conventional dual-chamber (DR)-ICD.

Methods and Results—

Two hundred forty-nine patients with standard ICD indications but no requirement for antibradycardia pacing were randomized to receive an A+-ICD (n=124) or a DR-ICD (n=125). Implantation details, need for ICD system revision, long-term sensing, documented arrhythmia episodes, and the respective rhythm discrimination during follow-up were analyzed. The implantation time was significantly shorter in the A+-ICD group (67±30 vs 79±30 minutes,
P
=0.003). Mean P-wave amplitudes were 3.5±0.8 mV (A+-ICD) and 3.2±0.6 mV (DR-ICD) and remained stable during the follow-up period of 12 months. Surgical revision was necessary in 13 patients in the DR-ICD and 10 in the A+-ICD group. All 593 ventricular tachyarrhythmia episodes were correctly discriminated. Sensitivity and specificity of supraventricular tachyarrhythmia discrimination were not different between the study groups.

Conclusions—
The novel A+-ICD system can be implanted faster and is equivalent to a standard DR-ICD with regard to the detection of ventricular tachyarrhythmias and supraventricular tachyarrhythmias. It represents a useful alternative to obtain atrial sensing.

Clinical Trial Registration—

URL:
http://www.clinicaltrials.gov
. Unique identifier: NCT00324662.
Isoproterenol Administration During General Anesthesia for the Evaluation of Children With Ventricular Preexcitation
Authors: Moore Jeremy P. , Kannankeril Prince J. , Fish Frank A. 
Published: December 2010

Background—
Rapid anterograde conduction in the setting of ventricular preexcitation is associated with an increased risk of sudden cardiac death. The effect of isoproterenol in this setting is unclear, particularly in younger anesthetized patients. The aim of this study was to determine the effect of isoproterenol on accessory-pathway conduction in children undergoing general anesthesia and its role in the risk-stratification process.

Methods and Results—

The records of 151 pediatric patients with preexcitation undergoing electrophysiologic study under propofol anesthesia during a 5-year period were reviewed. Data included accessory-pathway effective refractory period, minimum 1:1 accessory pathway conduction with atrial pacing, and shortest preexcited R-R interval in atrial fibrillation. Measurements were repeated after administration of low-dose isoproterenol (mean, 0.013 μg/kg per min; range, 0.003 to 0.027). All accessory-pathway characteristics were significantly shortened with isoproterenol (
P
<0.001). Accessory-pathway effective refractory period increased modestly with age, both in the baseline state (
r
=0.172,
P
=0.04) and with isoproterenol (
r
=0.267,
P
<0.01) as did minimum 1:1 accessory pathway conduction with atrial pacing (
r
=0.178,
P
=0.034, and
r
=0.175,
P
<0.01, respectively). Accessory-pathway effective refractory period ≤250 ms was observed in only 5% of patients at baseline vs 25% after isoproterenol, and Shortest preexcited R-R interval in atrial fibrillation ≤250 ms was noted in 16% vs 41%. Tachycardia was induced in 48 of 151 patients before and in 102 of 151 after isoproterenol.

Conclusions—
In anesthetized children with ventricular preexcitation, accessory pathways display shorter conduction properties at younger ages and important adrenergic sensitivity at all ages. Use of low-dose isoproterenol resulted in a substantial increase in the number of patients who would otherwise meet typical criteria for ablation.
The Effect of the Sea Ice Freshwater Flux on Southern Ocean Temperatures in CCSM3: Deep-Ocean Warming and Delayed Surface Warming
Authors: Kirkman Clark H. , Bitz Cecilia M. 
Published: December 2010

Abstract
This study explores the role of sea ice freshwater and salt fluxes in modulating twenty-first-century surface warming in the Southern Ocean via analysis of sensitivity experiments in the Community Climate System Model, version 3 (CCSM3). In particular, the role of a change in these fluxes in causing surface cooling, expanding sea ice, and increasing deep oceanic storage of heat in the Southern Ocean is investigated. The results indicate that in response to the doubling of CO2 concentrations in the atmosphere in CCSM3, net freshwater input from sea ice to the ocean increases south of 58°S (owing to less growth) and decreases from 48° to 58°S (owing to less melt). The freshwater source from changing precipitation in the model is considerably less than from sea ice south of 58°S, but it serves to compensate for the reduction in sea ice melt near the ice edge, leaving almost no net freshwater flux change between about 48° and 58°S. As a result, freshwater input principally from sea ice reduces ocean convection, which in turns reduces the entrainment of heat into the mixed layer and reduces the upward heat transport along isopycnals below about 1000 m. The reduced upward heat transport (from all sources) causes deep-ocean heating south of 60°S and below 500-m depth, with a corresponding surface cooling in large parts of the Southern Ocean in the model. These results indicate that changing sea ice freshwater and salt fluxes are a major component of the twenty-first-century delay in surface warming of the Southern Ocean and weak reduction in Antarctic sea ice in model projections.