bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sex moderates the association between symptoms of anxiety, but not obsessive compulsive disorder, and error‐monitoring brain activity: A meta‐analytic review
Authors: Moser Jason S. , Moran Tim P. , Kneip Chelsea , Schroder Hans S. , Larson Michael J. 
Published: December 2015

AbstractSex differences in cognition and emotion are particularly active areas of research. Much of this work, however, focuses on mean‐level differences between the sexes on cognitive and/or emotional variables in isolation. In this article, we are primarily concerned with how sex affects associations between cognition and emotion, or cognition‐emotion interactions. Specifically, the purpose of this paper is to shed light on a gap in our understanding of how sex affects the relationship between error monitoring, a core component of cognitive control, and anxiety. Using meta‐analysis, we show that the relationship between symptoms of anxiety and a neurophysiological marker of error monitoring—the error‐related negativity (ERN)—is significantly greater in women than men such that women, but not men, with higher levels of anxiety show a larger ERN. This sex difference held true across studies of anxiety‐specific symptoms but not studies of obsessive‐compulsive symptoms. These findings underscore the need to consider sex in studies of anxiety and the ERN as well as support growing evidence indicating that obsessive‐compulsive problems are distinguishable from other anxiety‐specific problems across multiple levels of analysis. Overall, we conclude that ignoring sex in studies of cognition‐emotion interactions is unacceptable. Rather, future research that continues to tackle questions related to sex differences in associations between cognition and emotion will more likely lead to advancements in basic and applied sciences of relevance to health and human behavior.
Increasing awareness of sex differences in airway diseases
Authors: Raghavan Deepa , Jain Raksha 
Published: December 2015

AbstractThere is growing epidemiologic data demonstrating sex differences with respect to prevalence and progression of airway diseases, including asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF) and non‐CF‐related bronchiectasis. In asthma, for example, young boys have increased exacerbations and higher morbidity than girls which distinctly reverses after adolescence and into adulthood. In COPD, a disease that was historically considered an illness of men, the number of women dying per year is now greater than in men. Finally, women with CF‐related bronchiectasis have a decreased median life expectancy relative to men and a higher risk of respiratory infections despite equal prevalence of the disease. A number of studies now exist demonstrating mechanisms behind these sex differences, including influences of genetic predisposition, sex hormones and comorbidities. The notable sex disparity has potential diagnostic, therapeutic and prognostic implications and for the practicing respiratory or general physician, a familiarity with these distinctions may augment effective management of patients with airway diseases. This review seeks to concisely summarize the data regarding gender‐based differences in airway diseases, outline the current understanding of contributing factors and discuss therapeutic implications for clinicians.
The Phenotypic and Functional Features of Human M2 Macrophages Generated Under Low Serum Conditions
Authors: Sakhno L. V. , Shevela E. Ya. , Tikhonova M. A. , Ostanin A. A. , Chernykh E. R. 
Published: December 2015

AbstractThe phenotypic and functional features of human M2 macrophages, in particular, their immunosuppressive activity, can considerably vary depending on M2 polarizing stimulus. This study was aimed at the investigation of cytokine production and pro‐apoptogenic/inhibitory molecule expression in macrophages generated with GM‐CSF using either standard conditions (M1) or deficiency of serum/growth factors (M2‐LS cells). In contrast to M1, M2‐LS cells were characterized by an enhanced content of CD206+, B7‐H1+, FasL+ and TRAIL+ cells along with a decreased production of IFN‐γ, IL‐5, IL‐6, IL‐13, TNF‐α, IL‐17 and MCP‐1. In addition, M2‐LS exhibited a lower T cell stimulatory activity in MLC that was associated with the higher numbers of apoptotic and the lower numbers of proliferating T cells. B7‐H1 plays a key role in M2‐LS‐mediated cytotoxic effects as the neutralization of B7‐H1 reduces the apoptosis‐inducing activity of M2‐LS, while the blocking of CD206 and TRAIL reduces the cytostatic activity of M2 macrophages.
The Active Metabolite of Vitamin D3 as a Potential Immunomodulator
Authors: Szymczak I. , Pawliczak R. 
Published: December 2015

AbstractIn the past, vitamin D was known for its classical, skeletal action as a regulator of calcium and bone homoeostasis. Currently, vitamin D was found to have a role in numerous physiological processes in the human body; thus, vitamin D has pleiotropic activity. The studies carried out in the past two decades showed the role of vitamin D in the regulation of immune system functions. Basically, these effects may be mediated not only via endocrine mechanism of circulating calcitriol but also via paracrine one (based on cell–cell communication that leads to production of signal inducing the changes in nearby/adjacent cells and modulating their differentiation or behaviour) and intracrine mechanism (the action of vitamin D inside a cell) of 1,25‐dihydroxycholecalciferol (1,25(OH)2D3) synthetized from its precursor 25‐hydroxyvitamin D3 (25(OH)D3). Both vitamin D receptor (VDR) and 25‐hydroxyvitamin D3 1‐α‐hydroxylase (CYP27B1) are expressed in several types of immune cells (i.e. antigen presenting cells, T and B cells), and thus, they are able to synthetize the bioactive form of vitamin D that modulates both the innate and adaptive immune system. This review discusses the role of vitamin D as regulator of immune system, and our understanding of how vitamin D regulates both adaptive and innate immunity as well as inflammatory cascade on the cellular level.
Kainate receptor pore‐forming and auxiliary subunits regulate channel block by a novel mechanism
Authors: Brown Patricia M. G. E. , Aurousseau Mark R. P. , Musgaard Maria , Biggin Philip C. , Bowie Derek 
Published: December 2015

Key points
Kainate receptor heteromerization and auxiliary subunits, Neto1 and Neto2, attenuate polyamine ion‐channel block by facilitating blocker permeation.
Relief of polyamine block in GluK2/GluK5 heteromers results from a key proline residue that produces architectural changes in the channel pore α‐helical region.
Auxiliary subunits exert an additive effect to heteromerization, and thus relief of polyamine block is due to a different mechanism.
Our findings have broad implications for work on polyamine block of other cation‐selective ion channels.
AbstractChannel block and permeation by cytoplasmic polyamines is a common feature of many cation‐selective ion channels. Although the channel block mechanism has been studied extensively, polyamine permeation has been considered less significant as it occurs at extreme positive membrane potentials. Here, we show that kainate receptor (KAR) heteromerization and association with auxiliary proteins, Neto1 and Neto2, attenuate polyamine block by enhancing blocker permeation. Consequently, polyamine permeation and unblock occur at more negative and physiologically relevant membrane potentials. In GluK2/GluK5 heteromers, enhanced permeation is due to a single proline residue in GluK5 that alters the dynamics of the α‐helical region of the selectivity filter. The effect of auxiliary proteins is additive, and therefore the structural basis of polyamine permeation and unblock is through a different mechanism. As native receptors are thought to assemble as heteromers in complex with auxiliary proteins, our data identify an unappreciated impact of polyamine permeation in shaping the signalling properties of neuronal KARs and point to a structural mechanism that may be shared amongst other cation‐selective ion channels.
Signaling Responses After Varying Sequencing of Strength and Endurance Training in a Fed State
Authors: Jones Thomas W. , Walshe Ian H. , Hamilton David L. , Howatson Glyn , Russell Mark , Price Oliver J. , Gibson Alan St Clair , French Duncan N. 
Published: December 2015

Purpose:To compare anabolic signaling responses to differing sequences of concurrent strength and endurance training in a fed state.Methods:Eighteen resistance-trained men were randomly assigned to the following experimental conditions: strength training (ST), strength followed by endurance training (ST-END), or endurance followed by strength training (END-ST). Muscle tissue samples were taken from the vastus lateralis before each exercise protocol, on cessation of exercise, and 1 h after cessation of strength training. Tissue was analyzed for total and phosphorylated (p-) signaling proteins linked to the mTOR and AMPK networks.Results:Strength-training performance was similar between ST, ST-END, and END-ST. p-S6k1 was elevated from baseline 1 h posttraining in ST and ST-END (both P < .05). p-4E-BP1 was significantly lower than baseline post-ST (P = .01), whereas at 1 h postexercise in the ST-END condition p-4E-BP1 was significantly greater than postexercise (P = .04). p-ACC was elevated from baseline both postexercise and 1 h postexercise (both P < .05) in the END-ST condition. AMPK, mTOR, p38, PKB, and eEF2 responded similarly to ST, ST-END, and END-ST. Signaling responses to ST, ST-END, and END were largely similar. As such it cannot be ascertained which sequence of concurrent strength and endurance training is most favorable in promoting anabolic signaling.Conclusions:In the case of the current study an acute bout of concurrent training of differing sequences elicited similar responses of the AMPK and mTOR networks.
Whole-Genome Sequences of Novel Porcine Circovirus Type 2 Viruses Detected in Swine from Mexico and the United States
Authors: Harmon Karen M. , Gauger Phillip C. , Zhang Jianqiang , Piñeyro Pablo E. , Dunn Derek D. , Chriswell Amy J. 
Published: December 2015

ABSTRACT
A unique porcine circovirus type 2 capsid protein (ORF2) sequence was detected in swine samples submitted to the Iowa State University Veterinary Diagnostic Laboratory. The complete genome sequences of four viruses, one from Mexico and three from the United States, were determined to further characterize this novel PCV2 genotype.
Draft Genome Sequence of
Pedobacter
sp. Strain Hv1, an Isolate from Medicinal Leech Mucosal Castings
Authors: Ott Brittany M. , Beka Lidia , Graf Joerg , Rio Rita V. M. 
Published: December 2015

ABSTRACT

The
Pedobacter
sp. Hv1 strain was isolated from the medicinal leech,
Hirudo verbana,
mucosal castings. These mucosal sheds have been demonstrated to play a role in horizontal symbiont transmission. Here, we report the draft 4.9 Mbp genome sequence of
Pedobacter
sp. strain Hv1.
Genome Sequence of Bradyrhizobium tropiciagri Strain CNPSo 1112
T
, Isolated from a Root Nodule of
Neonotonia wightii
Authors: Delamuta Jakeline Renata Marçon , Gomes Douglas Fabiano , Ribeiro Renan Augusto , Chueire Ligia Maria Oliveira , Souza Renata Carolini , Almeida Luiz Gonzaga Paula , Vasconcelos Ana Tereza Ribeiro , Hungria Mariangela 
Published: December 2015

ABSTRACT

CNPSo 1112
T
is a nitrogen-fixing symbiont of perennial soybean, a tropical legume forage. Its draft genome indicates a large genome with a circular chromosome and 9,554 coding sequences (CDSs). Operons of nodulation, nitrogen fixation, and uptake hydrogenase were present in the symbiotic island, and the genome encompasses several CDSs of stress tolerance.
Draft Genome Sequence of
Caloranaerobacter
sp. TR13, an Anaerobic Thermophilic Bacterium Isolated from a Deep-Sea Hydrothermal Vent
Authors: Zhou Meixian , Xie Yunbiao , Dong Binbin , Liu Qing , Chen Xiaoyao 
Published: December 2015

ABSTRACT

Here, we report the draft 2,261,881-bp genome sequence of
Caloranaerobacter
sp. TR13, isolated from a deep-sea hydrothermal vent on the East Pacific Rise. The sequence will be helpful for understanding the genetic and metabolic features, as well as potential biotechnological application in the genus
Caloranaerobacter
.
Moment problems in an infinite number of variables
Authors: Alpay Daniel , Jorgensen Palle E. T. , Kimsey David P. 
Published: December 2015

Let [Formula: see text]. Given a closed set [Formula: see text] and [Formula: see text], where [Formula: see text] denotes the set of tuples of nonnegative integers [Formula: see text] with [Formula: see text] for finitely many [Formula: see text], the [Formula: see text]-moment problem on [Formula: see text] entails determining whether or not there exists a measure [Formula: see text] on [Formula: see text] so that [Formula: see text] and [Formula: see text] We prove that [Formula: see text] exists if and only if a natural analogue of the Riesz–Haviland functional [Formula: see text] is [Formula: see text]-positive, i.e. if [Formula: see text] is any polynomial which is nonnegative for all [Formula: see text], then [Formula: see text] We will also provide a sufficient condition for [Formula: see text] to be unique, an analogue of a celebrated theorem of K. Schmüdgen and an application to stochastic processes.
CRISIS-DRIVEN INNOVATION: THE CASE OF HUMANITARIAN INNOVATION
Authors: BESSANT JOHN , RUSH HOWARD , TRIFILOVA ANNA 
Published: December 2015

Innovation is often presented as a survival issue and this provides a powerful metaphor to focus attention on the need to manage it effectively. But in the humanitarian context it takes on a very literal meaning. Crises, whether natural or man-made, require rapid problem solving if agencies and aid workers are to avoid the huge negative impacts of such disasters.That makes consideration of how innovation takes place in this sector an urgent challenge. How can the humanitarian sector best organise to enable innovation and what are the roles for key actors — donors, agencies, and most importantly ‘users’? Our paper summarises the nature of the challenge and reviews experience so far in humanitarian innovation (HI).There is a second issue which we also explore. Arguably crisis conditions provide a “laboratory” for exploring alternative approaches and generating novel innovation trajectories which might diffuse more widely — the concept of “reverse innovation.” Are there lessons which could be learned for mainstream innovation management? And if so, what are the mechanisms which might enable such learning and experience exchange to take place?
Abstract A13: Endothelial podosome rosettes regulate vascular branching in tumor angiogenesis
Authors: Seano Giorgio , Chiaverina Giulia , Gagliardi Paolo Armando , Blasio Laura di , Puliafito Alberto , Bouvard Claire , Sessa Roberto , Tarone Guido , Sorokin Lydia , Helley Dominique , Jain Rakesh K. , Serini Guido , Bussolino Federico , Primo Luca 
Published: December 2015

Abstract
The mechanism, by which angiogenic endothelial cells break the physical barrier of vascular basement membrane and consequently sprout, forming new vessels in mature tissues, is unclear. We discovered that angiogenic endothelium is characterized by the presence of functional podosome rosettes. These extracellular matrix-degrading and adhesive structures are precursor of de novo branching points and represent a key event in the formation of new blood vessels. VEGF-A stimulation induces the formation of endothelial podosome rosettes by up-regulating integrin α6β1; in contrast, the binding of α6β1 integrin to vascular basement membrane laminin impairs the formation of podosome rosettes by restricting α6β1 integrin to focal adhesions and hampering its translocation to podosomes. Inhibition of podosome rosette formation by α6β1 blockade or genetic deletion affects vessel branching. The control exerted by α6β1 integrin on tumor blood vessels branching as a consequence of podosome rosette inhibition in endothelial cells recalls the previously proposed notion of vascular normalization by suggesting endothelial podosome rosettes as a new target to normalize tumor vasculature.
Citation Format: Giorgio Seano, Giulia Chiaverina, Paolo Armando Gagliardi, Laura di Blasio, Alberto Puliafito, Claire Bouvard, Roberto Sessa, Guido Tarone, Lydia Sorokin, Dominique Helley, Rakesh K. Jain, Guido Serini, Federico Bussolino, Luca Primo. Endothelial podosome rosettes regulate vascular branching in tumor angiogenesis. [abstract]. In: Proceedings of the AACR Special Conference: Tumor Angiogenesis and Vascular Normalization: Bench to Bedside to Biomarkers; Mar 5-8, 2015; Orlando, FL. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(12 Suppl):Abstract nr A13.
Abstract A25: Molecular characterization of cyclin-dependent kinase 1 pathway in newly established epithelial ovarian cancer cell lines
Authors: Cho Hanbyoul , Sabrgaliyeva Assel , Yang Woo Kyeom , Kim Sol , Shin Ha-Yeon , Lee Eun Ju , Kim Jae-hoon 
Published: December 2015

Abstract
Background: Epithelial ovarian cancer (EOC) is a heterogeneous gynecologic tumor. To better understand the biological pathways involved in the development of EOC, we performed mRNA expression profiling on newly established EOC cell lines and studied the common characteristics in EOC cells.
Methods: Five newly established EOC cell lines were characterized by transcript profiling. Microarray analyses were validated using quantitative real-time PCR (RT-PCT), immunoblotting, and GEO dataset. Subsequently, we investigated the possible functions of S100A14 in EOC by small interfering RNA (siRNA) approaches.
Results: A total of 239 genes represented by 24,957 probes were identified from microarray analysis, of which 98 and 141 genes are up- (&gt; 2 fold, p &lt; 0.05) or down-regulated (&lt; 3 fold, p &lt; 0.05), respectively, in EOC cell lines compare to human ovarian surface epithelial cells. Interestingly, our data showed upregulation of 11 genes which are associated with the CDK1 pathway. In RT-PCR and immunoblotting, Cdk1 and cyclin B1 expression was significantly increased in EOC cells and tissues compared to benign or normal ovarian surface epitheliums.
Cdk1 knockdown by siCdk1 or Cdk1 inhibitor, RO-3306, inhibited cell growth and arrested the cell cycle at G2/M phase with increased pro-apoptotic signals and decreased anti-apoptotic signals.
Conclusions: These results suggest that elevated expression of Cdk1/cyclinB1 is important to EOC development and progression, providing new insight into the biology of EOC.
Citation Format: Hanbyoul Cho, Assel Sabrgaliyeva, Woo Kyeom Yang, Sol Kim, Ha-Yeon Shin, Eun Ju Lee, Jae-hoon Kim. Molecular characterization of cyclin-dependent kinase 1 pathway in newly established epithelial ovarian cancer cell lines. [abstract]. In: Proceedings of the AACR Special Conference: Tumor Angiogenesis and Vascular Normalization: Bench to Bedside to Biomarkers; Mar 5-8, 2015; Orlando, FL. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(12 Suppl):Abstract nr A25.
Abstract B05: An immune modulatory role for the Fes protein tyrosine kinase
Authors: Alotaibi Faizah Mesfer , Zhang Connie , Basta Sam , Greer Peter A. 
Published: December 2015

Abstract
The Fes protein tyrosine kinase is abundantly expressed in phagocytic immune cells, including tumor associated macrophages. In addition to the C-terminal kinase and central SH2 domains, Fes contains an N-terminal F-BAR domain that confers unique membrane binding and bending properties which implicate it in the regulation of dynamic membrane-cytoskeletal remodeling processes associated with phagocytosis, receptor endocytosis, vesicular trafficking and cross-talk between receptor systems. In addition to roles in signaling downstream from a variety of cytokine receptors, including those for IL-3, -4, -5, and GM-CSF, Fes has also been implicated in regulating signaling downstream from the TLR-4 receptor for LPS. Fes knockout mice display enhanced sensitivity to LPS, and this was shown to be associated with increased NF-κB signaling and TNFα production from Fes-/- macrophages. Recent studies have also implicated Fes in cross-talk between MHC-I and the NF-κB and IRF-3 pathways in macrophages. Activation of these pro-inflammatory NF-κB and IRF-3 pathways so called Signal 3 - in antigen presenting cells (APCs) is associated with more robust activation of T cells. Interestingly, tumor onset in the MMTV-Neu transgenic mouse model of breast cancer is significantly delayed in Fes-/-, and this was associated with increased frequency of T and B lymphocytes in the premalignant mammary glands.
These observations suggest that Fes contributes to the regulation of signaling downstream from the MHC-I and TLR receptors such that Fes disruption in TLR-engaged APCs would lead to enhanced activation of CD8+ T cells through increased Signal 3 from the T-cell receptor-engaged APCs.
Using a lymphocytic choriomeningitis virus (LCMV) model of immune activation we show that LPS stimulated Fes-/- macrophages promote more robust activation of CD8+ T cells than Fes+/+ macrophages. Furthermore, LPS stimulated Fes-/- macrophages show increased phosphorylation of TBK-1 and IRF-3. We also observed that Fes co-localizes with MHC-I in dynamic vesicular structures within macrophages. These observations are consistent with a model where Fes regulates Signal 3 in APCs through roles in cross-talk between MHC-I and the NF-kB and IRF-3 signaling pathways. This suggests that Fes plays an immune checkpoint role at the level of Signal 3, and that Fes inhibition could promote tumor immunity through increased Signal 3 driven T cell activation.
Citation Format: Faizah Mesfer Alotaibi, Connie Zhang, Sam Basta, Peter A. Greer. An immune modulatory role for the Fes protein tyrosine kinase. [abstract]. In: Proceedings of the AACR Special Conference: Tumor Angiogenesis and Vascular Normalization: Bench to Bedside to Biomarkers; Mar 5-8, 2015; Orlando, FL. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(12 Suppl):Abstract nr B05.
Abstract B15: In vivo analysis of repeated siRNA silencing on protein expression levels
Authors: Aliabadi Hamidreza Montazeri , Mahdipoor Parvin , Uludag Hasan 
Published: December 2015

Abstract
An ever increasing number of anticancer drugs are under investigation, and enter the clinical setting targeting different tumor survival and/or growth mechanisms; however, development of resistance against the mechanism of action of even the most promising drugs seems to be inevitable and remains a major concern. RNA interference (RNAi) have shown considerable promise in silencing proteins involved in tumor vascularization, as well as intracellular pathways involved in cell proliferation and/or survival. Despite the apparent efficacy of this powerful tool (especially in vitro), our information about the factors affecting siRNA efficiency and the possibility of resistance development against the silencing effect are limited at best. This study focused on determining the possibility of resistance development against siRNA treatment as a result of repeated exposure to siRNA in vivo. Our preliminary experiments in vitro revealed an unaffected siRNA cellular internalization and reproducible silencing efficiency of selected targets. The expression level of other mediators involved in breast cancer cell survival and proliferation (notably survivin, JUN, JAK2, NFkB and STAT3) were, however, altered in siRNA treated cells. In vivo experiments in a xenograft model demonstrated a similar silencing efficiency at the mRNA level after each repeated dose, with little, if any, apparent resistance development to the siRNA therapy. We conclude that cells would respond to repeated siRNA treatments in a similar fashion after a temporary initial alteration.
Citation Format: Hamidreza Montazeri Aliabadi, Parvin Mahdipoor, Hasan Uludag. In vivo analysis of repeated siRNA silencing on protein expression levels. [abstract]. In: Proceedings of the AACR Special Conference: Tumor Angiogenesis and Vascular Normalization: Bench to Bedside to Biomarkers; Mar 5-8, 2015; Orlando, FL. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(12 Suppl):Abstract nr B15.