bluuebunny/crossref_metadata_2025_split huggingface dataset:
A COACHING WORKSHOP IMPROVES COACH INTENTION BUT DOES NOT TRANSLATE TO IMPLEMENTATION OF A ACL INJURY PREVENTION PROGRAM
Authors: Frank B , Register-Mihalik J , Marshall S , Padua D 
Published: March 2014

BackgroundThere is limited evidence describing methods and challenges for implementing anterior cruciate ligament (ACL) injury prevention programs (IPP) in a “real-world” context.ObjectiveEvaluate the effects of a ACL IPP workshop on elite-division youth soccer coaches' behavioral determinants to implement a ACL IPP, and describe coaches' subsequent ACL IPP implementation compliance.DesignDescriptive study.SettingElite-division youth soccer club.ParticipantsA convenient sample of 34 soccer coaches (age=34.6±9.1 yrs) of elite-division youth soccer club teams.InterventionsWe administered a workshop aimed at increasing coaches' behavioral determinants to implement a ACL IPP. Coaches were provided with instructional materials following the workshop.Main outcome measurementsCoaches' behavioral determinants regarding ACL IPP using pre/post-workshop surveys and coaches' subsequent rate and fidelity of implementation of the ACL IPP during the following soccer season.ResultsWilcoxon signed-rank tests indicated the workshop increased coach attitude toward; conducting a ACL IPP (P=.020), substituting a ACL IPP for a warm-up (P=.007), and improving player cutting and landing technique by implementing a ACL IPP (P=.001). The workshop increased coaches' perceived behavioral control; coaches felt more comfortable in their ability to teach their team a ACL IPP (P=.002) and more confident leading a ACL IPP if given instructions (P=.025). The workshop increased coaches' intent to implement a ACL IPP the next season (P<.001); for 15 minutes (P=.008) and 20 minutes (P=.011) prior to the start of a training session. Only 53% of the club's teams implemented the ACL IPP, with implementers demonstrating high variability in program fidelity.ConclusionsACL IPP workshops can effectively increase coach attitudes, perceived behavioral control, and intent to implement a ACL IPP. However, amplification of behavioral determinants does not appear to directly translate to high-level implementation compliance. Future research should investigate supplementary strategies to facilitate optimal ACL IPP implementation to improve compliance.
Are there gender differences in service use for mental disorders across countries in the European Union? Results from the EU-World Mental Health survey
Authors: Kovess-Masfety Vivane , Boyd Anders , van de Velde Sarah , de Graaf Ron , Vilagut Gemma , Haro Josep Maria , Florescu Silvia , O'Neill Siobhan , Weinberg Lauren , Alonso Jordi ,   the EU-WMH investigators
Published: March 2014

BackgroundWomen are more likely than men to use mental healthcare (MHC) due to differences in the types of problems and help-seeking behaviours. The consistency of this relationship across European countries, whose MHC organisation differs substantially, is unknown.MethodsLifetime MHC-use and the type of MHC provider were assessed in 37 289 participants from the EU-World Mental Health (EU-WMH) survey, including 10 European countries (Northern Ireland, The Netherlands, Belgium, Germany, France, Spain, Italy, Portugal, Bulgaria and Romania). Lifetime mood/anxiety disorders (DSM-IV) and severity were evaluated using the CIDI V.3.0.ResultsMHC use was significantly higher for women than men in every country except for Romania (overall OR=1.80, 95% CI1.64 to 1.98), while remaining so after adjusting for socioeconomic characteristics (age, income level, employment status, education, marital status; adjusted OR=1.87, 95% CI 1.69 to 2.06) and country-level indicators (MHC provision, private household out-of-pocket expenditure, and Gender Gap Index; adjusted OR=1.89, 95% CI 1.71 to 2.08). Compared with men, women were also more likely to consult general practitioners (GP) versus specialised MHC (OR=1.32, 95% CI 1.12 to 1.56) with high between-country variability. In participants with mood disorder, the gender relationship in MHC use and type of MHC did not change. Conversely, in participants with anxiety disorder, no significant gender relationship in MHC use was observed (adjusted OR=1.21, 95% CI 0.99 to 1.47). Finally, men with severe mental health problems had a significantly higher odds of MHC use (OR=14.70) when compared with women with similar levels (OR=8.95, p for interaction=0.03) after adjusting for socioeconomic characteristics and country-level indicators.ConclusionsWomen use MHC and GPs more frequently than men, yet this depends on the type and severity of mental health problems.
Unemployment insurance and deteriorating self-rated health in 23 European countries
Authors: Ferrarini Tommy , Nelson Kenneth , Sjöberg Ola 
Published: March 2014

BackgroundThe global financial crisis of 2008 is likely to have repercussions on public health in Europe, not least through escalating mass unemployment, fiscal austerity measures and inadequate social protection systems. The purpose of this study is to analyse the role of unemployment insurance for deteriorating self-rated health in the working age population at the onset of the fiscal crisis in Europe.MethodsMultilevel logistic conditional change models linking institutional-level data on coverage and income replacement in unemployment insurance to individual-level panel data on self-rated health in 23 European countries at two repeated occasions, 2006 and 2009.ResultsUnemployment insurance significantly reduces transitions into self-rated ill-health and, particularly, programme coverage is important in this respect. Unemployment insurance is also of relevance for the socioeconomic gradients of health at individual level, where programme coverage significantly reduces health risks attached to educational attainment.ConclusionsUnemployment insurance mitigated adverse health effects both at individual and country-level during the financial crisis. Due to the centrality of programme coverage, reforms to unemployment insurance should focus on extending the number of insured people in the labour force.
Identification of mTORC2 as a Necessary Component of HRG/ErbB2-Dependent Cellular Transformation
Authors: Lin Miao-chong J. , Rojas Katherine S. , Cerione Richard A. , Wilson Kristin F. 
Published: March 2014

Abstract
Overexpression of the receptor tyrosine kinase HER2/ErbB2 (ERBB2) has been linked to a poor prognosis for patients with breast cancer; thus, its activity is a central target for cancer therapy. Likewise, overexpression of heregulin (HRG/NRG1), a growth factor responsible for ErbB2 activation, has also been shown to be a driver of breast cancer progression. Although ErbB2 inhibitors offer a major advancement in the treatment of ErbB2-dependent breast cancers, patients are highly susceptible to developing clinical resistance to these drugs. Therefore, a detailed understanding of the molecular mechanism that underlies HRG/ErbB2-induced tumorigenesis is essential for the development of effective therapeutic strategies for this subset of patients with breast cancer. Here, it was demonstrated that HRG promoted anchorage-independent breast cancer cell growth more potently than EGF, and that the HRG-dependent activation of phosphoinositide 3-kinase and mTORC1 are necessary events for cell transformation. Functional evaluation of two distinct mTOR (MTOR) inhibitors, rapamycin and INK-128, on HRG-dependent signaling activities, uncovered a necessary role for mTORC2 in the regulation of the AKT/TSC2/mTORC1 axis by affecting the phosphorylation of AKT at the PDK1(PDPK1)-dependent site (T308) as well as at the mTORC2-dependent site (S473). The elimination of Rictor (RICTOR), a critical component of mTORC2, is detrimental to both the activation of mTORC1 and HRG-mediated cellular transformation. Similar results were obtained in multiple breast cancer model systems, highlighting an important role for mTORC2 in HRG/ErbB2-dependent breast cancer.
Implications: These findings suggest the potential benefits of targeting mTORC2 in HRG/ErbB2-induced breast cancer. Mol Cancer Res; 12(6); 940–52. ©2014 AACR.
Antitumor Effects of Cisplatin Combined with Tecemotide Immunotherapy in a Human MUC1 Transgenic Lung Cancer Mouse Model
Authors: Kao Chiao-Jung , Wurz Gregory T. , Monjazeb Arta M. , Vang Daniel P. , Cadman Timothy B. , Griffey Stephen M. , Wolf Michael , DeGregorio Michael W. 
Published: March 2014

Abstract
The goals of the present study were to define the effects of simultaneous cisplatin/tecemotide therapy on tumor development in a human mucin 1 (MUC1) transgenic lung cancer mouse model and to examine the effects of radiotherapy (RTX) on splenocytes, serum cytokines, and immune response to tecemotide. Two hundred twenty-six human MUC1 transgenic C57BL/6 mice were used in five studies designed to assess (i) serum cytokine and immune responses following four weekly 10-μg doses of tecemotide; (ii) the effects of simultaneous administration of cisplatin (2.5 mg/kg × 2 doses/cycle × 4 cycles) and tecemotide (2 cycles × 8 weekly 10-μg doses/cycle) therapy on tumor development, serum cytokines, and immune response; (iii) the dose–response effects of RTX on lymphocyte counts 16 hours following doses of 2 to 8 Gy; (iv) the time course of lymphocyte recovery from 16 hours to 20 days following 8-Gy RTX; and (v) the effects of simultaneous administration of RTX (8 Gy) and tecemotide on the immune response to tecemotide (four weekly 10-μg doses). Serum cytokines were analyzed by multiplex immunoassay, IFNγ immune responses by enzyme-linked immunosorbent spot (ELISpot), and lung tumor foci by lung whole mounts. Simultaneous cisplatin/tecemotide therapy resulted in significant and additive reduction in lung tumor foci compared with control mice, with significantly elevated serum IFNγ levels and specific IFNγ immune responses observed in both tecemotide and tecemotide + cisplatin–treated mice. Finally, neither cisplatin nor radiation interfered with the immune response to tecemotide. Cancer Immunol Res; 2(6); 581–9. ©2014 AACR.
Arterial Wall Stress Controls NFAT5 Activity in Vascular Smooth Muscle Cells
Authors: Scherer Clemens , Pfisterer Larissa , Wagner Andreas H. , Hödebeck Maren , Cattaruzza Marco , Hecker Markus , Korff Thomas 
Published: March 2014

Background

Nuclear factor of activated T‐cells 5 (
NFAT
5) has recently been described to control the phenotype of vascular smooth muscle cells (
VSMC
s). Although an increase in wall stress or stretch (eg, elicited by hypertension) is a prototypic determinant of
VSMC
activation, the impact of this biomechanical force on the activity of
NFAT
5 is unknown. This study intended to reveal the function of
NFAT
5 and to explore potential signal transduction pathways leading to its activation in stretch‐stimulated
VSMC
s.

Methods and Results

Human arterial
VSMC
s were exposed to biomechanical stretch and subjected to immunofluorescence and protein‐biochemical analyses. Stretch promoted the translocation of
NFAT
5 to the nucleus within 24 hours. While the protein abundance of
NFAT
5 was regulated through activation of c‐Jun N‐terminal kinase under these conditions, its translocation required prior activation of palmitoyltransferases.
DNA
microarray and ChiP analyses identified the matrix molecule tenascin‐C as a prominent transcriptional target of
NFAT
5 under these conditions that stimulates migration of
VSMC
s. Analyses of isolated mouse femoral arteries exposed to hypertensive perfusion conditions verified that
NFAT
5 translocation to the nucleus is followed by an increase in tenascin‐C abundance in the vessel wall.

Conclusions

Collectively, our data suggest that biomechanical stretch is sufficient to activate
NFAT
5 both in native and cultured
VSMC
s where it regulates the expression of tenascin‐C. This may contribute to an improved migratory activity of
VSMC
s and thus promote maladaptive vascular remodeling processes such as hypertension‐induced arterial stiffening.
Caregiver Burden
Authors: Abdollahpour Ibrahim , Nedjat Saharnaz , Noroozian Maryam , Salimi Yahya , Majdzadeh Reza 
Published: March 2014

Objective: People having dementia need help and supervision to perform their activities of daily living. This responsibility is usually imposed on family members who endure a great burden, leading to undesirable health outcomes. The aims of our study were to measure caregivers’ health as well as identify its adjusted relevant predictors. Methods: One hundred and fifty three registered patients and their caregivers from Iranian Alzheimer Association were included in this cross-sectional study through sequential sampling. Self-rated health (SRH) was measured using a single question with Likert-type scale ranging from very bad (1) to very good (5). The multiple linear regression model was applied to determine the adjusted associations between independent variables under study and SRH. Results: The mean caregiver SRH level was 3.03. Of the participant caregivers, 29% were either unsatisfied or very unsatisfied with their health level. In the final regression model, SRH showed a direct significant association with the patient’s number of children but an inverse significant association with the marital status (married patients), patient’s age, and caregiver burden. Conclusions: Caregiver burden was not only significantly associated with poor SRH after removing the effect of the other covariates but it was also recognized as the strongest predictor of caregivers’ SRH. Therefore, it seems that development of intervention programs, in order to reduce caregiver burden, can be considered as important step in promoting caregivers’ health level.
Structural and Functional Brain Changes in the Default Mode Network in Subtypes of Amnestic Mild Cognitive Impairment
Authors: Li Xin , Cao Miao , Zhang Junying , Chen Kewei , Chen Yaojing , Ma Chao , Fleisher Adam , He Yong , Zhang Zhanjun ,   BABRI Study Group
Published: March 2014

Background: Various amnestic mild cognitive impairment (aMCI) subtypes have been identified as single domain (SD) or multiple domain (MD), with differential probabilities of progression to Alzheimer disease (AD). Detecting the differences in the alterations in gray matter (GM) and intrinsic brain activity between the subtypes of aMCI help to understand their pathophysiological mechanisms and was conducive to construct such potential biomarkers to monitor the progression of aMCI. Methods: In all, 22 normal controls (NCs), 18 patients with SD-aMCI, and 17 patients with MD-aMCI participated in the study. The amplitude of low-frequency fluctuations (ALFFs) during rest represented intrinsic brain activity. Voxel-based morphometry analysis was used to measure the GM volume. Results: The MD-aMCI showed reduced GM in hippocampus (Hip), parahippocampal gyrus (PHG), and other regions than SD-aMCI. The SD-aMCI had reduced GM only in Hip and PHG than in NC. The MD-aMCI showed decreased ALFF in posterior cingulate cortex (PCC) and precuneus and increased ALFF in anterior cingulate cortex (ACC), PHG, and Hip compared with both SD-aMCI and NC. However, no ALFF difference was found between SD-aMCI and NC. Neuropsychological measures were correlated with ALFF in PCC and ACC only in the MD-aMCI. Conclusions: Patients with MD-aMCI displayed more severe GM atrophy and ALFF changes than patients with SD-aMCI. The results suggested that aMCI is heterogeneous and that MD-aMCI may be a prodromal stage which is more close to AD.
Human papillomavirus awareness among HIV-infected drug users in two urban areas
Authors: Rosa-Cunha Isabella , Hooton Thomas M , Cardenas Gabriel A , Del Rio Carlos , Bonney Loida E , Pereyra Margaret , Metsch Lisa R 
Published: March 2014

Summary Human papillomavirus (HPV) is the cause of cervical and anal cancer. Human immunodeficiency virus (HIV) infection and cocaine use are associated with increased risk for HPV infection and associated diseases, but little is known about HIV-infected drug users' awareness of HPV. We investigate HPV awareness among HIV-infected, sexually-active crack cocaine users from two inner-city hospitals in Florida and Georgia during their inpatient stays. Multivariate logistic regression analysis was used to examine potential correlates of HPV awareness. We interviewed 215 participants (110 women; 105 men) about their awareness of HPV infection. Overall, only 25% of respondents reported having heard of HPV. The odds of having heard of HPV were greater for respondents having a high-school degree or higher, having ever gone to an HIV provider for HIV care, and having two or more sexual partners. Despite increased susceptibility to HPV infection and HPV-related cancers, our study findings suggest that sexually-active HIV-infected crack cocaine users have little awareness of HPV and highlight the need for programmes targeting HPV education for HIV-infected crack cocaine drug users.
Idelalisib, a selective inhibitor of phosphatidylinositol 3-kinase-δ, as therapy for previously treated indolent non-Hodgkin lymphoma
Authors: Flinn Ian W. , Kahl Brad S. , Leonard John P. , Furman Richard R. , Brown Jennifer R. , Byrd John C. , Wagner-Johnston Nina D. , Coutre Steve E. , Benson Don M. , Peterman Sissy , Cho Yoonjin , Webb Heather K. , Johnson David M. , Yu Albert S. , Ulrich Roger G. , Godfrey Wayne R. , Miller Langdon L. , Spurgeon Stephen E. 
Published: March 2014

Key PointsThis clinical study assessed idelalisib, a selective PI3Kδ inhibitor, in 64 patients with relapsed, indolent non-Hodgkin lymphoma. Idelalisib treatment rapidly induced durable disease responses in heavily pretreated patients with a favorable safety profile.
PPAR Gamma agonists regulate tobacco smoke-induced toll like receptor 4 expression in alveolar macrophages
Authors: Yin Yan , Hou Gang , Li Erran , Wang Qiuyue , Kang Jian 
Published: March 2014

Abstract

Background
Peroxisome proliferator-activated receptor-gamma (PPARγ) is a ligand-activated transcription factor that exerts multiple biological effects. Growing evidence suggests that PPARγ plays an important role in inflammation; however, the effects of this transcription factor on the inflammation caused by smoking are unclear.

Methods
We measured the expression of inflammatory cytokines (leukotriene B4, LTB4 and interleukin 8, IL-8), PPARγ and toll-like receptors (TLR2 and TLR4) in alveolar macrophages (AMs) harvested from rats exposed to cigarette smoke (CS) for 3 months in vivo. Some of the rats were pre-treated with rosiglitazone (PPARγ agonist, 3 mg/kg/day, ip), rosiglitazone (3 mg/kg/day, ip) + BADGE (bisphenol A diglycidyl ether, a PPARγ antagonist, 30 mg/kg/day, ig), or BADGE alone (30 mg/kg/day, ig). We also measured the expression of PPARγ, TLR2, TLR4 and nuclear factor-kappaB (NF-κB) in AMs gained from normal rats, which exposed to 5% CSE (cigarette smoke extract) for 12hrs, respectively pretreated with PBS, rosiglitazone (30 uM), rosiglitazone (30 uM) + BADGE (100 uM), 15d-PGJ2 (PPARγ agonist, 5 uM), 15d-PGJ2 (5 uM) + BADGE (100 uM), or BADGE (100 uM) alone for 30 min in vitro.

Results

In vivo, rosiglitazone counteracted CS-induced LTB4 and IL-8 release and PPARγ downregulation, markedly lowering the expression of TLR4 and TLR2. In vitro, both rosiglitazone and 15d-PGJ2 inhibited CS-induced inflammation through the TLR4 signaling pathway.

Conclusions
These results suggest that PPARγ agonists regulate inflammation in alveolar macrophages and may play a role in inflammatory diseases such as COPD.
Billions of basepairs of recently expanded, repetitive sequences are eliminated from the somatic genome during copepod development
Authors: Sun Cheng , Wyngaard Grace , Walton D Brian , Wichman Holly A , Mueller Rachel Lockridge 
Published: March 2014

AbstractBackgroundChromatin diminution is the programmed deletion of DNA from presomatic cell or nuclear lineages during development, producing single organisms that contain two different nuclear genomes. Phylogenetically diverse taxa undergo chromatin diminution — some ciliates, nematodes, copepods, and vertebrates. In cyclopoid copepods, chromatin diminution occurs in taxa with massively expanded germline genomes; depending on species, germline genome sizes range from 15 – 75 Gb, 12–74 Gb of which are lost from pre-somatic cell lineages at germline – soma differentiation. This is more than an order of magnitude more sequence than is lost from other taxa. To date, the sequences excised from copepods have not been analyzed using large-scale genomic datasets, and the processes underlying germline genomic gigantism in this clade, as well as the functional significance of chromatin diminution, have remained unknown.ResultsHere, we used high-throughput genomic sequencing and qPCR to characterize the germline and somatic genomes ofMesocyclops edax, a freshwater cyclopoid copepod with a germline genome of ~15 Gb and a somatic genome of ~3 Gb. We show that most of the excised DNA consists of repetitive sequences that are either 1) verifiable transposable elements (TEs), or 2) non-simple repeats of likely TE origin. Repeat elements in both genomes are skewed towards younger (i.e. less divergent) elements. Excised DNA is a non-random sample of the germline repeat element landscape; younger elements, and high frequency DNA transposons and LINEs, are disproportionately eliminated from the somatic genome.ConclusionsOur results suggest that germline genome expansion inM. edaxreflects explosive repeat element proliferation, and that billions of base pairs of such repeats are deleted from the somatic genome every generation. Thus, we hypothesize that chromatin diminution is a mechanism that controls repeat element load, and that this load can evolve to be divergent between tissue types within single organisms.
Identification and characterization of cancer stem cells in human head and neck squamous cell carcinoma
Authors: Han Jing , Fujisawa Toshio , Husain Syed R , Puri Raj K 
Published: March 2014

Abstract

Background
Current evidence suggests that initiation, growth, and invasion of cancer are driven by a small population of cancer stem cells (CSC). Previous studies have identified CD44+ cells as cancer stem cells in head and neck squamous cell carcinoma (HNSCC). However, CD44 is widely expressed in most cells in HNSCC tumor samples and several cell lines tested. We previously identified a small population of CD24+/CD44+ cells in HNSCC. In this study, we examined whether this population of cells may represent CSC in HNSCC.

Methods
CD24+/CD44+ cells from HNSCC cell lines were sorted by flow cytometry, and their phenotype was confirmed by qRT-PCR. Their self-renewal and differentiation properties, clonogenicity in collagen gels, and response to anticancer drugs were tested in vitro. The tumorigenicity potential of CD24+/CD44+ cells was tested in athymic nude mice in vivo.

Results
Our results show that CD24+/CD44+ cells possessed stemness characteristics of self-renewal and differentiation. CD24+/CD44+ cells showed higher cell invasion in vitro and made higher number of colonies in collagen gels compared to CD24-/CD44+ HNSCC cells. In addition, the CD24+/CD44+ cells were more chemo-resistant to gemcitabine and cisplatin compared to CD24-/CD44+ cells. In vivo, CD24+/CD44+ cells showed a tendency to generate larger tumors in nude mice compared to CD24-/CD44+ cell population.

Conclusion
Our study clearly demonstrates that a distinct small population of CD24+/CD44+ cells is present in HNSCC that shows stem cell-like properties. This distinct small population of cells should be further characterized and may provide an opportunity to target HNSCC CSC for therapy.