bluuebunny/crossref_metadata_2025_split huggingface dataset:
A scoping review protocol to map the research foci trends in tobacco control over the last decade
Authors: Halas Gayle , Schultz Annette S H , Rothney Janet , Goertzen Leah , Wener Pamela , Katz Alan 
Published: January 2015

IntroductionTobacco dependence and smoke exposure have been global epidemics with health consequences recognised by the US Surgeon General since the 1960s and 1970s, respectively. During this period, a vast body of research evidence has emerged including many reviews of primary research studies targeting various tobacco control strategies. Published review studies synthesise primary evidence, providing a rich source for mapping the broad range of topics and research foci along with revealing areas of evidence deficits. In this paper, we outline our scoping review protocol to systematically review published review articles specific to tobacco control and primary prevention over the last 10 years.Methods and analysisUsing Arksey and O'Malley's scoping review methodology as a guide, our scoping review of published reviews begins by searching several databases: PubMed, Scopus, the Cochrane Library, the Cumulative Index to Nursing and Allied Health Literature (CINAHL), PsycInfo and the Educational Resources Information Centre (ERIC). Our multidisciplinary team has formulated search strategies and two reviewers will independently screen eligible studies for final study selection. Bibliographic data and abstract content will be collected and analysed using a tool developed iteratively by the research team.Ethics and disseminationA scoping review of published review articles is a novel approach for examining the breadth of literature regarding tobacco control strategies and, as a secondary analysis, does not require ethics approval. We anticipate results will identify research gaps as well as novel ideas for primary prevention research specific to tobacco control strategies concerning intervention, programming and policy. Although this is our first step in establishing a foundation for a research agenda, we will be disseminating results through journals and conferences targeting primary care providers and tobacco control.
Use of wind-up fetal Doppler versus Pinard for fetal heart rate intermittent monitoring in labour: a randomised clinical trial
Authors: Byaruhanga R , Bassani D G , Jagau A , Muwanguzi P , Montgomery A L , Lawn J E 
Published: January 2015

ObjectivesIn resource-poor settings, the standard of care to inform labour management is the partograph plus Pinard stethoscope for intermittent fetal heart rate (FHR) monitoring. We compared FHR monitoring in labour using a novel, robust wind-up handheld Doppler with the Pinard as a primary screening tool for abnormal FHR on perinatal outcomes.DesignProspective equally randomised clinical trial.SettingThe labour and delivery unit of a teaching hospital in Kampala, Uganda.ParticipantsOf the 2042 eligible antenatal women, 1971 women in active term labour, following uncomplicated pregnancies, were randomised to either the standard of care or not.InterventionIntermittent FHR monitoring using Doppler.Primary outcome measuresIncidence of FHR abnormality detection, intrapartum stillbirth and neonatal mortality prior to discharge.ResultsAge, parity, gestational age, mode of delivery and newborn weight were similar between study groups. In the Doppler group, there was a significantly higher rate of FHR abnormalities detected (incidence rate ratio (IRR)=1.61, 95% CI 1.13 to 2.30). However, in this group, there were also higher though not statistically significant rates of intrapartum stillbirths (IRR=3.94, 0.44 to 35.24) and neonatal deaths (IRR=1.38, 0.44 to 4.34).ConclusionsRoutine monitoring with a handheld Doppler increased the identification of FHR abnormalities in labour; however, our trial did not find evidence that this leads to a decrease in the incidence of intrapartum stillbirth or neonatal death.Trial registration numberClinical Trails.gov (1000031587).
Prevalence of smoking restrictions and child exposure to secondhand smoke in cars and homes: a repeated cross-sectional survey of children aged 10–11 years in Wales
Authors: Moore Graham F , Moore Laurence , Littlecott Hannah J , Ahmed Nilufar , Lewis Sophia , Sulley Gillian , Jones Elen , Holliday Jo 
Published: January 2015

ObjectiveSmall increases in smoking restrictions in cars and homes were reported after legislation prohibiting smoking in public places. Few studies examine whether these changes continued in the longer term. This study examines changes in restrictions on smoking in cars and homes, and child exposure to secondhand smoke (SHS) in these locations, since 2008 postlegislation surveys in Wales.SettingState-maintained primary schools in Wales (n=75).ParticipantsChildren aged 10–11 years (year 6) completed CHETS (CHild exposure to Environmental Tobacco Smoke) Wales surveys in 2007 (n=1612) and 2008 (n=1605). A replication survey (CHETS Wales 2) was conducted in 2014, including 1601 children.Primary outcome variableChildren's reports of whether smoking was allowed in their car or home and exposure to SHS in a car or home the previous day.ResultsThe percentage of children who reported that smoking was allowed in their family vehicle fell from 18% to 9% in 2014 (OR=0.42; 95% CI 0.33 to 0.54). The percentage living in homes where smoking was allowed decreased from 37% to 26% (OR=0.30; 95% CI 0.20 to 0.43). Among children with a parent who smoked, one in five and one in two continued to report that smoking was allowed in their car and home. The percentage reporting SHS exposure in a car (OR=0.52; 95% CI 0.38 to 0.72) or home (OR=0.44; 95% CI 0.36 to 0.53) the previous day also fell. Children from poorer families remained less likely to report smoking restrictions.ConclusionsSmoking in cars and homes has continued to decline. Substantial numbers of children continue to report that smoking is allowed in cars and homes, particularly children from poorer families. A growing number of countries have legislated, or plan to legislate, banning smoking in cars carrying children. Attention is needed to the impact of legislation on child health and health inequalities, and reducing smoking in homes.
Placebo effects in trials evaluating 12 selected minimally invasive interventions: a systematic review and meta-analysis
Authors: Holtedahl Robin , Brox Jens Ivar , Tjomsland Ole 
Published: January 2015

ObjectivesTo analyse the impact of placebo effects on outcome in trials of selected minimally invasive procedures and to assess reported adverse events in both trial arms.DesignA systematic review and meta-analysis.Data sources and study selectionWe searched MEDLINE and Cochrane library to identify systematic reviews of musculoskeletal, neurological and cardiac conditions published between January 2009 and January 2014 comparing selected minimally invasive with placebo (sham) procedures. We searched MEDLINE for additional randomised controlled trials published between January 2000 and January 2014.Data synthesisEffect sizes (ES) in the active and placebo arms in the trials’ primary and pooled secondary end points were calculated. Linear regression was used to analyse the association between end points in the active and sham groups. Reported adverse events in both trial arms were registered.ResultsWe included 21 trials involving 2519 adult participants. For primary end points, there was a large clinical effect (ES≥0.8) after active treatment in 12 trials and after sham procedures in 11 trials. For secondary end points, 7 and 5 trials showed a large clinical effect. Three trials showed a moderate difference in ES between active treatment and sham on primary end points (ES ≥0.5) but no trials reported a large difference. No trials showed large or moderate differences in ES on pooled secondary end points. Regression analysis of end points in active treatment and sham arms estimated an R2of 0.78 for primary and 0.84 for secondary end points. Adverse events after sham were in most cases minor and of short duration.ConclusionsThe generally small differences in ES between active treatment and sham suggest that non-specific mechanisms, including placebo, are major predictors of the observed effects. Adverse events related to sham procedures were mainly minor and short-lived. Ethical arguments frequently raised against sham-controlled trials were generally not substantiated.
The boarding experience from the patient perspective: the wait
Authors: Liu Shan , Milne Leslie , Yun Brian , Walsh Kathleen 
Published: January 2015

Study objectiveWe sought to better understand the experience of being a boarder patient.MethodsWe conducted a qualitative study between March and August 2012 to examine the experience of boarding in an urban, teaching hospital emergency department (ED). We included boarder patients and selected patients based on a convenience sample. Interviews were semistructured, consisting of eight main open-ended questions. Interviews were transcribed; codes were generated and then organised into categorises and subsequently into one theme. We concluded analysis when we achieved thematic saturation. Our institutional review board approved this study.ResultsOur final sample included 18 patients. The average age was 62.3 years. Patients characterised waiting as central to their experience as a boarder patient. One patient stated, “Well if you have to wait for a bed you have to wait for a bed, it's terrible.” Three categories exemplified this waiting experience: (1) there was often lack of communication; (2) patients experienced frustration during this waiting period; and yet (3) patients often differentiated the experience of waiting from the care they were receiving.ConclusionsBeing a boarder patient was characterised as a waiting experience associated with poor communication and frustration. However, patients may still differentiate their feelings towards the wait from those towards the medical care they are receiving. Our data add more reason to eradicate the practice of ED boarding.
Proteins of the mitotic checkpoint and spindle are related to chromosomal instability and unfavourable prognosis in patients with myelodysplastic syndrome
Authors: Genga Kelly Roveran , Filho Francisco Dário Rocha , Ferreira Francisco Valdeci de Almeida , de Sousa Juliana Cordeiro , Studart Fernando Sergio , Magalhães Silvia Maria Meira , Heredia Fabíola Fernandes , Pinheiro Ronald Feitosa 
Published: January 2015

AimsTo study the immunoexpression of proteins related to the mitotic checkpoint (cell division cycle 20 (CDC20), mitotic arrest deficient 2 (MAD2)) and the mitotic spindle (Aurora-B) in patients with myelodysplastic syndrome (MDS).MethodsProtein expression was analysed in bone marrow tissue samples from 40 patients with MDS using immunohistochemistry. Prognostic markers (transfusion dependency, depth of cytopenias, chromosomal abnormalities and survival) were also studied.ResultsHigher MAD2 expression was observed among patients with platelets <50×109/L than among patients with platelets ≥50×109/L (42.6±22.8% vs 22.7±19.1%, respectively). Higher CDC20 expression was identified among patients with three dysplasias compared with patients who presented with one or two dysplasias (33.9±24.1% vs 10.5±5.7% vs 12.8±7.8%, respectively), among patients who exhibited a complex versus non-complex karyotype (50.0±30.2% vs 18.4±14%, respectively) and among patients with platelets <50×109/L vs platelets ≥50×109/L (38.2±26.2% vs 16.1±12.4%, respectively). Higher Aurora-B expression was found in patients with an abnormal versus normal karyotype (21.2±13.2% vs 7.5±5.0%, respectively). High expression of MAD2 and CDC20 (≥50%) was associated with severe thrombocytopenia. We also found statistically significant differences in the overall survival rate when comparing different degrees of CDC20, MAD2 and Aurora-B protein expression.ConclusionsTo the best of our knowledge, this is the first report to demonstrate that these proteins are associated with chromosomal abnormalities and poor prognosis in patients with MDS.
Associations of financial strain and income with depressive and anxiety disorders
Authors: Dijkstra-Kersten Sandra M A , Biesheuvel-Leliefeld Karolien E M , van der Wouden Johannes C , Penninx Brenda W J H , van Marwijk Harm W J 
Published: January 2015

BackgroundPrevious research has shown socioeconomic inequality in prevalence and onset of depressive disorders. It is not yet clear whether perceived financial strain is associated with depressive and/or anxiety disorders in addition to an objective indicator, such as income. This study examines whether financial strain is associated with the prevalence and onset/recurrence of depressive and/or anxiety disorders, above income.MethodsData are from the Netherlands Study of Depression and Anxiety. Associations between financial strain, income and presence of depressive and/or anxiety disorder at baseline were assessed among 2937 participants (18–65 years). Impact of financial strain and income on 4-year onset/recurrence of depressive and/or anxiety disorders were examined among 1250 participants without a depressive or anxiety disorder at baseline. Depressive and anxiety disorders were determined with the Composite-International-Diagnostic-Interview. Financial strain and income were assessed in an interview.ResultsParticipants with mild or severe financial strain had higher odds of being depressed (OR=1.68, 95% CI 1.35 to 2.09; OR=3.88, 95% CI 2.58 to 5.81) or remitted (OR=1.56, 95% CI 1.24 to 1.96; OR=1.99, 95% CI 1.27 to 3.11) at baseline compared with healthy controls, after adjusting for income. Mild or severe financial strain was not associated with onset/recurrence of depressive and/or anxiety disorders during follow-up (OR=1.08, 95% CI 0.83 to 1.42; OR=1.05, 95% CI 0.64 to 1.73).ConclusionsFinancial strain was associated with having a depressive and/or anxiety disorder, above the effect of income. Healthcare and social services should be alert to this association, even for higher income households. However, financial strain and income were not related with 4-year onset/recurrence of depressive and/or anxiety disorders.
Partial ablation of a para‐ureteral pseudocyst without ureteronephrectomy in a cat
Authors: Rossanese Matteo 
Published: January 2015

A three‐year‐old, male neutered, domestic shorthair cat was presented eight weeks after a road traffic accident with abdominal pain, lethargy and anorexia. Clinical examination was suggestive of a mass in the right retroperitoneal space. Survey radiographs and abdominal ultrasonography confirmed the presence of a cavitated fluid‐filled lesion in the left retroperitoneal area consistent with a suspected paraureteral pseudocyst. Based on these findings, an exploratory laparotomy was performed. Surgical management included partial resection and omentalisation of the pseudocyst without ureteronephrectomy. The patient recovered well after surgery and the clinical signs resolved completely after 24 hours. One, three and six months after surgery, the cat was reportedly well. In the presence of a healthy kidney with maintained renal function, an attempt to preserve the kidney and ureter should be made.
Polymorphic CAG Repeat and Protein Expression of Androgen Receptor Gene in Colorectal Cancer
Authors: Huang Rui , Wang Guiyu , Song Yanni , Wang Feng , Zhu Bing , Tang Qingchao , Liu Zheng , Chen Yinggang , Zhang Qian , Muhammad Shan , Wang Xishan 
Published: January 2015

Abstract
Although somatic alterations in CAG repeats in the androgen receptor (AR) gene have been suggested to predispose to colorectal cancer, less is known about AR in colorectal cancer carcinogenesis. Because of lack of relevant analysis on CAG repeat length and AR expression in colorectal cancer, we aimed to investigate the prognostic value of polymorphic CAG and protein expression of the AR gene in patients with colorectal cancer. A case–control study was carried out on 550 patients with colorectal cancer and 540 healthy controls to investigate whether polymorphic CAG within the AR gene is linked to increased risk for colorectal cancer. Polymorphic CAG and AR expression were analyzed to clarify their relationship with clinicopathologic and prognostic factors in patients with colorectal cancer. The study showed that the AR gene in patients with colorectal cancer had a longer CAG repeat sequence than those in the control group, as well as increased risk for colorectal cancer among females (P = 0.013), males (P = 0.002), and total colorectal cancer population (P &lt; 0.001), respectively. AR expression exhibited a significant difference in long CAG repeat sequence among males (P &lt; 0.001), females (P &lt; 0.001), and total colorectal cancer study population (P &lt; 0.001). Both long CAG repeat sequence and negative AR expression were associated with a short 5-year overall survival (OS) rate in colorectal cancer. Long CAG repeat sequences and the absence of AR expression were closely related to the development of colorectal cancer. Both long CAG and decreased AR expression were correlated with the poor 5-year OS in patients with colorectal cancer. Mol Cancer Ther; 14(4); 1066–74. ©2015 AACR.
The Selective PI3K Inhibitor XL147 (SAR245408) Inhibits Tumor Growth and Survival and Potentiates the Activity of Chemotherapeutic Agents in Preclinical Tumor Models
Authors: Foster Paul , Yamaguchi Kyoko , Hsu Pin P. , Qian Fawn , Du Xiangnan , Wu Jianming , Won Kwang-Ai , Yu Peiwen , Jaeger Christopher T. , Zhang Wentao , Marlowe Charles K. , Keast Paul , Abulafia Wendy , Chen Jason , Young Jenny , Plonowski Artur , Yakes F. Michael , Chu Felix , Engell Kelly , Bentzien Frauke , Lam Sanh T. , Dale Stephanie , Yturralde Olivia , Matthews David J. , Lamb Peter , Laird A. Douglas 
Published: January 2015

Abstract
Dysregulation of PI3K/PTEN pathway components, resulting in hyperactivated PI3K signaling, is frequently observed in various cancers and correlates with tumor growth and survival. Resistance to a variety of anticancer therapies, including receptor tyrosine kinase (RTK) inhibitors and chemotherapeutic agents, has been attributed to the absence or attenuation of downregulating signals along the PI3K/PTEN pathway. Thus, PI3K inhibitors have therapeutic potential as single agents and in combination with other therapies for a variety of cancer indications. XL147 (SAR245408) is a potent and highly selective inhibitor of class I PI3Ks (α, β, γ, and δ). Moreover, broad kinase selectivity profiling of &gt;130 protein kinases revealed that XL147 is highly selective for class I PI3Ks over other kinases. In cellular assays, XL147 inhibits the formation of PIP3 in the membrane, and inhibits phosphorylation of AKT, p70S6K, and S6 in multiple tumor cell lines with diverse genetic alterations affecting the PI3K pathway. In a panel of tumor cell lines, XL147 inhibits proliferation with a wide range of potencies, with evidence of an impact of genotype on sensitivity. In mouse xenograft models, oral administration of XL147 results in dose-dependent inhibition of phosphorylation of AKT, p70S6K, and S6 with a duration of action of at least 24 hours. Repeat-dose administration of XL147 results in significant tumor growth inhibition in multiple human xenograft models in nude mice. Administration of XL147 in combination with chemotherapeutic agents results in antitumor activity in xenograft models that is enhanced over that observed with the corresponding single agents. Mol Cancer Ther; 14(4); 931–40. ©2015 AACR.
The Genetics of Splicing in Neuroblastoma
Authors: Chen Justin , Hackett Christopher S. , Zhang Shile , Song Young K. , Bell Robert J.A. , Molinaro Annette M. , Quigley David A. , Balmain Allan , Song Jun S. , Costello Joseph F. , Gustafson W. Clay , Van Dyke Terry , Kwok Pui-Yan , Khan Javed , Weiss William A. 
Published: January 2015

Abstract
Regulation of mRNA splicing, a critical and tightly regulated cellular function, underlies the majority of proteomic diversity and is frequently disrupted in disease. Using an integrative genomics approach, we combined both genomic data and exon-level transcriptome data in two somatic tissues (cerebella and peripheral ganglia) from a transgenic mouse model of neuroblastoma, a tumor that arises from the peripheral neural crest. Here, we describe splicing quantitative trait loci associated with differential splicing across the genome that we use to identify genes with previously unknown functions within the splicing pathway and to define de novo intronic splicing motifs that influence splicing from hundreds of bases away. Our results show that these splicing motifs represent sites for functional recurrent mutations and highlight novel candidate genes in human cancers, including childhood neuroblastoma.
Significance: Somatic mutations with predictable downstream effects are largely relegated to coding regions, which comprise less than 2% of the human genome. Using an unbiased in vivo analysis of a mouse model of neuroblastoma, we have identified intronic splicing motifs that translate into sites for recurrent somatic mutations in human cancers. Cancer Discov; 5(4); 380–95. ©2015 AACR.
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Systemic Agonistic Anti-CD40 Treatment of Tumor-Bearing Mice Modulates Hepatic Myeloid-Suppressive Cells and Causes Immune-Mediated Liver Damage
Authors: Medina-Echeverz José , Ma Chi , Duffy Austin G. , Eggert Tobias , Hawk Nga , Kleiner David E. , Korangy Firouzeh , Greten Tim F. 
Published: January 2015

Abstract
Immune-stimulatory mAbs are currently being evaluated as antitumor agents. Although overall toxicity from these agents appears to be moderate, liver toxicities have been reported and are not completely understood. We studied the effect of systemic CD40 antibody treatment on myeloid cells in the spleen and liver. Naïve and tumor-bearing mice were treated systemically with agonistic anti-CD40 antibody. Immune cell subsets in the liver and spleen, serum transaminases, and liver histologies were analyzed after antibody administration. Nox2−/−, Cd40−/−, and bone marrow chimeric mice were used to study the mechanism by which agonistic anti-CD40 mediates its effects in vivo. Suppressor function of murine and human tumor-induced myeloid-derived suppressor cells (MDSC) was studied upon CD40 ligation. Agonistic CD40 antibody caused liver damage within 24 hours after injection in two unrelated tumor models and mice strains. Using bone marrow chimeras, we demonstrate that CD40 antibody–induced hepatitis in tumor-bearing mice was dependent on the presence of CD40-expressing hematopoietic cells. Agonistic CD40 ligation–dependent liver damage was induced by the generation of reactive oxygen species. Furthermore, agonistic CD40 antibody resulted in increased CD80-positive and CD40-positive liver CD11b+Gr-1+ immature myeloid cells. CD40 ligation on tumor-induced murine and human CD14+HLA-DRlow peripheral blood mononuclear cells from patients with cancer reduced their immune suppressor function. Collectively, agonistic CD40 antibody treatment activated tumor-induced myeloid cells, caused myeloid-dependent hepatotoxicity, and ameliorated the suppressor function of murine and human MDSC. Collectively, our data suggest that CD40 may mature immunosuppressive myeloid cells and thereby cause liver damage in mice with an accumulation of tumor-induced hepatic MDSC. Cancer Immunol Res; 3(5); 557–66. ©2015 AACR.