bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of a behaviour change intervention on the diets and physical activity levels of women attending Sure Start Children’s Centres: results from a complex public health intervention
Authors: Baird Janis , Jarman Megan , Lawrence Wendy , Black Christina , Davies Jenny , Tinati Tannaze , Begum Rufia , Mortimore Andrew , Robinson Sian , Margetts Barrie , Cooper Cyrus , Barker Mary , Inskip Hazel 
Published: July 2014

ObjectivesThe UK government's response to the obesity epidemic calls for action in communities to improve people's health behaviour. This study evaluated the effects of a community intervention on dietary quality and levels of physical activity of women from disadvantaged backgrounds.DesignNon-randomised controlled evaluation of a complex public health intervention.Participants527 women attending Sure Start Children's Centres (SSCC) in Southampton (intervention) and 495 women attending SSCCs in Gosport and Havant (control).InterventionTraining SSCC staff in behaviour change skills that would empower women to change their health behaviours.OutcomesMain outcomesdietary quality and physical activity.Intermediate outcomesself-efficacy and sense of control.Results1-year post-training, intervention staff used skills to support behaviour change significantly more than control staff. There were statistically significant reductions of 0.1 SD in the dietary quality of all women between baseline and follow-up and reductions in self-efficacy and sense of control. The decline in self-efficacy and control was significantly smaller in women in the intervention group than in women in the control group (adjusted differences in self-efficacy and control, respectively, 0.26 (95% CI 0.001 to 0.50) and 0.35 (0.05 to 0.65)). A lower decline in control was associated with higher levels of exposure in women in the intervention group. There was a statistically significant improvement in physical activity in the intervention group, with 22.9% of women reporting the highest level of physical activity compared with 12.4% at baseline, and a smaller improvement in the control group. The difference in change in physical activity level between the groups was not statistically significant (adjusted difference 1.02 (0.74 to 1.41)).ConclusionsWhile the intervention did not improve women's diets and physical activity levels, it had a protective effect on intermediate factors—control and self-efficacy—suggesting that a more prolonged exposure to the intervention might improve health behaviour. Further evaluation in a more controlled setting is justified.
Is there a causal link between knee loading and knee osteoarthritis progression? A systematic review and meta-analysis of cohort studies and randomised trials
Authors: Henriksen Marius , Creaby Mark W , Lund Hans , Juhl Carsten , Christensen Robin 
Published: July 2014

ObjectiveWe performed a systematic review, meta-analysis and assessed the evidence supporting a causal link between knee joint loading during walking and structural knee osteoarthritis (OA) progression.DesignSystematic review, meta-analysis and application of Bradford Hill's considerations on causation.Data sourcesWe searched MEDLINE, Scopus, AMED, CINAHL and SportsDiscus for prospective cohort studies and randomised controlled trials (RCTs) from 1950 through October 2013.Study eligibility criteriaWe selected cohort studies and RCTs in which estimates of knee joint loading during walking were used to predict structural knee OA progression assessed by X-ray or MRI.Data analysesMeta-analysis was performed to estimate the combined OR for structural disease progression with higher baseline loading. The likelihood of a causal link between knee joint loading and OA progression was assessed from cohort studies using the Bradford Hill guidelines to derive a 0–4 causation score based on four criteria and examined for confirmation in RCTs.ResultsOf the 1078 potentially eligible articles, 5 prospective cohort studies were included. The studies included a total of 452 patients relating joint loading to disease progression over 12–72 months. There were very serious limitations associated with the methodological quality of the included studies. The combined OR for disease progression was 1.90 (95% CI 0.85 to 4.25; I2=77%) for each one-unit increment in baseline knee loading. The combined causation score was 0, indicating no causal association between knee loading and knee OA progression. No RCTs were found to confirm or refute the findings from the cohort studies.ConclusionsThere is very limited and low-quality evidence to support for a causal link between knee joint loading during walking and structural progression of knee OA.Trial registration numberCRD42012003253
Adding liraglutide to the backbone therapy of biguanide in patients with coronary artery disease and newly diagnosed type-2 diabetes (the AddHope2 study): a randomised controlled study protocol
Authors: Anholm Christian , Kumarathurai Preman , Klit Malene S , Kristiansen Ole P , Nielsen Olav W , Ladelund Steen , Madsbad Sten , Sajadieh Ahmad , Haugaard Steen B 
Published: July 2014

IntroductionNewly diagnosed type 2 diabetes mellitus (T2DM) in patients with coronary artery disease (CAD) more than doubles the risk of death compared with otherwise matched glucose tolerant patients. The biguanide metformin is the drug of choice in treatment of T2DM and has shown to ameliorate cardiovascular morbidity in patients with T2DM and myocardial infarction (MI). The incretin hormone, glucagon-like peptide-1 (GLP-1) improves β-cell function, insulin sensitivity and causes weight loss and has been suggested to have beneficial effects on cardiac function. The GLP-1 receptor agonist (GLP-1RA), liraglutide, is currently used for treatment of T2DM but its potential effect on cardiac function has not been investigated in detail. We hypothesised that liraglutide added to metformin backbone therapy in patients with CAD and newly diagnosed T2DM will improve β-cell function and left ventricular systolic function during dobutamine stress.Methods and analyses40 patients with CAD and newly diagnosed T2DM will receive the intervention liraglutide+metformin and placebo+metformin in this investigator-initiated, double blind, randomised, placebo-controlled, cross-over 12 plus 12 weeks intervention study with a 2-week washout period. The primary cardiovascular end point is changes in left ventricular ejection fraction during stress echocardiography. The primary endocrine end point is β-cell function evaluated during a frequently sampled intravenous glucose tolerance test. Secondary end points include heart rate variability, diurnal blood pressure, glucagon suppression and inflammatory response (urine, blood and adipose tissue).Ethics and disseminationThis study is approved by the Danish Medicines Agency, the Danish Dataprotection Agency and the Regional Committee on Biomedical Research Ethics of the Capital Region of Denmark. The trial will be carried out under the guidance from the GCP unit at Copenhagen University Hospital of Bispebjerg and in accordance with the ICH-GCP guidelines and the Helsinki Declaration.Trial registrations numberClinicaltrials.gov ID:NCT01595789, EudraCT: 2011-005405-78.
Wealth, income, and health before and after retirement
Authors: Geyer Siegfried , Spreckelsen Ove , von dem Knesebeck Olaf 
Published: July 2014

BackgroundIt was supposed that associations of wealth and health might be higher after retirement than in the economically active periods of life, but no comparisons were available. Most studies on wealth were based on net worth, a measure combining several elements of wealth into an index. We examined associations between different elements of wealth and health by comparing retired women and men with economically active ones.MethodData were drawn from the German Socio-Economic Panel, a nationwide longitudinal survey project. Two waves (2002 and 2007) included indicators of wealth in addition to household income and education. Wealth was not depicted by an index. Instead, debts, property of life insurances, home ownership and assets were considered separately with their associations with self-rated health. Two data sets were used to examine whether the results were occasional, or whether they can be replicated.ResultsAssociations of income and education emerged in respondents in their active periods of life. In most cases indicators of wealth were associated with subjective health. In retired respondents home ownership was the only indicator yielding consistent associations with health, but their sizes turned out as rather moderate.ConclusionsContrary to expectation, the associations of wealth and health were inconsistent in the retired study population. These results were obtained in a country with national pension schemes, and it has to be examined whether the findings can be generalised to other countries. The inconsistent findings of indicators of wealth are calling the utility of net worth into question.
Malarial Infection in HIV Infected Pregnant Women Attending a Rural Antenatal Clinic in Nigeria
Authors: Houmsou R. S. , Wama B. E. , Elkanah S. O. , Garba L. C. , Hile T. D. , Bingbeng J. B. , Kela S. L. , Amuta E. U. 
Published: July 2014

Malaria still remains a challenging infection affecting the lives of several HIV infected pregnant women in sub-Saharan Africa. This study was undertaken to determine malarial infection in HIV infected pregnant women in relation to sociodemographic and obstetrical factors. The study also assessed relationship between malarial infection and haemoglobin level, CD4+ counts, and ART regimen, as well as predisposing risk factors that influenced occurrence of malarial infection in the women. Thick and thin blood smears were prepared and stained with Giemsa. Haemoglobin level was determined using a hematology analyzer, while the flow cytometry was used to measure CD4+ counts. Sociodemographic and obstetrical parameters were obtained through the administration of questionnaires. Of the 159 HIV infected pregnant women examined, 33.3% (59/159) had malarial infection. Malarial infection was significantly higher in pregnant women who were divorced, 40.24% (33/82) (χ2=5.72; P=0.05), were at their first trimester (4–12 weeks), 54.8% (17/31) (χ2=14.85; P=0.01), had CD4+ = [201–500 cells/μL], 42.42% (42/99) (χ2=10.13; P=0.00), and those that had severe anaemia (<8 dg/L), 100.00% (χ2= 45.75; P=0.00). However, risk factors that influenced the occurrence of malarial infection in the pregnant women were occupation (farming) (AOR=0.226; P=0.03), marital status (divorced) (AOR=2.80; P=0.02), gestation (first trimester) (AOR=0.33; P=0.00), haemoglobin level (Hb < 8 dg/L) (AOR=0.02; P=0.00), and CD4+ counts (low CD4+) (OR=0.40; P=0.05). The study reported endemicity of malaria in HIV infected pregnant women living in rural areas of Benue State, Nigeria. Malarial infection was higher in women that were divorced, and at their first trimester, had low CD4+ count, and had severe anaemia. Farming, divorce, gestation, severe anaemia, and low CD4+ counts were predisposing risk factors that influenced malaria occurrence in the HIV infected pregnant women. It is advocated that HIV infected pregnant women should be properly and thoroughly educated on malaria preventive measures in rural areas so as to avoid unpleasant effect of malaria during their pregnancies.
Hypoxia Provokes Base Excision Repair Changes and a Repair-Deficient, Mutator Phenotype in Colorectal Cancer Cells
Authors: Chan Norman , Ali Mohsin , McCallum Gordon P. , Kumareswaran Ramya , Koritzinsky Marianne , Wouters Bradly G. , Wells Peter G. , Gallinger Steven , Bristow Robert G. 
Published: July 2014

Abstract
Regions of acute and chronic hypoxia exist within solid tumors and can lead to increased rates of mutagenesis and/or altered DNA damage and repair protein expression. Base excision repair (BER) is responsible for resolving small, non–helix-distorting lesions from the genome that potentially cause mutations by mispairing or promoting DNA breaks during replication. Germline and somatic mutations in BER genes, such as MutY Homolog (MUTYH/MYH) and DNA-directed polymerase (POLB), are associated with increased risk of colorectal cancer. However, very little is known about the expression and function of BER proteins under hypoxic stress. Using conditions of chronic hypoxia, decreased expression of BER proteins was observed because of a mechanism involving suppressed BER protein synthesis in multiple colorectal cancer cell lines. Functional BER was impaired as determined by MYH- and 8-oxoguanine (OGG1)–specific glycosylase assays. A formamidopyrimidine-DNA glycosylase (Fpg) Comet assay revealed elevated residual DNA base damage in hypoxic cells 24 hours after H2O2 treatment as compared with normoxic controls. Similarly, high-performance liquid chromatography analysis demonstrated that 8-oxo-2′-deoxyguanosine lesions were elevated in hypoxic cells 3 and 24 hours after potassium bromate (KBrO3) treatment when compared with aerobic cells. Correspondingly, decreased clonogenic survival was observed following exposure to the DNA base damaging agents H2O2 and MMS, but not to the microtubule interfering agent paclitaxel. Thus, a persistent downregulation of BER components by the microenvironment modifies and facilitates a mutator phenotype, driving genetic instability and cancer progression.
Implications: Aberrant BER is a contributing factor for the observed genetic instability in hypoxic tumor cells. Mol Cancer Res; 12(10); 1407–15. ©2014 AACR.
Elevated levels of D-dimers increase the risk of ischaemic and haemorrhagic stroke
Authors: Castelnuovo Augusto Di , Agnoli Claudia , Curtis Amalia de , Giurdanella Maria Concetta , Sieri Sabina , Mattiello Amalia , Matullo Giuseppe , Panico Salvatore , Sacerdote Carlotta , Tumino Rosario , Vineis Paolo , Gaetano Giovanni de , Donati Maria Benedetta , Iacoviello Licia 
Published: July 2014

SummaryElevated D-dimer levels are reportedly associated with coronary artery disease. It was the study objective to investigate the association of baseline D-dimer levels with strokes that occurred in the European Prospective Investigation into Cancer and Nutrition-Italy cohort. Using a nested case-cohort design, a centre-–stratified sample of 832 subjects (66 % women, age 35–71) was selected as subcohort and compared with 289 strokes in a mean follow-up of nine years. D-dimers were measured by an automated latex-enhanced immunoassay (HemosIL-IL). The multivariable hazard ratios were estimated by a Cox regression model using Prentice method. Individuals with elevated D-dimer levels had significantly higher risk of incident stroke. It was evident from the second quartile (D-dimers > 100 ng/ml) and persisted almost unchanged for higher D-dimers (hazard ratio [HR] 2.10, 95 % confidence interval [CI]: 1.28–3.47; 2.42, 95 %CI: 1.44–4.09 and 2.10, 95 %CI: 1.27–3.48 for the second, third or fourth quartile compared with the lowest quartile, respectively). The association was independent of several confounders, including triglycerides and C-reactive protein. No differences were observed in men and women (P for interaction= 0.46), in hypertensive or non-hypertensive subjects (P for interaction= 0.88) or in subjects with low (< 1 mg/l) or elevated (≥ 1 mg/l) C-reactive protein (P for interaction=0.35). After stratification for stroke type, the hazard ratio for every standard deviation increase was statistically significant both for ischaemic (1.21; 95 %CI: 1.01 to 1.45) and haemorrhagic (1.24; 95 %CI: 1.00 to 1.65) strokes. In conclusion, our data provide clear evidence that elevated levels of D-dimers are potential risk factors not only for ischaemic but also for haemorrhagic strokes.
Complement depletion with humanised cobra venom factor: Efficacy in preclinical models of vascular diseases
Authors: Fritzinger David , Gorsuch Brian , Stahl Gregory , Vogel Carl-Wilhelm 
Published: July 2014

SummaryThe complement system is an intrinsic part of the immune system and has important functions in both innate and adaptive immunity. On the other hand, inadvertent or misdirected complement activation is also involved in the pathogenesis of many diseases, contributing solely or significantly to tissue injury and disease development. Multiple approaches to develop pharmacological agents to inhibit complement are currently being pursued. We have developed a conceptually different approach of not inhibiting but depleting complement, based on the complement-depleting activities of cobra venom factor (CVF), a non-toxic cobra venom component with structural and functional homology to complement component C3. We developed a humanised version of CVF by creating human complement component C3 derivatives with complement-depleting activities of CVF (humanised CVF) as a promising therapeutic agent for diseases with complement pathogenesis. Here we review the beneficial therapeutic effect of humanised CVF in several murine models of vascular diseases such as reperfusion injury.
Protective effects of aliskiren and valsartan in mice with diabetic nephropathy
Authors: Wang Weidong , Qiu Liru , Howard Allison , Solis Nathaniel , Li Chunling , Wang Xiaoxin , Kopp Jeffrey B. , Levi Moshe 
Published: July 2014

Aim: We investigated whether aliskiren, a direct renin inhibitor, provided protection in a model of diabetic nephropathy in mice and compared its protective effects to valsartan, an angiotensin II type 1 receptor blocker. Materials and methods: Hyperglycemia was induced with streptozotocin (STZ, 40 mg/kg/day × 5 days) injection in DBA/2J mice fed on a high fat diet. Mice were treated with either aliskiren (25 mg/kg/day) or valsartan (8 mg/kg/day) for 6 weeks. Results: Aliskiren and/or valsartan treatment significantly attenuated albuminuria, urinary nephrin excretion and glomerulosclerosis. Aliskiren and/or valsartan prevented reduction of podocin and WT1 protein abundance in diabetic mice. Aliskiren and/or valsartan significantly prevented increased expression of profibrotic growth factors (TGFβ, CTGF and PAI-1), proinflammatory cytokines (MCP-1, TNFα and IL-1β), endoplasmic reticulum (ER) stress markers (CHOP and XBP-1) and lipid accumulation in the kidney of diabetic animals. Aliskiren showed similar efficacy compared to valsartan therapy and dual treatment in some aspects has synergistic protective effects. Conclusion: Our study indicates that aliskiren and/or valsartan protects against diabetic kidney disease through multiple mechanisms, including decreasing podocyte injury, activation of profibrotic growth factors and proinflammatory cytokines, ER stress and accumulation of lipids.
The microRNA-132/212 family fine-tunes multiple targets in Angiotensin II signalling in cardiac fibroblasts
Authors: Eskildsen Tilde V , Schneider Mikael , Sandberg Maria B , Skov Vibe , Brønnum Hasse , Thomassen Mads , Kruse Torben A , Andersen Ditte C , Sheikh Søren P 
Published: July 2014

Introduction: MicroRNAs (miRNAs) are emerging as key regulators of cardiovascular development and disease; however, the cardiac miRNA target molecules are not well understood. We and others have described the Angiotensin II (AngII)-induced miR-132/212 family as novel regulators of cardiovascular function including regulation of cardiac hypertrophy, heart failure and blood pressure possibly through AT1R signalling. However, the miR-132/212 targets in the heart remain unknown. Materials and methods: To understand the role of these miRNAs in cardiac signalling networks, we undertook comprehensive in silico and in vitro experiments to identify miR-132/212 molecular targets in primary rat cardiac fibroblasts. Results: MiR-132/212 overexpression increased fibroblast cell size and mRNA arrays detected several hundred genes that were differentially expressed, including a wide panel of receptors, signalling molecules and transcription factors. Subsequent comprehensive in silico analysis identified 24 target genes, of which 22 genes were qPCR validated. We identified seven genes involved in AngII signalling pathways. Conclusion: We here report novel insight of an extensive network of molecular pathways that fine-tuned by miR-132/212, suggesting a role for this miRNA family as master signalling switches in cardiac fibroblasts. Our data underscore the potential for miRNA tools to manipulate a large array of molecules and thereby control biological function.
Human CD68 promoter GFP transgenic mice allow analysis of monocyte to macrophage differentiation in vivo
Authors: Iqbal Asif J. , McNeill Eileen , Kapellos Theodore S. , Regan-Komito Daniel , Norman Sophie , Burd Sarah , Smart Nicola , Machemer Daniel E. W. , Stylianou Elena , McShane Helen , Channon Keith M. , Chawla Ajay , Greaves David R. 
Published: July 2014

Key PointsCD68-GFP reporter mice show GFP transgene expression in both monocytes and tissue resident macrophage populations. Adoptively transferred CD68-GFP monocytes maintain GFP expression after recruitment in an ongoing inflammatory response.
Sleep architecture and cognitive changes in olanzapine-treated patients with depression: A double blind randomized placebo controlled trial
Authors: Lazowski Lauren K , Townsend Ben , Hawken Emily R , Jokic Ruzica , du Toit Regina , Milev Roumen 
Published: July 2014

Abstract

Background
Disturbance in sleep quality is a symptom of Major Depressive Disorder (MDD) and Bipolar Disorder (BD) and thus improving quality of sleep is an important aspect of successful treatment. Here, a prospective, double-blind, randomized, placebo-controlled study examined the effect of olanzapine (an atypical antipsychotic) augmentation therapy on sleep architecture, specifically slow wave sleep (SWS), in the treatment of depression. The effect of olanzapine augmentation therapy on other features of sleep (e.g., sleep continuity) and depression (e.g., illness severity and cognitive function) were also determined.

Methods
Patients currently experiencing a major depressive episode and who were on a stable medication were included. Sleep architecture was measured by overnight ambulatory polysomnography. Illness severity was determined using the Montgomery-Asberg Depression Rating Scale (MADRS). Cognitive function was examined using Cambridge Neuropsychological Test Automated Battery (CANTAB): Spatial Working Memory (SWM), Spatial Span (SSP), and Reaction Time (RTI) tasks. Polysomnographs, clinical measures and cognitive tests were administered at baseline, after 2–4 days of treatment and after 28–31 days of treatment. Twenty-five patients participated in the study (N = 10, N = 15 for placebo and olanzapine treated groups respectively).

Results
The primary objective of the study was to assess the objective (polysomnographic) changes in sleep quality, defined as changes in SWS, following olanzapine treatment for depression. Latency to but not duration of SWS was found to significantly differ between olanzapine- and placebo-treated participants (Hedge’s g: 0.97, 0.13 respectively). A significant improvement in olanzapine-treated participants over placebo-treated participants was observed in secondary outcome measures, including sleep efficiency, total sleep time, and sleep latency. Secondary objectives assessed the subjective changes in sleep quality parameters and correlated them with measures of illness severity and changes in cognition. MADRS scores were significantly improved in olanzapine-treated participants over time but not more than placebo treatment. There was no significant difference between olanzapine- and placebo-treated participants in SWM, SSP or RTI tasks.

Conclusions
Olanzapine augmentation treatment generally did not improve SWS but did improve sleep continuity and depression. Olanzapine may be one of few medications that improve sleep continuity, thus directly targeting symptoms of depression.

Trial registration
ClinicalTrials.gov, NCT00520507.