bluuebunny/crossref_metadata_2025_split huggingface dataset:
Factors affecting the compliance of Israeli women with screening for intimate partner violence
Authors: Ben Natan Merav , Abramov Luda , Dhokarker Avigail , Israelov Etery 
Published: April 2013

Violence against women has become a frequent occurrence. In Israel, some 200 000 women are subjected to various types of violence by their intimate partners annually. Routine screening for intimate partner violence is endorsed by the Ministry of Health in Israel; however, screening rates in health‐care settings remain problematic. This study aimed to examine whether the model based on the Theory of Reasoned Action (TRA) succeeds in predicting women's intention to comply with screening for intimate partner violence.A questionnaire based on the literature review and research model was administered to a convenience sample of 200 married women. Although only 4.5% (n = 9) of respondents were screened for violence at various health‐care institutions over the past year, 75% (n = 150) of women declared that they intend to cooperate with screening. A positive correlation was found between women's marriage duration, beliefs concerning violence, attitudes towards screening, family member support for compliance with screening—and women's intention to comply with screening. The TRA succeeds in partially predicting women's intention to comply with screening.
New insights into osteoporosis: the bone–fat connection
Authors: Kawai M. , de Paula F. J. A. , Rosen C. J. 
Published: April 2013

Kawai M, de Paula FJA, Rosen CJ (Osaka Medical Center and Research Institute for Maternal and Child Health, Izumi, Osaka, Japan; University of São Paulo, Ribeirão Preto, SP, Brazil; and Maine Medical Center Research Institute, Scarborough, ME, USA). New insights into osteoporosis: the bone–fat connection (Review). J Intern Med 2012; 272: 317–329.Abstract.  Osteoporosis and obesity are chronic disorders that are both increasing in prevalence. The pathophysiology of these conditions is multifactorial and includes genetic, environmental and hormonal determinants. Although it has long been considered that these are distinct disorders rarely found in the same individual, emerging evidence from basic and clinical studies support an important interaction between adipose tissue and the skeleton. It is proposed that adiposity may influence bone remodelling through three mechanisms: (i) secretion of cytokines that directly target bone, (ii) production of adipokines that influence the central nervous system thereby changing sympathetic impulses to bone and (iii) paracrine influences on adjacent skeletal cells. Here we focus on the current understanding of bone–fat interactions and the clinical implications of recent studies linking obesity to osteoporosis.
Targeting T‐cell migration in inflammatory bowel disease
Authors: Marsal J. , Agace W. W. 
Published: April 2013

AbstractCrohn's disease and ulcerative colitis are chronic inflammatory disorders of the gastrointestinal tract and are collectively referred to as inflammatory bowel disease (IBD). IBD is a major cause of lifetime morbidity, has a severe impact on quality of life of patients (equivalent to that of rheumatoid arthritis, asthma, migraine or diabetes) and constitutes a substantial economic burden to the healthcare system. The introduction of anti‐tumour necrosis factor (TNF) antibodies has dramatically improved the treatment of IBD, but approximately one‐third of patients are nonresponders and another 30–50% will eventually lose the therapeutic effect or become intolerant to these antibodies. Thus, there is an urgent and unmet need for new therapies. The aetiologies of the different forms of IBD have not been fully elucidated but there is strong evidence implicating T cells and T‐cell migration to the gut in initiating and perpetuating the intestinal inflammatory process and tissue destruction. In recent years, progress in basic science has shed light on the mechanisms regulating T‐cell migration to the gut and new therapeutics targeting these pathways have been developed. It is interesting that some of the factors directing the localization of T cells to the gut have been shown to be relatively organ specific, potentially enabling new T‐cell‐targeted treatments to demonstrate improved safety whilst preserving therapeutic efficacy. Here, fundamental aspects of the gut immune system, the generation of tissue‐tropic effector T cells and the mechanisms of T‐cell trafficking to the gut mucosa will be reviewed. In addition, the role of these processes in IBD and how they have been exploited for the development of novel therapies for IBD will be discussed.
Lipoprotein(a): resurrected by genetics
Authors: Kronenberg F. , Utermann G. 
Published: April 2013

AbstractPlasma lipoprotein(a) [Lp(a)] is a quantitative genetic trait with a very broad and skewed distribution, which is largely controlled by genetic variants at the LPA locus on chromosome 6q27. Based on genetic evidence provided by studies conducted over the last two decades, Lp(a) is currently considered to be the strongest genetic risk factor for coronary heart disease (CHD). The copy number variation of kringle IV in the LPA gene has been strongly associated with both Lp(a) levels in plasma and risk of CHD, thereby fulfilling the main criterion for causality in a Mendelian randomization approach. Alleles with a low kringle IV copy number that together have a population frequency of 25–35% are associated with a doubling of the relative risk for outcomes, which is exceptional in the field of complex genetic phenotypes. The recently identified binding of oxidized phospholipids to Lp(a) is considered as one of the possible mechanisms that may explain the pathogenicity of Lp(a). Drugs that have been shown to lower Lp(a) have pleiotropic effects on other CHD risk factors, and an improvement of cardiovascular endpoints is up to now lacking. However, it has been established in a proof of principle study that lowering of very high Lp(a) by apheresis in high‐risk patients with already maximally reduced low‐density lipoprotein cholesterol levels can dramatically reduce major coronary events.
Severity of overactive bladder symptoms and response to dose escalation in a randomized, double‐blind trial of solifenacin (SUNRISE)
Authors: Cardozo Linda , Amarenco Gerard , Pushkar Dmitry , Mikulas Jura , Drogendijk Ted , Wright Mark , Compion Gerhard ,   SUNRISE Study Group
Published: April 2013

What's known on the subject? and What does the study add?
Antimuscarinics are effective and well tolerated for treatment of OAB. Studies have found that a flexible dosing strategy can be effective in improving OAB symptoms with minimal impact on tolerability.
This study confirms these findings with two doses of solifenacin, and shows that improved outcomes can be achieved by increasing solifenacin dose (from 5 to 10 mg) in patients with more severe symptoms.
Objective
To determine the relationship between severity of baseline overactive bladder (OAB) symptoms and requests for solifenacin dose increases, and the efficacy of 5 and 10 mg solifenacin doses in relieving OAB symptoms in patients who requested a dose increase.
Patients and Methods
In a 16‐week clinical study, patients with OAB were randomized to double‐blind treatment with solifenacin or placebo once daily.
At week 8, all patients could request a dose increase; these patients entered a second phase of 8 weeks in which those in the solifenacin group were randomized to either 5 or 10 mg doses.
The primary efficacy variable was mean change in the number of urgency episodes with or without incontinence per 24 h, measured using the Patient Perception of Intensity of Urgency Scale (PPIUS; grades 3 and 4).
Results
Of 591 patients receiving solifenacin at 8 weeks, 275 (46.5%) requested a dose increase to 10 mg, and were further randomized to receive 10 mg (n = 140) or to remain on 5 mg (n = 135).
Patients who requested a dose increase at week 8 generally had more severe OAB symptoms at baseline and a smaller response at week 8 to the initial solifenacin 5 mg dosage than those who did not.
Greater reductions in the mean number of severe urgency episodes (PPIUS grades 3 and 4) were observed from week 8 to the end of treatment for patients requesting a dose increase and randomized to 10 mg solifenacin compared with those randomized to remain on 5 mg (mean reductions –0.9 vs –0.4, respectively), although these did not reach statistical significance.
Statistically significant reductions were observed in mean total urgency score (TUS; –2.7 vs –0.6; P = 0.010), mean maximum PPIUS urgency rating (–0.3 vs –0.1; P = 0.034) and mean micturition frequency (–0.8 vs –0.1; P = 0.037). For all other OAB variables, greater changes were observed in the solifenacin 10 mg group but these did not reach statistical significance.
Of those who requested a dose increase, eight (5.7%) patients randomized to receive 10 mg and one (0.7%) patient randomized to remain on 5 mg reported new or worsening cases of dry mouth.
Conclusions
Increasing the solifenacin dose to 10 mg further improved OAB symptoms in patients who requested a dose increase after 8 weeks' treatment with 5 mg solifenacin.
The present study supports the view that patients with severe OAB symptoms benefit from a higher antimuscarinic dose.
Combined Dominant Frequency and Complex Fractionated Atrial Electrogram Ablation After Circumferential Pulmonary Vein Isolation of Atrial Fibrillation
Authors: KUMAGAI KOJI , SAKAMOTO TAMOTSU , NAKAMURA KEIJIRO , NISHIUCHI SUGURU , HAYANO MAMORU , HAYASHI TATSUYA , SASAKI TAKEHITO , AONUMA KAZUTAKA , OSHIMA SHIGERU 
Published: April 2013

Dominant Frequency‐Based Ablation of Atrial FibrillationIntroductionAtrial substrates with high‐dominant frequency (DF) and complex fractionated atrial electrogram (CFAE) sites have sources maintaining atrial fibrillation (AF) and are potential AF ablation targets. This study aimed to evaluate an approach of circumferential pulmonary vein isolation (PVI) followed by a DF and CFAE site ablation.Methods and ResultsFifty consecutive AF patients (23 paroxysmal, 9 persistent, and 18 longstanding persistent) underwent ablation, using NavX. When AF continued after circumferential PVI, high‐DF sites of ≥8 Hz and then continuous left atrial (LA) CFAE sites defined by fractionated intervals (FI) of ≤50 milliseconds including the coronary sinus and right atrium were targeted. A total of 45.1% of high‐DF and 48.1% of continuous CFAE sites significantly decreased after PVI (P < 0.001). The mean LA DF and FI significantly decreased and prolonged, respectively, after PVI (P < 0.001). Only 14.1% of all high‐DF sites after PVI overlapped with continuous CFAE sites. AF terminated at high‐DF sites in 11 (22%) patients and continuous CFAE sites in 1 (2%). AF could be induced in only 8% of patients after the procedure. The mean LA DF value before ablation was significantly lower in those without recurrence (P = 0.003). AF freedom on antiarrhythmic drugs was 96% and 59%, respectively, in the paroxysmal and nonparoxysmal AF patients (89% persistent and 44% longstanding persistent) after 1 procedure over a 12‐month follow‐up.ConclusionsA combined high‐DF and continuous CFAE site ablation in all chambers after circumferential PVI may be effective in the paroxysmal and persistent AF patients.
Effects of Electrical Stimulation of Carotid Baroreflex and Renal Denervation on Atrial Electrophysiology
Authors: LINZ DOMINIK , MAHFOUD FELIX , SCHOTTEN ULRICH , UKENA CHRISTIAN , NEUBERGER HANS‐RUPRECHT , WIRTH KLAUS , BÖHM MICHAEL 
Published: April 2013

Renal Denervation and Baroreflex StimulationIntroductionThis study was designed to compare the effect of electrical baroreflex stimulation (BRS) at an intensity used in hypertensive patients and renal denervation (RDN) on atrial electrophysiology. BRS and RDN reduce blood pressure and global sympathetic drive in patients with resistant hypertension. Whereas RDN decreases sympathetic renal afferent nerve activity, leading to decreased central sympathetic drive, BRS modulates autonomic balance by activation of the baroreflex, resulting in both reduced sympathetic drive and increased vagal activation. Increased vagal tone potentially shortens atrial refractoriness resulting in a stabilization of reentry circuits perpetuating atrial fibrillation (AF).Methods and ResultsIn normotensive anesthetized pigs (n = 12), we compared the acute effect of BRS and RDN on blood pressure, atrial effective refractory period (AERP), and inducibility of AF. Electrical BRS was titrated to result in comparable heart rate and blood pressure reduction compared to irreversible RDN. BRS resulted in a rapid and pronounced shortening of AERP (from 162 ± 8 milliseconds to 117 ± 16 milliseconds, P = 0.001) associated with increased AF‐inducibility from 0% to 82%. This shortening in AERP was completely reversible after stopping BRS. After administration of atropine, AF‐inducibility during BRS was attenuated. Ventricular repolarization was not modulated by BRS. In RDN, AF was not inducible; however, it did not prevent BRS‐induced shortening of AERP.ConclusionRDN and BRS resulting in comparable blood pressure and heart rate reductions differently influence atrial electrophysiology. Vagally mediated shortening of AERP, resulting in increased AF‐inducibility, was observed with BRS but not with RDN.
Akt‐mediated anti‐apoptotic effects of substance P in Anti‐Fas‐induced apoptosis of human tenocytes
Authors: Backman Ludvig J. , Danielson Patrik 
Published: April 2013

AbstractSubstance P (SP) and its receptor, the neurokinin‐1 receptor (NK‐1 R), are expressed by human tenocytes, and they are both up‐regulated in cases of tendinosis, a condition associated with excessive apoptosis. It is known that SP can phosphorylate/activate the protein kinase Akt, which has anti‐apoptotic effects. This mechanism has not been studied for tenocytes. The aims of this study were to investigate if Anti‐Fas treatment is a good apoptosis model for human tenocytes in vitro, if SP protects from Anti‐Fas‐induced apoptosis, and by which mechanisms SP mediates an anti‐apoptotic response. Anti‐Fas treatment resulted in a time‐ and dose‐dependent release of lactate dehydrogenase (LDH), i.e. induction of cell death, and SP dose‐dependently reduced the Anti‐Fas‐induced cell death through a NK‐1 R specific pathway. The same trend was seen for the TUNEL assay, i.e. SP reduced Anti‐Fas‐induced apoptosis via NK‐1 R. In addition, it was shown that SP reduces Anti‐Fas‐induced decrease in cell viability as shown with crystal violet assay. Protein analysis using Western blot confirmed that Anti‐Fas induces cleavage/activation of caspase‐3 and cleavage of PARP; both of which were inhibited by SP via NK‐1 R. Finally, SP treatment resulted in phosphorylation/activation of Akt as shown with Western blot, and it was confirmed that the anti‐apoptotic effect of SP was, at least partly, induced through the Akt‐dependent pathway. In conclusion, we show that SP reduces Anti‐Fas‐induced apoptosis in human tenocytes and that this anti‐apoptotic effect of SP is mediated through NK‐1 R and Akt‐specific pathways.
Imaging haematopoietic cells recruitment to an acute wound in vivo identifies a role for c‐Met signalling
Authors: FALENTA K. , RODAWAY A. , JONES G.E. , WELLS C.M. 
Published: April 2013

SummaryWe have used a direct in vivo imaging strategy to investigate the role of c‐Met signalling and kinase activity during the immune response to wounding. Our assay utilizes the optical translucent properties of the zebrafish embryo and demonstrates the versatility of microscopy‐based approach to the screening of compounds for inhibition of the wounding response. We have focussed on the c‐Met pathway as little is known about the influence of c‐Met signalling in immune responses, although it has been suggested that the c‐Met tyrosine kinase receptor signalling pathway may be involved in cytokine secretion and directional migration in immune cells. Using both imaging of fixed zebrafish embryos in combination with digital time lapse microscopy of neutrophils recruited to a wound site, we find that pharmacological inhibition of c‐Met, using a specific inhibitor, modulates the immune response in zebrafish embryos. We have found that inhibition of c‐Met does not prevent the inflammatory response but does appear to limit recruitment and retention of immune cells at the wound site. This work demonstrates the versatility of using direct imaging assays for inhibitor studies and suggests that the HGF/c‐Met signalling cascade plays an important role in the migration of haematopoietic cells in vivo.
Hypoglycaemic episodes and risk of dementia in diabetes mellitus: 7‐year follow‐up study
Authors: Lin C.‐H. , Sheu W. H.‐H. 
Published: April 2013

AbstractObjectiveWe investigated the risk of dementia in patients with type 2 diabetes with or without prior hypoglycaemic episodes.Subjects and SettingOne million subjects randomly selected from the National Health Insurance Research Database, Taiwan.ResultsA total of 15 404 diabetic subjects without prior dementia and a mean age of 64.2 years were enrolled in the study. About 2% (n = 289) of participants had at least one episode of hypoglycaemia in a 3‐year period; these subjects were older and more likely to be women and also had higher rates of insulin use and comorbidities compared to those without hypoglycaemia. During a total of 7 years of follow‐up (mean and median follow‐up, 3.8 and 4.8 years, respectively), 1106 patients with diabetes (7.2%) developed dementia. The incidence rate of dementia was higher in diabetic subjects with [29.9 per 1000 person‐years (95% CI 22.1–39.2)] compared to those without [11.1 per 1000 person‐years (95% CI 10.3–11.8)] hypoglycaemic episodes. The crude rate ratio (RR) and age‐ and gender‐adjusted RR values for dementia were 2.76 (95% CI 2.06–3.70, P < 0.001) and 1.60 (95% CI 1.19–2.14, P = 0.002), respectively, in diabetic subjects with hypoglycaemia compared to those without hypoglycaemia. Results of Cox proportional hazards analysis revealed that hypoglycaemia, older age, female gender and insulin use were independent predictors of dementia.ConclusionAdult diabetic patients with prior hypoglycaemia had a significantly increased risk of dementia. The influence of hypoglycaemic episodes on brain function warrants further investigation.
Prevalence and extent of subclinical atherosclerosis in patients with psoriasis
Authors: Yiu K.‐H. , Yeung C.‐K. , Zhao C.‐T. , Chan J. C. , Siu C.‐W. , Tam S. , Wong C.‐S. , Yan G. H. , Yue W. S. , Khong P.‐L. , Chan H. H. , Tse H.‐F. 
Published: April 2013

AbstractObjectivePatients with psoriasis are prone to premature atherosclerosis and increased risk of cardiovascular disease events. However, the prevalence and extent of atherosclerosis in patients with psoriasis are unknown.DesignA cross‐sectional study.Setting and subjectsThe prevalence and extent of coronary and carotid atherosclerosis were compared in 70 patients with psoriasis (46 ± 9 years, 71% male) without known cardiovascular disease or joint involvement and 51 age‐ and gender‐matched healthy control subjects (45 ± 7 years, 71% male). Systemic inflammation was assessed by the level of high‐sensitivity C‐reactive protein (hs‐CRP). Coronary atherosclerosis was determined by the coronary calcification score (CCS) measured by multi‐detector computed tomography. Carotid atherosclerosis was assessed by high‐resolution ultrasound‐derived carotid intima–media thickness (cIMT).ResultsPatients with psoriasis had a higher prevalence of coronary atherosclerosis (CCS > 0; 28.6% vs. 3.9%, P < 0.01), and a higher degree of coronary atherosclerosis estimated by the mean CCS (67.4 ± 349.2 vs. 0.5 ± 3.0, P < 0.05) compared with controls. Similarly, cIMT was significantly greater in patients with psoriasis than in control subjects (0.73 ± 0.11 mm vs. 0.67 ± 0.08 mm, P < 0.01). Multiple logistic regression revealed that psoriasis [odd ratio (OR): 10.54, 95% confidence interval (CI) 1.89–58.67, P < 0.01] and serum total cholesterol level (OR 2.10, 95% CI 1.01–4.37) were associated with the presence of coronary atherosclerosis (CCS > 0). By contrast, only age was independently associated with increased cIMT. Amongst participants with no traditional cardiovascular disease risk factors, hs‐CRP level was higher in patients with psoriasis than in controls.ConclusionThe present results demonstrate early‐onset, diffuse arterial atherosclerosis in coronary and carotid arteries in patients with psoriasis, but not in age‐ and gender‐matched control subjects. Low‐grade inflammation could explain the presence of premature atherosclerosis in patients with psoriasis.
Biofilm infections, their resilience to therapy and innovative treatment strategies
Authors: Römling U. , Balsalobre C. 
Published: April 2013

AbstractBiofilm formation of microorganisms causes persistent tissue and foreign body infections resistant to treatment with antimicrobial agents. Up to 80% of human bacterial infections are biofilm associated; such infections are most frequently caused byStaphylococcus epidermidis,Pseudomonas aeruginosa,Staphylococcus aureusandEnterobacteria such asEscherichia coli. The accurate diagnosis of biofilm infections is often difficult, which prevents the appropriate choice of treatment. As biofilm infections significantly contribute to patient morbidity and substantial healthcare costs, novel strategies to treat these infections are urgently required. Nucleotide second messengers, c‐di‐GMP, (p)ppGpp and potentially c‐di‐AMP, are major regulators of biofilm formation and associated antibiotic tolerance. Consequently, different components of these signalling networks might be appropriate targets for antibiofilm therapy in combination with antibiotic treatment strategies. In addition, cyclic di‐nucleotides are microbial‐associated molecular patterns with an almost universal presence. Their conserved structures sensed by the eukaryotic host have a widespread effect on the immune system. Thus, cyclic di‐nucleotides are also potential immunotherapeutic agents to treat antibiotic‐resistant bacterial infections.
TLR4 expression on monocyte subsets in myocardial infarction
Authors: Tapp L. D. , Shantsila E. , Wrigley B. J. , Montoro‐Garcia S. , Lip G. Y. H. 
Published: April 2013

AbstractBackgroundMonocyte toll‐like receptor 4 (TLR4) has been implicated in the pathogenesis of atherosclerosis with increased levels in myocardial infarction. The aim of this study was to assess the numbers of TLR4+ monocytes in each monocyte subset in MI, the expression of TLR4 and association with markers of monocyte activation, inflammation, myocardial damage and postmyocardial infarction (MI) cardiac contractility.MethodsSurface expression of TLR4 and numbers of TLR4‐expressing monocytes were quantified by flow cytometry of venous blood in 50 patients with ST‐elevation MI (STEMI), 48 with non‐STEMI (NSTEMI) and 40 with stable coronary artery disease (CAD). These parameters were measured on days 1, 3, 7 and 30 post‐MI in STEMI patients. Three monocyte subsets were defined as CD14++ CD16− CCR2+ (Mon1), CD14++ CD16+ CCR2+ (Mon2) and CD14+ CD16++ CCR2− (Mon3). Plasma inflammatory cytokines were assessed using cytometric bead arrays.ResultsThere was a significant increase in counts of TLR4+ Mon1 and Mon2 in STEMI patients and TLR4+ Mon2 in NSTEMI patients compared with controls with CAD. Monocyte TLR4+ expression was similar between the groups, and was not changed during follow‐up in STEMI patients. Plasma interleukin‐6 (IL6) levels correlated positively with TLR4+ Mon2 count (r = 0.54, P < 0.001), but negatively with TLR4 expression on Mon2 (r = −0.33, P = 0.021).ConclusionFollowing treatment of acute MI, TLR4 expression by individual monocyte subsets is unchanged. An increase in TLR4+ Mon1 and Mon2 count in patients with STEMI and TLR+ Mon2 count in those with NSTEMI is due to an increase in monocyte subset count and not to changes in TLR4 expression. Monocyte counts but not TLR4 expression correlate positively with plasma IL6 levels. We suggest that TLR4 expression may not be a reliable marker of monocyte activation in MI.