bluuebunny/crossref_metadata_2025_split huggingface dataset:
Low cardiorespiratory fitness is a strong predictor for clustering of cardiovascular disease risk factors in children independent of country, age and sex
Authors: Anderssen Sigmund A. , Cooper Ashley R. , Riddoch Chris , Sardinha Luis B. , Harro Maarike , Brage Søren , Andersen Lars B. 
Published: July 2007

Background and design Few studies have investigated the association between maximal cardiorespiratory capacity (fitness) and the clustered cardiovascular disease (CVD) risk in children and youth from culturally diverse countries. This cross-sectional study examined the association between fitness and clustered CVD risk in children and adolescents from three European countries. Methods Participants were 2845 randomly selected school children aged 9 or 15 years from Portugal ( n = 944), Denmark ( n = 849) and Estonia ( n = 1052). Cardiorespiratory fitness was determined during a maximal test on a cycle ergometer. CVD risk factors selected to assess the degree of clustering were the total cholesterol/high-density lipoprotein cholesterol ratio, plasma triglycerides, insulin resistance (homeostasis model assessment), sum of four skinfolds, and systolic blood pressure. Results There was a strong association between cardiorespiratory fitness and the clustering of CVD risk factors. The odds ratios for clustering in each quartile of fitness, using the quartile with the highest fitness as reference, were 13.0 [95% confidence interval (CI) 8.8-19.1]; 4.8 (95% CI 3.2-7.1) and 2.5 (95% CI 1.6-3.8), respectively, after adjusting for country, age, sex, socio-economic status, pubertal stage, family history of CVD and diabetes. In stratified analyses by age group, sex and country, similar strong patterns were observed. Conclusion Low cardiorespiratory fitness is strongly associated with the clustering of CVD risk factors in children independent of country, age and sex.
Primary risk factors influence risk of recurrent myocardial infarction/death from coronary heart disease: results from the Stockholm Heart Epidemiology Program (SHEEP)
Authors: Leander Karin , Wiman Björn , Hallqvist Johan , Andersson Tomas , Ahlbom Anders , de Faire Ulf 
Published: July 2007

Background Prognosis after a first myocardial infarction (MI) is influenced by primary risk factors as well as secondary risk factors. There is still a lack of follow-up studies of well-characterized patient cohorts assessing the relative importance of these factors. Design A cohort of 1635 patients (aged 45-70 years) surviving at least 28 days after a first MI were followed for 6-9 years with regard to recurrent MI/fatal coronary heart disease (CHD). Data were collected through questionnaires, physical examinations, and medical records. Methods Hazard ratios (HR) with 95% confidence intervals (CI) for different risk factors were calculated using the Cox proportional hazard model. Results Of the primary risk factors, diabetes in both sexes was the most important predictor of recurrent MI/fatal CHD, multivariate-adjusted HR in men 1.6 (95% CI; 1.0-2.4) and in women 2.5 (95% CI; 0.9-6.9). Other primary risk factors with prognostic influence were job strain, HR 1.5 (95% CI; 1.0-2.1), and central obesity, HR 1.4 (95% CI; 1.0-2.0), in men and a low level of apolipoprotein A1, HR 2.3 (95% CI; 1.1-5.0), and high-density lipoprotein cholesterol, HR 1.9 (95% CI; 0.9-4.1), in women. The secondary risk factors most detrimental for prognosis were heart failure in men, HR 2.2 (95% CI; 1.2-4.0), and a high peak acute cardiac enzyme level in women, HR 4.4 (95% CI; 2.0-9.7). Conclusions Long-term follow-up of patients who survived at least 28 days after a first MI shows that several primary cardiovascular risk factors, particularly diabetes, contribute to the increased risk of recurrent MI/fatal CHD.
Secondary prevention programmes for coronary heart disease: a meta-regression showing the merits of shorter, generalist, primary care-based interventions
Authors: Clark Alexander M. , Hartling Lisa , Vandermeer Ben , Lissel Sue L. , McAlister Finlay A. 
Published: July 2007

Background The aim of this study was to determine which programme characteristics influence the effectiveness of secondary prevention programmes for Coronary Heart Disease. Design The study follows a meta-regression design. Methods We conducted a meta-regression within a systematic review of randomized trials comparing secondary prevention programmes versus usual care. The primary outcome was all-cause mortality. Studies were identified by searching multiple electronic databases, bibliographies of published studies, contact with experts, and references provided by the United States Centers for Medicare and Medicaid Services. Primary authors of all relevant trials were surveyed for detailed information on programme characteristics. Forty-six unique trials were identified (18 821 patients). The pooled all-cause mortality risk ratio (RR) for programmes was 0.87 [95% confidence interval (CI) 0.79-0.97]. Programmes containing less than 10 h of patient contact with health professionals reduced all-cause mortality (RR 0.80, 95% CI 0.68-0.95) as effectively as programmes with more contact time. Programmes provided in general practice settings were effective at reducing all-cause mortality (RR 0.76, 95% CI 0.63-0.92) and compared favourably with the effectiveness of hospital-based programmes. Other characteristics, including specialist versus generalist provision, did not appreciably impact programme effectiveness. Conclusions Shorter secondary prevention programmes, those based in general practice, and those staffed by generalists are at least as effective in reducing all cause mortality in patients with coronary heart disease as longer programmes, hospital-based programmes, and programmes staffed by specialists.
Symptoms of anxiety and depression in patients with stable coronary heart disease: prognostic value and consideration of pathogenetic links
Authors: Rothenbacher Dietrich , Hahmann Harry , Wüsten Bernd , Koenig Wolfgang , Brenner Hermann 
Published: July 2007

Background We evaluated the association of symptoms of anxiety and depression with fatal and non-fatal cardiovascular disease events among patients with coronary heart disease and considered several potential underlying pathogenetic links. Design This was a prospective cohort study. Methods In this study, including coronary heart disease patients undergoing an in-patient rehabilitation program, symptoms of anxiety and depression were evaluated with the Hospital Anxiety and Depression Scale (HADS). Fatal and non-fatal cardiovascular disease events were determined during a 3-year follow-up. Results Of the 1052 patients with CHD 16.1% showed a borderline and 8.3% a manifest anxiety symptoms score, whereas 11.8 and 5.9% showed a borderline and manifest depressive symptoms score, respectively. During the 3-year follow-up fatal and non-fatal cardiovascular disease events were observed in 73 (6.9%) patients. After adjustment for covariates, patients having manifest anxiety symptoms had a statistically significant hazard ratio (HR) of 2.32 [95% confidence interval (CI) 1.14-4.74] for a cardiovascular disease event, and patients with depressive symptoms had an HR of 1.47 (95% CI 0.62-3.51) compared to other patients. In a model considering anxiety and depressive symptom scores simultaneously, the hazard ratio for a cardiovascular disease event associated with anxiety symptoms increased to 3.31 (95% CI 1.32-8.27), whereas the hazard ratio associated with depressive symptoms decreased (HR 0.62; 95% CI 0.20-1.87). We found a positive association of increased anxiety scores with body mass index and systolic blood pressure. Conclusions The study suggests an important role especially for symptoms of anxiety for long-term prognosis of patients with known coronary heart disease. It furthermore suggests that several pathogenetic links may partly explain the increased risk.
Association between intelligence and coronary heart disease mortality: a population-based cohort study of 682 361 Swedish men
Authors: Silventoinen Karri , Modig-Wennerstad Karin , Tynelius Per , Rasmussen Finn 
Published: July 2007

Background Socio-economic position and intelligence predict coronary heart disease but their mutual associations are not yet well understood. We investigated associations between intelligence and coronary heart disease mortality and explored if they are confounded or modified by socio-economic position. Design This was a cohort-based follow-up study. Methods Data on intelligence, systolic and diastolic blood pressures and body mass index were measured at conscription examination at age 18 years in 682 361 Swedish men born 1951-1965. Data on parental and own education and social position were derived from censuses in 1960, 1970, 1980 and 1990. Follow-up data up to end of 2001 were derived from the Swedish Cause of Death Register and 737 coronary heart disease deaths were observed. Data were analyzed by Cox regression and conditional logistic regression models. Results An inverse association was found between intelligence and coronary heart disease mortality after adjustment for parental and own education and social position, body mass index and blood pressure (hazard ratio 0.92; 95% confidence interval 0.88-0.96). These associations were of similar strengths within all socio-economic categories and also found within 215 brother pairs discordant for coronary heart disease mortality and intelligence (odds ratio 0.76; 95% confidence interval 0.58-1.00). Conclusions Intelligence is associated with coronary heart disease mortality independently of socio-economic position. Health education messages should be tailored according to intellectual performance of the recipients, but also other factors are important for socio-economic coronary heart disease inequalities.
Subclinical coronary atherosclerosis is more pronounced in men and women with lower socio-economic status: associations in a population-based study Coronary atherosclerosis and social status
Authors: Dragano Nico , Verde Pablo Emilio , Moebus Susanne , Stang Andreas , Schmermund Axel , Roggenbuck Ulla , Möhlenkamp Stefan , Peter Richard , Jöckel Karl-Heinz , Erbel Raimund , Siegrist Johannes ,   for the Heinz Nixdorf Recall Study
Published: July 2007

Background Social inequalities of manifest coronary heart diseases are well documented in modern societies. Less evidence is available on subclinical atherosclerotic disease despite the opportunity to investigate processes underlying this association. Therefore, we examined the relationship between coronary artery calcification as a sign of subclinical coronary atherosclerosis, socio-economic status and established cardiovascular risk factors in a healthy population. Design Cross-sectional. Methods In a population-based sample of 4487 men and women coronary artery calcification was assessed by electron beam computed tomography quantified by the Agatston score. Socio-economic status was assessed by two indicators, education and income. First, we investigated associations between the social measures and calcification. Second, we assessed the influence of cardiovascular risk factors on this association. Results After adjustment for age, men with 10 and less years of formal education had a 70% increase in calcification score compared with men with high education. The respective increase for women was 80%. For income the association was weaker (among men 20% higher for the lowest compared with the highest quartile; and among women 50% higher, respectively). Consecutive adjustment for cardiovascular risk factors significantly attenuated the observed association of socio-economic status with calcification. Conclusions Social inequalities in coronary heart diseases seem to influence signs of subclinical coronary atherosclerosis as measured by coronary artery calcification. Importantly, cumulation of major cardiovascular risk factors in lower socio-economic groups accounted for a substantial part of this association.
Illicit drugs and cardiac arrhythmias in athletes
Authors: Furlanello Francesco , Serdoz Laura Vitali , Cappato Riccardo , De Ambroggi Luigi 
Published: July 2007

The current management of athletes with cardiac arrhythmias has become complicated by the widespread use of illicit drugs, which can be arrhythmogenic.The World Anti-Doping Agency annually updates a list of prohibited substances and methods banned by the International Olympic Committee that includes different classes of substances namely, anabolic androgenic steroids, hormones and related substances, β2-agonists, diuretics, stimulants, narcotics, cannabinoids, glucocorticosteroids, alcohol, β-blockers and others. Almost all illicit drugs may cause, through a direct or indirect arrhythmogenic effect, a wide range of cardiac arrhythmias (focal or reentry type, supraventricular and/or ventricular) that can even be lethal and which are frequently sport activity related.A large use of illicit drugs has been documented in competitive athletes, but the arrhythmogenic effect of specific substances is not precisely known. Precipitation of cardiac arrhythmias, particularly in the presence of a latent electrophysiologic substrate including some inherited cardiomyopathies, at risk of sudden death or due to long-term consumption of the substances, should raise the suspicion that illicit drugs may be a possible cause and lead cardiologists to investigate carefully this relationship and appropriately prevent the clinical consequences.
Phenotypic consequences of variation across the aldosterone synthase and 11‐beta hydroxylase locus in a hypertensive cohort: data from the MRC BRIGHT Study
Authors: Freel E. M. , Ingram M. , Friel E. C. , Fraser R. , Brown M. , Samani N. J. , Caulfield M. , Munroe P. , Farrall M. , Webster J. , Clayton D. , Dominiczak A. F. , Davies E. , Connell J. M. C. 
Published: July 2007

SummaryBackground  Aldosterone is an important cardiovascular hormone; 15% of hypertensive subjects have alteration in aldosterone regulation, defined by a raised ratio of aldosterone to renin (ARR). Studies of the aldosterone synthase gene (CYP11B2) have focused on a single nucleotide polymorphism in the 5′promoter region (–344 C/T). In normotensive subjects, the T allele associates with raised levels of the 11‐deoxysteroids, deoxycorticosterone and 11‐deoxycortisol which are substrates for 11β‐hydroxylase, encoded by the adjacent and homologous gene, CYP11B1. We have speculated that this altered 11β‐hydroxylase efficiency leads to increased ACTH drive to the adrenal gland to maintain cortisol production and reported herein the association between the –344 C/T single nucleotide polymorphism (SNP) and adrenal steroid production in subjects with essential hypertension.Methods  The CYP11B2–344 C/T polymorphism was genotyped and urinary excretion of adrenal steroid metabolites was measured (by GCMS) in 511 unrelated hypertensives from the Medical Research Council (MRC) British Genetics of Hypertension (BRIGHT) study.Results  Thirty‐five per cent of subjects were homozygous for the –344T allele whilst 16% were CC homozygotes. There was no difference in cortisol excretion rate between the two genotype groups but the index of adrenal 11β‐hydroxylation (ratio of tetrahydrodeoxycortisol/total cortisol) was significantly higher in the TT group (P < 0·005) than in the CC group. Excretion rates of the major urinary metabolite of aldosterone (tetrahydroaldosterone) correlated strongly with the ACTH‐regulated steroids, cortisol (r = 0·437, P < 0·0001) and total androgen metabolites (r = 0·4, P < 0·0001) in TT but not CC subjects.Conclusions  Hypertensives homozygous for the –344 T allele of CYP11B2 demonstrate altered 11β‐hydroxylase efficiency (CYP11B1); this is consistent with the hypothesis of a genetically determined increase in adrenal ACTH drive in these subjects. The correlation between excretion of aldosterone and cortisol metabolites and suggests that, in TT subjects, ACTH exerts an important common regulatory influence on adrenal corticosteroid production in subjects with hypertension.
Polycystic ovaries and the polycystic ovary syndrome phenotype in women with active acromegaly
Authors: Kaltsas Gregory A. , Androulakis Ioannis I. , Tziveriotis Kostas , Papadogias Dimitrios , Tsikini Aggeliki , Makras Polysois , Dimitriou Konstantina , Stathopoulou Alexandra , Piaditis George 
Published: July 2007

SummaryBackground  Previous retrospective studies have suggested that women with acromegaly may present with menstrual irregularity and symptoms/signs of hyperandogenism, a phenotype similar to that of the polycystic ovary syndrome (PCOS).Objective  The aim of this study was to investigate prospectively the presence of the PCOS phenotype (PCOSP) and polycystic ovaries (PCO) on ultrasonography in women with active acromegaly.Design  Women within the reproductive age range (21–43 years) with active acromegaly of recent onset and/or previous surgical and/or medical therapy were studied.Main outcome measures  Subjects underwent a physical examination; fasting bloods for androgens, pituitary hormones and metabolic parameters; an oral glucose tolerance test (OGTT) to estimate disease activity and insulin resistance; and a transvaginal ultrasound.Results  Six women had newly diagnosed acromegaly, and eight still had active disease following previous surgical and/or medical treatment. Seven women were found to have PCO and six fulfilled the criteria for PCOSP; six of these women, five with PCOSP, had a pituitary macroadenoma. Women with PCOSP had significantly increased mean ovarian volumes and characteristic ovarian morphology compared to women without PCOSP (P < 0·05), higher levels of IGF‐1 and testosterone and lower SHBG levels that did not reach statistical significance. A positive correlation between IGF‐1 and mean ovarian volume was identified only in women with PCOSP (r = 0·851, P < 0·05).Conclusions  PCO and PCOSP are relatively common in women with acromegaly and may account for some of the symptoms related to gonadal dysfunction irrespective of the size of the pituitary tumour. It is likely that IGF‐1 alone or in combination with GH and/or insulin resistance may be involved.
Repeated intratunical injection of adenovirus expressing transforming growth factor‐β1 in a rat induces penile curvature with tunical fibrotic plaque: a useful model for the study of Peyronie’s disease
Authors: Piao Shuguang , Ryu Ji‐Kan , Shin Hwa‐Yean , Zhang Luwei , Song Sun U. , Han Jee‐Young , Park Seok Hee , Kim Joon Mee , Kim In‐Hoo , Kim Seong‐Jin , Suh Jun‐Kyu 
Published: July 2007

SummaryThis study was undertaken to establish a Peyronie’s disease model with penile curvature by using recombinant transforming growth factor‐β1 (TGF‐β1) protein or adenovirus (ad‐TGF‐β1). Four‐month‐old male Sprague–Dawley rats were divided into seven groups (n = 18 per group): G1 received a single injection of saline into the tunica albuginea (0.1 mL); G2, repeated injections of ad‐LacZ (days 0, 3, and 6; 1 × 1010 particles/0.1 mL respectively); G3, a single injection of recombinant TGF‐β1 protein (700 ng/0.1 mL); G4, repeated injections of recombinant TGF‐β1 protein (days 0, 3 and 6; 700 ng/0.1 mL respectively); G5, a single injection of low‐dose ad‐TGF‐β1 (1 × 1010 particles/0.1 mL); G6, a single injection of high‐dose ad‐TGF‐β1 (3 × 1010 particles/0.1 mL); and G7, repeated injections of low‐dose ad‐TGF‐β1 (days 0, 3, and 6; 1 × 1010 particles/0.1 mL respectively). Penile curvature was evaluated 30, 45 and 60 days after treatment, and the penis was then harvested for histological examination. Repeated injection of low‐dose ad‐TGF‐β1 not only induced fibrous scar in the tunica, which lasted up to 60 days after injection, but also resulted in significant penile curvature by artificial erection test 45 days after treatment. A peculiar histological finding in this group was trapping of inflammatory cells in the tunica, subsequent fibrosis, and formation of cartilage and calcification as well as loss of elastin fibres. This model involving repeated injection of ad‐TGF‐β1 may contribute to further investigation of the pathogenesis of Peyronie’s disease and the development of new therapeutics targeting this pathway.
Alkali‐labile sites in sperm cells from Sus and Ovis species
Authors: Cortés‐Gutiérrez Elva I. , Dávila‐Rodríguez Martha I. , López‐Fernández Carmen , Fernández José Luis , Gosálvez Jaime 
Published: July 2007

SummaryConstitutive alkali‐labile sites (ALSs) have been investigated using a protocol of DNA breakage detection–fluorescence in situ hybridization (DBD–FISH) in sperm cells from Sus domesticus (pig), Ovis gmelini musimon (mouflon) and Ovis aries (sheep). The results were compared with those obtained using leucocytes from the same species. Whole comparative genomic hybridization (W‐CGH) showed that most of the constitutive ALSs in somatic and germ line cells in all species examined were constrained to particular repetitive satellite DNA sequences located in the pericentromeric constitutive heterochromatin of each chromosome. However, their relative abundance was different among cells of the same organism (leucocytes/sperm cells), and this trend was not maintained when the different species were compared. Thus, in mouflon, the density of ALSs in leucocytes when compared with that observed in sperm cells indicated abundance of the order of eight times less. In sheep, both leucocytes and sperm cells exhibited a large quantity of ALSs, being of the order of four times more abundant in sperm cells. In the pig genome, leucocytes showed a high abundance of ALSs (of the order of 12 times more that in sperm cells) but only involved the metacentric chromosomes of the karyotype. ALSs were not present in the acrocentric chromosomes. Contrary to mouflon and sheep, ALSs were relatively scarce in sperm cells from pig. These results suggest that ALSs are a transient structural feature in the cells of any organisms and point to a non‐universal model of chromatin organization in sperm cells among mammals.
Localization and expression of spermadhesin PSP‐I/PSP‐II subunits in the reproductive organs of the boar
Authors: García E. M. , Vázquez J. M. , Parrilla I. , Ortega M. D. , Calvete J. J. , Sanz L. , Martínez E. A. , Roca J. , Rodríguez‐Martínez H. 
Published: July 2007

SummaryThe epithelial localization and expression of the spermadhesin PSP‐I and PSP‐II subunits were determined in the testis, ductus epididymes (caput, corpus and cauda), seminal vesicles and bulbourethral glands of mature boars, using immunohistochemical, western blotting and RT‐PCR methods. Immunohistochemistry showed positive labelling for PSP‐I and PSP‐II antibodies in the epithelium of seminal vesicles in all males tested. Positive immunolabelling, but with variable intensity, was also present in the epididymal epithelium (caput, corpus and cauda), although varying largely among segments and boars. Immunoreactivity was nearly or completely absent in the seminiferous epithelium and the bulbourethral gland, although SDS‐PAGE and western blotting revealed the presence of PSP‐I and PSP‐II immunoreactive bands in all the tissue extracts, including the testis and the bulbourethral gland. mRNA amplification by RT‐PCR using primers specific for PSP‐I and PSP‐II showed a trend similar to that observed for western blotting, i.e. intensity variation between tissues (even between segments of the same epididymis) and among boars. Our results indicate that the seminal vesicles are the main source of PSP‐I and PSP‐II spermadhesins, although epididymal segments, testis and the bulbourethral gland also participate in the expression of both proteins.