How do scientists perceive the current publication culture? A qualitative focus group interview study among Dutch biomedical researchers.

OBJECTIVE: To investigate the biomedical scientist's perception of the prevailing publication culture. DESIGN: Qualitative focus group interview study. SETTING: Four university medical centres in the Netherlands. PARTICIPANTS: Three randomly selected groups of biomedical scientists (PhD, postdoctoral staff members and full professors). MAIN OUTCOME MEASURES: Main themes for discussion were selected by participants. RESULTS: Frequently perceived detrimental effects of contemporary publication culture were the strong focus on citation measures (like the Journal Impact Factor and the H-index), gift and ghost authorships and the order of authors, the peer review process, competition, the funding system and publication bias. These themes were generally associated with detrimental and undesirable effects on publication practices and on the validity of reported results. Furthermore, senior scientists tended to display a more cynical perception of the publication culture than their junior colleagues. However, even among the PhD students and the postdoctoral fellows, the sentiment was quite negative. Positive perceptions of specific features of contemporary scientific and publication culture were rare. CONCLUSIONS: Our findings suggest that the current publication culture leads to negative sentiments, counterproductive stress levels and, most importantly, to questionable research practices among junior and senior biomedical scientists

Cardiovascular autonomic function is associated with (micro-)albuminuria in elderly Caucasian subjects with impaired glucose tolerance or type 2 diabetes: the Hoorn Study

OBJECTIVE: To determine whether impaired cardiovascular autonomic function correlates with albuminuria in an age-, sex-, and glucose tolerance-stratified sample of an elderly (50-75 years of age) Caucasian population and to determine whether this association is independent of other determinants of albuminuria. RESEARCH DESIGN AND METHODS: We studied 536 subjects, 256 with normal glucose tolerance, 143 with impaired glucose tolerance (IGT), and 137 with type 2 diabetes. Microalbuminuria was defined as an albumin-to-creatinine ratio of > or =3.0 and 30 mg/mmol) were grouped as having albuminuria. In bivariate analyses, albuminuria was associated with age, waist-to-hip ratio, systolic and diastolic blood pressure, calculated glomerular filtration rate, and glucose tolerance status. The mean CAFS was higher in subjects with versus without albuminuria (7.5 vs. 5.9, P<0.001). Multiple logistical regression analyses revealed that the CAFS was independently associated with albuminuria in subjects with IGT or type 2 diabetes with an odds ratio (95% CI) of 1.19 (1.02-1.39) per point increase in the CAFS. CONCLUSIONS: Impaired cardiovascular autonomic function is independently associated with (and thus a possible contributor to) the presence of albuminuria in subjects with IGT or type 2 diabetes

Microvascular function is impaired in ankylosing spondylitis and improves after tumour necrosis factor a blockade

Objectives: Ankylosing spondylitis (AS) is associated with increased cardiovascular morbidity and mortality. Microvascular function has been linked to several risk factors for cardiovascular disease. Inflammation in AS may cause microvascular dysfunction. To test this, we assessed microvascular function in (a) patients with AS compared to healthy controls and (b) patients with AS before and after 1 month of anti-tumour necrosis factor (TNF)alpha treatment with etanercept. Methods: A total of 15 consecutive patients with AS, who were scheduled for etanercept treatment according to the Assessment in Ankylosing Spondylitis (ASAS) group guidelines, and 12 healthy controls matched for age and sex, were recruited. Endothelium-dependent and independent vasodilatation in skin were evaluated with laser Doppler fluxmetry after iontophoresis of acetylcholine and sodium nitroprusside, respectively. Videomicroscopy was used to measure recruitment of skin capillaries after arterial occlusion. Results: Compared to healthy controls, patients with AS had impaired endothelium-dependent vasodilatation and capillary recruitment. Following anti-TNF alpha treatment, microvascular function improved significantly for endothelium-dependent vasodilatation (p = 0.03) and capillary recruitment (p = 0.006). A significant correlation was observed between changes in endothelium-dependent vasodilatation and changes in erythrocyte sedimentation rate (ESR) (r = -0.56; p = 0.03). Conclusion: Microvascular dysfunction is present in patients with AS with active disease, but improves as inflammation regresses after TNF alpha blockad

S-Adenosylmethionine and 5-Methyltetrahydrofolate are associated with endothelial function after controlling for confounding by homocysteine: the Hoorn study

): 48.57 microm (21.16; 75.98) and -32.15 microm (-59.09; -5.20), but high homocysteine was not (-15.11 microm (-42.99; 12.78). High SAM and low 5-MTHF were also significantly associated with high and low NMD, respectively. NMD explained the association of 5-MTHF with FMD but not of SAM. No interactions were observed for diabetes or cardiovascular risk factors. CONCLUSIONS: In this elderly population, both SAM and 5-MTHF are associated with endothelial and smooth muscle cell function. The effect of homocysteine on endothelial function is relatively small compared with SAM and 5-MTHF. The relative impact of SAM, 5-MTHF, and homocysteine, and the mechanisms through which these moieties may affect endothelial and smooth muscle cell function need clarification. Both SAM and 5-MTHF are associated with endothelial and smooth muscle cell function whereas the effect of homocysteine is relatively small compared with SAM and 5-MTH

Rheumatoid arthritis versus diabetes as a risk factor for cardiovascular disease: a cross-sectional study, the CARRE Investigation.

Objectives: Patients with rheumatoid arthritis (RA) have an increased cardiovascular risk, but the magnitude of this risk is not known precisely. A study was undertaken to investigate the associations between RA and type 2 diabetes (DM2), a well-established cardiovascular risk factor, on the one hand, and cardiovascular disease (CVD) on the other. Methods: The prevalence of CVD (coronary, cerebral and peripheral arterial disease) was determined in 353 randomly selected outpatients with RA (diagnosed between 1989 and 2001, aged 50-75 years; the CARRÉ study) and in participants of a population-based cohort study on diabetes and CVD (the Hoorn study). Patients with RA with normal fasting glucose levels from the CARRÉ study (RA, n = 294) were compared with individuals from the Hoorn study with normal glucose metabolism (non-diabetic, n = 258) and individuals with DM2 (DM2, n = 194). Results: The prevalence of CVD was 5.0% (95% CI 2.3% to 7.7%) in the non-diabetic group, 12.4% (95% CI 7.5% to 17.3%) in the DM2 group and 12.9% (95% CI 8.8% to 17.0%) in those with RA. With non-diabetic individuals as the reference category, the age- and gender-adjusted prevalence odds ratio (OR) for CVD was 2.3 (95% CI 1.1 to 4.7) for individuals with DM2 and 3.1 (95% CI 1.6 to 6.1) for those with RA. There was an attenuation of the prevalences after adjustment for conventional cardiovascular risk factors (OR 2.0 (95% CI 0.9 to 4.5) and 2.7 (95% CI 1.2 to 5.9), respectively). Conclusions: The prevalence of CVD in RA is increased to an extent that is at least comparable to that of DM2. This should have implications for primary cardiovascular prevention strategies in RA

Endothelial dysfunction and low-grade inflammation are associated with greater arterial stiffness over a 6-year period

Endothelial dysfunction and low-grade inflammation are associated with cardiovascular disease. Arterial stiffening plays an important role in cardiovascular disease and, thus, may be a mechanism through which endothelial dysfunction and/or low-grade inflammation lead to cardiovascular disease. We investigated the associations between, on the one hand, biomarkers of endothelial dysfunction (soluble endothelial selectin, thrombomodulin, and both vascular and intercellular adhesion molecules 1 and von Willebrand factor) and of low-grade inflammation (C-reactive protein, serum amyloid A, interleukin 6, interleukin 8, tumor necrosis factor-α and, soluble intercellular adhesion molecule 1) and, on the other hand, arterial stiffness over a 6-year period, in 293 healthy adults (155 women). Biomarkers were combined into mean z scores. Carotid, femoral, and brachial arterial stiffness and carotid-femoral pulse wave velocity were determined by ultrasonography. Measurements were obtained when individuals were 36 and 42 years of age. Associations were analyzed with generalized estimating equation and adjusted for sex, height, and mean arterial pressure. The endothelial dysfunction z score was inversely associated with femoral distensibility (β:-0.51 [95% CI:-0.95 to-0.06]) and compliance coefficients (β:-0.041 [95% CI:-0.076 to-0.006]) but not with carotid or brachial stiffness or carotid-femoral pulse wave velocity. The low-grade inflammation z score was inversely associated with femoral distensibility (β:-0.51 [95% CI:-0.95 to-0.07]) and compliance coefficients (β:-0.050 [95% CI:-0.084 to-0.016]) and with carotid distensibility coefficient (β:-0.910 [95% CI:-1.810 to-0.008]) but not with brachial stiffness or carotid-femoral pulse wave velocity. Biomarkers of endothelial dysfunction and low-grade inflammation are associated with greater arterial stiffness. This provides evidence that arterial stiffening may be a mechanism through which endothelial dysfunction and low-grade inflammation lead to cardiovascular disease