Barrbishop5252

ry products of the CL during early pregnancy holds the promise of improving the efficacy and safety of ART based on programmed FET cycles.

A better understanding of the critical roles of the secretory products of the CL during early pregnancy holds the promise of improving the efficacy and safety of ART based on programmed FET cycles.

An interplay between thrombo-inflammatory and atherogenic mechanisms is recognized in cardiovascular disease pathogenesis (CVD) in antiphospholipid syndrome (APS). Herein, we examine associations of growth differentiation factor-15 (GDF-15), a pro-inflammatory cytokine identified as potent CVD risk biomarker in the general population, with subclinical atherosclerosis in APS.

We measured plasma GDF-15 levels by an electrochemiluminescence immunoassay (cut-off 1200 pg/mL) and examined carotid intima-media thickness (IMT) and the presence of carotid and femoral plaques using vascular ultrasound in 80 patients with APS (44 primary, 36 systemic lupus erythematosus (SLE)/APS) and 40 healthy controls. We calculated the aGAPSSCVD, a revised adjusted Global APS Score (aGAPSS) to predict CVD, including lupus anticoagulant, anticardiolipin and anti-beta2glycoprotein-I antibodies, and hypertension, dyslipidemia, obesity, diabetes and smoking.

GDF-15 levels were higher in APS patients vs. controls adjusting for age and gender (absolute difference 281 (95% CI 141-421) pg/mL, p < 0.001). find protocol GDF-15 levels ≥1200 pg/mL were associated with higher mean IMT of right and left carotid (beta coefficient 0.068 (95% CI 0.020, 0.116), p = 0.006) compared with GDF-15 levels <1200 pg/mL. GDF-15 was independently associated with mean IMT adjusting for gender and aGAPSSCVD (beta coefficient 0.059 (95% CI 0.008-0.110, p = 0.024), and additionally for statin (p = 0.025) and hydroxychloroquine use (p = 0.011). GDF-15 levels ≥1200 pg/mL were associated with 2.4 higher odds for atherosclerotic plaques (OR = 2.438 (95% CI 0.906, 6.556), p = 0.078), while this effect reduced adding more covariates in the model.

GDF-15 is independently associated with subclinical atherosclerosis in APS patients suggesting its potential role in CVD risk stratification in APS.

GDF-15 is independently associated with subclinical atherosclerosis in APS patients suggesting its potential role in CVD risk stratification in APS.

Epidemiological studies have demonstrated a positive association between chronic lymphocytic leukaemia (CLL) and non-melanoma skin cancer (NMSC). We hypothesized that shared genetic risk factors between CLL and NMSC could contribute to the association observed between these diseases.

We examined the association between (i) established NMSC susceptibility loci and CLL risk in a meta-analysis including 3100 CLL cases and 7667 controls and (ii) established CLL loci and NMSC risk in a study of 4242 basal cell carcinoma (BCC) cases, 825 squamous cell carcinoma (SCC) cases and 12802 controls. Polygenic risk scores (PRS) for CLL, BCC and SCC were constructed using established loci. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs).

Higher CLL-PRS was associated with increased BCC risk (OR4th-quartile-vs-1st-quartile = 1.13, 95% CI 1.02-1.24, Ptrend = 0.009), even after removing the shared 6p25.3 locus. No association was observed with BCC-PRS and CLL risk (Ptrend = 0.68). These findings support a contributory role for CLL in BCC risk, but not for BCC in CLL risk. Increased CLL risk was observed with higher SCC-PRS (OR4th-quartile-vs-1st-quartile = 1.22, 95% CI 1.08-1.38, Ptrend = 1.36 × 10-5), which was driven by shared genetic susceptibility at the 6p25.3 locus.

These findings highlight the role of pleiotropy regarding the pathogenesis of CLL and NMSC and shows that a single pleiotropic locus, 6p25.3, drives the observed association between genetic susceptibility to SCC and increased CLL risk. The study also provides evidence that genetic susceptibility for CLL increases BCC risk.

These findings highlight the role of pleiotropy regarding the pathogenesis of CLL and NMSC and shows that a single pleiotropic locus, 6p25.3, drives the observed association between genetic susceptibility to SCC and increased CLL risk. The study also provides evidence that genetic susceptibility for CLL increases BCC risk.The link between viral respiratory infection and non-pulmonary organ-specific injury, including cardiac injury, has become increasingly appreciated during the current coronavirus disease 2019 (COVID-19) pandemic. Even prior to the pandemic, however, the association between acute infection with influenza and elevated cardiovascular risk was evident. The recently published results of the NHLBI-funded INfluenza Vaccine to Effectively Stop CardioThoracic Events and Decompensated (INVESTED) trial, a 5200 patient comparative effectiveness study of high-dose vs. standard-dose influenza vaccine to reduce cardiopulmonary events and mortality in a high-risk cardiovascular population, found no difference between strategies. However, the broader implications of influenza vaccine as a strategy to reduce morbidity in high-risk patients remain extremely important, with randomized controlled trial and observational data supporting vaccination in high-risk patients with cardiovascular disease. Given a favourable risk-benefit profile and widespread availability at generally low cost, we contend that influenza vaccination should remain a centrepiece of cardiovascular risk mitigation and describe the broader context of underutilization of this strategy. Few therapeutics in medicine offer seasonal efficacy from a single administration with generally mild, transient side effects, and exceedingly low rates of serious adverse effects. Infection control measures such as physical distancing, hand washing, and the use of masks during the COVID-19 pandemic have already been associated with substantially curtailed incidence of influenza outbreaks across the globe. Appending annual influenza vaccination to these measures represents an important public health and moral imperative.