A microfluidic device has been developed that can adsorb proteins from solution, hold them with negligible denaturation, and release them on command. The active element in the device is a 4-nanometer-thick polymer film that can be thermally switched between an antifouling hydrophilic state and a protein-adsorbing state that is more hydrophobic. This active polymer has been integrated into a microfluidic hot plate that can be programmed to adsorb and desorb protein monolayers in less than 1 second. The rapid response characteristics of the device can be manipulated for proteomic functions, including preconcentration and separation of soluble proteins on an integrated fluidics chip.

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Cardiac contractility modulation (CCM) is the application of nonexcitatory electrical signals to the myocardium, during the absolute refractory period of the action potential, to elicit a positive inotropic effect without increasing myocardial oxygen consumption. These effects are independent of QRS duration; consequently, CCM device therapy might benefit symptomatic patients with reduced left ventricular ejection fraction who are not candidates for cardiac resynchronization therapy. Preclinical studies have demonstrated a rapid positive inotropic effect of CCM, which seems to be mediated by modulation of cardiomyocyte Ca(2+) fluxes and alterations in the phosphorylation of cardiac phospholamban. In vivo translational and clinical studies that utilized double biphasic voltage pulses to the right ventricular aspect of the interventricular septum have demonstrated positive global effects on cardiac reverse remodelling and contractility. Long-term application of CCM seems to improve patients' exercise tolerance and quality of life. These benefits are apparently accomplished with an acceptable safety profile; however, to date, no data have demonstrated reductions in hospitalizations for heart failure or mortality. CCM is currently available in Europe and ongoing studies are attempting to identify the ideal target population and accumulate additional outcome data.

Background Vascular-endothelial dysfunction may play an important role in the progression of heart failure. We hypothesize that elevated levels of vascular markers, placental growth factor (PlGF) and soluble Fms like tyrosine kinase-1 (sFlt-1) are associated with adverse outcomes in patients with heart failure (HF). We also assessed possible triggers of sFlt-1 elevation in animal HF models. Methods and Results We measured plasma PlGF and sFlt-1 in 791 HF patients undergoing elective coronary angiogram. Median (IQR) PlGF and sFlt-1 levels were 24 (20–29) pg/ml and 382 (277–953) pg/ml, respectively. After five years of follow up, and after using receiver operator characteristic curves to determine optimal cutoffs, high levels of sFlt-1 (≥ 280 pg/ml; adjusted hazard ratio (HR) = 1.47, 95% confidence interval (CI) 1.03–2.09, p=0.035) but not PlGF (≥25 pg/ml; adjusted HR = 1.26, 95%CI 0.94–1.71, p=0.12) were associated with adverse cardiovascular outcomes. In addition, significant elevation of sFlt-1 levels was observed in left anterior descending artery ligation and transverse aortic constriction HF mouse models after 4 and 8 weeks of follow up, suggesting vascular stress and ischemia as triggers for sFlt-1 elevation in HF. Conclusions Circulating sFlt-1 is generated as a result of myocardial injury and subsequent HF development. Elevated levels of sFlt-1 are associated with adverse outcomes in stable patients with HF.