Neuropeptide Y (NPY) is an abundant sympathetic co-transmitter, widely found in the central and peripheral nervous systems and with diverse roles in multiple physiological processes. In the cardiovascular system it is found in neurons supplying the vasculature, cardiomyocytes and endocardium, and is involved in physiological processes including vasoconstriction, cardiac remodeling, and angiogenesis. It is increasingly also implicated in cardiovascular disease pathogenesis, including hypertension, atherosclerosis, ischemia/infarction, arrhythmia, and heart failure. This review will focus on the physiological and pathogenic role of NPY in the cardiovascular system. After summarizing the NPY receptors which predominantly mediate cardiovascular actions, along with their signaling pathways, individual disease processes will be considered. A thorough understanding of these roles may allow therapeutic targeting of NPY and its receptors.

Hydrogel iontronic devices can emulate biological functions and communicate with living matter. But the fabrication of miniature, soft iontronic devices according to modular designs has not been achieved. In this work, we report the use of surfactant-supported assembly of freestanding microscale hydrogel droplets to construct various iontronic modules, circuits, and biointerfaces. Chemical modifications of silk fibroin produced a pair of oppositely charged hydrogels. Microscale assembly of various combinations of hydrogel droplets produced iontronic diodes, npn- and pnp-type transistors, and diverse reconfigurable logic gates. Through the incorporation of poly(amino acid)s, we have demonstrated a droplet-based synthetic synapse with ionic polymer–mediated long-term plasticity. Further, our iontronic transistor can serve as a biocompatible sensor to record electrophysiological signals from sheets of human cardiomyocytes, paving a way to the building of miniature bioiontronic systems.

Advances in the development of tiny devices with sizes below a few cubic millimeters require a corresponding decrease in the volume of driving power sources. To be minimally invasive, prospective power sources in biomedical devices must be fabricated from soft materials. Previous endeavors with droplet-based devices have produced promising miniature power sources; however, a droplet-based rechargeable battery has remained out of reach. Here we report a microscale soft flexible lithium-ion droplet battery (LiDB) based on the lipid-supported assembly of droplets constructed from a biocompatible silk hydrogel. Capabilities such as triggerable activation, biocompatibility and biodegradability and high capacity are demonstrated. We have used the LiDB to power the electrophoretic translocation of charged molecules between synthetic cells and to mediate the defibrillation and pacing of ex vivo mouse hearts. By the inclusion of magnetic particles to enable propulsion, the LiDB can function as a mobile energy courier. Our tiny versatile battery will thereby enable a variety of biomedical applications.

We tested the hypothesis that the known reduction in myocardial functional reserve in preterm-born young adults is an independent predictor of exercise capacity (peak VO₂) and heart rate recovery (HRR). We recruited 101 normotensive young adults (n = 47 born preterm; 32.8 ± 3.2 weeks’ gestation and n = 54 term-born controls). Peak VO₂ was determined by cardiopulmonary exercise testing (CPET), and lung function assessed using spirometry. Percentage predicted values were then calculated. HRR was defined as the decrease from peak HR to 1 min (HRR₁) and 2 min of recovery (HRR₂). Four-chamber echocardiography views were acquired at rest and exercise at 40% and 60% of CPET peak power. Change in left ventricular ejection fraction from rest to each work intensity was calculated (EFΔ40% and EFΔ60%) to estimate myocardial functional reserve. Peak VO₂ and per cent of predicted peak VO₂ were lower in preterm-born young adults compared with controls (33.6 ± 8.6 vs. 40.1 ± 9.0 mL/kg/min, P = 0.003 and 94% ± 20% vs. 108% ± 25%, P = 0.001). HRR₁ was similar between groups. HRR₂ decreased less in preterm-born young adults compared with controls (−36 ± 13 vs. −43 ± 11 b.p.m., P = 0.039). In young adults born preterm, but not in controls, EFΔ40% and EFΔ60% correlated with per cent of predicted peak VO₂ (r² = 0.430, P = 0.015 and r² = 0.345, P = 0.021). Similarly, EFΔ60% correlated with HRR₁ and HRR₂ only in those born preterm (r² = 0.611, P = 0.002 and r² = 0.663, P = 0.001). Impaired myocardial functional reserve underlies reductions in peak VO₂ and HRR in young adults born moderately preterm. Peak VO₂ and HRR may aid risk stratification and treatment monitoring in this population.

Exercise is advised for young adults with elevated blood pressure, but no trials have investigated efficacy at this age. We aimed to determine whether aerobic exercise, self-monitoring and motivational coaching lowers blood pressure in this group. The study was a single-centre, open, two-arm, parallel superiority randomized clinical trial with open community-based recruitment of physically-inactive 18–35 year old adults with awake 24 h blood pressure 115/75mmHg-159/99 mmHg and BMI<35 kg/m². The study took place in the Cardiovascular Clinical Research Facility, John Radcliffe Hospital, Oxford, UK. Participants were randomized (1:1) with minimisation factors sex, age (<24, 24–29, 30–35 years) and gestational age at birth (37 weeks) to the intervention group, who received 16-weeks aerobic exercise training (three aerobic training sessions per week of 60 min per session at 60–80% peak heart rate, physical activity self-monitoring with encouragement to do 10,000 steps per day and motivational coaching to maintain physical activity upon completion of the intervention. The control group were sign-posted to educational materials on hypertension and recommended lifestyle behaviours. Investigators performing statistical analyses were blinded to group allocation. The primary outcome was 24 h awake ambulatory blood pressure (systolic and diastolic) change from baseline to 16-weeks on an intention-to-treat basis. Clinicaltrials.gov registered on March 30, 2016 (NCT02723552). Enrolment occurred between 30/06/2016-26/10/2018. Amongst the 203 randomized young adults (n = 102 in the intervention group; n = 101 in the control group), 178 (88%; n = 76 intervention group, n = 84 control group) completed 16-week follow-up and 160 (79%; n = 68 intervention group, n = 69 control group) completed 52-weeks follow-up. There were no group differences in awake systolic (0·0 mmHg [95%CI, -2·9 to 2·8]; P = 0·98) or awake diastolic ambulatory blood pressure (0·6 mmHg [95%CI, -1·4. to 2·6]; P = 0·58). Aerobic training increased peak oxygen uptake (2·8 ml/kg/min [95%CI, 1·6 to 4·0]) and peak wattage (14·2watts [95%CI, 7·6 to 20·9]) at 16-weeks. There were no intervention effects at 52-weeks follow-up. These results do not support the exclusive use of moderate to high intensity aerobic exercise training for blood pressure control in young adults. Wellcome Trust, British Heart Foundation, National Institute for Health Research, Oxford Biomedical Research Centre.