Comparison between piezoelectric and magnetic strategies for wearable energy harvesting

This paper introduces the design and fabrication of energy harvesters for the power generation from human body motion. Two alternative strategies are compared: piezoelectric and magnetic inductive. The generated energy is used to supply body sensors including accelerometers and temperature sensors and RF module. Two prototypes of the magnetic based generator and of the piezoelectric generator are built and tested with shaker at resonance condition and by dedicated bench reproducing joints rotation during walking. The experimental results show that the magnetic prototype can generate 0.7mW from human body motion, while the piezo harvester generates 0.22 and 0.33μW respectively for flexion and extension at angular velocity lower than 1rad/s and 45° amplitude

Experimental and numerical characterization of a gravitational electromagnetic energy harvester

In this paper, the dynamic experimental identification of an inductive energy harvester for the conversion of vibration energy into electric power is presented. Recent advances and requirements in structural monitoring and vehicle diagnostic allow defining Autonomous Internet of Things (AIoT) systems that combine wireless sensor nodes with energy harvester devices properly designed considering the specific duty cycle. The proposed generator was based on an asymmetrical magnetic suspension and was addressed to structural monitoring applications on vehicles. The design of the interfaces of the electric, magnetic, and structural coupled systems forming the harvester are described including dynamic modeling and simulation. Finally, the results of laboratory tests were compared with the harvester dynamic response calculated through numerical simulations, and a good correspondence was obtained

Haar wavelet-based adaptive finite volume shallow water solver

This paper presents the formulation of an adaptive finite volume (FV) model for the shallow water equations. A Godunov-type reformulation combining the Haar wavelet is achieved to enable solutiondriven resolution adaptivity (both coarsening and refinement) by depending on the wavelet’s threshold value. The ability to properly model irregular topographies and wetting/drying are transferred from the (baseline) FV uniform mesh model, with no extra notable efforts. Selected hydraulic tests are employed to analyse the performance of the Haar wavelet FV shallow water solver considering adaptivity and practical issues including choice for the threshold value driving the adaptivity, mesh convergence study, shock and wet/dry front capturing abilities. Our findings show that Haar wavelet-based adaptive FV solutions offer great potential to improve the reliability of multiscale shallow water models

Cardiomyocyte and vascular smooth muscle independent 11β-hydroxysteroid dehydrogenase 1 amplifies infarct expansion, hypertrophy and the development of heart failure following myocardial infarction in male mice

Global deficiency of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), an enzyme that regenerates glucocorticoids within cells, promotes angiogenesis, and reduces acute infarct expansion after myocardial infarction (MI), suggesting that 11β-HSD1 activity has an adverse influence on wound healing in the heart after MI. The present study investigated whether 11β-HSD1 deficiency could prevent the development of heart failure after MI and examined whether 11β-HSD1 deficiency in cardiomyocytes and vascular smooth muscle cells confers this protection. Male mice with global deficiency in 11β-HSD1, or with Hsd11b1 disruption in cardiac and vascular smooth muscle (via SM22α-Cre recombinase), underwent coronary artery ligation for induction of MI. Acute injury was equivalent in all groups. However, by 8 weeks after induction of MI, relative to C57Bl/6 wild type, globally 11β-HSD1-deficient mice had reduced infarct size (34.7 ± 2.1% left ventricle [LV] vs 44.0 ± 3.3% LV, P = .02), improved function (ejection fraction, 33.5 ± 2.5% vs 24.7 ± 2.5%, P = .03) and reduced ventricular dilation (LV end-diastolic volume, 0.17 ± 0.01 vs 0.21 ± 0.01 mL, P = .01). This was accompanied by a reduction in hypertrophy, pulmonary edema, and in the expression of genes encoding atrial natriuretic peptide and β-myosin heavy chain. None of these outcomes, nor promotion of periinfarct angiogenesis during infarct repair, were recapitulated when 11β-HSD1 deficiency was restricted to cardiac and vascular smooth muscle. 11β-HSD1 expressed in cells other than cardiomyocytes or vascular smooth muscle limits angiogenesis and promotes infarct expansion with adverse ventricular remodeling after MI. Early pharmacological inhibition of 11β-HSD1 may offer a new therapeutic approach to prevent heart failure associated with ischemic heart disease

Cinaciguat prevents the development of pathologic hypertrophy in a rat model of left ventricular pressure overload

Pathologic myocardial hypertrophy develops when the heart is chronically pressure-overloaded. Elevated intracellular cGMP-levels have been reported to prevent the development of pathologic myocardial hypertrophy, therefore we investigated the effects of chronic activation of the cGMP producing enzyme, soluble guanylate cyclase by Cinaciguat in a rat model of pressure overload-induced cardiac hypertrophy. Abdominal aortic banding (AAB) was used to evoke pressure overload-induced cardiac hypertrophy in male Wistar rats. Sham operated animals served as controls. Experimental and control groups were treated with 10 mg/kg/day Cinaciguat (Cin) or placebo (Co) p.o. for six weeks, respectively. Pathologic myocardial hypertrophy was present in the AABCo group following 6 weeks of pressure overload of the heart, evidenced by increased relative heart weight, average cardiomyocyte diameter, collagen content and apoptosis. Cinaciguat did not significantly alter blood pressure, but effectively attenuated all features of pathologic myocardial hypertrophy, and normalized functional changes, such as the increase in contractility following AAB. Our results demonstrate that chronic enhancement of cGMP signalling by pharmacological activation of sGC might be a novel therapeutic approach in the prevention of pathologic myocardial hypertrophy

Improved heart function follows enhanced inflammatory cell recruitment and angiogenesis in 11 beta HSD1-deficient mice post-MI

AIMS: Mice unable to locally regenerate corticosterone due to deficiency of 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1) have enhanced angiogenesis during acute myocardial infarct healing. The present study investigates the hypotheses that in these mice (i) inflammation and angiogenic signalling are promoted and (ii) longer-term remodelling and function are improved. METHODS AND RESULTS: Myocardial infarction (MI) was induced by coronary artery ligation in 11βHSD1(−/−) and wild-type (C57BL/6) mice. Studies were terminated 2, 4, 7, and 28 days post-surgery. Increased vessel density (CD31 immunoreactivity) on the infarct border was confirmed 7 days after MI in 11βHSD1(−/−) hearts (P < 0.05) and was accompanied by improved ejection fraction (ultrasound) compared with C57BL/6. During wound healing, recruitment of neutrophils (at 2 days after MI) and macrophages (from 4 days after MI) and expression of monocyte-chemoattractant protein-1 was increased in 11βHSD1(−/−) compared with C57BL/6 hearts (P < 0.05). Recruitment of alternatively activated YM1-positive macrophages was particularly enhanced in the period preceding increased vessel density and was accompanied by increased expression of pro-angiogenic IL-8. By 28 days post-MI, when the infarct scar had matured, higher vessel density was maintained in 11βHSD1(−/−) hearts and vessels were smooth-muscle coated. Infarct scars were thicker (P < 0.001) in 11βHSD1(−/−) compared with C57BL/6 hearts and ejection fraction was higher (P < 0.05). CONCLUSION: Increased vessel density in healing infarcts of mice deficient in 11(−/−)HSD1 follows recruitment of pro-reparative macrophages and increased pro-angiogenic signalling. Mature infarcts show less thinning and cardiac function is improved relative to wild-type mice, suggesting that 11βHSD1 may be a novel therapeutic target after MI