Optimization of permanent magnet type of retarder using 3-D finite element method and direct search method

3-D optimization method using the combined experimental design method and direct search method is developed to apply to the optimal design of a permanent magnet type of retarder. It is shown that the braking torque is increased by using the optimization method. The CPU time can be considerably reduced by utilizing the initial values obtained by the experimental design method </p

Allogeneic Mesenchymal Stem Cells as a Treatment for Aging Frailty

As life expectancy is projected to increase in the ensuing decades, individuals of older age continue to exceed the previous generation’s lifespan. Advancing age is associated with a reduction in physical and mental functional capacity, and chronic inflammation is a major factor contributing to this decline. A heightened inflammatory state can lead to exhaustion, weakness, weight loss, slow gate speed, and an overall decrease in activity level. These phenotypes define the onset of the disease process known as frailty. Frailty is a growing epidemic, which severely undermines a person’s ability to deal with outside stressors, and increases their rate of hospitalization, institutionalization, and mortality. Current interventions focus on preventative care by improving exercise capacity, strength, nutritional supplementation, diet, and mobility. However, a biological cure has heretofore remained elusive. Here, we introduce the novel therapeutic principle that mesenchymal stem cell (MSC) therapy may represent a safe, practical, and efficacious both the treatment and prevention of frailty in individuals of advancing age. To date, a phase I safety trial reveals an excellent safety profile and suggests that mesenchymal stem cells can ameliorate signs and symptoms of frailty. These early studies lay the groundwork for future large-scale clinical trials of this exciting and novel therapeutic concept that has the potential to expand health span in the aging population

Left atrial diastasis strain slope is a marker of hemodynamic recovery in post-ST elevation myocardial infarction: the Laser Atherectomy for STemi, Pci Analysis with Scintigraphy Study (LAST-PASS)

BackgroundLeft atrial (LA) mechanics are strongly linked with left ventricular (LV) filling. The LA diastasis strain slope (LADSS), which spans between the passive and active LA emptying phases, may be a key indicator of the LA–LV interplay during diastole.AimThis study aimed to investigate the LA–LV interdependencies in post-ST elevation myocardial infarction (STEMI), with particular focus on the LADSS.Materials and methodsPatients with post-anterior STEMI who received primary percutaneous coronary intervention underwent contrast cardiac magnetic resonance imaging (MRI) during acute (5–9 days post-STEMI) and chronic (at 6 months) phases. The LADSS was categorized into three groups: Groups 1, 2, and 3 representing positive, flat, and negative slopes, respectively. Cross-sectional correlates of LADSS Group 2 or 3 compared to Group 1 were identified, adjusting for demographics, LA indices, and with or without LV indices. The associations of acute phase LADSS with the recovery of LV ejection fraction (LVEF) and scar amount were investigated.ResultsSixty-six acute phase (86.4% male, 63.1 ± 11.8 years) and 59 chronic phase cardiac MRI images were investigated. The distribution across LADSS Groups 1, 2, and 3 in the acute phase was 24.2%, 28.9%, and 47.0%, respectively, whereas in the chronic phase, it was 33.9%, 22.0%, and 44.1%, respectively. LADSS Group 3 demonstrated a higher heart rate than Group 1 in the acute phase (61.9 ± 8.7 vs. 73.5 ± 11.9 bpm, p &lt; 0.01); lower LVEF (48.7 ± 8.6 vs. 41.8 ± 9.9%, p = 0.041) and weaker LA passive strain rate (SR) (−1.1 ± 0.4 vs. −0.7 [−1.2 to −0.6] s−1, p = 0.037) in the chronic phase. Chronic phase Group 3 exhibited weaker LA passive SR [relative risk ratio (RRR) = 8.8, p = 0.012] than Group 1 after adjusting for demographics and LA indices; lower LVEF (RRR = 0.85, p &lt; 0.01), higher heart rate (RRR = 1.1, p = 0.070), and less likelihood of being male (RRR = 0.08, p = 0.058) after full adjustment. Acute phase LADSS Groups 2 and 3 predicted poor recovery of LVEF when adjusted for demographics and LA indices; LADSS Group 2 remained a predictor in the fully adjusted model (β = −5.8, p = 0.013).ConclusionThe LADSS serves both as a marker of current LV hemodynamics and its recovery in post-anterior STEMI. The LADSS is an important index of LA–LV interdependency during diastole.Clinical Trial Registrationhttps://clinicaltrials.gov/, identifier NCT03950310

Insights Into Signaling in Cell-Based Therapy for Heart Disease

Over the past several decades, stem cell therapy for heart disease has been translated from the bench to the bedside and in clinical trials improves cardiac structure and function in both ischemic and nonischemic cardiac disease. Although the regenerative effects of stem cells in cardiac disease are mediated by both paracrine and cell-to-cell contact mechanisms, many of the downstream signaling pathways remain to be fully elucidated. This review outlines what is currently known about the main signaling pathways involved in mesenchymal stem cell and cardiac stem cell survival, proliferation, and migration and mechanisms of action to repair the damaged heart. </jats:p

Abstract 35: Transendocardial Mesenchymal Stem Cell Injection Demonstrates Reverse Remodeling Effects of Global LV Volumes and Enhanced Lateral Papillary Muscle Shortening

Rationale: Secondary mitral regurgitation (MR) carries a poor prognosis despite improvements in surgical and transcatheter interventions. Mesenchymal stem cell (MSC) therapy for heart disease reduces infarct size and left ventricle (LV) dilatation, reverses remodeling, and improves regional contractility and functional capacity. However, it is unknown if the benefits of MSC therapy on LV structure and function apply to lateral papillary muscle shortening, an important predictor of secondary MR severity. Hypothesis: Test the hypothesis that administration of MSCs promotes interpapillary muscle distance (IPMD) shortening. Methods/Results: This retrospective analysis draws on results from autologous or allogeneic MSC injection therapies in a Göttingen swine model of chronic ischemic cardiomyopathy (ICM). MRI was used to measure end-diastolic volume (EDV), end-systolic volume (ESV), diastolic/systolic IPMD, and IPMD shortening. NOGA mapping and angiographic tracings of left ventriculography allowed for assessment of the effect of injection localized to papillary muscles (defined as injection within cardiac segments 4, 6, 10 and 12 in the 16-segment model). Three months after stem cell injection, EDV increased in both placebo- (12.2±3.6 mL; p=0.002) and MSC- (10.2±2.6 mL; p=0.03) treated swine. ESV increased only in placebo- (7.1±2.2 mL; p=0.003) but not MSC- treated swine. Systolic IPMD was maintained with MSC therapy (1.20±0.74 mm; p=0.33) but increased in placebo (1.83±0.60 mm; p=0.01). Systolic IPMD was preserved whether MSC injection was localized to papillary muscle (0.53±0.49 mm; p=0.44) or not (0.22±0.40 mm; p=0.24). Notably, IPMD shortening was significantly greater in MSC- (8.1±5.6%; p=0.02) but not placebo-injected (4.7±5.0%; p=0.69) swine. There were no between group differences in IPMD shortening (p=0.08). Conclusion: This study is the first to show that transendocardial MSC injections significantly enhanced IPMD shortening and lateral interpapillary muscle contraction in a model of chronic ICM. This effect was independent of injection site