The contribution of postural control and bilateral coordination to the impact of dual tasking on gait

The simultaneous performance of a cognitive task while walking typically alters the gait pattern. In some populations, these alterations have been associated with an increased risk of falls, motivating study of this response from the clinical perspective. The mechanisms responsible for these effects are not fully understood. The concurrent requirement to control upright posture and stepping, a bilaterally coordinated rhythmic task, may be the cause of this so-called dual-tasking effect. To evaluate this possibility, the present study was designed to isolate the individual contribution of these two demands by assessing the effects of cognitive loading on standing (i.e., postural control without bilateral coordination of stepping), cycling (i.e., bilateral coordination similar to stepping, but with minimal postural demands), and walking. We also investigated the effects of aging and parkinsonism on the performance of these three tasks in response to cognitive loading, also referred to as a dual task. Twenty-one healthy young adults, 15 healthy older adults, and 18 patients with Parkinson’s disease were assessed while walking, standing, and cycling, with and without an additional cognitive load. In the young adults, the performance on the two motor tasks that involved bilateral coordination deteriorated significantly in response to the dual task, while standing was not impacted. Similar results, although less robust, were observed among the healthy older adults. In contrast, among the patients with Parkinson’s disease, the dual-task costs, i.e., the impact of the simultaneously performed cognitive task on the gait pattern, were high in all motor tasks. These findings suggest that walking is especially vulnerable to cognitive loading, in part, because of the unique sensitivity of bilateral coordination of limb movements to the effects of dual tasking.     

Modulation of cardiac macrophages by phosphatidylserine-presenting liposomes improves infarct repair

Herein we investigated a new strategy for the modulation of cardiac macrophages to a reparative state, at a predetermined time after myocardial infarction (MI), in aim to promote resolution of inflammation and elicit infarct repair. The strategy employed intravenous injections of phosphatidylserine (PS)-presenting liposomes, mimicking the anti-inflammatory effects of apoptotic cells. Following PS-liposome uptake by macrophages in vitro and in vivo, the cells secreted high levels of anti-inflammatory cytokines [transforming growth factor β (TGFβ) and interleukin 10 (IL-10)] and upregulated the expression of the mannose receptor--CD206, concomitant with downregulation of proinflammatory markers, such as tumor necrosis factor α (TNFα) and the surface marker CD86. In a rat model of acute MI, targeting of PS-presenting liposomes to infarct macrophages after injection via the femoral vein was demonstrated by magnetic resonance imaging (MRI). The treatment promoted angiogenesis, the preservation of small scars, and prevented ventricular dilatation and remodeling. This strategy represents a unique and accessible approach for myocardial infarct repair.     

Molecular Imaging of Healing After Myocardial Infarction

The progression from acute myocardial infarction (MI) to heart failure continues to be a major cause of morbidity and mortality. Potential new therapies for improved infarct healing such as stem cells, gene therapy, and tissue engineering are being investigated. Noninvasive imaging plays a central role in the evaluation of MI and infarct healing, both clinically and in preclinical research. Traditionally, imaging has been used to assess cardiac structure, function, perfusion, and viability. However, new imaging methods can be used to assess biological processes at the cellular and molecular level. We review molecular imaging techniques for evaluating the biology of infarct healing and repair. Specifically, we cover recent advances in imaging the various phases of MI and infarct healing such as apoptosis, inflammation, angiogenesis, extracellular matrix deposition, and scar formation. Significant progress has been made in preclinical molecular imaging, and future challenges include translation of these methods to clinical practice.     

Circulating endothelial progenitor cells in patients with dysfunctional versus normally functioning congenitally bicuspid aortic valves

Patients with bicuspid aortic valve (BAV) may gradually develop significant valve dysfunction, whereas others remain free of dysfunction. Factors that determine the prognosis of BAV remain unclear. Because endothelial progenitor cells (EPCs) have a role in the repair of endothelial surfaces after injury, we hypothesized that EPCs may also be involved in preventing BAV degeneration. Accordingly, we compared EPC level and function in patients with BAV with versus without valve dysfunction. The study group included 22 patients with BAV and significant valve dysfunction (at least moderate aortic regurgitation and/or at least moderate aortic stenosis). The control group included 28 patients with BAV without valve dysfunction. All patients had 1 blood sample taken. Proportion of peripheral mononuclear cells expressing vascular endothelial growth factor receptor 2, CD133 and CD34 was evaluated by flow cytometry. EPC colony-forming units (CFUs) were grown from peripheral mononuclear cells, characterized, and counted after 7 days of culture. The 2 groups had similar clinical characteristics except for higher prevalence of hypertension in the dysfunctional valve group. Number of EPC CFUs was smaller in the dysfunctional valve group (32 CFUs/plate, 15 to 42.5, vs 48 CFUs/plate, 30 to 62.5, respectively, p = 0.01), and the migratory capacity of the cells in this group was decreased. In addition, the proportion of cells coexpressing vascular endothelial growth factor receptor 2, CD133, and CD34 tended to be smaller in the dysfunctional valve group. In conclusion, patients with BAV and significant valve dysfunction appear to have circulating EPCs with impaired functional properties. These findings require validation by further studies.