Poor Motor Competence Affects Functional Capacities and Healthcare in Children and Adolescents with Obesity.

BACKGROUND: From a young age, children learn different motor skills known as fundamental motor skills. The acquisition of these skills is crucial for the future development of context-tailored actions that could improve adherence to physical activity (PA) practice. Motor competence and function deficits have been associated with pediatric obesity. We reviewed the literature data regarding motor competence in pediatrics and impaired motor performance in children and adolescents with obesity. METHODS: We assessed the abstracts of the available literature (n = 110) and reviewed the full texts of potentially relevant articles (n = 65) that were analyzed to provide a critical discussion. RESULTS: Children and adolescents with obesity show impaired motor performance, executive functions, postural control, and motor coordination. Children's age represents a crucial point in the development of motor skills. Early interventions are crucial to preventing declines in motor proficiency and impacting children's PA and overall fitness levels. CONCLUSIONS: To involve children, the PA protocol must be fun and tailored in consideration of several aspects, such as clinical picture, level of physical fitness, and motor skills. A supervised adapted exercise program is useful to personalized PA programs from an early pediatric age.

Mesoangioblasts, vessel-associated multipotent stem cells, repair the infarcted heart by multiple cellular mechanisms: a comparison with bone marrow progenitors, fibroblasts, and endothelial cells.

OBJECTIVE: To test the potential of mesoangioblasts (Mabs) in reducing postischemic injury in comparison with bone marrow progenitor cells (BMPCs), fibroblasts (Fbs), and embryonic stem cell-derived endothelial cells (ECs), and to identify putative cellular protective mechanisms. METHODS AND RESULTS: Cells were injected percutaneously in the left ventricular (LV) chamber of C57BL/6 mice, 3 to 6 hours after coronary ligation, and detected in the hearts 2 days and 6 weeks later. Echocardiographic examinations were performed at 6 weeks. LV dilation was reduced and LV shortening fraction was improved with Mabs and BMPCs but not with ECs and Fbs. Donor cell colonization of the host myocardium was modest and predominantly in the smooth muscle layer of vessels. Capillary density was higher in the peripheral infarct area and apoptotic cardiomyocytes were fewer with Mabs and BMPCs. Mabs and BMPCs, but not Fbs or ECs, promoted survival of cultured cardiocytes under low-oxygen in culture. This activity was present in Mab-conditioned medium and could be replaced by a combination of basic fibroblast growth factor (bFGF), insulin-like growth factor (IGF)-1, and hepatocyte growth factor (HGF), all of which are produced by these cells. Conditioned medium from Mabs, but not from Fbs, stimulated proliferation of smooth muscle cells in vitro. CONCLUSIONS: Mabs appear as effective as BMPCs in reducing postinfarction LV dysfunction, likely through production of antiapoptotic and angiogenic factors.

Myocardial infarction: animal models.

Among the cardiovascular pathologies, ischemic heart disease is the leading cause of congestive heart failure as well as permanent premature disabilities. Reperfusion of a previously ischemic heart is a standard clinical procedure. Even if beneficial, reperfusion triggers an inflammatory response that contributes to the acute extension of ischemic injury and later participates in the reparative processes of the damaged myocardium. Occlusion of a major coronary artery in small rodents, followed or not followed by reperfusion, has proven to be a good model to assess the relevance of pathophysiological processes and drug effects in the setting of myocardial ischemia. Models involving reperfusion appear to be particularly suitable to study the inflammatory response, which is much more marked than with permanent ischemia. Ischemia/reperfusion of the myocardium in wild-type and transgenic animals (mostly mice) allows the possibility of testing the vast array of mediators that orchestrate the sequelae of inflammation, including tumor necrosis factor (TNF). Moreover, this model allows testing of the protective effects of anti-inflammatory drugs in experimental myocardial infarction.

A nonerythropoietic derivative of erythropoietin protects the myocardium from ischemia-reperfusion injury.

The cytokine erythropoietin (EPO) protects the heart from ischemic injury, in part by preventing apoptosis. However, EPO administration can also raise the hemoglobin concentration, which, by increasing oxygen delivery, confounds assignment of cause and effect. The availability of EPO analogs that do not bind to the dimeric EPO receptor and lack erythropoietic activity, e.g., carbamylated EPO (CEPO), provides an opportunity to determine whether EPO possesses direct cardioprotective activity. In vivo, cardiomyocyte loss after experimental myocardial infarction (MI) of rats (40 min of occlusion with reperfusion) was reduced from approximately 57% in MI-control to approximately 45% in animals that were administered CEPO daily for 1 week (50 microg/kg of body weight s.c.) with the first dose administered intravenously 5 min before reperfusion. CEPO did not increase the hematocrit, yet it prevented increases in left ventricular (LV) end-diastolic pressure, reduced LV wall stress in systole and diastole, and improved LV response to dobutamine infusion compared with vehicle-treated animals. In agreement with the cardioprotective effect observed in vivo, staurosporine-induced apoptosis of adult rat or mouse cardiomyocytes in vitro was also significantly attenuated ( approximately 35%) by CEPO, which is comparable with the effect of EPO. These data indicate that prevention of cardiomyocyte apoptosis, in the absence of an increase in hemoglobin concentration, explains EPO's cardioprotection. Nonerythropoietic derivatives such as CEPO, devoid of the undesirable effects of EPO, e.g., thrombogenesis, could represent safer and more effective alternatives for treatment of cardiovascular diseases, such as MI and heart failure. Furthermore, these findings expand the activity spectrum of CEPO to tissues outside the nervous system.

Eplerenone, a selective aldosterone blocker, improves diastolic function in aged rats with small-to-moderate myocardial infarction.

BACKGROUND: The incidence of cardiovascular diseases increases rapidly with age, and the elderly suffer higher morbidity and mortality. Aldosterone blockers have shown benefits in patients with left ventricular (LV) dysfunction and heart failure after myocardial infarction (MI). However, aldosterone blockade efficacy has not been explored in aged animals with MI. Methods and results Small-to-moderate MI was induced by coronary artery ligation in 16-month old rats, divided into 3 groups: sham-operated (control, n = 9), MI (n = 9), and MI fed a diet containing eplerenone (120 mg/kg/day, MI+Eplerenone, n = 9) given 18 days postsurgery and up to sacrifice 3 months later. At sacrifice, untreated MI rats did not show overt systolic dysfunction but they had (1) echocardiographic evidences of impaired relaxation (increase of E wave deceleration time and of isovolumic relaxation time, decrease of peak E wave velocity), (2) hemodynamically impaired LV relaxation (LV -dP/dt from 7413 +/- 720 to 4956 +/- 475 mm Hg/s, P < .05), and (3) significant increase of collagen content in LV interstitium (from 4.27 +/- 0.23 to 5.34 +/- 0.24%, P < .01) and in aorta (from 19 +/- 1 to 24 +/- 2%, P < .05). Eplerenone normalized echocardiographic and hemodynamic evidences of diastolic dysfunction, as well as myocardial interstitial collagen and aortic fibrosis (all parameters statistically different from untreated MI). CONCLUSION: In aged rats with small to moderate MI, eplerenone normalized diastolic relaxation, possibly through a reduction of interstitial fibrosis.