Comportamento alimentar entre estudantes de medicina de uma Universidade privada em Campo Grande – Mato Grosso do Sul / Eating behavior among medical students in a private university in Campo Grande - Mato Grosso do Sul

A preocupação com a autoimagem incentivada pela mídia, aliada ao estresse cotidiano propicia desvios de comportamento alimentar e insatisfação corporal. Este estudo teve como objetivo identificar a prevalência de transtornos alimentares e de insatisfação corporal em estudantes de medicina do sexo feminino da Universidade Uniderp na cidade de Campo Grande – MS e correlacionar com os índices de massa corporal. É um estudo transversal com amostra aleatória representativa de 154 estudantes, utilizando como método de estudo o Índice de Massa Corporal (IMC); o Eating Attitudes Test (EAT-26) e o Body Shape Questionnaire modificado. Todos os dados colhidos foram tabulados no Excel para análise de frequência e cruzamento de variáveis. Como resultado foi obtido a média de 20,15% de peso elevado, 30,5% de estudantes com comportamento de risco para Transtornos Alimentares Comportamentais (TCA) e 47,4% de prevalência de insatisfação corporal. 47,4% das acadêmicas tiveram ambos os resultados normais. É evidenciado que as acadêmicas de medicina que apresentaram risco para o desenvolvimento ou progressão de TCA colhem repercussões danosas tanto na saúde física quanto mental. Conclui-se que equilibrando a rotina extensa com hábitos saudáveis tende a reduzir o desencadeamento de distúrbios, não prejudicando a saúde e o exercício da carreira médica futuramente

Stem Cell Therapies for Renal Diseases

Kidney disease is a public health priority, due to its morbidity and mortality with limited therapeutic options. Stem cell therapies are undergoing investigation to improve the regenerative capacity of the kidney. The mechanisms underlying the reparative effects of stem cells include antiinflammatory, immunomodulatory, antiapoptotic, and pro-angiogenic properties. Stem cell clinical trials have shown efficacy in improving kidney transplantation success, whereas variable responses have been observed in acute and chronic kidney diseases, depending on various variables including disease background, cell type, route of administration, and patient population. In this article, we review the state of the stem cell therapy field in kidney disease

Mesenchymal Stem Cell-Based Therapy for Cardiovascular Disease: Progress and Challenges

Administration of mesenchymal stem cells (MSCs) to diseased hearts improves cardiac function and reduces scar size. These effects occur via the stimulation of endogenous repair mechanisms, including regulation of immune responses, tissue perfusion, inhibition of fibrosis, and proliferation of resident cardiac cells, although rare events of transdifferentiation into cardiomyocytes and vascular components are also described in animal models. While these improvements demonstrate the potential of stem cell therapy, the goal of full cardiac recovery has yet to be realized in either preclinical or clinical studies. To reach this goal, novel cell-based therapeutic approaches are needed. Ongoing studies include cell combinations, incorporation of MSCs into biomaterials, or pre-conditioning or genetic manipulation of MSCs to boost their release of paracrine factors, such as exosomes, growth factors, microRNAs, etc. All of these approaches can augment therapeutic efficacy. Further study of the optimal route of administration, the correct dose, the best cell population(s), and timing for treatment are parameters that still need to be addressed in order to achieve the goal of complete cardiac regeneration. Despite significant progress, many challenges remain. [Display omitted] Administering mesenchymal stem cells (MSCs) to the injured heart improves cardiac function and reduces scar size, primarily by stimulating endogenous repair mechanisms. We review the progress, challenges, and potential of MSC-based therapy, and we propose that combining MSCs with other cell type(s) improves therapeutic efficacy

Attenuation of frailty in older adults with mesenchymal stem cells

•Frailty is a syndrome characterized by exhaustion, weight loss, a feeling of slowing down, and low levels of activity.•Frailty is associated with chronic inflammation and depletion or impairment of endogenous precursor and stem cells.•Interventions such as nutritional supplementation, physical exercise have shown inconsistent and modest benefits.•Use of allogeneic mesenchymal stem cells (MSCs) is a novel approach that addresses the pathophysiology of the syndrome.•Clinical studies show that MSCs are safe and potentially efficacious, ameliorating signs and symptoms of frailty. Aging frailty is a syndrome characterized by a progressive decline in health and clinical symptoms of exhaustion, weight loss, a feeling of slowing down, and a decrease in functional capacity. The biological substrate for frailty is sarcopenia, which is potentiated by chronic inflammation and depletion or impairment of endogenous precursor and stem cells. Current interventions focus on interdisciplinary approaches which include nutritional supplementation, physical exercise, and cognitive intervention. Clinical studies of these preventative approaches have shown inconsistent and modest benefits, further highlighting the unmet clinical need. A variety of pharmacologic and biologic therapies are currently being tested to treat aging. Cell-based therapy represents an attractive option that addresses the pathophysiology of the syndrome. Human allogeneic mesenchymal stem cells (MSCs) which possess immunomodulatory and tissue reparative properties, have been tested in Phase I and Phase II trials. These small early stage studies reveal that allogeneic MSCs administered to frail older adults are feasible to administer, safe and potentially efficacious, ameliorating signs and symptoms of frailty. These studies have formed the basis for larger ongoing trials. Here we review the pathobiology of frailty, and the potential for developing biological strategies to treat this important syndrome

Mechanism of Action of Mesenchymal Stem Cells (MSCs): impact of delivery method

Mesenchymal stromal cells (MSCs; AKA mesenchymal stem cells) stimulate healing and reduce inflammation. Promising therapeutic responses are seen in many late-phase clinical trials, but others have not satisfied their primary endpoints, making translation of MSCs into clinical practice difficult. These inconsistencies may be related to the route of MSC delivery, lack of product optimization, or varying background therapies received in clinical trials over time. Here we discuss the different routes of MSC delivery, highlighting the proposed mechanism(s) of therapeutic action as well as potential safety concerns. PubMed search criteria used: MSC plus: local administration; routes of administration; delivery methods; mechanism of action; therapy in different diseases. Direct injection of MSCs using a controlled local delivery approach appears to have benefits in certain disease states, but further studies are required to make definitive conclusions regarding the superiority of one delivery method over another

Stem Cells and Myocardial Repair

The rising prevalence of cardiovascular disease and the limited treatment options necessitate new therapeutic approaches to stimulate cardiac repair. Stem cell administration has emerged as a novel treatment for cardiovascular disease and over the last two decades has been successfully translated from in vitro and preclinical studies to clinical trials. A variety of cell types have been administered in clinical trials to treat heart disease, with some demonstrating promising results to repair the damaged heart. However, their efficacy remains controversial and defining the ideal cell type, cell dose, route and timing of delivery and ideal patient population, remains a challenge. Here, we discuss lessons learned from previous clinical trials and propose future directions of cell-based therapy for cardiac disease

Abstract 15869: Antiarrhythmic Effects of Mesenchymal Stromal Cells in a Post-Infarct Swine Model of Ventricular Tachycardia

Abstract only Introduction: Mesenchymal Stromal Cells (MSC) reduce scar burden in models of ischemic cardiomyopathy. It is unknown whether MSCs exert antiarrhythmic effects. Hypothesis: MSCs reduce inducibility of monomorphic VT (mmVT) or prolong VT cycle length by ≥20 msec in a post-infarct swine model of VT. Methods: Two groups of 8 Yorkshire Swine underwent a 180-minute occlusion of the LAD. Group 1 (n=8) pigs underwent initial MRI scan, electrophysiology study (EPS), and 3D electroanatomic mapping (EAM) with injection of open-label MSCs (200M cells) around the borderzone of the infarct, using a NOGA Myostar catheter (J&J) guided by EAM. Group 1 pigs had repeat EAM, and final EPS 8 weeks later. Group 2 pigs (n=8) were randomized between placebo and MSC and underwent sequential MSC injections (100M cells/procedure), 7 weeks apart, followed by final EPS and MRI 7 weeks later. Scar% = total scar/myocardial mass (grams). Results: MmVT was induced in 5 of 8 (62.5%) at initial EPS (i-EPS) in Group 1 pigs and 3 of 8 (37.5%) at final EPS (f-EPS). In Group 2 all 4 MSC-treated swine had inducible mmVT during i-EPS but only 2 had mmVT at f-EPS. Overall, 9 of 12 MSC-treated pigs had mmVT initially and 5 of 12 pigs had mmVT at f-EPS (p=0.12). For MSC-treated pigs with persistently inducible mmVT (Groups 1 & 2), the baseline VT CL increased in all pigs by ≥20msec and increased from 216 ± 17 msec initially to 274 ± 35 msec at f-EPS (p = 0.001). In Group 1, Scar% was unchanged (22.2±1.6% to 20.5±2.1%) after single MSC treatment (p=0.17). In Group 2 MSC-treated pigs, Scar% decreased from 25.8±2.0% to 17.9±0.6% after 2 MSC treatments (p=0.014). In pigs with mmVT at i-EPS, the scar% was 24.4±1.2%, compared with 19.3±2.0% in pigs without i-EPS inducible mmVT (p=0.025). In pigs with mmVT at f-EPS, scar% was 22.5±1.8% compared with 18.1±1.6% in pigs without mmVT at f-EPS (p=0.048). Placebo-treated pigs showed no change in scar% (22.5±2.6% to 22.4±2.9%, p=0.44) and no change in VT inducibility (3 of 4 pigs at i-EPS and f-EPS). Conclusions: This study demonstrates that MSC injection reduced myocardial scar and either suppressed induction of VT or prolonged VT cycle length, consistent with an antiarrhythmic effect. Lower scar burden was associated with non-inducibility of VT, either at baseline or final EPS

Preclinical comparative assessment of a dedicated pediatric poly‐L‐lactic‐acid‐based bioresorbable scaffold with a low‐profile bare metal stent

Background Polymer‐based bioresorbable scaffolds (PBBS) have been assessed for coronary revascularization with mixed outcomes. Few studies have targeted pediatric‐specific scaffolds. We sought to assess safety, efficacy, and short‐term performance of a dedicated drug‐free PBBS pediatric scaffold compared to a standard low‐profile bare metal stent (BMS) in central and peripheral arteries of weaned piglets. Methods Forty‐two devices (22 Elixir poly‐L‐lactic‐acid‐based pediatric bioresorbable scaffolds [BRS] [6 × 18 mm] and 20 control BMS Cook Formula 418 [6 × 20 mm]) were implanted in the descending aorta and pulmonary arteries (PAs) of 14 female Yucatan piglets. Quantitative measurements were collected on the day of device deployment and 30 and 90 days postimplantation to compare device patency and integrity. Results The BRS has a comparable safety profile to the BMS in the acute setting. Late lumen loss (LLL) and percent diameter stenosis (%DS) were not significantly different between BRS and BMS in the PA at 30 days. LLL and %DS were greater for BRS versus BMS in the aorta at 30 days postimplantation (LLL difference: 0.96 ± 0.26; %DS difference: 16.15 ± 4.51; p < .05). At 90 days, %DS in the aortic BRS was less, and PA BRS LLL was also less than BMS. Histomorphometric data showed greater intimal proliferation and area stenosis in the BRS at all time points and in all vessels. Conclusions A dedicated PBBS pediatric BRS has a favorable safety profile in the acute/subacute setting and demonstrates characteristics that are consistent with adult BRSs

Abstract Mo102: Swine Model of Heart Failure with Preserved Ejection Fraction Driven by Lipoprotein Lipase Inhibition and Enhanced Cardiac Low-Density Lipoprotein Receptor Expression

Abstract only Background: Heart failure with preserved ejection fraction (HFpEF) poses an escalating public health threat, marked by growing incidence and high mortality. In the cardiometabolic phenogroup of HFpEF that includes diabetes and obesity, intramyocardial lipid content is a prognostic indicator of diastolic dysfunction and adverse outcome. Our group recently reported a mouse model of cardiometabolic HFpEF wherein myocardial lipotoxicity was induced by systemic inhibition of lipoprotein lipase (LPL) with Poloxamer 407 (P407) and cardiac overexpression of the LDL receptor (LDLR), conditions that have been documented in clinical HFpEF. The model demonstrates myocardial lipid accumulation, fibrosis, arrhythmia, and diastolic dysfunction. To reproduce this model in large animals we implemented the same protocol in pigs. Methods: Female Yorkshire swine (~25 Kg) were subjected to one of two protocols including: 1) single intracoronary (i.c.) injection of 10 13 AAV9-cTnT-LDLR particles and biweekly intraperitoneal (i.p.) P407 at 1g/Kg, (high dose, n=2), or 2) Double i.c. injections of 10 13 AAV9-cTnT-LDLR particles and biweekly i.p. P407 at 0.25g/Kg) (low dose, n=2). Cardiac structure and function were evaluated by MRI, and hemodynamics measured by PV-Loop at baseline, 4, 8, and 12 weeks. Blood was collected biweekly for complete blood count (CBC), basic biochemistry, and liver and lipid panels. Tissues were collected for protein and histopathological analysis. Results: In both strategies, the animals developed high LDL-cholesterol and cardiac hypertrophy with preserved EF. High dose P407 led to higher triglycerides, VLDL, HDL, liver injury (ALT > 200U/L), and steatosis at 4 weeks. One of the 2 pigs died at 3 weeks. Low dose P407 and high dose viral particles induced HFpEF at ~12 weeks with increased LV mass, relative wall thickness, end-diastolic pressure, and tau. Serum LDL-C accumulated from an initial value of 161 to 344.5mg/dL at 12 weeks. No significant liver injury was present until week 12 (ALT<88 U/L, AST<59 U/L). Both strategies did not exhibit abnormalities in CBC or other biochemical parameters. Conclusions: Low dose inhibition of LPL combined with cardiac overexpression of LDLR confers HFpEF in swine

Effectiveness of growth hormone-releasing hormone agonists (GHRH‐A) in chronic kidney disease-induced heart failure with preserved ejection fraction

Background: Therapies that improve morbidity and mortality in heart failure with preserved ejection fraction (HFpEF) are lacking. Growth hormone releasing hormone analogues (GHRH-A) reverse fibrosis and improve cardiac function in ischemic and non-ischemic animal models. We tested the hypothesis that GHRH-A treatment ameliorates chronic kidney disease (CKD)-induced HFpEF in a large animal model. Methods: Female Yorkshire pigs (n=16) underwent 5/6 nephrectomy via renal artery embolization, which induced HFpEF, and 12-weeks later received daily subcutaneous injections of GHRH-A (n=8) or placebo (n=8). Kidney function, renal and cardiac MRI, pressure-volume loops, and electrical stimulation were assessed at baseline, 12-weeks, and 16-18 weeks post-embolization. Results: The CKD model was confirmed by increased creatinine and BUN. HFpEF was demonstrated at 12 weeks by maintenance of ejection fraction associated with increased left ventricular mass, relative wall thickening, end-diastolic pressure (EDP), end-diastolic pressure-volume relationship (EDPVR), and tau. After 6 weeks of treatment, diastolic function improved in the GHRH-A group, evidenced by normalization of EDP (p=0.03) associated with improved diastolic compliance as measured by EDP/EDV ratio (p=0.018). Conclusion: A beneficial effect of GHRH-A in diastolic function was observed in a CKD large animal model that manifests the characteristics of HFpEF. These findings have important therapeutic implications for the HFpEF syndrome