Walking speed as a predictor of community mobility and quality of life after stroke

Background: Community mobility (CM) is considered a part of community reintegration that enhances Quality of Life (QoL). Achieving an appropriate gait speed is essential in attaining an independent outdoor ambulation and satisfactory CM.

Objective: The aim of this study was to identify whether gait speed is a predictor of CM and QoL in patients with stroke following a multimodal rehabilitation program (MRP).

Methods: This was a baseline control trial with 6-months follow-up in an outpatient rehabilitation setting at a university hospital. Twenty-six stroke survivors completed the MRP (24 sessions, 2 days/wk, 1 hr/session). The MRP consisted of aerobic exercise, task-oriented exercises, balance exercises and stretching. Participants also performed an ambulation program at home. Outcome variables were: walking speed (10-m walking test) and QoL (physical and psychosocial domains of Euroquol and Sickness Impact Profile).

Results: At the end of the intervention, comfortable and fast walking speed increased by an average of 0.16 (SD 0.21) (*p < .05) and 0.40 (SD 0.51) (**p < .001) m/s, respectively. After the intervention, all participants achieved independent outdoor ambulation with an increase of 34.14 of walking minutes/day in the community and a decrease of sitting time of 95.45 minutes/day. Regarding QoL there were increased mean scores on the physical and psychosocial dimensions of Euroquol and the Sickness Impact Profile, respectively (**p < .001).

Conclusions: The results suggest that improved walking speed after the MRP is associated with CM and higher scores in QoL. These findings support the need to implement rehabilitation programs to promote increased speed.     

Eutanasia: ¿es esta la ley que necesitamos?

La Ley de Eutanasia española introduce un nuevo derecho que se incorpora a la cartera de servicios del sistema sanitario, como una prestación cuya aplicación se garantiza en el plazo de 40 días. Desde la experiencia clínica se argumenta que, sin el derecho efectivo a unos cuidados paliativos de calidad, y con el actual déficit en las ayudas a la dependencia, esta ley puede ser un mensaje coactivo para aquellas personas especialmente frágiles y dependientes, que se sientan como una pesada carga para su familia y para la sociedad.Se razona de qué modo fundamentar el derecho a morir en la dignidad de la persona, puede tener repercusiones sociales inesperadas.El texto normativo muestra debilidades propias de una ley apresurada y sin apoyo de órganos consultivos. Hay cuestiones pendientes de aclarar en su aplicación dentro del contexto de la medicina de familia. Se concluye que esta nueva norma planteará más problemas de los que pretende resolver.Palabras clave: Eutanasia, Suicidio asistido, Medicina de familia, Cuidados paliativos, Bioética     

Reversión de sobrepeso y obesidad en población infantil de Vilafranca del Penedès: Programa ACTIVA’T (2012)

Objective

To assess a 6-month nutritional and physical activity intervention program on the nutritional status of overweight or obese and not very active 8-14 years old children by means of a controlled pre-post design (ACTIVA’T program).

Insulin Resistance Is Associated With Diminished Endoplasmic Reticulum Stress Responses in Adipose Tissue of Healthy and Diabetic Subjects

We recently showed that insulin increased ER stress in human adipose tissue. The effect of insulin resistance on ER stress is not known. It could be decreased, unchanged, or increased, depending on whether insulin regulates ER stress via the metabolic/phosphoinositide 3-kinase (PI3K) or alternate signaling pathways. To address this question, we examined effects of lipid-induced insulin resistance on insulin stimulation of ER stress. mRNAs of several ER stress markers were determined in fat biopsies obtained before and after 8-h hyperglycemic-hyperinsulinemic clamping in 13 normal subjects and in 6 chronically insulin-resistant patients with type 2 diabetes mellitus (T2DM). In normal subjects, hyperglycemia-hyperinsulinemia increased after/before mRNA ratios of several ER stress markers (determined by ER stress pathway array and by individual RT-PCR). Lipid infusion was associated with inhibition of the PI3K insulin-signaling pathway and with a decrease of hyperinsulinemia-induced ER stress responses. In chronically insulin-resistant patients with T2DM, hyperglycemic-hyperinsulinemia did not increase ER stress response marker mRNAs. In summary, insulin resistance, either produced by lipid infusions in normal subjects or chronically present in T2DM patients, was associated with decreased hyperinsulinemia-induced ER stress responses. This suggests, but does not prove, that these two phenomena were causally related.     

Mutations in TIMM50 cause severe mitochondrial dysfunction by targeting key aspects of mitochondrial physiology

3‐Methylglutaconic aciduria (3‐MGA‐uria) syndromes comprise a heterogeneous group of diseases associated with mitochondrial membrane defects. Whole‐exome sequencing identified compound heterozygous mutations in TIMM50 (c.[341 G>A];[805 G>A]) in a boy with West syndrome, optic atrophy, neutropenia, cardiomyopathy, Leigh syndrome, and persistent 3‐MGA‐uria. A comprehensive analysis of the mitochondrial function was performed in fibroblasts of the patient to elucidate the molecular basis of the disease. TIMM50 protein was severely reduced in the patient fibroblasts, regardless of the normal mRNA levels, suggesting that the mutated residues might be important for TIMM50 protein stability. Severe morphological defects and ultrastructural abnormalities with aberrant mitochondrial cristae organization in muscle and fibroblasts were found. The levels of fully assembled OXPHOS complexes and supercomplexes were strongly reduced in fibroblasts from this patient. High‐resolution respirometry demonstrated a significant reduction of the maximum respiratory capacity. A TIMM50‐deficient HEK293T cell line that we generated using CRISPR/Cas9 mimicked the respiratory defect observed in the patient fibroblasts; notably, this defect was rescued by transfection with a plasmid encoding the TIMM50 wild‐type protein. In summary, we demonstrated that TIMM50 deficiency causes a severe mitochondrial dysfunction by targeting key aspects of mitochondrial physiology, such as the maintenance of proper mitochondrial morphology, OXPHOS assembly, and mitochondrial respiratory capacity.