Applying learning strategy questionnaires: problems and possibilities

This article discusses measuring learning strategies by means of questionnaires. In ‘multi-method’ research, in which think-aloud measures are compared with questionnaires, low or moderate correlations are found. A conclusion often drawn is that learners are not able to verbally report on their learning activities. Alternative explanations concern two other possibilities: first, that different learning strategies may be measured by the two methods; second, that the measuring methods may be aimed at different learning tasks. Keeping these prerequisites in mind, we constructed a task-specific questionnaire directly based on a taxonomy for coding think-aloud protocols in text studying. We found a higher correlation (r=.51) between the questionnaire and think-aloud protocols than is regularly reported. A case-study, in which four students answered the questionnaire while thinking aloud, led to new insights into why a questionnaire may lead to somewhat different ratings of activities than the think-aloud method. Based on these results, task-specific questionnaires may be improved. Our studies involved a fair comparison between a questionnaire and think-aloud protocols. We cautiously conclude that if task-specific questionnaires are meticulously constructed and examined in new ways, they might become reasonably adequate alternatives for the labor-intensive think-aloud method in measuring learners’ learning strategies

Thrombospondins in the heart: potential functions in cardiac remodeling

Cardiac remodeling after myocardial injury involves inflammation, angiogenesis, left ventricular hypertrophy and matrix remodeling. Thrombospondins (TSPs) belong to the group of matricellular proteins, which are non-structural extracellular matrix proteins that modulate cell–matrix interactions and cell function in injured tissues or tumors. They interact with different matrix and membrane-bound proteins due to their diverse functional domains. That the expression of TSPs strongly increases during cardiac stress or injury indicates an important role for them during cardiac remodeling. Recently, the protective properties of TSP expression against heart failure have been acknowledged. The current review will focus on the biological role of TSPs in the ischemic and hypertensive heart, and will describe the functional consequences of TSP polymorphisms in cardiac disease

Cardiomyopathy and Response to Enzyme Replacement Therapy in a Male Mouse Model for Fabry Disease

Fabry disease is an X-linked disorder of glycosphingolipid metabolism that results in progressive accumulation of neutral glycosphingolipids, (predominately globotriaosylceramide; GL-3) in lysosomes, as well as other cellular compartments and the extracellular space. Our aim was to characterize the cardiac phenotype of male knock-out mice that are deficient in alpha-galactosidase A activity, as a model for Fabry disease and test the efficacy of Enzyme Replacement Therapy with agalsidase-beta. Male mice (3–4 months of age) were characterized with awake blood pressure and heart rate measurements, cardiac echocardiography and electrocardiography measurements under light anesthesia, histological studies and molecular studies with real-time polymerase chain reaction. The Fabry knock-out mouse has bradycardia and lower blood pressure than control wild type (CB7BL/6J) mice. In Fabry knock-out mice, the cardiomyopathy associated mild hypertrophy at echography with normal systolic LV function and mild diastolic dysfunction. Premature atrial contractions were more frequent in without conduction defect. Heart weight normalized to tibial length was increased in Fabry knock-out mice. Ascending aorta dilatation was observed. Molecular studies were consistent with early stages of cardiac remodeling. A single dose of agalsidase-beta (3 mg/kg) did not affect the LV hypertrophy, function or heart rate, but did improve the mRNA signals of early cardiac remodeling. In conclusion, the alpha-galactosidase A deficient mice at 3 to 4 months of age have cardiac and vascular alterations similar to that described in early clinical stage of Fabry disease in children and adolescents. Enzyme replacement therapy affects cardiac molecular remodeling after a single dose