This comes with being discouraged from physical activity because of these perceived limitations imposed by their medical condition. Participation and barriers
Participation is involvement in life situations and everyday activities. Participation includes self-care, productivity, and leisure. In fact, communication, mobility, education, home life, leisure, and social relationships require participation, and indicate the extent to which children function in their environment. Barriers can exist on three levels: micro, meso, and macro. First, the barriers at the micro level involve the person. Barriers at the micro level include the childs physical limitations (motor, sensory and cognitive impairments) or their subjective feelings regarding their ability to participate. For example, the child may not participate in group activities due to lack of confidence. Second, barriers at the meso level include the family and community. These may include negative attitudes of people toward disability or lack of support within the family or in the community. One of the main reasons for this limited support appears to be the result of a lack of awareness and knowledge regarding the childs ability to engage in activities despite his or her disability. Third, barriers at the macro level incorporate the systems and policies that are not in place or hinder children with CP. These may be environmental barriers to participation such as architectural barriers, lack of relevant assistive technology, and transportation difficulties due to limited wheelchair access or public transit that can accommodate children with CP.
About 50% of diabetics with diabetic cardiomyopathy show pathologic evidence for microangiopathy such as sub-endothelial and endothelial fibrosis, compared to only 21% of non-diabetic heart failure patients. Over the years, several hypotheses were postulated to explain the endothelial dysfunction observed in diabetes. It was hypothesized that the extracellular hyperglycemia leads to an intracellular hyperglycemia in cells unable to regulate their glucose uptake, most predominantly, endothelial cells. Indeed, while hepatocytes and myocytes have mechanisms allowing them to internalize their glucose transporter, endothelial cells do not possess this ability. The consequences of increased intracellular glucose concentration are fourfold, all resulting from increasing concentration of glycolytic intermediates upstream of the rate-limiting glyceraldehyde-3-phosphate reaction which is inhibited by mechanisms activated by increased free radical formation, common in diabetes. Four pathways, enumerated below all explain part of the diabetic complications. First, it has been widely reported since the 1960s that hyperglycemia causes an increase in the flux through aldose reductase and the polyol pathway. Increased activity of the detoxifying aldose reductase enzyme leads to a depletion of the essential cofactor NADH, thereby disrupting crucial cell processes. Second, increasing fructose 6-phosphate, a glycolysis intermediate, will lead to increased flux through the hexosamine pathway. This produces N-acetyl glucosamine that can add on serine and threonine residues and alter signaling pathways as well as cause pathological induction of certain transcription factors. Third, hyperglycemia causes an increase in diacylglycerol, which is also an activator of the Protein Kinase C (PKC) signaling pathway.