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After more than twenty years of research, the molecular events of apoptotic cell death can be succinctly stated; different pathways, activated by diverse signals, increase the activity of proteases called caspases that rapidly and irreversibly dismantle condemned cell by cleaving specific substrates. In this time the ideas that apoptosis protects us from tumourigenesis and that cancer chemotherapy works by inducing apoptosis also emerged. Currently, apoptosis research is shifting away from the intracellular events within the dying cell to focus on the effect of apoptotic cells on surrounding tissues. This is producing counterintuitive data showing that our understanding of the role of apoptosis in tumourigenesis and cancer therapy is too simple, with some interesting and provocative implications. Here, we will consider evidence supporting the idea that dying cells signal their presence to the surrounding tissue and, in doing so, elicit repair and regeneration that compensates for any loss of function caused by cell death. We will discuss evidence suggesting that cancer cell proliferation may be driven by inappropriate or corrupted tissue-repair programmes that are initiated by signals from apoptotic cells and show how this may dramatically modify how we view the role of apoptosis in both tumourigenesis and cancer therapy.
Sicherheit im Fährverkehr
(2012)
People with type 2 Diabetes have an elevated risk for developing cardiovascular disease (CVD) for which dyslipidemia is the major contributor. Diabetic patients have characteristic pattern of dyslipidemia with decreased level of high density lipoprotein cholesterol (HDL-C) and elevated triglycerides (TG) level. However, in diabetes mellitus, low density lipoprotein cholesterol (LDL-C) which is used as one of the markers for the risk of CVD, is underestimated so in such cases the levels of non-High density lipoprotein cholesterol (non-HDL-C) can be a stronger predictor of CVD as it strongly correlates with atherogenic lipoproteins. Therefore, an attempt has been made to evaluate the level of non-HDL-C as a newer marker for the risk of cardiovascular disease and to fi nd out the pattern of dyslipidemia in diabetes mellitus. The present study comprised of 82 type 2 Diabetic cases and 81 non-diabetic controls. Among the diabetics, the majority of the subjects (61.0%) were HDL-C dyslipidemic. However, among the controls, the maximum numbers of individuals (40.7%) were TG dyslipidemic. Diabetics have signifi cantly elevated ratio of total cholesterol to high density lipoprotein cholesterol (TC/HDL-C) and the signifi cant increased levels of non-high density lipoprotein cholesterol (non-HDL-C) compared to controls which can be used as markers of dyslipidemia and can also be used to predict the risk of cardiovascular disease in type 2 Diabetes Mellitus.