104,254 research outputs found
Advanced glycosylation end-products and the pathogenesis of accelerated atherosclerosis in diabetes
No full textAdvanced glycation end products and vascular inflammation: implications for accelerated atherosclerosis in diabetes
No full textAbstract
The formation of advanced glycation end products (AGEs) is an important biochemical abnormality that accompanies diabetes mellitus
and, likely, inflammation in general. Here we summarize and discuss recent studies indicating that the effects of AGEs on vessel wall
homeostasis may account for the rapidly progressive atherosclerosis associated with diabetes mellitus. Driven by hyperglycemia and oxidant
stress, AGEs form to a greatly accelerated degree in diabetes. Within the vessel wall, collagen-linked AGEs may ‘‘trap’’ plasma proteins,
quench nitric oxide (NO) activity and interact with specific receptors to modulate a large number of cellular properties. On plasma low
density lipoproteins (LDL), AGEs initiate oxidative reactions that promote the formation of oxidized LDL. Interaction of AGEs with
endothelial cells as well as with other cells accumulating within the atherosclerotic plaque, such as mononuclear phagocytes and smooth
muscle cells (SMCs), provides a mechanism to augment vascular dysfunction. Specifically, the interaction of AGEs with vessel wall
components increases vascular permeability, the expression of procoagulant activity and the generation of reactive oxygen species (ROS),
resulting in increased endothelial expression of endothelial leukocyte adhesion molecules. AGEs potently modulate initiating steps in
atherogenesis involving blood-vessel wall interactions, triggering an inflammatory-proliferative process and, furthermore, critically
contribute to propagation of inflammation and vascular perturbation in established disease. Thus, a better understanding of the biochemical
mechanisms by which AGEs contribute to such processes in the vessel wall could be relevant to devise preventive and therapeutic strategies
for diabetic atherosclerosis
Stem cells for the cell and molecular therapy of type 1 diabetes mellitus (T1D): the gap between dream and reality.
No full textIn spite of intense research, over the past 2-3 decades, targeted to validating methods for the cure of T1D, based on cell substitution therapy in the place of exogenously administered insulin injections, achievement of the final goal continues to remain out of reach. In fact, aside of very limited clinical success of the few clinical trials of pancreatic islet cell transplantation in totally immunosuppressed patients with T1D, the vast majority of these diabetic patients invariably is insulin-dependent. New advances for cell and molecular therapy for T1D, including use of stem cells, are reviewed and discussed in an attempt to clearly establish where we are and where are we may go for the final cure for T1DM
Trabsplantation of microencapsulated human islet in non immunosuppressed diabetic patients.
No full textAdvanced glycosylation end-products and the pathogenesis of accelerated atherosclerosis in diabetes
No full text
In Vitro Cultured Human Islet Cell Monolayers : Stemness Markers and Insulin Recovery upon Streptozotocin exposure.
No full textWe have investigated long-term in vitro–cultured human islet-derived cell monolayers (CM) to determine their
suitability as source of newly generated b-cells. Initial loss of the islet three-dimensional architecture resulted in
rearrangement of pancreatic hormone and key transcriptional factor expression, or decreased insulin secretion,
or declined glucose-stimulated insulin release, reflecting reversal to an immature precursor stage. However,
upon exposure to several streptozotocin (STZ) concentrations, CM showed glucose-stimulated insulin release
recovery and an increased synthesis of insulin mRNA. Possibly, this outcome could derive from eventual
‘‘stemness’’ properties of such cell populations, unfolded by subtoxic STZ-induced CM damage. To test this
hypothesis, we have examined messenger and protein expression of embryonic stem cell markers (Nanog, Sox-2,
Oct-4A), which varied in CM versus control whole human islets. Moreover, different STZ concentrations were
shown to modulate marker expression in CM. All together our data preliminarily seem to indicate that CM
may generate reconstituted insulin-producing cells likely due to their intrinsic, preexisting stemness properties
S. Pasquinelli, G. Rusmini (a cura di), “Badare non basta. Il lavoro i cura: attori, progetti, politiche”
No full textRecensione al volume di S. Pasquinelli, G. Rusmini (a cura di), “Badare non basta. Il lavoro i cura: attori, progetti, politiche” .Book Review: S. Pasquinelli, G. Rusmini (a cura di), “Badare non basta. Il lavoro i cura: attori, progetti, politiche”
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