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Metformin Treatment in Post-stroke Period Prevents Nitrative Stress and Restores Angiogenic Signaling in the Brain in Diabetes.
Abstract We have shown that diabetes impedes vascular repair and causes vasoregression in the brain after stroke but mechanisms underlying this response are still unclear. We hypothesized that excess peroxynitrite formation in diabetic ischemia/reperfusion injury (I/R) inactivates the p85 subunit of PI3K by nitration and diverts the PI3K-Akt-survival signal to the p38MAPkinase-apoptosis pathway. Nitrotyrosine (NY), Akt and p38 activity, p85 nitration and caspase-3 cleavage were measured in brains from control, diabetic (GK) or GK rats treated with metformin subjected to sham or stroke surgery and in brain microvas...
Source: Diabetes - December 18, 2014 Category: Endocrinology Authors: Abdelsaid M, Prakash R, Li W, Coucha M, Hafez S, Johnson MH, Fagan SC, Ergul A Tags: Diabetes Source Type: research

Diabetic microangiopathy: impact of impaired cerebral vasoreactivity and delayed angiogenesis after permanent middle cerebral artery occlusion on stroke damage and cerebral repair in mice.
Abstract Diabetes increases the risk of stroke by 3, increases related mortality and delays recovery. We aimed to characterize functional and structural alterations in cerebral microvasculature before and after experimental cerebral ischemia in a mouse model of type 1 diabetes. We hypothesized that pre-existing brain microvascular disease in diabetics might partly explain increased stroke severity and impact on outcome.Diabetes was induced in 4-week-old C57Bl/6J mice by intraperitoneal injections of streptozotocin (60 mg/kg). After 8 weeks of diabetes, the vasoreactivity of the neurovascular network to CO2 was abo...
Source: Diabetes - October 6, 2014 Category: Endocrinology Authors: Poittevin M, Bonnin P, Pimpie C, Rivière L, Sebrié C, Dohan A, Pocard M, Charriaut-Marlangue C, Kubis N Tags: Diabetes Source Type: research

Metformin Treatment in the Period After Stroke Prevents Nitrative Stress and Restores Angiogenic Signaling in the Brain in Diabetes
Diabetes impedes vascular repair and causes vasoregression in the brain after stroke, but mechanisms underlying this response are still unclear. We hypothesized that excess peroxynitrite formation in diabetic ischemia/reperfusion (I/R) injury inactivates the p85 subunit of phosphoinositide 3-kinase (PI3K) by nitration and diverts the PI3K–Akt survival signal to the p38–mitogen-activated protein kinase apoptosis pathway. Nitrotyrosine (NY), Akt and p38 activity, p85 nitration, and caspase-3 cleavage were measured in brains from control, diabetic (GK), or metformin-treated GK rats subjected to sham or stroke surg...
Source: Diabetes - April 23, 2015 Category: Endocrinology Authors: Abdelsaid, M.; Prakash, R.; Li, W.; Coucha, M.; Hafez, S.; Johnson, M. H.; Fagan, S. C.; Ergul, A. Tags: Pharmacology and Therapeutics Source Type: research

Diabetic Microangiopathy: Impact of Impaired Cerebral Vasoreactivity and Delayed Angiogenesis After Permanent Middle Cerebral Artery Occlusion on Stroke Damage and Cerebral Repair in Mice
Diabetes increases the risk of stroke by three, increases related mortality, and delays recovery. We aimed to characterize functional and structural alterations in cerebral microvasculature before and after experimental cerebral ischemia in a mouse model of type 1 diabetes. We hypothesized that preexisting brain microvascular disease in patients with diabetes might partly explain increased stroke severity and impact on outcome. Diabetes was induced in 4-week-old C57Bl/6J mice by intraperitoneal injections of streptozotocin (60 mg/kg). After 8 weeks of diabetes, the vasoreactivity of the neurovascular network to CO2 was abo...
Source: Diabetes - February 24, 2015 Category: Endocrinology Authors: Poittevin, M.; Bonnin, P.; Pimpie, C.; Riviere, L.; Sebrie, C.; Dohan, A.; Pocard, M.; Charriaut-Marlangue, C.; Kubis, N. Tags: Pathophysiology Source Type: research

Neuroimaging and Neurolaw: Drawing the Future of Aging
Vincenzo Tigano1, Giuseppe Lucio Cascini2, Cristina Sanchez-Castañeda3, Patrice Péran4 and Umberto Sabatini5* 1Department of Juridical, Historical, Economic and Social Sciences, University of Magna Graecia, Catanzaro, Italy 2Department of Experimental and Clinical Medicine, University of Magna Graecia, Catanzaro, Italy 3Department of Clinical Psychology and Psychobiology, University of Barcelona, Barcelona, Spain 4ToNIC, Toulouse NeuroImaging Center, Université de Toulouse, Inserm, UPS, Toulouse, France 5Department of Medical and Surgical Sciences, University of Magna Graecia, Catanzaro, ...
Source: Frontiers in Endocrinology - April 7, 2019 Category: Endocrinology Source Type: research

Mechanistic Evidence in Support of Alpha1-Antitrypsin as a Therapeutic Approach for Type 1 Diabetes
Utilizing endogenous molecules as a therapeutic approach is almost unequivocally superior to engineered or synthetic molecules. However, one rarely encounters an anti-inflammatory, cytoprotective, immunomodulatory and wound-healing molecule that has been available for use for decades. α1-antitrypsin (AAT), a circulating protein that rises more than 4-fold during acute-phase responses, has been administered for a rare genetic deficiency at large doses, for life. Aside from advances in insulin therapy, medical research in type 1 diabetes (T1D) has predominantly focused on autoimmunity—controlling the adaptive imm...
Source: Journal of Diabetes Science and Technology - October 28, 2014 Category: Endocrinology Authors: Fleixo-Lima, G., Ventura, H., Medini, M., Bar, L., Strauss, P., Lewis, E. C. Tags: Review Articles Source Type: research

One special question to start with: Can HIF/NFkB be a target in inflammation?
Abstract Hypoxia and Inflammation are strictly interconnected with important consequences at clinical and therapeutic level. While cell and tissue damage due to acute hypoxia mostly leads to cell necrosis, in chronic hypoxia, cells that are located closer to vessels are able to survive adapting their phenotype through the expression of a number of genes, including proinflammatory receptors for alarmins. These receptors are activated by alarmins released by necrotic cells and generate signals for master transcription factors such as NFkB, AP1, etc. which control hundreds of genes for innate immunity and damage repa...
Source: Endocrine, Metabolic and Immune Disorders Drug Targets - March 16, 2015 Category: Endocrinology Authors: Russo MA, Sansone L, Carnevale I, Limana F, Runci A, Polletta L, Perrone GA, De Santis E, Tafani M Tags: Endocr Metab Immune Disord Drug Targets Source Type: research