Opposing tissue-restricted roles for microRNAa during atherogenesis. Hehenberger K, Hansson A. CD36 is significantly correlated with adipophilin in human carotid lesions and inversely correlated with plasma ApoAI. Oxidative stress and diabetic complications. Impairment of both nitric oxide-mediated and EDHF-type relaxation in small mesenteric arteries from rats with streptozotocin-induced diabetes.

Inhibition of microRNAa prevents endothelial dysfunction and atherosclerosis in mice. Mitochondrial dysfunction in diabetes: Figure 4 integrates the cascade of deleterious factors that impact on diabetic granulation tissue onset. Role of microparticles on atherothrombosis. Molecular and cellular biology of endothelin and its receptors.

The role of insulin in wound healing is well known by its anabolic effect on wound protein balance, favoring synthesis and preventing degradation [78, 79]. So, it is the pattern of clinical complications, including the wound itself.

The nitrate ester ITF relaxes isolated canine arteries and veins.

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Angiogenesis, arteriogenesis, and diabetes: Clin Chem Lab Med. Willkam effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. British J Clinical Pharmacol, ; Magentic tagging of cell-derived microparticles: Role of nitric oxide in wound healing. A case of perforating ulcers of both feet associated with diabetes and ataxic symptoms. Intensive insulin treatment increases donor site wound protein synthesis in burn patients.

Cells harvested and cultured from hypoperfused granulation tissues orchestrate a molecular program of arrest and senescence Jorge Berlanga, manuscript in preparation.


William Benessiano

In contrast to acute wounds in non-diabetic subjects, the inflammatory reaction in diabetics appears currculum [93] and sharply delays granulation tissue formation and maturation [94]. National Center for Biotechnology Information, U.

Lack of insulin receptor expression derives in reduced skin proliferation and abnormal differentiation in vivo []. Biology of the Diabetic Wound.

Chronic treatment with the Calcium channel inhibitor RO potentiates endothelium-dependent relaxations in the aorta of the hypertensive salt sensitive dahl rat. Figure 4 integrates the cascade of deleterious factors that impact on diabetic granulation benessisno onset.

Aside from the glucose-mediated direct cytotoxic effect on keratinocytes, AGE modification of type-I collagen and other ECM proteins impairs the integrin-mediated adhesion of keratinocytes to the basement matrix, and could wipliam contribute to the pathogenesis of diabetic re-epithelialization failure [].

Ann Clin Lab Sci. Since limb salvage is always a worthwhile goal and diabetic foot ulceration involves predisposing factors that can be diagnosed and clinically graded; primary care ulcer prevention plans, podiatric assistance, optimal glycemic control and educational programs, will be always far more socially rewarding.

william benessiano curriculum vitae

We are also investigating the vascular impact of other components e. Insulin-degrading activity in wound fluid. Interactions between endothelin-1 and endothelium-derived relaxing factor in human arteries and veins.

william benessiano curriculum vitae

In particular, we identified circulating microvesicles as the trigger for endothelial dysfunction in patients with coronary artery and related diseases. Chapman and Hall, London,pp Fund Clin Pharmacol 4: Trandolapril plus verapamil inhibit the coronary vasospasm induced by hypoxia following ischemia-reperfusion injury in dogs.


Circulation of endothelial —derived prothrombotic microparticles following cis-platine induced stroke.

Recent experiments beneasiano the negative effect of null mutation of the Slug transcription factor on its function as a downstream EGFR catalytic mediator for wound re-epithelialization.

Circulating immune complexes do not affect microparticle flow cytometry analysis in acute coronary syndrome.

Br J Pharmacol Proteomic analysis of secretory proteins and vesicles in vascular research. Thus, the challenge that represents the diabetic wound healing failure is the clinical gross expression of an outstanding array of biochemical and cellular disorders [7]. Years later, Goldstein also announced that cells obtained from insulin-dependent or insulin-independent diabetics not only exhibit abnormal replicative capacity in vitrobut that the aging process appeared more precociously than in non-diabetic counterparts [18].

In support to the glucagon-like peptide-1 action is the study by Ta et al.

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