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Abstract: Cardiovascular complications are the leading cause of morbidity and mortality in patients with diabetes mellitus; up to 80% of deaths in patients with diabetes are closely associated with vascular disease. The ability of the organism to form a collateral network of blood vessels constitutes an important response to vascular occlusive disease and determines to a large part the clinical consequences and severity of tissue ischemia. The development of new vessels is significantly reduced in diabetic patients with coronary or peripheral artery disease. This probably contributes to the severe course of limb ischemia in diabetic patients, in which peripheral artery disease often results in foot ulceration and lower extremity amputation. Diabetic retinopathy remains one of the major causes of acquired blindness in developed nations. This is true despite the development of laser treatment, which can prevent blindness in the majority of those who develop macular edema or proliferative diabetic retinopathy. The hallmark of diabetic retinopathy is the lack of microvessels in the macula, leading to hypoxia, associated with peripheral retinal neovascularization that may ultimately cause severe vitreous cavity bleeding and/or retinal detachment. The factors that stimulate retinal blood vessel growth have not been fully defined, but there is accumulating evidence that the renin-angiotensin-bradykinin system may be involved in a number of retinal vascular disorders, including retinopathy of prematurity and proliferative diabetic retinopathy. Only a few studies have specifically evaluated the effect of diabetes on angiogenesis in ischemic vascular disease and in the retina. Moreover, the mechanisms by which diabetes could both limit the formation of new blood vessels in most organs and simultaneously induce proliferative diabetic retinopathy remain largely undefined. In the present review, we aimed to briefly describe the main molecular mechanisms involved in the ischemia-induced angiogenesis, and their alterations in diabetes. Possible therapeutic strategies to restore angiogenesis in diabetic patients are also listed. [Copyright &y& Elsevier]

Objective. – We assessed the efficacy of topical methylprednisolone or lidocaine for prevention of postoperative sore throat.Study design. – Randomised, prospective in single blind study.Patients and methods. – Sixty patients ASA 1 or 2 undergoing tracheal intubation for dental surgery received before intubation either topical lidocaine 5% (15 puffs) or aerosolized methylprednisolone (80 mg). Postoperative pain was assessed by the patients using a VAS and a specific scoring system for sore throat, cough and hoarseness. Evaluations were performed immediately after emergence from anaesthesia, 1 h later, at time of the first postoperative drink, at time of the first postoperative meal and 24 h after surgery.Results. – Patients receiving methylprednisolone showed slightly better scores for sore throat and cough 1 h after surgery.Conclusion. – Topical methylprednisolone may therefore be a useful adjuvant in the prevention of sore throat after intubation. [Copyright &y& Elsevier]

Cell-based therapy is a promising option for treatment of cardiovascular diseases. Based on experimental studies demonstrating that bone marrow-derived mononuclear cells (BMMNCs) improve the functional recovery after ischemia, clinical trials were initiated to address this new therapeutic concept. BMMNCs improve neovascularization of ischemic tissue by a broad repertoire of potential therapeutic actions. Whereas initial studies documented that the cells incorporate and differentiate to cardiovascular cells, other studies suggested that short-time paracrine mechanisms mediate the beneficial effects. Here, we hypothesized that BMMNCs have a phagocytic ability, and switch to a proangiogenic phenotype after engulfment of apoptotic cells. Activation of such angiogenic program may be pivotal in the beneficial effect of BMMNCs-based therapy. In vitro, wildtype (WT) BMMNCs ingestion of apoptotic cells upregulated the release of proangiogenic factors VEGF and HGF by 15- and 5-fold, respectively. In contrast, BMMNCs collected from mice deficient in MFG-E8, a protein that is required for attachment and engulfment of apoptotic cells by phagocytes, displayed lower phagocytic ability, leading to decrease in VEGF and HGF release. The capacity of BMMNCs to differentiate into cells with endothelial phenotype was similar in control and MFG-E8-deficient cells. In an in vivo model of mice myocardial infaction (MI), transplantation of WT BMMNCs increased fractionnal shortening (120 % of untreated control, p<0.05), 14 days after MI. Size of the infarct scar was reduced by 30 % (p<0.05 vs untreated control), and capillary density in the infarct border zone was raised by 10 % (p<0.05 vs untreated control) in the WT BMMNCs group. In contrast, transplantation of MFG-E8 deficient BMMNCs displayed no significant effect on cardiac function, infarct size or angiogenesis in the ischemic myocardium. Four days after MI, VEGF protein levels were raised by 1.4 fold in the myocardium of WT BMMNCs treated animals compared to untreated controls (p<0.05), while treatment with MFG-E8 deficient BMMNCs failed to raise VEGF levels. Taken together, these results suggest that phagocytosis of apoptotic cells reprograms BMMNCs into a proangiogenic phenotype. Hence, the therapeutic effect of transplanted BMMNCs depends, at least in part, on their phagocytic ability. [Copyright &y& Elsevier]

Abstract: Electroneuromyography (ENMG) is the gold standard tool in evaluating peripheral neuropathies, and it is essential to the diagnosis and the location of the involvement, as well as the assessment of the severity and the prognosis of the lesion. However, it has also limitations. It is highly examiner dependant and because it is unpleasant, the assessment of some nerves and muscles is limited. The evaluation of proximal nerve and deep muscles is difficult to perform. Magnetic resonance imaging and echography represent a fast growing field in demyelinating and motor neuropathy assessment, while these imaging procedures are now well validated in myopathies. In this article, we discuss sensitivity, specificity and prognostic data brought up by these new imaging tools compared to ENMG and the significant future prospects they offer. [Copyright &y& Elsevier]

Abstract: It has long been believed that cerebral lesions were irreversible in the adult human brain. However, the spontaneous improvement in functional outcome observed in the following weeks after cerebral ischemia suggests plasticity phenomenons involving postischemic neuronal network reorganization. Regarding the large prevalence of stroke in industrialized countries, and the few available treatments, the understanding of cerebral plasticity has become an important issue but also a potential source of new therapeutic approaches in stroke. Thus, “constraint induced therapy” and repetitive transcranial magnetic stimulation (rTMS) are based on the concept of local but also remote consequences of the ischemic focal lesion. Cell-therapy is based on the capacity of stem cells to respond to hypoxic signals and adapt their phenotype to the host organ, but above all to release cytokines locally and boost endogeneous repair mechanisms. We could consider to perform in the future a sequential treatment with fibrinolysis, stem cell therapy, repetitive transcranial magnetic stimulation and constraint-induced therapy in the same patient. [Copyright &y& Elsevier]