The low-energy SW therapy induces therapeutic lymphangiogenesis by up-regulating VEGF-C and bFGF, and improves lymphoedema in a rat-tail model, suggesting that low-energy SW therapy could be a non-invasive and effective strategy for lymphoedema in humans.

The mortality rate after major amputation in hemodialysis patients was high, and major amputation had a huge negative effect on patients' walking ability.

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Aim: Nitroglycerin-mediated vasodilatation (NMD) provides insight into the NTG-induced bioactivity of smooth muscle. It is plausible that in dysfunctional smooth muscle cells, the response to nitroglycerin may become blunted. The relationship between impaired brachial artery NMD and subsequent cardiovascular events is not well established. Methods: We examined brachial artery flow-mediated dilatation (FMD) and NMD using ultrasound in 93 subjects (71 7 years, including 26 with peripheral artery disease (PAD), 37 with aortic aneurysms, 10 with PAD complicated with aneurysms, and 20 without evident arterial disease). Brachial artery responses to hyperemia and nitroglycerin were measured every minute after cuff deflation and nitroglycerin administration. Time courses of vasodilatation were assessed and maximal FMD and NMD were measured. Results: The time courses in response to NTG were sigmoidal and maximal diameter reached 7.2 1.6 minutes after NTG was administered sublingually. The mean FMD was 2.3±2.0% and the mean NMD was 17.6 7.1%. Subjects were prospectively followed for an average of 47 13 months. Eighteen subjects had an event during follow-up; events included myocardial infarction (five), unstable angina pectoris (four), stroke (two), aortic dissection (one), ruptured aortic aneurysm (three), symptomatic abdominal aortic aneurysm (two), and lower limb ischemia requiring revascularization (one). NMD and FMD were significantly lower in subjects with events than in those without an event. In a Cox proportional-hazards model, lower FMD as well as lower NMD independently predicted future cardiovascular events. Conclusion: Brachial artery nitroglycerin-mediated vasodilatation may add information to conventional risk stratification.

Objective: Exogenously administered CO interferes with PMN recruitment to the inflamed organs. The mechanisms of COdependent modulation of vascular proadhesive phenotype, a key step in PMN recruitment, are unclear. Methods: We assessed the effects/mechanisms of CO liberated from a water-soluble CORM-3 on modulation of the proadhesive phenotype in hCMEC/D3 in an in vitro model of endotoxemia. To this end, hCMEC/D3 were stimulated with LPS (1 lg/mL) for six hours. In some experiments hCMEC/D3 were pretreated with CORM-3 (200 lmol/L) before LPS-stimulation. PMN rolling/ adhesion to hCMEC/D3 were assessed under conditions of laminar shear stress (0.7 dyn/cm 2 ). In parallel, expression of adhesion molecules E-selectin, ICAM-1, and VCAM-1 (qPCR), activation of transcription factors, NF-jB and AP-1 (ELISA), and MAPKsignaling (expression/phosphorylation of p38, ERK1/2, and JNK1/ 2; western blot) were assessed. Results: The obtained results indicate that CORM-3 pretreatment reduces PMN rolling/adhesion to LPS-stimulated hCMEC/D3 (p < 0.05). Decreased PMN rolling/adhesion to hCMEC/D3 was associated with CORM-3-dependent inhibition of MAPK JNK1/2 activation (Tyr-phosphorylation), inhibition of transcription factor, AP-1 (c-Jun phosphorylation), and subsequent suppression of VCAM-1 expression (p < 0.05).Conclusions: These findings indicate that CORM-3 pretreatment interferes with JNK/AP-1 signaling and suppresses LPS-induced upregulation of the proadhesive phenotype in hCMEC/D3.

We report our experience of two cases of refractory cellulitis caused by peripheral micro-arteriovenous fistulas (AVFs) in the lower extremity. The micro-AVFs were so small that they could not be located accurately; further, the patients’ symptoms differed markedly from those previously reported for AVF. AVF is known to cause ischemic symptoms. In contrast, micro-AVF causes congestive symptoms and remains undetected in the majority of patients. Identification of this pathology is crucial to enable effective treatment by the ligation of the incompetent perforator vein that increases venous hypertension, leading to congestive symptoms.

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