Sneddon’s syndrome (SS) is a rare non-inflammatory thrombotic vasculopathy characterized by the combination of cerebrovascular disease with livedo racemosa(LR). The Orpha number for SS is ORPHA820. It has been estimated that the incidence of SS is 4 per 1 million per annum in general population and generally occurs in women between the ages of 20 and 42 years. LR may precede the onset of stroke by years and the trunk and/or buttocks are involved in nearly all patients. The cerebrovascular manifestations are mostly secondary to ischemia (transient ischemic attacks and cerebral infarct). Other neurological symptoms range from headache, cerebral hemorrhage, seizures, cognitive and psychiatric disturbances. The involved internal organs include heart, kidney, and eyes. Histological findings of skin are characteristic and the involved vessels are small to medium-sized arteries at the border of dermis to subcutis with a distinct histopathological time course. The main diagnostic criteria are general LR with typical histopathological findings on skin biopsy and focal neurological deficits. The pathogenesis is related to hypercoagulable state and intrinsic small-vessel vasculopathy. The optimal management remains an unsolved problem and long-term anticoagulation have been recommended for cerebral ischemic events based on the presumed pathogenesis. There are controversial results in treatment of SS with immunomodulatory agents. The aim of this review is to comprehensively discuss this disease.

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These data suggest that vascular tissue from the metabolically dysregulated obese Zucker rat exhibits attenuated endothelin-1 peptide production and elevated endothelin receptor levels. Since elevated insulin levels have been linked to increased endothelin receptor expression, it is plausible that hyperinsulinemia upregulates endothelin receptors contributing to elevated vasoconstrictor responses to endothelin-1 in this model of obesity and hypertension.

BackgroundCardiac Lipoma is a rare entity constituting approximately 10-19 % of primary tumors of the heart and pericardium. To our best knowledge, such a large cardiac lipoma with septal enhancement in our case has never been reported before.Case presentationHere we present a rare case of a 65-year-old symptomatic female with an unusual giant cardiac lipoma. Due to the enhancement of the tumor septa, it was first diagnosed as liposarcoma and thought to be unresectable. Debulking surgery was performed to release patient’s symptoms.ConclusionsThe patient ultimately underwent complete tumor resection with uneventful postoperative evolution. The postoperative pathological diagnosis is cardiac lipoma.

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Abstract-The vasodilatory capacity of insulin has been widely reported, yet some investigators have not noted this effect.Because insulin has been shown to enhance endothelin release, we speculated that endothelin could be attenuating insulin-evoked vasodilation. We examined the effect of ex vivo insulin perfusion on vascular resistance by using the Sprague-Dawley rat mesenteric vascular bed. In methoxamine-preconstricted preparations, insulin (3.0 pmol/L to 10 nmol/L) evoked a concentration-dependent decrease in perfusion pressure (PP) with a maximal response of 42.0Ϯ9.2%, whereas continuous exposure to 10 nmol/L insulin induced a 51.8Ϯ3.5% relaxation. Further exposure to 10 nmol/L insulin resulted in the generation of endothelin and a subsequent loss of the vasodilatory response. Indomethacin had no effect on vascular responses. The vasodilatory response was significantly inhibited by nitric oxide synthase inhibition (20.5Ϯ4.2%; PϽ0.01) and calcium-activated potassium channel blockade (28.5Ϯ3.7%; PϽ0.05). Endothelial denudation attenuated the vasodilatory component (20.3Ϯ7.1%; PϽ0.01) and altered the biphasic pattern of the response. The decline in insulin-evoked vasodilation was significantly prevented by an endothelin-A antagonist (BQ123), an endothelin-B antagonist (BQ788), and nonselective endothelin blockade with both BQ123 and BQ788. These results demonstrate that the endothelium is intimately involved in regulating the vascular response to insulin. Insulin promotes the release of nitric oxide and endothelium-derived hyperpolarizing factor. During sustained exposure to higher concentrations, this vasodilatory effect is countered by the pathological generation of endothelin. Key Words: insulin Ⅲ nitric oxide Ⅲ vasodilation Ⅲ endothelin Ⅲ endothelium Ⅲ mesenteric arteries T he ability of insulin to induce vasodilation is integral to the regulation of skeletal muscle blood flow and glucose delivery. [1][2][3] Insulin-mediated vasodilation is impaired in insulin-resistant patients, suggesting a close relation between insulin resistance and hypertension. 4,5 However, despite the potential significance, the mechanism(s) underlying direct vascular effects of insulin remain controversial. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] Several studies in animals and humans attribute the vasodilatory effect of insulin to enhanced generation of endotheliumderived nitric oxide (EDNO). 2,[11][12][13][14][15][16] On the contrary, there have been reports supporting an endothelium-independent mechanism. 5-10 Incubation with insulin has been shown to reduce cytosolic-free calcium levels 6 and to increase the expression of the sodium pump gene, leading to hyperpolarization of vascular smooth muscle (VSM) cells. 7 Insulin enhancement of vascular ␤-adrenergic responsiveness has also been reported in normotensive animals and humans. 8,9 In the perfused rat mesenteric vascular bed (MVB), insulinevoked vasodilation has been linked to the activation of calcitonin gene-related peptide receptors on the VSM cells. 10 Inte...

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