[Emergency small-sized stent placement following aortic true lumen obliteration of Stanford type B acute aortic dissection].

Acute aortic obstruction induced by acute aortic dissection frequently causes life-threatening organ ischemia. Although early reperfusion of lower extremities, renal and mesenteric artery is necessary, surgical treatment such as graft replacement is invasive and may result in myonephropathic-metabolic syndrome (MNMS), which leads to loss of limb and life. We herein report a case of stent placement as a less invasive treatment for true lumen obliteration associated with Stanford type B aortic dissection in a patient with chronic renal failure on hemodialysis. Ten mm metallic stents were placed in the obliterated true lumen of the descending aorta in order to perfuse peripheral organs within 5 hours after occurrence. It relieved symptoms of visceral organ and leg ischemia. On the postoperative day 14, abdominal discomfort after meal, hypertension in the upper extremity and headache appeared. Chest and abdominal computed tomography (CT) revealed stenosis of the true lumen proximal to the stents. On the other hand, the diameter of the true lumen was inversely dilated distal to the stents. Bilateral axillo-femoral artery bypass was performed with relief of upper extremity hypertension and visceral organ ischemia. The patient otherwise had an uneventful course and was discharged on the postoperative day 37. Our experience suggests that emergency stent placement can provide an option that is less invasive, more effective and prompt treatment for patients with visceral organ and leg ischemia resulting from acute aortic dissection.

[A report of three surgical cases in a family of Marfan syndrome].

A family of 3 patients with Marfan syndrome was reported. All of them had surgical interventions in cardiovascular disorders such as DeBakey type I, III aortic dissection and thoracoabdominal aortic aneurysm. In 2 patients, multiple surgical treatments were performed for aneurysmal dilatation of the distal false lumen or another lesions of the treated aorta. Since cardiovascular lesions of Marfan syndrome are systemic and progressive, the postoperative long term follow-up, including systemic evaluation of the arterial system, is essential to detect the latent cardiovascular complications. Careful examining the family with Marfan syndrome is necessary to discover any cardiovascular abnormalities in these people early.

Soluble interleukin-6 receptor alpha inhibits the cytokine-Induced fractalkine/CX3CL1 expression in human vascular endothelial cells in culture.

Soluble form of IL-6 receptor alpha (sIL-6R) is known to serve as an agonist, without exogenous IL-6, on endothelial cells which do not express IL-6R but have only IL-6 receptor beta chain, gp130. We investigated the effect of sIL-6R on fractalkine expression in human umbilical vein endothelial cells (HUVECs) in culture. sIL-6R markedly inhibited HUVEC fractalkine/CX3CL1 expression induced by interleukin (IL)-1alpha, tumor necrosis factor (TNF)-alpha, or interferon (IFN)-gamma. IL-1alpha-induced fractalkine expression was inhibited by sIL-6R in time- and concentration-dependent manners. The experiment using actinomycin D indicated that sIL-6R lowered the stability of fractalkine mRNA. The inhibitory effect of sIL-6R was reversed by anti-gp130 neutralizing antibody. sIL-6R inhibited adhesion of mononuclear cells (MNCs) to HUVEC monolayers stimulated with IFN-gamma, but it did not inhibit the adhesion to monolayers stimulated with IL-1alpha. MNC chemotactic activity of conditioned medium of HUVEC stimulated with IL-1alpha or IFN-gamma was inhibited by co-treatment with sIL-6R. sIL-6R may play a regulatory role in immune responses by modulating the interaction between leukocytes and the vascular endothelium.

Synergistic stimulation, by tumor necrosis factor-alpha and interferon-gamma, of fractalkine expression in human astrocytes.

Fractalkine is a CX3C chemonkine that appears to be a neuron-to-microglia signal molecule in the central nervous system. We studied the expression of fractalkine in normal human astrocytes in culture, by using semi-quantitative reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. We found that tumor-necrosis factor alpha (TNF-alpha) and interferon-gamma (IFN-gamma) synergistically enhance the expression of fractalkine. The expression of both fractalkine mRNA and protein was increased in time- and concentration-dependent manners in the cells co-stimulated with TNF-alpha and IFN-gamma. Cycloheximide, an inhibitor of protein synthesis, and dexamethasone had no effect on the synergy of the stimulation of fractalkine expression. We conclude that normal human astrocytes produce fractalkine by co-stimulation with pro-inflammatory cytokines and it may serve as a potential signal for immune and inflammatory responses in the central nervous system.