Vein of Galen malformation.
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Biomedical subjects
Publications and source records attributed to Mark S Landis.
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PURPOSE: To assess the efficacy and durability of percutaneous transluminal angioplasty (PTA)/stent placement for treatment of chronic mesenteric ischemia (CMI). MATERIALS AND METHODS: A retrospective review of patients treated from January 1986 to August 2003 was conducted. Twenty-nine patients (mean age, 62 years) were treated for clinical symptoms consistent with CMI. Clinical diagnosis was verified with angiographic assessment and PTA with or without stent placement was performed based on angiographic and/or pressure gradient findings. Outcomes were estimated with the Kaplan-Meier method. RESULTS: A total of 63 interventions were performed in 29 patients during the study period. Of these 63 interventions, 46 PTA and 17 stent implantation procedures were performed. Thirty-four interventions were performed for SMA stenosis/occlusion, 17 interventions for celiac artery stenosis/occlusion, and four interventions were performed on aorto-mesenteric graft stenoses. Technical success was 97%, and clinical success (defined as clinical resolution of symptoms) was 90% (26 of 29 patients). Mean duration of follow-up was 28.3 months. Primary patency for all interventions at 3, 6, and 12 months was 82.7% (95% CI: 68.7-96.7), 78.9% (66.7-91.1), and 70.1% (55.1-85.6), respectively. Primary assisted patency for all interventions at 3, 6, and 12 months was 87.9% (79.0-95.3), 87.9% (79.2-95.1), and 87.9% (77.3-98.3), respectively. An average of 1.9 interventions per patient was required. One major complication occurred (3.4%). There were three minor complications (10.3%). CONCLUSIONS: Percutaneous intervention for CMI is safe with durable early and midterm clinical success. However, repeated intervention is often required for improved primary assisted patency.
Liver X receptor alpha (LXRalpha), is a nuclear hormone receptor that is activated by oxysterols and plays a crucial role in regulating cholesterol and lipid metabolism in liver and cholesterol efflux from lipid-loaded macrophages. Here we show that treatment of human peripheral blood monocytes or monocytic THP-1 cells with the LXR ligand 22(R)-hydroxycholesterol (22(R)-HC), in combination with 9-cis-retinoic acid (9cRA), a ligand for the LXR heterodimerization partner retinoid X receptor (RXR), results in the specific induction of the potent pro-apoptotic and pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha). Promoter analysis, inhibitor studies, and order-of-addition experiments demonstrated that TNF-alpha induction by 22(R)-HC and 9cRA occurs by a novel two-step process. The initial step involves 22(R)-HC-dependent induction of TNF-alpha mRNA, and intracellular accumulation of TNF-alpha protein, mediated by binding of LXRalpha/RXRalpha to an LXR response element at position -879 of the TNF-alpha promoter. Subsequent cell release of TNF-alpha protein occurs via a separable 9cRA-dependent, LXRalpha-independent step that requires de novo transcription and protein synthesis. Our findings reveal a potentially new dimension of the physiological role of LXRalpha and identify a unique multistep pathway of TNF-alpha production that may be of consequence to the normal function of LXR in monocyte/macrophages and in disease conditions such as atherosclerosis.