PURPOSE: The purpose of this study was to report on splenic artery aneurysms (SAAs) treated by transcatheter embolization in our single-center institution and to evaluate the clinical outcomes of patients with SAA by aneurysm location. MATERIALS AND METHODS: The original medical records and imaging results of 52 patients with SAA treated in our center between January 1, 1995 and December 31, 2013 were reviewed. Of these cases, 7 patients (13.5%) underwent surgery, 4 patients (7.5%) underwent serial observation, and 1 patient had stent insertion only, leaving 40 patients (78.9%) who underwent endovascular treatment using a coil, with or without N-butyl-2-cyanoacrylate. RESULTS: Aneurysms were located in the distal third of the splenic artery in 27 patients (67.5%), in the middle third in 9 cases (22.5%), and in the proximal third in 4 cases (10%). Of the 40 included patients, 25 were female (62.5%). Twenty-eight patients (70%) were asymptomatic. The mean aneurysm diameter was 2.48 cm (range, 0.8-6.0 cm). Complications involved pancreatitis (n=1) and early spleen infarction (n=29: <1/3 in 14, 1/3-2/3 in 10, and >2/3 in 5). Postembolization syndrome was noted in 26 patients (65%). There were no significant differences by aneurysm location in the postoperative increase in the values of white blood cells, amylase, lipase, and C-reactive protein (P=0.067, P=0.881, P=0.891, and P=0.188, respectively). CONCLUSION: At our institution, endovascular management is safe, has high technical success, and represents the first-line treatment for SAA, regardless of aneurysm location.
Amylases ; Aneurysm* ; C-Reactive Protein ; Embolization, Therapeutic ; Enbucrilate ; Female ; Humans ; Infarction ; Leukocytes ; Lipase ; Medical Records ; Pancreatitis ; Spleen ; Splenic Artery* ; Stents

Waldenstr m's macroglobulinemia(WM) is a disorder of malignant proliferation of plasmacyoid lymphocytes and monoclonal immunoglobulin M. The renal complications of WM are less common and severe than that of multiple myeloma. We present a case of WM which involved the kidney as massive proteinuria, hematuria and renal failure. A biopy specimen of the kidney reveals the intraglomerular hyaline thrombi of immunoglobulin M paraprotein. Three cycles of plasmapheresis and systemic chemotherapy with chlorambucil and prednisolone show improvement in his renal manifestations. We suppose the glomerulonephritis caused by hyaline thrombi in WM may be reversible, at least in its early stage.

Sumoylation, the conjugation of a small ubiquitin-like modifier (SUMO) protein to a target, has diverse cellular effects. However, the functional roles of the SUMO modification during myogenesis have not been fully elucidated. Here, we report that basal sumoylation of histone deacetylase 1 (HDAC1) enhances the deacetylation of MyoD in undifferentiated myoblasts, whereas further sumoylation of HDAC1 contributes to switching its binding partners from MyoD to Rb to induce myocyte differentiation. Differentiation in C2C12 skeletal myoblasts induced new immunoblot bands above HDAC1 that were gradually enhanced during differentiation. Using SUMO inhibitors and sumoylation assays, we showed that the upper band was caused by sumoylation of HDAC1 during differentiation. Basal deacetylase activity was not altered in the SUMO modification-resistant mutant HDAC1 K444/476R (HDAC1 2R). Either differentiation or transfection of SUMO1 increased HDAC1 activity that was attenuated in HDAC1 2R. Furthermore, HDAC1 2R failed to deacetylate MyoD. Binding of HDAC1 to MyoD was attenuated by K444/476R. Binding of HDAC1 to MyoD was gradually reduced after 2 days of differentiation. Transfection of SUMO1 induced dissociation of HDAC1 from MyoD but potentiated its binding to Rb. SUMO1 transfection further attenuated HDAC1-induced inhibition of muscle creatine kinase luciferase activity that was reversed in HDAC1 2R. HDAC1 2R failed to inhibit myogenesis and muscle gene expression. In conclusion, HDAC1 sumoylation plays a dual role in MyoD signaling: enhancement of HDAC1 deacetylation of MyoD in the basally sumoylated state of undifferentiated myoblasts and dissociation of HDAC1 from MyoD during myogenesis.
Creatine Kinase, MM Form ; Gene Expression ; Histone Deacetylase 1 ; Histone Deacetylases ; Histones ; Luciferases ; Muscle Cells ; Muscle Development ; Myoblasts ; Myoblasts, Skeletal ; Sumoylation ; Transfection