Fracture of a Renal Artery Stent after PTAS in a Patient with Atherosclerotic Ostial Stenosis

Renovascular hypertension occurs in 1~5% of the patients with hypertension. Renal artery stenosis (RAS) is a potentially curable cause of hypertension, and the main cause of ostial RAS is atherosclerosis. Revascularization by endovascular stent placement is one of the favorable treatments for ostial RAS that is without severe nephropathy. The complications of endovascular stents include hematoma at the inguinal region, femoral pseudoaneurysm, renal artery perforation, dissection, stent dislocation, stent fracture and so on. Fracture of a renal artery stent is a very unusual condition and it has rarely been reported in the literature. We experienced a case of renal artery stent fracture in 77-year-old male patient after right renal arterial stenting due to RAS. The fracture was found by chance during an evaluation for peripheral artery disease.

Mycophenolic Acid Induced Apoptotic Signal Transduction in Molt-4 T-cells

PURPOSE: Mycophenolic acid (MPA), a selective inhibitor of inosine monophosphate dehydrogenase (IMPDH), is the active metabolite of the immunosuppressive drug, mycophenolate mofetil (MMF). MMF is used to prevent an immune- mediate rejection response following organ transplantation via the inhibition of the IMPDH and GTP biosynthesis pathway. This study was designed to elucidate the mechanism by which MPA exerts its cytotoxic effect on human T lymphocytic and monocytic cell lines. METHODS: MOLT-4 and U937 cell lines were treated with MPA. Cell viability, expression of Bcl2 family proteins and Fas/Fas-L, effects of antioxidants and intracellular Ca2+ regulating agents and apoptosis were measured using a variety of microscopic and biochemical techniques. RESULTS: MPA induced the death of U937 and MOLT-4 cells in dose and time dependent manners, which was revealed an apoptosis with a characteristic ladder pattern of DNA fragmentation. In addition, BAPTA/AM, an intracellular Ca2+ chelator protected MOLT-4 cells from MPA treated apoptosis, although it did not have an additive with thapsigargin, and increases cytosolic Ca2+ stores. However, antioxidants including reduced glutathione (GSH) and N-acetyl-L-cysteine (NAC) did not inhibit the apoptosis of cells by MPA. Furthermore, guanosine suppressed MPA induced apoptosis of MOLT-4 lymphocytes, although adenosine did not. MPA also increased the catalytic activity of caspase family cysteine proteases including caspase-8, 9 and 3 proteases in MOLT-4 cells. Sequential activation indicated that the cleavage of caspase-8 and 9 precedes those of caspase-3. CONCLUSION: The results suggest that MPA induces the apoptotic death of MOLT-4 lymphocytes via the activations of caspase family proteases and the depletion of GTP.

Bacterial Endotoxin, Lipopolysaccaride, and Induced Activation of Stress-Activated Protein Kinase and Generation of Nitric Oxide

BACKGROUND: Previously, it has been suggested that lipopolysaccaride (LPS) stimulates the activation of the transcriptional factor activator protein (AP-1) which is in part regulated by activation of the c-Jun N-terminal kinase (JNK) / stress-activated protein kinase (SAPK) in the murine macrophage cell line RAW 264.7. METHODS: Consistent with this notion, we find that treatment of LPS on RAW 264.7 cells induces the generation of nitric oxide (NO) and results in the activation of JNK and treated with NO donors and NO inhibitors. RESULTS: NO donors including sodium nitroprusside (1 mM), GSNO (0.2 mM), or SNAP (0.5 mM) treatment of the macrophage cell line markedly induces the activation of JNK. However NGMMA (2 mM), a competitive inhibitor of NO, does not inhibit the activation of JNK induced by LPS. SIN-1, NO, and superoxide donor induce an activation of JNK that is slightly decreased by treatment with sodium dismutase whereas the activation of JNK is significantly augmented by adding sodium dismutase with catalase. C2 ceramide suppresses the generation of NO induced by LPS, but significantly increases the activity of JNK in vivo. LPS can induce the activation of JNK at 30 min after stimulation in RAW 264.7 cells. Exposure to SNP does not affect the enzymatic activity of JNK, immunoprecipitates, JNK, and c-Jun N-terminal proteins. CONCLUSIONS: These data suggest that even though NO is one of the major activators of JNK induced by LPS, there is, at least, an NO-independent JNK activation, signaling a pathway for LPS. Also, there may be an undefined NO-sensitive JNK-regulator (s) in vivo.

A Case of Congenital Lymphedema

Congenital lymphedema is a rare disorder of unknown etiology which affects the extremities, preponderantly the lower extremities, at or immediately after birth. We experienced a case of congenital lymphedema in a newborn with generalized edema on the left lower extremity. We performed lymphangioscintigraphy and MRI for diagnosis. Microlymphaticovenous anastomosis was done on 16 days after birth and the patient showed clinical improvement. We report this case with brief review of the related literature.