Abstract-The phosphoinositide 3-kinase [PI(3)K] pathway is a key signaling pathway important for replication of mammalian cells. In this study, we examined the role of PI(3)K in smooth muscle cell (SMC) replication after balloon catheter injury of rat carotid arteries. Protein kinase B (PKB), a downstream target of PI(3)K, was phosphorylated at 30 and 60 minutes after injury and to a lesser degree after 6 hours and 1 and 2 days but not after 7 days. Wortmannin (10 g per rat), a PI(3)K inhibitor, given to rats 60 and 5 minutes before and 11 hours after balloon injury, reduced the levels of phosphorylated PKB. SMC replication quantified between 24 to 48 hours was significantly reduced compared with control replication, as were the levels of cyclin D 1 . Wortmannin was also administered to rats between days 7 and 8 and between days 7 and 9 after balloon catheter injury. A reduction in levels of phosphorylated PKB was detected, but no decrease in the replication of intimal SMCs was observed in either experiment. These data demonstrate that the PI ( Key Words: balloon injury Ⅲ smooth muscle cell replication Ⅲ protein kinase B Ⅲ wortmannin B alloon injury to the rat carotid artery initiates smooth muscle cell (SMC) replication in a predictable manner. Our previous data suggest that the replication of intimal and medial cells is controlled by different mechanisms. For example, the extracellular signal-regulated kinase (ERK)1/2 cascade is involved in the early proliferative response of the artery after mechanical injury, inasmuch as PD98095, a mitogen-activated protein kinase kinase (MEK)1 inhibitor, significantly blocked ERK1/2 phosphorylation and SMC replication 48 hours after injury. In contrast, the MEK1 inhibitor was not able to block intimal SMC replication after 7 days. 1 These data have led us to suggest that other signaling pathways may be important for intimal cell replication.Phosphoinositide 3-kinase [PI(3)K] is activated by many growth factors, and there is good evidence that this pathway is involved in the entry of cells into S phase. 2-4 Activation of PI(3)K leads to the generation of phosphatidylinositol 3,4-diphosphate and phosphatidylinositol 3,4,5-triphosphate in the cell membrane. These phospholipids form a binding site for proteins with a pleckstrin homology domain, such as protein kinase B (PKB), and in doing so a cryptic phosphorylation site is exposed. These sites are then phosphorylated by phosphoinositide-dependent kinases (PDKs), thus leading to their activation. Once activated, PKB phosphorylates several substrates, including glycogen synthase kinase-3␤ 5 and glucose transporter 4. 6 PKB is also known to be involved in regulating cell survival and cell replication. [7][8][9][10]

Early occurrence of anastomotic false aneurysm is characteristic of BD. Further investigation is necessary to establish effective postoperative treatment.

Temporary IVC filters were effective for the prevention of fatal pulmonary embolism. However, our experience of a high incidence of complications related to temporary filters suggests that this device has limited indications and supports the need for innovative design of temporary filters.

AAV ANCA-associated vasculitis ACR American College of Rheumatology ADA adalimumab ANCA anti-neutrophil cytoplasmic antibody AZA azathioprine bDMARDs biologic disease-modifying anti-rheumatic drugs c-ANCA cytoplasmic ANCA CG cryoglobulin CHCC Chapel Hill Consensus Conference Cr creatinine CT computed tomography CRP C-reactive protein CyA cyclosporine CV cryoglobulinemic vasculitis CY cyclophosphamide DMARDs disease-modifying anti-rheumatic drugs * a The aorta and its primary branches corresond to the aorta (ascending, arch, thoracic descending, abdominal descending), primary branches of the aorta (including the coronary artery), and pulmonary artery. * b Multiple lesions are defined as those that involve two or more of the above arteries or sites or two or more segments of the aorta. * c Hypertrophic lesions are detected by ultrasonography (macaroni sign of the common carotid artery), contrast-enhanced CT, contrastenhanced MRI (circumferential contrast enhancement of the arterial wall), and PET-CT (circumferential FDG uptake of the arterial wall). * d Stenotic lesions and dilated lesions are detected by chest radiography (wave-like deformation of the descending aorta), CT angiography, MR angiography, echocardiography (aortic insufficiency), and angiography. They are accompanied by dilatation of the ascending aorta and frequently also by aortic insufficiency. In the chronic stage, circumferential calcification of the arterial wall is visualized by CT, and the development of collateral circulation is detected by CT angiography and MR angiography Points of attention in imaging diagnosis: Contrast-enhanced CT is performed in the late phase of contrast enhancement. CT angiography is performed in the early phase of contrast enhancement with 3-dimensional image processing. Angiography is usually performed when other procedures such as endovascular treatment and coronary artery angiography or left ventriculography are simultaneously intended. C. Conditions to be included in the differential diagnoses of Takayasu arteritis Arteriosclerosis, congenital vascular anomaly, inflammatory abdominal aortic aneurysm, infectious aneurysm, syphilitic mesaortitis, giant cell arteritis (temporal arteritis), vascular Behçet's disease, IgG4-related diseases. Definite: At least 1 of the items in A + any of the conditions in B are observed, and conditions in C can be excluded.

Compared to OS patients, EVAR patients with massive neck atheroma tend to develop late-phase complications possibly related to cholesterol crystal embolisation. The clinical features of massive neck atheroma patients receiving EVAR should be carefully monitored even after hospital discharge.