Objective To study the clinical effect of endovascular treatment on complex TASC-D type aortoiliac occlusive disease (AIOD). Methods Clinical data of 27 patients (35 limbs) of the TASC-D type AIOD were collected in Department of Cardiovascular Surgery and were retrospectively analyzed. According to the Fontaine staging and the corresponding imaging examination before surgery, the therapy programme was worked out. Two limbs received thrombectomies, and 33 limbs received endovascular treatments including 5 limbs received percutaneous transluminal angioplasty (PTA), 24 limbs received percutaneous transluminal angioplasty stenting (PTAS), and 4 limbs underwent catheter-directed thrombolysis. Patients were followed up for 3 to 36 months regularly by telephone or outpatient after operation. The clinical symptoms, ankle brachial index (ABI), complications and cumulative primary patency rates were evaluated. Results The overall success rate of endovascular treatment was 90.9% (30/33). Two limbs treated with PTAS and one limb with catheter-directed thormbolysis showed a poor outcome. ABI increased from (0.40 ± 0.15) prehospital to (0.82±0.20) for 1 month. After therapy for one year, the primary patency rate was 93.3%(28/30). At 24 months, the primary patency rate was 83.3%(25/30), and limb salvage rate was 94.3%(33/35). One limb resulted in above ankle amputation 10 days after admission to hospital, and 1 limb underwent toe amputation in 2 months after operation. Conclusion Endovascular therapy is a safe and effective method for TASC-D AIOD, which shows satisfactory clinical outcomes with short-term to mid-term patency rates.

As one of the immediate-early(IE)proteins of herpes simplex virus type 1(HSV-1),ICP22 is a multifunctional viral regulator that localizes in the nucleus of infected cells.It is required in experimental animal systems and some nonhuman cell lines,but not in Vero or HEp-2 cells.ICP22 is extensively phosphorylated by viral and cellular kinases and nucleotidylylated by casein kinase Ⅱ.It has been shown to be required for efficient expression of early(E)genes and a subset of late(L)genes.ICP22,in conjunction with the UL13 kinase,mediates the phosphorylation of RNA polymerase Ⅱ.Both ICP22 and UL13 are required for the activation of ode2,the degradation of cyclins A and B and the acquisition of a new cdc2 partner,the UL42 DNA polymerase processivity factor.The cdc2-UL42 complex mediates postranscriptional modification of topoisomerase Ⅱa in an ICP22-dependent manner to promote L gene expression.In addition,ICP22 interacts with cdk9 in a Us3 kinase dependent fashion to phosphorylate RNA polymerase Ⅱ.