The clinical application of 16-slice CT coronary angiography (CTCA) and the impact of plaques differently characterized on assessing coronary artery stenosis were evaluated. Thirty-eight patients with coronary artery disease diagnosed by conventional coronary angiography (CAG) un- derwent 16-slice CTCA (collimation: 16×0.75 mm; rotation time: 420 msec; kernel: 35f; effective current: 500 mAs; tube voltage: 120 kV). The interval between CTCA and CAG was within one month. CTCA was evaluated by consensus of two independent experienced radiologists unknowing CAG findings. Original images, maximum intensity projections and multiplanar reconstructions were used to assess coronary artery stenosis. For a determined plaque an attenuation value≥130 HU was considered as calcified, and ＜130 HU noncalcified. The plaques were then classified into significant calcification (extensive calcification), medium calcification (small isolated calcification) and noncal- cification. The diagnostic accuracy of 16-slice CTCA findings as well as to detect ≥50% stenoses caused by plaques was evaluated respectively regarding CAG as the standard of reference. In com- parison with CAG findings, the sensitivity, specificity, positive and negative predictive value derived from CTCA for mild stenosis (＜50%) were 72.7%, 38.5%, 50%, 62.5%, respectively; for moderate stenosis (50%-75%) 82.4%, 72.7%, 70%, 84.2%, resepctively; and for severe coronary stenosis (＞75%) 85%, 90.5%, 81%, 92.7% respectively. With the increase of stenoses degree, the value of CTCA was greater. For the classification of the plaque calcification with ≥50% stenosis CTCA at- tained the sensitivity, specificity, positive and negative predictive value for severe calcificatoin 73.3%, 22.2%, 61.1% and 33.3%, respectively; for moderate calcification 70%, 55.6%, 63.6% and 62.5%, respectively; for noncalcification 93.8%, 85.7%, 93.8% and 85.7% respectively. CTCA was restricted in assessing coronary artery stenosis in the presence of calcification, but CTCA value was much im-proved in assessing non-calcified stenosis. It was concluded that 16-slice CTCA could provide useful information about coronary artery stenosis, especially for severe stenosis (≥50%) and non-calcified plaque. Since CTCA is a noninvasive technique, it may be useful in screening coronary artery dis-ease.

ObjectiveTo explore the mechanisms of Astragali Radix-Curcumae Rhizoma （HQ-EZ） in alleviating hypercoagulability and inhibiting tumor growth and metastasis by modulating the formation of neutrophil extracellular traps （NETs） via the complement component 5a （C5a）/C5a receptor （C5aR） pathway. MethodForty male C57BL/6 mice were randomized into four groups： Blank， model， HQ-EZ （8.2 g·kg^-1）， and PMX53 （1 mg·kg^-1）. The mouse model of Lewis lung cancer was established in other three groups except the blank group. Mice were administrated with corresponding drugs from day 3 after modeling. Specifically， the HQ-EZ decoction was administrated for 14 consecutive days， while intraperitoneal injection of PMX53 was implemented on days 3， 6， 9， 12， and 15. Mouse body weight and tumor diameter were measured every two days. On the next day of the last administration， lung microCT was performed to observe the tumor metastasis in vivo. Blood samples were collected from the eyeball after anesthetization， and tumor and lungs were collected after the mice were sacrificed. Tumor weight was measured to calculate the tumor growth inhibitory rate. Enzyme-linked immunosorbent assay was employed to measure the levels of C5a， neutrophil elastase （NE）， citrullinated histone-H3 （Cit-H3）， myeloperoxidase （MPO）， matrix metallopeptidase-9 （MMP-9）， NETs， von Willebrand Factor （vWF）， tissue factor （TF）， and P-selectin in the serum and tumor tissue. Terminal-deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling was conducted to assess apoptosis in the tumor tissue. Hematoxylin-eosin staining was conducted to observe lung metastasis， and immunofluorescence （IF） was employed to observe the expression of NETs in the tumor tissue. Western blot was employed to determine the protein levels of C5aR， MPO， and Cit-H3 in the tumor tissue. ResultCompared with the blank group， the model group had nodules in the lung， increased areas with low X-ray transmittance， appearance of nodular foci and multiple hemorrhagic foci in the lungs， and darkening lung color. Furthermore， the modeling elevated the serum levels of C5a， NETs and related proteins， vWF， TF， and P-selectin （P<0.01）. Compared with the model group， HQ-EZ and PMX53 reduced the lung metastases， areas with low X-ray transmittance， and nodules in the lungs and lightened the lung color. Compared with the model group， the two drug intervention groups showed flat tumor growth curves， decreased tumor weight （P<0.01）， increased apoptosis of tumor cells （P<0.01）， lowered levels of C5a， NETs and related proteins， vWF， TF， and P-selectin both in the serum and tumor tissue （P<0.05）， and down-regulated protein levels of C5aR， MPO， and Cit-H3 （P<0.05）. ConclusionHQ-EZ inhibited the expression of NETs by suppressing the C5a/C5aR pathway， thereby alleviating hypercoagulability and inhibiting tumor growth and metastasis.