Objective:To explore the relationship between YKL-40 and the proliferation of breast cancer and its mechanism.Methods:The expression of YKL-40 in breast cancer MCF-7 cells was detected by immunofluorescence assay.Fluorescence microscope was used to observe the conversion efficiency,and Real-time PCR was used to screen the most effective YKL-40 siRNA.Expression levels of PI3K,P-PI3K,AKT,P-AKT of the PI3K/AKT pathway associated proteins was test by Western blot.At the same time,MTT and flow cytometry were validated by YKL-40 siRNA treatment of human breast cancer MCF-7 ceils,the differences of 24h,48h and 72h groups of cell proliferation ability and cell cycle.Result:MCF-7 cell express YKL-40 protein,mainly located in the cytoplasm.Real-time PCR show that siRNA01,siRNA02,siRNA03 compared with NC group YKL-40 gene silencing effect is remarkable.Among of them the strongest silencing effect is siRNA02 (P＜0.01),Western blot show the experimental group than the control group,Total PI3K and AKT remain unchanged while P-PI3K,P-AKT expression decreased (P＜0.05).In the experimental group,the number of G1 cells in the control group was increased (P＜0.01),while the S phase cells decreased (P＜0.01).MTT results showed that the experimental group compared with the control group,the proliferation ability is decreased(P＜0.01).Conclusions This study suggests that YKL-40 can be used as the upstream regulatory factor of PI3K/AKT signaling pathway and affect the process of cell cycle in breast cancer,and then regulate the proliferation of breast cancer,YKL-40 may be a crucial target for the treatment of breast cancer.

The fine structure of enoxaparin sodium samples with different degree of 1,6-anhydro derivatives were analyzed with polyacrylamide gel electrophoresis, high performance liquid chromatography, ultraviolet spectroscopy, infrared spectroscopy and nuclear magnetic resonance spectroscopy. A further study of anticoagulation activity of enoxaparins was performed, including those on their inhibition activities of coagulation factor Xa (FXa) and thrombin (FIIa). The results showed that the anti-FXa and -FIIa activities of enoxaparins with different degree of 1,6-anhydro derivatives (20.0%-39.7%) with similar structure characteristics, had decreasing tendency when the degree of 1,6-anhydro derivatives increased. Especially, the anti-FXa activity was sensitive to the change of the degree of 1,6-anhydro derivatives.

Background: and Purpose Despite administration of evidence-based therapies, residual risk of stroke recurrence persists. This study aimed to evaluate the residual risk of recurrent stroke in acute ischemic stroke or transient ischemic attack (TIA) with adherence to guideline-based secondary stroke prevention and identify the risk factors of the residual risk. Methods: Patients with acute ischemic stroke or TIA within 7 hours were enrolled from 169 hospitals in Third China National Stroke Registry (CNSR-III) in China. Adherence to guideline-based secondary stroke prevention was defined as persistently receiving all of the five secondary prevention medications (antithrombotic, antidiabetic and antihypertensive agents, statin and anticoagulants) during hospitalization, at discharge, at 3, 6, and 12 months if eligible. The primary outcome was a new stroke at 12 months. Results: Among 9,022 included patients (median age 63.0 years and 31.7% female), 3,146 (34.9%) were identified as adherence to guideline-based secondary prevention. Of all, 864 (9.6%) patients had recurrent stroke at 12 months, and the residual risk in patients with adherence to guidelinebased secondary prevention was 8.3%. Compared with those without adherence, patients with adherence to guideline-based secondary prevention had lower rate of recurrent stroke (hazard ratio, 0.85; 95% confidence interval, 0.74 to 0.99; P=0.04) at 12 months. Female, history of stroke, interleukin-6 ≥5.63 ng/L, and relevant intracranial artery stenosis were independent risk factors of the residual risk. Conclusions There was still a substantial residual risk of 12-month recurrent stroke even in patients with persistent adherence to guideline-based secondary stroke prevention. Future research should focus on efforts to reduce the residual risk.