AIM: To explore the long-term efficacy of Q-factor guided laser epithelial keratomleusis ( LASEK ) for myopia and astigmatism with positive Q-factor.
METHODS: There were 158 eyes which were myopia and astigmatism with positive Q- factor taken in two groups randomly: 86 eyes accepted Q - factor guided LASEK as observation group and 72 eyes accepted routine LASEK as control group. The difference between the two groups about all data was similar. The uncorrected visual acuity ( UCVA ) and the best corrected visual acuity ( BCVA ) as well as diopter, ocular tension, corneal topography, Keratometry value K, aspherical factor Q, Higher-order aberrations ( HOA ) , corneal thickness by ultrasound and, contrast sensitivity ( CS ) , Haze were examined and compared before and after surgery. All the cased were followed up for 14d, 1, 3, 6, 12mo. And there were no statistical difference among the data before surgery.
RESULTS: After 12mo there were no statistical difference between the two groups about UCVA and BCVA. But the safety index of observation group was 1.10, that of control group was 1. 07. The validity index of observation group was 1. 06, that of control group was 0.99. The HOA of observation group was 0. 45±0. 17μm, and that of control group was 0. 72±0.25μm, there was statistically significant difference (t=-8. 193,P=0. 000). Q factor of observation group was 0. 41±0. 17, that of control group was 0. 77±0. 22, there was significant difference (t=11. 377,P = 0. 028). The contrast sensitivity of 3mo post surgery of patients in the observation group returned to the level of before surgery. But in the control group the contrast sensitivity of the patients did not returned until 6mo.
CONCLUSION:Q-factor guided LASEK for myopia and astigmatism with positive Q-factor is stable, safe and effective. The operation allow for reducing the high order aberrations, maintaining the most asphericity of cornea, saving more in corneal tissue, which cause faster recovery of contrast sensitivity, less haze and better visual quality.

Calycosin （CA）， a functional phytoestrogenic isoflavone extracted from Chinese herb Astragali Radix， is characterized by high efficiency， low toxicity， and multiple targets and has multiple pharmacological activities such as anti-oxidation， anti-radiation， anti-bacteria， cardio-cerebrovascular protection， and immunity enhancement. A number of studies have proved its significant anti-tumor effect， making it expected to become a potential component for the treatment of malignant tumors. Research shows that CA exerts the anti-tumor effect via multiple mechanisms like inducing tumor cell apoptosis and inhibiting tumor cell proliferation， migration， and invasion. It has been proved to be effective in suppressing breast cancer， colorectal cancer， lung cancer， cervical cancer， ovarian cancer， nasopharyngeal cancer， and other common malignant tumors. Its anti-tumor activity is mainly related to the regulation of B-cell lymphoma-2 （Bcl-2） family genes， microRNA （miRNA）， and estrogen receptor β （ERβ） to trigger tumor cell apoptosis. Its anti-proliferation activity is mainly reflected in the regulation of cyclin family， WD repeat-containing protein 7 （WDR7-7）， and Ewing sarcoma-associated transcript 1 （EWSAT1）. By blocking the epithelial mesenchymal transformation （EMT）， vascular endothelial growth factor （VEGF）， matrix metalloproteinases （MMPs）， CA inhibits tumor cell metastasis and invasion. In addition， it inhibits tumors by regulating autophagy marker Beclin-1 induced tumor cell autophagy and increases the sensitivity to chemotherapy drugs， thus improving the treatment effect. Although there are many reports about the wide range of applications and good effects of CA in anti-tumor， the systematic review of its anti-tumor mechanism is still lacking. Therefore， this study reviewed the anti-tumor effects and mechanisms of CA， aiming to provide reference for researchers and clinical workers.

Betulinic acid （BA） is a lupane pentacyclic triterpene extracted from a variety of Chinese herbs such as Betulae Platyphyllae Cortex， Astragali Radix， Paeoniae Radix Alba， Jujubae Fructus， Sanguisorbae Radix， Eucommiae Cortex， Glycrrhizae Radix et Rhizoma， Aucklandiae Radix， and Ziziphi Spinosae Semen. It has attracted wide attention from doctors because of its low toxicity， high efficacy， and multiple functions. BA has been found to possess a significant anti-tumor biological activity， and it is expected to become a potential drug for the treatment of malignant tumors. So far， a number of studies have shown that BA is able to promote apoptosis， inhibit proliferation， metastasis and invasion， and induce cell cycle arrest via multiple mechanisms， thus resisting various malignant tumors such as ovarian cancer， breast cancer， gastric cancer， lung cancer， colorectal cancer， and prostate cancer. It exerts the anti-tomor effect by regulating the expression of cancer suppressor genes p53 and p21， triggering the generatoipn of reactive oxygen species （ROS）， down-regulating the expression of nuclear transcription factor-κB （NF-κB）， adjusting the B lymphocytoma-2 （Bcl-2） family to cause tumor cell apoptosis， and regulating transcription factor Sp1/3/4 to induce apoptosis. Its anti-proliferative activity is mainly achieved via the regulation of cyclin B， cyclin D and cyclin dependent kinases CDK and CDC. Its efficacy in inhibiting metastasis and invasion is mainly realized by regulating matrix metalloproteinase （MMP） and matrix metalloproteinase inhibitor （TIMP）， up-regulating E-cadherin， down-regulating N-cadherin and blocking the epithelial-mesenchymal transformation （EMT）. In addition， BA also induces cell cycle arrest， affects tumor metabolic reprogramming， and activates autophagy to inhibit tumor. Although there are a large number of studies on BA against tumors and its efficacy has been proved strong， the systematic review on its anti-tumor effect is still lacking. Therefore， this study reviewed the anti-tumor effect and mechanism of BA， in order to provide reference for its subsenquent research.

Objective::To observe the intervention effect of Yiqi Huoxue recipe (YQHX) on ventricular remodeling in rats with chronic heart failure, in order to explore its mechanism. Method::Among 40 male SD rats, 10 were randomly selected as the sham operation group. The left anterior descending coronary artery ligation was performed to construct the chronic heart failure(CHF) rat model. After modeling, they were randomly divided into model group, captopril group(13.5 mg·kg^-1·d^-1) and YQHX group (20 g·kg^-1·d^-1), and orally given the corresponding drugs. After 8 weeks of intervention, cardiac tissues were collected, body mass and heart mass were weighed, and echocardiography were performed to detect the changes in cardiac structure. Masson staining was performed to determine the myocardial interstitial collagen volume fraction. Western blot was used to detect the expression levels of mitochondrial fusion protein optic atrophy 1 (Opa1) and cleavage protein dynamic-related protein 1 (Drpl). The quantitative real-time fluorescence polymerase chain reaction(Real-time PCR)was applied to detect the expressions of Wnt/β-catenin pathway-related factors such as lipoprotein receptor-related protein 6 (LRP6), glycogen synthase kinase-3β (GSK-3β) and β-catenin. Result::Compared with the sham group, the left ventricular wall of the model group was significantly thickened (P<0.05), the cardiac cavity was significantly enlarged, and the content of collagen in the myocardial interstitium was increased (P<0.01). The expression level of Opal decreased, the expression level of Drp1 increased (P<0.05), the mRNA expression level of LRP6, GSK-3, and β-catenin increased (P<0.01). Compared with the model group, YQHX group can reduce ventricular wall thickening, heart chamber enlargement, myocardial interstitial collagen content, up-regulate the low expression of Opa1, but down-regulate the high expressions of Drpl, LRP6, GSK-3β, β-catenin(P<0.05, P<0.01). Conclusion::YQHX can effectively alleviate ventricular remodeling and improve mitochondrial energy metabolism in rats with CHF. The mechanism may be related to the inhibition of Wnt/β-catenin related factors.