It aimed to analyze the price disclosure system of genetic drugs in Australia.Based on the analysis of background and historical evolution,it tracked each step of price disclosure on the basis of descriptive statistics and analvsis so as to provide reterences for constructing the price disclosure system of genetic drugs led by market factor under the effective conduct of future medical reform policy in China.

Objective　To examine the expressions of estrogen receptor α (ERα), estrogen receptor β (ERβ) and pituitary-specific truncated estrogen receptor product-1 (TERP-1) in diethylstilbestrol (DES) induced prolactinoma of rats. Methods　Ovariectomised Wistar rats were subcutaneously implanted with an implant containing 20 mg DES. Rats were implanted with a blank implant as controls. Eight weeks later, serum prolactin level of rats was measured by RIA. Prolactin immunoreactive cells of anterior pituitary were detected by immunohistochemistry assay. ERα, ERβ and TERP-1 mRNAs in pituitaries were examined by RT-PCR. Results　Serum prolactin levels, pituitary weights and pituitary prolactin immunoreactive cell countings in experimental group rats were all obviously higher than those in control group (P＜0.001 respectively). ERα, ERβ and TERP-1 mRNAs were all transcripted in DES induced rat prolactinomas. ERα and TERP-1 mRNA levels were significantly higher in experimental group than those in control group (P＜0.001 and P＜0.05). Conclusion　Estrogen plays a direct role in regulating pituitary prolactin cells through estrogen receptors. Further functional studies will be required to determine whether coexpression of ER variants along with normal ER confers a pathophysiological role in pituitary hormone regulation and (or) tumor cell proliferation.

Objective:To evaluate the anxiety and depression symptoms of burning mouth syndrome (BMS), and to explore risk factors to BMS.Method:In this case-control study,147 patients with BMS and 140 sex-and age-matched healthy volunteers were recruited.Three questionnaires were used to collect information of psychical and mental condition.The Self-Rating Anxiety Scale (SAS)and Self-Rating Depression Scale (SDS)were applied to evaluate symptoms of anxiety and depression.The scores of SAS and SDS were statistically analyzed by t-test.The risk factors of BMS were statistically analyzed by Chi-square test and logistic regression analysis.Result:The scores of SAS and SDS were higher in the patients with BMS than in the controls [SAS:(44.4 ±9.9)vs. (35.7 ±6.2);SDS:(48.1 ±11.6)vs.(37.5 ±8.9)].The risk factors of BMS included ischemic stroke (OR =4.46,95%CI:1.87 -10.95),low level of education (OR =1.91,95%CI:1.04 -3.49),anxiety symptom (OR =8.12,95%CI:2.60 -25.37)and depression symptom (OR =2.57,95%CI:1.26 -5.27).Conclusion:BMS is a multi-factorial disease.It indicates that ischemic stroke,lower level of education,anxiety symptom and depression symptom are the risk factors of BMS.A positive association could be established between psychological alterations and BMS.According to these findings it can be assumed that mental factors should be taking into account in the etiologyof BMS.It should be advocated to treat BMS patients by psychotherapy.

OBJECTIVE: To investigate the effect of danusertib (Danu), an inhibitor of Aurora kinase, on the proliferation, cell cycle, apoptosis, and autophagy of hepatocellular carcinoma HepG2 cells and explore the underlying mechanisms. METHODS: MTT assay was used to examine the effect of Danu on the viability of HepG2 cells to determine the IC50 of Danu. The effect of Danu on cell cycle distribution, apoptosis and autophagy were determined using flow cytometry. Western blotting was used to detect the expressions of the proteins related to cell cycle, apoptosis and autophagy. Chloroquine was used to suppress Danuinduced autophagy to test the apoptosis-inducing effect of Danu. RESULTS: Danu significantly inhibited the proliferation of HepG2 cells with IC of 39.4 μmol and 14.4 μmol at 24 h and 48 h, respectively. Danu caused cell cycle arrest in G/M phase in HepG2 cells and led to polyploidy accumulation via up-regulating the expressions of p53 and p21 and down-regulating the expressions of cyclin B1 and DC2. Danu also caused apoptosis of HepG2 cells through up-regulating the expressions of Bax, Puma, cleaved caspase-3, cleaved caspase-9, cleaved PARP and cytochrome C and down-regulating the expressions of Bcl-xl and Bcl-2. Danu induced autophagy via activating AMPK signaling and inhibiting PI3K/PTEN/AKT/mTOR axis, and inhibition of Danu-induced autophagy with chloroquine enhanced the pro-apoptotic effect of Danu. CONCLUSIONS Danu inhibits cell proliferation and induces cell cycle arrest in G/M phase, apoptosis and cytoprotective autophagy in HepG2 cells.
Apoptosis ; drug effects ; Autophagy ; drug effects ; Benzamides ; pharmacology ; Carcinoma, Hepatocellular ; pathology ; Cell Cycle ; drug effects ; Cell Division ; drug effects ; Cell Proliferation ; drug effects ; Hep G2 Cells ; Humans ; Liver Neoplasms ; pathology ; Neoplasm Proteins ; metabolism ; Protein Kinase Inhibitors ; pharmacology ; Pyrazoles ; pharmacology