Animals ; Cadmium Compounds ; toxicity ; Cell Proliferation ; Cell Survival ; Cells, Cultured ; Cricetinae ; Cricetulus ; Fibroblasts ; drug effects ; metabolism ; Lactate Dehydrogenases ; metabolism ; Lung ; cytology ; Malondialdehyde ; metabolism ; Quantum Dots

Objective To establish a HPLC method for the determination of daphnetin, 7-OH coumarin and syringing in Zushima. Methods The separation was performed on YMC-Pack ODS (4.6 mm?250 mm, 5 ?m) column with a mobile phase consisting of methanol-0.5% acetic acid-water (19︰8︰1) as gradient elution at the flow rate of 1.0 mL/min. The dual detective wavelength was set at 327 nm and 266 nm. The column temperature was 30 ℃. Results Baseline separation was achieved for the analysis of the three index components. The average recoveries were 98.4%～100.2%. Conclusion This method is convenient, rapid and accurate. It can be used for quality control in production of Zushima.

This paper systematically stated the sexual moral problems of the repairment of ruptured hymen resulted form different reasons and the moral principles and requirements for the operator.

Objective To investigate the inhibitory effects of periplocin from cortex periplocae (CPP) on human lung cancer cell line QG56 and to discuss its mechanism. Methods QG56 cells were cultured in vitro. The final concentrations of CPP in control group were 1.25, 2.50, 5.00, 10.00 and 20.00μg/L. QG56 cells were treated with ascending concentration of CPP for 24 h, 48 h and 72 h. The cell proliferation was measured using MTT method. The morphological changes of QG56 cells were observed under inverted microscope. Flow cytometry (FCM) was used to detect the effects of CPP on cell cycle and cell apoptosis. The expression of apoptosis associated gene bax mRNA in QG56 cells was detected by RT-PCR. The expres-sion of bax protein before and after treatment of CPP was examined by SP immunocytochemistry. Results The inhibitory ef-fect of CPP on the proliferation of QG56 cells was increased with the increasing concentrations of CPP and the prolonged du-ration of treatment. The morphological changes were displayed in QG56 exposed to CPP. The results of FCM showed that CPP caused cell cycle arrest at G0/G1 phase. The apoptotic rate of QG56 cells was significantly increased after CPP treatment for 48 h (P<0.05). The expression of bax mRNA was increased in QG56 exposed to CPP. The result of immunocytochemis-try indicated that CPP up-regulated the expression of bax protein. Conclusion CPP showed significant inhibitory effect on human lung cancer cell lines QG56 through inducing cell cycle arrest and apoptosis.

Objective To investigate the effects of periplocin from Cortex Periplocae (CPP) on apoptosis of human lung cancer A549 cells and expression of survivin, and demonstrate its anti-tumor effect and the possible mechanism. Methods Inhibitory effect of CPP at different concentrations (1. 25, 2. 50, 5. 00, 10. 00, 20. 00 ng·mL-1 ) and for different time length (24, 48, 72 h) on A549 cell proliferation was tested by MTT method. Apoptosis rate of A549 cells treated with CPP at different concentrations (2. 50, 5. 00, 10. 00 ng·mL-1 ) were measured using flow cytometry (FCM) for 6, 12, 24, 48, 72 h, respectively. The morphological and ultrastructural changes of the apoptosis cells were observed by acridine orange/ ethidium bromide (AO/ EB) staining and transmission electron microscopy (TEM). The effects of CPP on mRNA and protein expression of apoptosis associated gene survivin were assessed by RT-PCR and Western blotting. Results CPP could significantly inhibit the growth of A549, and the inhibition rate reached (93. 46±2. 35)% . The results of FCM showed that the apoptosis rate of A549 cells treated with CPP was increased significantly as compared to the control group ( P<0. 05). Meanwhile, typical apoptotic peaks were detected. The characteristic morphological changes of apoptosis were observed in A549 exposed to CPP, including cell shrinkage, the nuclei became yellow-red by AO/ EB staining, and typical ultrastructural changes, including nuclear chromatin condensation along the nuclear membrane, vacuolar degeneration of cytoplasm observed by TEM. The result of RT-PCR indicated that survivin mRNA expression decreased obviously in A549 cells exposed to CPP. The protein expression of survivin in A549 cells treated with 10. 0 ng·mL-1 CPP(0. 251±0. 012)was weaker than that in control group(0. 928±0. 016). Conclusion CPP can induce apoptosis in human lung cancer cell lines A549, and the probable mechanism is related to the down-regulation of survivin mRNA and protein.

Objective To evaluate the therapeutic effects of metformin hydrochloride and rosiglitazone maleate tablets on insulin resistance and androgen concentration in obese and nonobese women with polycystic ovarian syndrome (PCOS).Methods Seventy women with PCOS were enrolled into this study according to the diagnostic criteria of Rotterdam conference (2003).The women with PCOS were divided into the over weight/obese group (body mass index ≥ 25 kg/m2,n =34) and the nonobese group (body mass index＜25 kg/m2,n =36).All women with PCOS took metformin hydrochloride and rosiglitazone maleate tablets twice daily for 3 months.The following indexes were measured before and after the treatment:height,weight,waist circumference,hip circumference,fasting plasma glucose,fasting plasma insulin,luteinizing hormone (LH),follicle stimulating hormone (FSH),total testosterone,free testosterone,follicular number and ovarian area,body mass index,waist to hip ratio,and homeostasis model assessment for insulin resistance (HOMA-IR) were calculated.Results (1) Compared with the nonobese group,dramatic increases in HOMA-IR and follicle number were observed in over weight/obese group(P＜0.05),while LH,LH/FSH,total testosterone,free testosterone showed no significant difference between two groups.(2) After the treatment with metformin hydrochloride and rosiglitazone maleate tablets,weight,body mass index,fasting plasma glucose,fasting plasma insulin,HOMA-IR significantly decreased in two groups (P ＜ 0.05).There were also significant declines of LH,LH/FSH,free testosterone,ovarian area,follicular number,especially in the over weight/ obese women with PCOS (P＜0.05),while total testosterone and FSH did not change significantly.(3) The incidence of gastrointestinal adverse reactions in nonobese and over weight/obese group was 9.3％ and 6.3％ respectively,and no liver toxicity,edema,hypoglycemia and other adverse reactions was observed during treatment.Conclusion Compared with the nonobese group,there were severer insulin resistance and more marked polycystic change of ovary in over weight/obese women with PCOS,while total testosterone and free testosterone showed no significant difference between two gruops.Metformin hydrochloride and rosiglitazone maleate tablets can ameliorate insulin resistance and polycystic ovary,and also reduce body mass index and free testosterone in women with PCOS particularly in the over weight/obese individuals.

The PDB culture medium was selected to ferment the endophyte strain, and the secondary metabolites of endophytic fungi Penicillium polonicum were studied. Combined application of Sephadex LH-20, ODS and HPLC chromatographies over the ethyl acetate extract of the fermented culture led to the isolation of 6 compounds. By spectral methods, the structures were elucidated as [3, 5-dihydroxy-2-(7-hydroxy-octanoyl)]-ethylphenylacetate (1), (3, 5-dihydroxy-2- octanoyl)-ethyl phenylacetate (2), (5, 7-di- hydroxy-9-heptyl)-isobenzo pyran-3-one (3), 3-(hydroxymethyl) 4-(1E)-1- propen-1-yl-(1R, 2S, 5R, 6S)-7-oxabicyclo [4.1.0] hept-3-ene-2, 5-diol (4), (E)-2-methoxy-3-(prop-1-enyl) phenol (5) and p-hydroxylphenylethanol (6).
Biological Factors ; chemistry ; metabolism ; Endophytes ; chemistry ; isolation & purification ; metabolism ; Fabaceae ; microbiology ; Fermentation ; Penicillium ; chemistry ; isolation & purification ; metabolism ; Secondary Metabolism

Adenocarcinoma ; genetics ; metabolism ; Angiomyolipoma ; etiology ; Antibiotics, Antineoplastic ; therapeutic use ; Astrocytoma ; etiology ; Brain Neoplasms ; etiology ; Breast Neoplasms ; genetics ; metabolism ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Humans ; Kidney Neoplasms ; etiology ; Lung Neoplasms ; genetics ; metabolism ; Mutation ; Sirolimus ; therapeutic use ; TOR Serine-Threonine Kinases ; antagonists & inhibitors ; metabolism ; Tuberous Sclerosis ; complications ; drug therapy ; genetics ; metabolism ; Tumor Suppressor Proteins ; genetics ; metabolism

ObjectiveTo investigate the effects of maternal rat with marginal iodine deficiency on the nerve and intelligence development in its offspring and the related mechanisms.MethodsThe rat model of marginal iodine deficiency was established on the basis of epidemiological characteristics and iodine metabolism characteristics of rats reported in literatures.Marginal iodine deficiency rats were given 3 μg iodine a day ; normal control rats were given 4 μg iodine daily ; iodine deficiency rats were given 1.2 μg iodine daily,respectively.Western blot was used to detect the protein levels of brain derived neurophic factor (BDNF) and early growth response factor 1 ( EGR1 ) in the hippocampus of 7 days newborn rats.Immunohistochemistry was used to measure c-jun and c-fos expressions in the hippocampal CA1 region of 40 days rats.Water maze method was used to measure the ability of learning and spatial memory.Results FT4 level in rats of marginal iodine deficiency group during pregnancy decreased by about 30％.Seven days after birth,the contents of EGR1 and BDNF proteins in the hippocampus of the offspring from marginal iodine deficiency group were significantly decreased compared with normal control group (both P ＜ 0.05 ).Forty-day-old newborn rats in marginal iodine deficiency group also showed significantly decreased c-jun and c-fos expressions in the hippocampal CA1 region ( both P＜0.05 ),along with a decreased trend of spatial learning and memory ability.Conclusions FT4 level will significantly decrease after pregnancy if rats have marginal iodine deficiency,affecting the expression of related proteins in the brain of newborn rats and having a negative impact on offspring brain development.

Objective To improve the quality of medical device clinical trial.Methods To analyze medical device clinical trials conducted in our hospital from 2006 to 2010,and proposed the strategy to strengthen medical device clinical trial management.Results Most of the medical devices clinical trials were class Ⅲ medical devices clinical validation in our hospital,Surgical departments undertook most of the clinical trials.Until July 2013,49 trials were done only 56％ of undertake the project.96％ of completed trials were approved for medical device registration certificate.Conclusions The quality of clinical trials must be improved,andthe quality control process in medical device clinical trial should be reinforced.