This paper firstly analyzed from three aspects:the necessity of pharmacognosy medical ethics educa-tion, and then illustrates the main content of the medicine ethics education , this paper expounds the method and form of medicine ethics education , and finally summarizes the medicine ethics education for clinical practice stage of medical students experience:the medical institutions about the medicine ethics instances of intuitive for training medical students , strengthening medical students learn the importance of pharmaceutical ethics in clinical practice stage , in order to enhance the medical students medical moral sentiment , lay the foundation for clinical drug safety work.

ObjectiveTo study the value of plasma corticotropin-releasing hormone (CRH) and the fetal fibronectin (fFN) in vaginal secretions and cervical length in predicting preterm labor.MethodsThe plasma CRH levels and fFN levels in vaginal secretions from 24 -37 weeks pregnant woman checked up in our hospital from Dec.2009 to Dec.2010 were detected by ELLISA method.The changes of these three indexes were observed with the pregnant time and were analyzed according to different pregnancy outcomes.Results Among the 112 cases of pregnant women,premature delivery in 54 cases,full-term birth 58 cases.At the 24 week of pregnancy,there were significant difference on the cervical length( [2.8 ±0.4]cm vs [3.3 ±0.5]cm,t =3.254,P =0.021 ) between premature delivery group and full-term birth group.At the 28 - 30 week,31 -32 week,33 - 34 week,35 - 36 week,the CRH were ( 162.33 ± 16.49 ) ng/L,(60.01:±: 14.56) ng/L;(352.12 ±61.01 )ng/L,( 118.04 ±53.74)ng/L; (364.55 ±56.71 )ng/L,( 122.95 ±71.41 )ng/L; (372.78 ±149.89)ng/L,(124.00 ± 19.05 )ng/L respectively in premature delivery group and full-term birth group,and there were significant differences on CRH at the four different pregnant time(t =3.687,6.875,8.652,8.524,respectively,P ＜ 0.05 ).It shows better sensitivity ( 97.92％ ),specificity ( 90.00％ ),positive predictive value(95.92％ ) and negative predictive value(94.73％ ) in predicting premature delivery by detection of CRH,fFN combined with cervical length.ConclusionDetection of plasma CRH,fFN combined with cervix length measurement can improve the predictability of premature and provide a good,reliable clinical basis for the early diagnosis and treatment for preterm premature.

OBJECTIVE:To improve the HPLC-fluorometric method in the determination of telmisartan in human plasma.METHODS:Using naproxen as internal standard,the plasma was extracted with ethyl acetate.The separation was performed on Symmetry C8 with mobile phase consisted of acetonitrile -0.01mol?L-1 potassium dihydrogen phosphate buffer solution(47∶53) at a flow rate of 1.0ml?min-1.The ?Ex was set at 305nm and the ?Em was set at 365nm,and the sample size was 20?L.RESULTS:The linear range of telmisartan was 2.5～200ng?mL-1(r=0.999 8),with the lowest detectable limit at 1ng?mL-1.The average recovery of extraction was (89.91?10.07)%.Both the intra-day RSD and inter-day RSD were less than 10%.The sample showed a good stability within 24 hours after three freeze-thaw cycles and extractions.CONCLUSI-ON:The method is simple,sensitive,accurate and reproducible,and suitable for the determination and pharmacokinetic study of telmisartan in human plasma.

OBJECTIVE: To screen for mutations of fragile X mental retardation 1 (FMR1) gene during early and middle pregnancy and provide prenatal diagnosis for those carrying high-risk CGG trinucleotide expansions. METHODS: Peripheral blood samples of 2316 pregnant women at 12 to 21(+6) gestational weeks were collected for the extraction of genomic DNA. CGG repeats of the FMR1 gene were detected by fluorescence PCR and capillary electrophoresis. Genetic counseling and prenatal diagnosis were provided for 3 women carrying the premutations. RESULTS: The carrier rate of CGG repeats of the FMR1 gene was 1 in 178 for the intermediate type and 1 in 772 for the premutation types. The highest frequency allele of CGG was 29 repeats, which accounted for 49.29%, followed by 30 repeats (28.56%) and 36 repeats (8.83%). In case 1, the fetus had a karyotype of 45,X, in addition with premutation type of CGG expansion of the FMR1 gene. Following genetic counseling, the couple chose to terminate the pregnancy through induced labor. The numbers of CGG repeats were respectively 70/- and 29/30 for the husband and wife. In case 2, amniocentesis was performed at 20 weeks of gestation. The number of CGG repeats of the FMR1 gene was 29/-. No abnormality was found in the fetal karyotype and chromosomal copy number variations. The couple chose to continue with the pregnancy. Case 3 refused prenatal diagnosis after genetic counseling and gave birth to a girl at full term, who had a birth weight of 2440 g and no obvious abnormality found during follow-up. CONCLUSION Pregnant women should be screened for FMR1 gene mutations during early and middle pregnancy, and those with high-risk CGG expansions should undergo prenatal diagnosis, genetic counseling and family study.
DNA Copy Number Variations ; Female ; Fragile X Mental Retardation Protein/genetics* ; Fragile X Syndrome/genetics* ; Genetic Counseling ; Humans ; Mutation ; Pregnancy ; Trinucleotide Repeat Expansion ; Trinucleotide Repeats

OBJECTIVE: To detect potential mutations of the PKHD1 gene in two pedigrees affected with infantile polycystic kidney disease. METHODS: Clinical data and peripheral venous blood samples were collected from the probands and their parents as well as fetal amniotic fluid cells. Genome DNA was extracted from the peripheral blood samples and amniotic fluid cells. Exons 32 and 61 of the PKHD1 gene were amplified with PCR and subjected to direct sequencing. RESULTS: The proband of pedigree 1 was found to carry c.4274T>G (p.Leu1425Arg) mutation in exon 32 and c.10445G>C (p.Arg3482Pro) mutation in exon 61 of the PKHD1 gene, which were inherited from her father and mother, respectively. The fetus has carried the c.4274T>G (p.Leu1425Arg) mutation. In pedigree 2, the wife and her husband had respectively carried a heterozygous c.5979_5981delTGG mutation and a c.9455delA mutation of the PKHD1 gene. No chromosomal aberration was found in the umbilical blood sample, but the genetic testing of their fetus was failed. Based on software prediction, all of the 4 mutations were predicted to be pathogenic. CONCLUSION PKHD1 c.4274T>G (p.Leu1425Arg), c.10445G>C (p.Arg3482Pro), c.5979_5981delTGG and c.9455delA were likely to be pathogenic mutations. The results have facilitated genetic counseling and prenatal diagnosis for the two pedigrees.
DNA Mutational Analysis ; Female ; Genetic Counseling ; Humans ; Mutation ; Pedigree ; Polycystic Kidney Diseases ; diagnosis ; genetics ; Pregnancy ; Prenatal Diagnosis ; Receptors, Cell Surface ; drug effects

OBJECTIVE: Utilize high-resolution chromosome analysis and microarray detection to determine the genetic etiology of infertility of a 32-year old female patient. METHODS: The peripheral blood of the patient was cultured for high-resolution chromosome G and C banding karyotype analysis, and then 750K SNP-Array chip detection was performed. RESULTS: Karyotype analysis results showed that the patient's karyotype was 45,XX,-13 [7]/46,XX,r(13) (p13q34) [185]/46,XX,dic r(13;13)(p13q34;p13q34) [14]/ 47,XX,+der(13;13;13;13) (p13q34;p13q34;p13q34; p13q34), dic r(13;13) [1]/ 46,XX [3]. The microarray results showed that the patient had a 3.3 Mb deletion in the 13q34 segment of chromosome 13, which may be related to infertility. CONCLUSION Infertility of the patient reported in this article may be related to the deletion of chromosome segment (13q34-qter).
Adult ; Chimera ; Chromosome Banding ; Chromosome Deletion ; Chromosome Disorders/genetics* ; Dacarbazine ; Female ; Humans ; Infertility/genetics* ; Ring Chromosomes

Metabolic reprogramming is a hallmark of cancer, including lung cancer. However, the exact underlying mechanism and therapeutic potential are largely unknown. Here we report that protein arginine methyltransferase 6 (PRMT6) is highly expressed in lung cancer and is required for cell metabolism, tumorigenicity, and cisplatin response of lung cancer. PRMT6 regulated the oxidative pentose phosphate pathway (PPP) flux and glycolysis pathway in human lung cancer by increasing the activity of 6-phospho-gluconate dehydrogenase (6PGD) and α-enolase (ENO1). Furthermore, PRMT6 methylated R324 of 6PGD to enhancing its activity; while methylation at R9 and R372 of ENO1 promotes formation of active ENO1 dimers and 2-phosphoglycerate (2-PG) binding to ENO1, respectively. Lastly, targeting PRMT6 blocked the oxidative PPP flux, glycolysis pathway, and tumor growth, as well as enhanced the anti-tumor effects of cisplatin in lung cancer. Together, this study demonstrates that PRMT6 acts as a post-translational modification (PTM) regulator of glucose metabolism, which leads to the pathogenesis of lung cancer. It was proven that the PRMT6-6PGD/ENO1 regulatory axis is an important determinant of carcinogenesis and may become a promising cancer therapeutic strategy.