OBJECTIVE:To improve the electronic prescription prior-review mode and increase the rate of qualified prescrip-tions. METHODS:The electronic prescription prior-review mode of our hospital was established by setting up outpatient and emer-gency electronic prescription review team,review evidence and enforcement measures. Aimed at these problems as low review effi-ciency at initial stage,non-unified standards and untimely feedback,quality control circle and internet tools WeChat were used to improve the mode and evaluate its effects. RESULTS:The electronic prescription prior-review mode of our hospital was improved by optimizing system settings,unifying review standard,one-to-one feedback and communication with WeChat public platform, etc. Average time of prescription prior-review had reduced from 50 s to 30.58 s;the rate of qualified prescriptions had increased from 86.77% to 95.30%;prescription review efficiency and the rate of qualified prescriptions had been improved significantly. CONCLUSIONS:The implementation and continuous improvement of electronic prescription prior-review mode can reduce the rate of unqualified prescriptions and promote rational drug use in outpatient and emergency department.

Adaptor Proteins, Signal Transducing ; genetics ; metabolism ; Adenosine Triphosphatases ; genetics ; metabolism ; DNA Mismatch Repair ; DNA Repair Enzymes ; genetics ; metabolism ; DNA-Binding Proteins ; genetics ; metabolism ; Endometrial Neoplasms ; etiology ; genetics ; metabolism ; pathology ; Female ; Genetic Predisposition to Disease ; Humans ; Lynch Syndrome II ; complications ; genetics ; metabolism ; pathology ; Mismatch Repair Endonuclease PMS2 ; MutL Protein Homolog 1 ; MutS Homolog 2 Protein ; genetics ; metabolism ; Mutation ; Nuclear Proteins ; genetics ; metabolism

Objective To evaluate the effect of suberoylanilide hydroxamic acid(SAHA) or/and paclitaxel(PTX) on lethality and autophagy of human ovarian cancer OC3 cells,and to explore whether the combination of the two drugs has a synergistic function.Methods The morphology of OC3 cells was treated with SAHA and/or PTX, and then the morphology of treated OC3 cells was observed under an inverted microscope, cell proliferation was detected by MTT assay and autoph-agy was analyzed by AO/EB double staining assay.The synergistic effect of SAHA and/or PTX was analyzed by factorial design and gold formula method.Results After treatment with SAHA and/or PTX, the morphology of OC3 cells in the combination group ( SAHA+PTX) displayed significant morphological changes.OC3 cells became less adherent and refrac-tive than in other groups.Cell proliferation by MTT assay demonstrated that the growth inhibition rate of the combination groups was higher than in groups treated with SAHA or PTX respectively( P<0.05) .Furthermore, the synergistic effect af-ter treatment with a combination of SAHA with PTX was proved by the factorial design and gold formula method.The auto-phagy rate of the combined groups was significantly higher than in single treatment groups (P<0.05) by AO/EB double staining.Conclusion SAHA and PTX can inhibit the survival of OC3 cells and induce its autophagy.The two drugs have synergistic antitumor effects.

AIM To investigate the protective effect of polydatin on ischemia-reperfusion (I-R) injury in cardiac muscle and the possible mechanism. METHODS Langendorff technique was used to make I-R injury in rats. Male Sprague-Dawley rats were randomly divided into control, model, polydatin(25, 50 and 75 μmol·L-1), glibenclamide(Gli, 10 μmol·L-1)+polydatin(50 μmol·L-1), 5-hydroxydecanoate(5-HD, 100 μmol·L-1)+polydatin(50 μmol·L-1), and atractyloside (Atr, 20 μmol·L-1)+polydatin(50 μmol·L-1) groups. The hearts in control group were perfused with K-H solution for 110 min. Model group hearts were subjected to 30 min no-flow global ischemia followed by 60 min of reperfusion. The hearts in 3 polydatin groups were perfused with K-H solution containing different concentrations of polydatin for 10 min before I-R. The hearts in Gli+polydatin and 5-HD+polydatin groups were perfused with K-H solution containing Gli or 5-HD for 5 min firstly, then perfused with K-H solution containing both polydatin and Gli or 5-HD for 10 min before I-R. The hearts in Atr+polydatin group were perfused with K-H solution containing polydatin for 10 min before I-R and perfused with K-H solution containing Atr for 15 min after I-R. The cardiac function, including left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (LVDP), the maximal rates of rise and decline of left ventricular pressure (±dp/dtmax), and coronary flow (CF), were recorded before, after 30 min no-flow global ischemia and, during 60 min reperfusion. Myocardial infarct size was assessed using 2, 3, 5-triphenyltetrazolium chloride method and myocardial ultrastructure was observed via transmission electron microscope after 60 min reperfusion. RESULTS There were no significant differences in cardiac functional parameters between control and model groups in pre-ischemia condition. Compared with model group, polydatin promoted a better recovery of cardiac function after I-R in a concentration-dependent manner. After 60 min of reperfusion, the values of LVDP, ±dp/dtmax and CF in polydatin groups were much higher, but LVEDP was lower than those in model group. Polydatin (50 μmol·L-1) also significantly reduced myocardial infarct size and relieved the I-R injury of myocardial ultrastructure. The protective effects of polydatin (50 μmol·L-1) on LVDP, LVEDP, ±dp/dtmax and CF, as well as the inhibitory effect on infarct size after I-R were abolished by Gli, 5-HD and Atr. CONCLUSION Polydatin has protective effect against I-R injury in rat hearts, which may be related with the opening of ATP-sensitive potassium channel located in both cell membrane and mitochondrial membrane, as well as inhibition of mitochondrial permeability transition pore opening.

Adult ; Antineoplastic Agents ; toxicity ; CD4-Positive T-Lymphocytes ; drug effects ; Female ; Humans ; Killer Cells, Natural ; drug effects ; Middle Aged ; Nurses ; statistics & numerical data ; Occupational Exposure ; T-Lymphocyte Subsets ; drug effects

Follicle-stimulating hormone (FSH) is synthesized and secreted by the anterior pituitary, which binds to its receptors expressed on the membrane of Sertoli cells in the testis to bring about spermatogenesis. With the development of DNA sequencing technology, FSH SNPs rs10835638 and FSHR SNPs rs6165, rs6166, and rs1394205 were detected, which might directly affect the expression of FSH and activity of FSHR, resulting in male spermatogenic dysfunction. This review focuses on the relationship of FSH and FSHR gene polymorphisms with male infertility.
Follicle Stimulating Hormone ; genetics ; Humans ; Infertility, Male ; genetics ; Male ; Polymorphism, Single Nucleotide ; Receptors, FSH ; genetics ; Sertoli Cells ; Spermatogenesis ; Testis

Objective To study whether carbon dioxide used to establish pneumoperitoneum has an influence on port-site and intraperitoneal implantation and metastasis of tumor cells. Methods R 15 hepatic cancer cells were injected into 30 Wistar rats’ peritoneal cavities 1 hour before operation, then the 30 Wistar rats were randomly divided into 3 groups: gasless group, helium group and carbon dioxide group. The suspension was exposed to the gas environment for 2 hours, all animals were killed after 28 days and the port-site and intraperitoneal implantation and metastasis of tumor cells were examined.Results On port-site, intestinal serous coat, mesentery, greater omentum and diaphragm, the weights of tumor cells, in carbon dioxide group were (326.7?230.3) mg, (626.2?215.9) mg, (476.2?204.8) mg,(2 536.5?906.7) mg and (384.5?149.9) mg respectively; in helium group were (235.6?107.3) mg, (414.2?148.4) mg, (261.8?92.6) mg, (1 633.4?247.3) mg and(220.0?57.9) mg; in gasless group were (145.0?42.4) mg, (221.5?108.2) mg, (212.5?109.6) mg, (797.5?335.9) mg and 113.0 mg.The weights of carbon dioxide group showed a significant increase, compared with helium group and gasless group (P 0.05). Conclusion The insufflation of carbon dioxide promotes intraperitoneal tumor implantation and growth compared with helium and gaslessness in a rat model.

OBJECTIVE To study the molecular mechanism of cisplatin(DDP)by which HeLa cell growth and proliferation are inhibited. METHODS Cultured HeLa cells were treated with DDP 0.02-75 μmol · L-1 for 24 or 48 h. CCK-8 assay was used to determine the cell proliferation. The wound scratch assay was used to detect the cell migration and invasion. Flow cytometry was used to detect the cell cycle arresting. q-PCR was used to test the expression of metastasis suppressor gene 1 (MTSS1)mRNA. Western blot was used to determine protein levels of MTSS1,phosphorylated-extra?cellular signal-regulated kinase(p-ERK) and phosphorylated-serine-threonine kinase(p-AKT). RESULTS Following the treatment with DDP for 24 or 48 h,the proliferation of HeLa cells was inhibited significantly (P<0.05),the value of the half inhibitory concentration (IC50) of cells was 4.14 and 11.82 μmol · L-1. Migration and invasion activity of HeLa cells were reduced according to the wound scratch assay(P<0.05). Flow cytometry results showed that the cell cycle was arrested at S phase. q-PCR results showed that MTSS1 mRNA expression changed with DDP in a concentration-dependent manner (r24 h=-0.965,P<0.01;r48 h=-0.953,P<0.01). Western blot showed that the protein levels of MTSS1,p-ERK and p-AKT expression declined significantly with the increase in DDP concentrations(p-ERK:r24 h=-0.875,P<0.01;r48 h=-0.966,P<0.01. p-AKT:r24 h=-0.831,P<0.01;r48 h=-0.863,P<0.01. MTSS1:r24 h=-0.969,P<0.01;r48 h=-0.988,P<0.01). CONCLUSION DDP treatment inhibits HeLa growth and proliferation by interfering with the MTSS1 expression and disturbing the activation of ERK and AKT signaling pathways.

Objective To detect the expression of metastasis sappressor 1(MTSS1) gene in cervical cancer tissue and to clarify its association with cervical cancer.Methods Totally 103 cases of cervical tissue were collected between Dec 2011 and Dec 2014 and classified according to biopsy and stage .Q-PCR and Western blotting were used to detect the expression of MTSS1 in normal cervical tissue and in different clinical stages of cervical cancer tissue .Results The expression of MTSS1 inⅡB-Ⅳstages of cervical cancer tissue was significantly higher than that of normal tissue or Ⅰ-ⅡA stages through q-PCR (P=0.000).Western blotting results showed that MTSS1 was positively expressed in normal cervical tissue at a rate of 23.3% or 53.3% in cervical cancer tissue.Moreover, the expression of MTSS1 was poorly correlated with age, tumor differentiation and lymphnode metastasis in cervical cancer tissue (P>0.05).The protein level of MTSS1 expressed in ⅡB-Ⅳ stages was significantly higher than that ofⅠ-ⅡA stages(P=0.005).Conclusion The expression of MTSS1 indicates the clinical stage of cervical cancer , suggesting that MTSS1 may play an important role in the development of cervical cancer .

Objective To evaluate the effect of SAHA or/and PTX on survival and apoptosis of human paclitaxel-resist-ant ovarian cancer OC3/P cells, and explore whether the combination of two drugs has a synergistic effect .Methods The morphology of OC3/P cells in different drug-groups was observed by inverted microscope .Cell viability was evaluated by MTT assay.The apoptosis rate was analyzed by Annexin V-FITC/PI assay.Results The morphology change of OC 3/P cells treated with different drug was observed by inverted microscope , and the change in combination group was more signif-icant than one drug alone group .The result of cell survival measured by MTT assay showed that inhibition rate of combina -tion group was more higher than one drug alone group (P<0.05).The analysis of factorial design and gold formula method all proved that the two drugs had synergy .Further the result of flow cytometry showed that apoptosis rate in combination group was significantly higher than SAHA or PTX alone group (P<0.05).Conclusion SAHA and PTX can inhibit the survival and induce apoptosis of OC 3/P cells, and two drugs have synergistic antitumor effects .