Objective To construct safety management barriers and protecting barriers to ensure patient safety.Methods The management barrier including the safety management system,work flow of safety nursing,and quality supervision system,as well as the protecting barrier including the hazardous medicines obstacle,three colored marks,and predicted alarm systems were developed and applied in clinical practice.Results This practice reduced the rate of adverse nursing events,enhanced nurses' ability to detect and correct errors,and controlled the risk factors of patient safety.Conclusion Constructing multiple barriers can ensure patient safety.It is suggested that nurses should detect the defects and consolidate the barriers consistently.

24 new cDNA sequences encoding cytochrome P450 were amplified respectively from deltamethrin susceptible and -resistant strains of the mosquito, Culex pipiens pallens, with a pair of degenerate primers according to the conservative amino acid sequences of CYP4 in insects by RT-PCR. Studies of molecular systematics show that the 24 new genes (alleles) belong to CYP4C, CYP4D, CYP4H and CYP4J subfamilies of the CYP4 family, and they were named by Cytochrome P450 Nomenclature Committee. Among the new genes (alleles), CYP4C23 may be a pseudogene, CYP4H13 has a retained intron 58 nucleotides in length, and CYP4J4V1 has a stop coden (TAG) in frame near the 3'-end.

To study the anticoagulant effect of Xiang-Qi-Tang (XQT),the mice model of endotoxemia was established to detect the expression of coagulation factors and their regulatory proteins in serum and aorta.The results showed that XQT could decrease the expression of TF and increase the expression of tPA in the aorta of mice with endotoxemia,and also decrease the expression of sEPCR in the serum.We further found that XQT caused the decrease of sEPCR through the regulation of PKC δ and ADAM17 to contribute the anticoagulation in mice.This study may provide a new strategy for treating endotoxin-induced disease and provide evidences for further researching the pharmacological action of XQT.

Objective To explore the application of amide proton transfer (APT) imaging in differentiating glioma from treatment effect and to evaluate the diagnostic efficiency of the quantitative APT-related parameters.Methods A total of 23 patients (15 males, 8 females, age: 13-80 years) with 27 lesions who had underwent APT imaging in Tongji Hospital(Wuhan, China) from October 2014 to June 2015 were enrolled in this prospective study.The scan protocols were MRI normal plain scanning, diffusion WI, contrast-enhancement T1WI and APT imaging.Both the magnetization transfer ratio (MTR) and the relative MTR (rMTR) of lesions were manually measured by drawing ROI in the functional post-processing workstation.The results were compared with those of pathologic examinations and radiographic follow-up (≥3 months).Mann-Whitney u test was used to analyze the data.Results Compared with contralateral white matter, the primary gliomas (n=12) and recurrent gliomas (n=8) manifested hyper-intensity, while the treatment induced injuries (n=7) showed iso-or hypo-intensity.The difference of MTR between tumors and treatment effects was significant (102.78(101.93,103.84) vs 100.17(99.94, 100.63);z=-3.76, P<0.01), so was the difference of rMTR between tumors and treatment effects (3.92%(2.69%,4.67%) vs 0.47%(-0.79%,1.11%);z=-3.43, P<0.01).Both those two quantitative parameters exhibited excellent diagnostic performance with the AUC of 0.986 and 0.943.The sensitivity, specificity and accuracy of MTR were 100%(20/20), 6/7 and 96.3%(26/27) in the threshold of 100.68, while those of rMTR were 95.0%(19/20), 6/7 and 92.6%(25/27) in the threshold of 1.66%.Conclusions Combined with the routine MRI images, APT imaging can provide excellent qualitative and quantitative information in differentiating glioma from treatment effect.Both MTR and rMTR are helpful for the differentiation with high sensitivity and specificity and can be used as non-invasive imaging biomarkers in evaluating treatment effect of glioma.

Pheretima,also called"earthworms",is a well-known animal-derived traditional Chinese medicine that is extensively used in over 50 Chinese patent medicines(CPMs)in Chinese Pharmacopoeia(2020 edi-tion).However,its zoological origin is unclear,both in the herbal market and CPMs.In this study,a strategy for integrating in-house annotated protein databases constructed from close evolutionary relationship-sourced RNA sequencing data from public archival resources and various sequencing al-gorithms(restricted search,open search,and de novo)was developed to characterize the phenotype of natural peptides of three major commercial species of Pheretima,including Pheretima aspergillum(PA),Pheretima vulgaris(PV),and Metaphire magna(MM).We identified 10,477 natural peptides in the PA,7,451 in PV,and 5,896 in MM samples.Five specific signature peptides were screened and then validated using synthetic peptides;these demonstrated robust specificity for the authentication of PA,PV,and MM.Finally,all marker peptides were successfully applied to identify the zoological origins of Brain Heart capsules and Xiaohuoluo pills,revealing the inconsistent Pheretima species used in these CPMs.In conclusion,our integrated strategy could be used for the in-depth characterization of natural peptides of other animal-derived traditional Chinese medicines,especially non-model species with poorly annotated protein databases.

ObjectiveTo investigate the mechanism by which Shenbai Jiedu prescription （SBJDF） inhibits the proliferation of colorectal cancer （CRC） HCT116 cells. MethodAfter 48 h treatment of HCT116 cells with SBJDF （0， 0.25， 0.5， 1， 2， 4 g·L^-1）， the viability of HCT116 cells were determined by methyl thiazolyl tetrazolium （MTT） colorimetry. Following the classification of cells into blank control group and SBJDF （1， 2， 4 g·L^-1） groups， the effect of SBJDF on HCT116 cell morphology was observed under an inverted microscope. The effects of SBJDF on the proliferation of HCT116 cells and mitochondrial membrane potential （Δψm） were detected by colony formation assay and JC-1 probe， respectively. The flow cytometry was then performed for determining cell cycle distribution and apoptosis. The effects of SBJDF on cell cycle-， apoptosis-， and nuclear factor kappa-B （NF-κB） signaling pathway-related proteins were determined by Western blot. ResultSBJDF effectively inhibited the vitality of HCT116 cells and changed their morphology in a concentration-dependent manner. Compared with the blank control group， SBJDF at 1， 2， 4 g·L^-1 significantly reduced cell colony formation （P<0.05， P<0.01），and SBJDF at 2 and 4 g·L^-1 arrested the HCT116 cell cycle at G₀/G₁ phase （P<0.05， P<0.01）. Compared with the blank control group， SBJDF at 1， 2， 4 g·L^-1 remarkably down-regulated the protein expression of CyclinD₁ （P<0.05， P<0.01）. SBJDF at 2 and 4 g·L^-1 lowered the CyclinA₂ and cyclin-dependent kinase 4 （CDK4） （P<0.05， P<0.01）. SBJDF at 4 g·L^-1 reduced the cyclin-dependent kinase 1 （CDK1） （P<0.01）. Compared with the blank control group， SBJDF at 2 and 4 g·L^-1 induced HCT116 cell apoptosis， down-regulated the protein expression of anti-apoptosis-related proteins Bcl-2 and Bcl-xl as well as the NF-κB signaling pathway-related proteins IκB kinase α （IKKα），inhibitor α of NF-κB （IκBα），and phospho-NF-κB p65 （p-p65） （P<0.05， P<0.01）， and diminished the mitochondrial membrane potential of HCT116 cells. ConclusionSBJDF inhibits the proliferation of HCT116 cells， which may be related to its inhibition of the activation of NF-κB signaling pathway and the induction of cell cycle arrest and apoptosis.

ObjectiveTo study the mechanism of Shenbai Jiedu prescription inhibiting the proliferation of HCT116 colorectal cancer （CRC） cells by regulating the phosphatase and tensin homolog deleted on chromosome ten （PTEN）/phosphatidylinositol 3-kinase （PI3K）/ protein kinase B （Akt） signaling pathway. MethodShenbai Jiedu prescription was extracted by water extraction and alcohol precipitation to prepare freeze-dried powder. HCT116 cells were cultured in vitro， and treated with different concentrations of Shenbai Jiedu prescription （2， 4， 8， 16 g·L^-1）. The inhibitory effect of Shenbai Jiedu prescription on the proliferation of HCT116 cells was tested by methyl thiazolyl tetrazolium （MTT）. Real-time quantitative PCR was used to detect the mRNA expression levels of PTEN， PI3K， Akt， glycogen synthase kinase-3β （GSK-3β）， c-Myc， survivin and Cyclin D₁. Western blot was employed to measure the protein expression levels of PTEN， phosphorylated PTEN （p-PTEN）， PI3K， Akt， phosphorylated Akt （p-Akt）， GSK-3β， phosphorylated GSK-3β （p-GSK-3β）， c-Myc， survivin and Cyclin D₁， β-catenin nuclear import was explored by immunofluorescence assay. ResultCompared with the control group， Shenbai Jiedu prescription inhibited the proliferation of HCT116 cells in a dose-dependent manner （P<0.01）. Compared with the control group， the mRNA expression levels of PTEN and GSK-3β were up-regulated whereas those of PI3K， Akt， c-Myc， survivin and CyclinD₁ were down-regulated after treatment with Shenbai Jiedu prescription （P<0.01）. The protein expression levels of PTEN， p-PTEN and GSK-3β were up-regulated whereas those of PI3K， Akt， p-Akt， GSK-3β， p-GSK-3β， c-Myc， survivin and CyclinD₁ were down-regulated （P<0.05， P<0.01）. Immunofluorescence assay showed that Shenbai Jiedu prescription suppressed β-catenin nuclear import in HCT116 cells. ConclusionShenbai Jiedu prescription inhibited the proliferation of HCT116 cells via the mechanism of regulating the PTEN/PI3K/Akt signaling pathway.