Objective:To develop a UPLC method for determining four glycosides in microctis folium.Methods:The UPLC deter-mination was performed on an Agilent SB -C18 (3.0 mm ×50 mm, 1.8 μm) colume with 0.05% acetonitrile -phosphate solution as the mobile phase.The detection wavelength was set at 320 nm.The flow rate was 0.3 ml· min-1.The column temperature was 25℃.Results:Narcissoside, isovitexin, kaempferol-3-rutinoside and isorhamnetin-3-O-glucoside all showed good linearity with the re-covery of 98.89%,99.03%, 97.00%and 97.41%, and RSD of 0.41%, 0.84%,0.44%and 0.80%, respectively (n=9).Con-clusion:The method is convenient with good stability , repeatability and sample recovery rate , which provides basis for the quality eval-uation and control of microctis folium.

Objective To probe into the effects of applying standardized nursing ward round in nursing management.Method The nursing ward round was regularly conducted to analyze and discuss the difficulties in intensive care.Results After formulating the nursing ward round,the qualification rate of the basic nursing,specific nursing,the nursing of critical paitents,nursing records and the patient's satisfaction were higher than those before the use of nursing ward round(P<0.05).Conclusion The standardized nursing ward round may strengthen the training of nurses' core ability and the initiative of studying,reduce medical disputes,and improve the satisfaction of patients together with the quality of nursing.

Objective:To establish a method for the separation and determination of ketoprofen enantiomer .Methods:A pre-col-umn derivation RP-HPLC method was used with L-alanine-β-naphthylamine ( L-Ala-β-NA) as the derivation reagent .The RP-HPLC conditions were as follows: a Hypersil ODS-2 column (250 mm ×4.6 mm,5 μm) was applied, the mobile phase was acetonitrile-0.025 mol· L-1 phosphate buffer solution (40∶60, v/v) and the flow rate was 1.0 ml· min-1 , the detection wavelength was set at 245 nm and the column temperature was 25℃.The injection volume was 10μl.Results:Base line separation was achieved for the sep-aration of enantiomer from ketoprofen , and the retention time for S-(+) -ketoprofen and the R-(-) -ketoprofen was 24.2 min and 26.0 min, respectively.Dexketoprofen within the range of 0.025-0.125 mg had a good linear relationship (r=0.998 1) and the aver-age recovery was 90.93%(RSD =4.10%, n=9 ).Conclusion:The method is simple, accurate and reliable, which can be applied in the separation and determination of ketoprofen .

Objective To investigate the correlation between chronic hepatic diseases and small intestinal inflammation.Methods Patients who received capsule endoscopy in The First Affiliated Hospital of Guangdong Pharmaceutical University were divided into groups of liver cirrhosis,non-alcoholic fatty liver disease(NAFLD),chronic hepatitis and non-hepatic disease according to clinic data from August 2011 to August 2015.The severity of small intestinal mucosal inflammation was graded according to Lewis Scoring system and incidence of small intestinal lesions in different groups and Lewis scores were compared.The liver function was also graded with liver noninvasive scoring systems.Then the correlation between liver function damage and small intestinal lesions was investigated.Results A total of 338 cases were enrolled in the study,including 25 cases of liver cirrhosis,47 cases of NAFLD,20 cases of chronic hepaitis and 246 cases of non-hepatic disease.There were 22 (88.0％),36 (76.6％),12 (60.0％) and 78 (31.7％) cases with lesions in small intestine in the four group respectively with significant differences(P＜0.001).Rate of small intestinal villi edema was significantly higher in liver cirrhosis group,NAFLD group,chronic hepatitis group than that in non-hepatic disease group(all P＜0.017).Small intestinal villi edema was found mainly in the upper and one third of middle parts in small intestine (P =0.033).Lewis scores of liver cirrhosis group (190.80±228.42)and NAFLD group(125.38± 191.31) were higher than those of non-hepatic disease group (42.91±97.69,P=0.021,P =0.034).Forns score,FIB-4 score,NAFLD-FS score and Child-Pugh score were positively correlated with Lewis score (correlation coefficient:0.247,0.244,0.223,0.284respectively,all P＜0.001).Conclusion Chronic hepatic diseases such as liver cirrhosis,NAFLD,chronic hepatitis might be risk factors for small intestinal mucosal inflammation,and the severity of chronic hepatic diseases may be positively correlated with that of small intestinal mucosal lesions.

AIM:To investigate whether angiotensin-(1-7) [Ang-(1-7)] protects H9c2 cardiac cells against high glucose (HG)-induced injury and inflammation by inhibiting the interaction between Toll-like receptor 4 (TLR4) acti-vation and necroptosis .METHODS:The expression levels of receptor-interacting protein 3 ( RIP3;an indicator of necrop-tosis) and TLR4 were determined by Western blot .Cell viability was measured by CCK-8 assay.The activity of lactate de-hydrogenase ( LDH) in the culture medium was measured with a commercial kit .The releases of interleukin-1β( IL-1β) and tumor necrosis factor-α( TNF-α) were measured by ELISA .The intracellular level of reactive oxygen species ( ROS) was analyzed by 2 ’ , 7 ’-dichlorfluorescein-diacetate ( DCFH-DA ) stating followed by photofluorography .Mitochondrial membrane potential ( MMP) was examined by rhodamine 123 staining followed by photofluorography .RESULTS:After the H9c2 cardiac cells were treated with HG (35 mmol/L glucose) for 24 h, the expression of RIP3 was obviously increased . Co-treatment of the cells with 30μmol/L TAK-242 (an inhibitor of TLR4) attenuated the up-regulation of RIP3 induced by HG.Furthermore, the expression of TLR4 was significantly increased after the cells were exposed to HG for 24 h, and co-treatment of the cells with 100μmol/L necrostatin-1 ( Nec-1;a specific inhibitor of necroptosis ) and HG for 24 h attenua-ted the up-regulation of TLR4 expression induced by HG .Moreover, 1μmol/L Ang-(1-7) simultaneously blocked the up-regulation of the RIP3 and TLR4 induced by HG.On the other hand, co-treatment of the cells with 1μmol/L Ang-(1-7), 30 μmol/L TAK-242 or 100 μmol/L Nec-1 and HG for 24 h attenuated HG-induced injuries and inflammatory response , leading to the increase in the cell viability , and the decreases in the activity of LDH , ROS generation , MMP loss as well as the releases of IL-1βand TNF-α.CONCLUSION:Ang-(1-7) protects H9c2 cardiac cells against HG-induced injury and inflammation by inhibiting the interaction between TLR 4 activation and necroptosis .

Objective To obtain the information of the 2009 influenza outbreak and the variations of influenza virus strains in quanzhou, and explore the relationship between the genetic variation of influenza virus and influenza epidemic. Methods During the influenza outbreak in quanzhou,one hundred and ninetyeight throat swabs specimens from the patients with influenza were collected. Viruses were isolated with MDCK cells and identified with serological test, followed by real-time RT-PCR. RNA of four influenza virus strains were extracted, then HA1 gene was amplified by RT-PCR. The purified PCR products were sequenced. The data were analyzed with the software DNAstar megalign. Results Total 98 pieces of H3N2 subtype influenza virus nucleic acid were detected in 198 throat swabs specimens,among which 62 influenza virus strains were identified as subtype influenza A( H3N2 ). The sequencing results of HA1 gene in these positive strains showed that their genetic characterization were more closed to strains A/Ningbo/333/2008 with a nucleotide homology of 98.7%, which was 96.8% as compared with A/Xiamen/70/2004. The amino acids sequences deduced from the nucleotide sequences in HA1 region of the isolated strain had 7 mutant sites compared with A/Brisbane/10/2007 vaccine strain. One variant amino acids were found located in the antigenic determinant sites A( 144 ), two were in the sites B( 158,189 ). Phylogenetic analysis also confirmed the difference in HAl domain. Conclusion The influenza virus strains causing the flu outbreak among some communities of quanzhou in 2009 are subtype influenza A ( H3N2 ), whose genetic characterization and antigenicity were different from the vaccine strain.

Objective To investigate the influenza H1N1 virus surveillance of 2009 in Quanzhou,and analyze the HA and NA gene of influenza H1N1 virus, explore its genetic variation and molecular characteristics. Methods During the influenza H1N1 virus surveillance in Quanzhou,specimens of throat swabs from the patients with influenza were collected, and detected by real-time RT-PCR. Viruses were isolated with MDCK cells and identified with serological test. Two influenza virus isolates were extracted, and their HA and NA genes were amplified by RT-PCR. The purified PCR products were sequenced. The data obtained were analyzed with the software DNAMAN. Results Of 1020, influenza H1N1 virus RNA was detected in 200 specimens, seasonal influenza virus RNA was detected in 70 specimens. A total of 29 influenza A H1N1 virus strains were isolated. The nucleotide homology in the HA gene was highly homologous with that of pandemic influenza virus in North America. The amino acids sequences deduced from the nucleotide sequences in HA region of the isolated strain had 22 variations compared with A/Brisbane/59/2007 vaccine strain recommend by WHO,the characteristics of α2,6 sialic acid receptor binding remained. The analysis of amino acids sequences of NA indicated that this virus possessed Oseltamivir sensitivity. Conclusion The causative influenza H1N1 strains in Quanzhou is highly homologous with that of pandemic influenza in North America, and it is antigenically and genetically different from the vaccine strain.

Objective To explore the effect of risk assessment tracking management in reducing unplanned extubation in patients with tracheal intubation.Methods From January to December 2015,120 patients with tracheal intubation in ICU were selected as the control group with routine nursing care of indwelling endotracheal intubation.From January to November 2016,120 patients with tracheal intubation were selected as the observation group,where the risk assessment and risk management were done on the basis of routine nursing as in the control group.The two groups were compared in terms of tracheal intubation and unplanned extubation related knowledge,the implementation of the risk assessment,the accuracy in risk assessment and the incidence of unplanned extubation.Result The tracheal intubation and unplanned extubation related knowledge in the observation group was lower than that of the control group (P＜0.001),The implementation rate of the risk assessment and the accuracy in risk assessment in the observation group were significantly higher than the control group,and the rate of unplanned extubation in the observation group was significantly lower than in the control group (all P＜0.01).Conclusion The implementation on risk assessment and extubation-preventing nursing quality tracing management can enhance the awareness and knowledge of preventing trachea cannula exodus,improve the quality of nursing and reduce the rate of unplanned extubation.

Aim To investigate the role of ATP-sensi-tive potassium channels-Akt pathway in exogenous hy-drogen sulfide( H2 S) inhibiting the high glucose( HG)-induced injury in H9c2 cardiac cells. Methods The expression level of Akt protein was tested by Western blot assay. The cell viability was measured by cell counter kit-8(CCK-8 assay). The number of apoptotic cells was tested by Hoechst 33258 nuclear staining fol-lowed by photofluorography. The intracellular levels of reactive oxygen species ( ROS ) were detected by DCFH-DA staining followed by photofluorography. Mi-tochondrial membrane potential ( MMP ) was examined by JC-1 staining followed by photofluorography. Results H9c2 cells were treated with 35 mmol·L-1 glucose (high glucose, HG) for 0 ~24 h respectively. After treating for 3 h, the expression level of phosphorated ( p )-Akt protein began to be obviously reduced, the maximum reduced expression level was observed after the cells were exposed to HG for 24 h. Pretreatment of the cells with 50 μmol · L-1 pinacidil ( Pin, a KATP channel opener) or 400 μmol·L-1 NaHS( a donor of H2 S) prior to exposure to HG considerably blocked the down regulation of p-Akt expression level induced by HG. However, pretreatment with 1 mmol · L-1 KATP channel blocker glibenclamide( Gli) obviously attenua-ted the inhibitory effect of NaHS on HG-induced down-regulation of p-Akt expression level. On the other hand, the protective effects of NaHS against the HG-induced cardiomyocyte injury were markedly blocked by 30 μmol·L-1 Ly294002(an inhibitor of Akt), as indicated by the decrease in cell viability and MMP dissipation as well as the increases in the number of apoptotic cells and ROS generation. Conclution KATP channels-Akt pathway mediates the protective effect of H2 S against the HG-induced cardiac injury.

AIM:To investigate whether the opening of ATP-sensitive K+(KATP) channels protects H9c2 car-diac cells against high glucose ( HG)-induced injury and inflammation by inhibiting the Toll-like receptor 4 ( TLR4 )/nu-clear factor-κB ( NF-κB) pathway.METHODS:The protein levels of TLR4 and NF-κB p65 were determined by Western blot.The levels of interleukin-1β(IL-1β) and tumor necrosis factor-α(TNF-α) were detected by ELISA.The cell viabil-ity was measured by CCK-8 assay.Mitochondrial membrane potential (MMP) was examined by rhodamine 123 (Rh 123) staining followed by photofluorography.The intracellular levels of reactive oxygen species ( ROS) were detected by 2′, 7′-
dichlorfluorescein-diacetate (DCFH-DA) staining followed by photofluorography.The number of apoptotic cells was ob-served by Hoechst 33258 nuclear staining followed by photofluorography.RESULTS: After the H9c2 cardiac cells were treated with HG (35 mmol/L glucose) for 24 h, the protein levels of TLR4 and phosphorylated NF-κB p65 ( p-NF-κB p65) were significantly increased.Pretreatment of the cells with 100 μmol/L diazoxide ( DZ, a KATP channel opener) for 30 min before exposure to HG considerably blocked the up-regulation of the TLR4 and p-NF-κB protein levels induced by HG.Moreover, co-treatment of the cells with 30 μmol/L TAK-242 (an inhibitor of TLR4) obviously inhibited the HG-in-duced up-regulation of the p-NF-κB p65 protein level.On the other hand, pretreatment of the cells with 100 μmol/L DZ had a clear myocardial protection effect, which attenuated the HG-induced cytotoxicity, inflammatory response, mitochon-drial damage, oxidative stress and apoptosis, evidenced by an increase in the cell viability, and decreases in the levels of IL-1βand TNF-α, MMP loss, ROS generation and the number of apoptotic cells.Similarly, co-treatment of H9c2 cardiac cells with 30μmol/L TAK-242 or 100μmol/L PDTC ( an inhibitor of NF-κB) and HG for 24 h also obviously reduced the above injuries and inflammation induced by HG.CONCLUSION: The opening of KATP channels protects H9c2 cardiac cells against HG-induced injury and inflammation by inhibiting the TLR4/NF-κB pathway.