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The reflective ability of nursing staff has been paid more and more attention, nurses' reflection can promote professional competence development, which also can improve clinical practice ability, knowledge expansion ability and innovation ability. Therefore this article reviews the current situation on nurses ′ reflection, the assessment tools, the modes, forms, methods and types, future prospects of clinical nurses reflective practice, in order to provide reference and basis for the relevant research on the reflection practice of clinical nursing staff in China.
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The reflective ability of nursing staff has been paid more and more attention, nurses' reflection can promote professional competence development, which also can improve clinical practice ability, knowledge expansion ability and innovation ability. Therefore this article reviews the current situation on nurses′ reflection, the assessment tools, the modes, forms, methods and types, future prospects of clinical nurses reflective practice, in order to provide reference and basis for the relevant research on the reflection practice of clinical nursing staff in China.
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This article summarized perioperative nursing experience of 6 patients underwent percutaneous microwave or radiofrequency ablation liver partition and portal vein embolization for planned hepatectomy(PALPP).The key points of nursing included:psychological counseling applied throughout the perioperative treatment;personalized preoperative biliary drainage;nursing intervention targeting at Enhanced Recovery After Surgery(ERAS);complication-directed prevention and nursing after microwave or radiofrequency ablation,portal vein embolization,and radical hepatectomy.All 6 patients were recovered and discharged successfully.
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Objective This study aims to evaluate the changes of Cdk5 expression at the time of 3 hours to 10 days after moderate brain injury by blunt force impact in a rat model,and to demonstrate its forensic significance.Methods To establish a rat model of blunt focal brain contusion,and to observe the changes of Cdk5 expression in brain tissue at different timepoints after brain injury by immunohistochemistry and Western blot.Results A low expression level of Cdk5 was observed in the brain tissue of both normal and sham control groups.The expression of Cdk5 increased after 3 and 6 hours,remarkably increased at 12 hours,and reached the maximal level at 24 hours after focal brain injury.The Cdk5 level gradually decreased 3 days,5 days,7 days,and 10 days and reached the normal level 7 and 10 days after the injury,with no statistical difference (P＞0.05) compared with the normal and sham control groups.Conclusion The expression of Cdk5 increased in the peripheral area of contusion tissue after blunt brain injury in rats,showing single peak change,and dropped to normal level with the time extension.The change of Cdk5 expression may provide a new reference index for the prediction of early brain contusion.
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Aim To study the effect of 6-(3-Benzyl-4-oxo-2-thioxo-thiazolidin-5-ylidenemethyl)-9-fluoro-3-methyl-10-(4-methyl-piperazin-1-yl)-2,3-dihydro-7-oxo-7-hydro-pyrido[1,2,3-de][1,4]benzoxazine (R3) on apoptosis of the human hepatocarcinoma SMMC-7721 cells (in vitro).Methods With different concentrations of R3 used to treat SMMC-7721 cells, esophageal squamous cell carcinoma EC-9706 cells, human colon adenocarcinoma cell line Caco-2 cells and in human L-02 hepatocytes (in vitro), and the inhibition effects of R3 on cell proliferation were examined by MTT assay.Cell apoptosis was determined using DAPI fluorescence staining and TUNEL method.The cell cycle was detected using flow cytometry with PI staining.Protein expression of p53 and caspase-3 was detected with Western blot analysis.Results Treatment with R3 (2~20 μmol·L-1) potently inhibited the proliferation of the cancer cells (the IC50 value at 24 h in SMMC-7721 cells, EC-9706cells and CaCO-2 cells was 3.893, 4.181 and 3.408 μmol·L-1, respectively).In contrast, R3 had weak cytotoxicity against L-02 cells with IC50 value of 38.96 μmol·L-1.Ofloxacin had weak cytotoxicity against SMMC-7721 cells with IC50 value of 240.137 μmol·L-1.Sunitinib had cytotoxicity against SMMC-7721 cells with IC50 value of 8.075 μmol·L-1.Treatment of SMMC-7721cells with different concentrations of R3 for 24 h increased the percentage of the apoptosis cells (P<0.05) and caused insufficient preparation for G1/S transition.In addition, R3 increased protein expression of p53, caspase-3 and the cleaved activated forms of caspase-3 in SMMC-7721 cells.Conclusion R3 as a kind of ofloxacin rhodanine derivatives exerts potent and selectively anticancer activity through the induction of apoptosis of SMMC-7721 cells.
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Nitrites play multiple characteristic functions in invasion and metastasis of hepatic cancer cells, but the exact mechanism is not yet known. Cancer cells can maintain the malignant characteristics via clearance of excess mitochondria by mitophagy. The purpose of this article was to determine the roles of nitrite, reactive oxygen species (ROS) and hypoxia inducing factor 1 alpha (HIF-1 α) in mitophagy of hepatic cancer cells. After exposure of human hepatocellular carcinoma SMMC-7721 cells to a serial concentrations of sodium nitrite for 24 h under normal oxygen, the maximal cell vitality was increased by 16 mg x (-1) sodium nitrite. In addition, the potentials of migration and invasion for SMMC-7721 cells were increased significantly at the same time. Furthermore, sodium nitrite exposure displayed an increase of stress fibers, lamellipodum and perinuclear mitochondrial distribution by cell staining with Actin-Tracker Green and Mito-Tracker Red, which was reversed by N-acetylcysteine (NAC, a reactive oxygen scavenger). DCFH-DA staining with fluorescent microscopy showed that the intracellular level of ROS concentration was increased by the sodium nitrite treatment. LC3 immunostaining and Western blot results showed that sodium nitrite enhanced cell autophagy flux. Under the transmission electron microscopy (TEM), more autolysosomes formed after sodium nitrite treatment and NAC could prevent autophagosome degradation. RT-PCR results indicated that the expression levels of COX I and COXIV mRNA were decreased significantly after sodium nitrite treatment. Meanwhile, laser scanning confocal microscopy showed that sodium nitrite significantly reduced mitochondrial mass detected by Mito-Tracker Green staining. The expression levels of HIF-1α, Beclin-1 and Bnip3 (mitophagy marker molecular) increased remarkably after sodium nitrite treatment, which were reversed by NAC. Our results demonstrated that sodium nitrite (16 mg x L(-1)) increased the potentials of invasion and migration of hepatic cancer SMMC-7721 cells through induction of ROS and HIF-1α mediated mitophagy.
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Aim To study the effect of (S) -1, 8-(2-methyl phosphate ethoxy )-6-fluorine-7-( 4-methyl- pi-perazine-1-base )-3-[ S-benzyls-based-4-( for nitroben-zene methylene group amino )-1 , 2 , 4-all triazole-3 base]-quinoline ( 1-H )-4-ketone ( M18 ) on apoptosis of hepatocarcinoma SMMC-7721 cells in vitro. Meth-ods With different concentrations of M18 at different time used to treat SMMC-7721 cells, human breast cancer MB-231cells, human colon cancer HCT-116 cells, human hepatocarcinoma HEPG-2 cells, mouse bone marrow mesenchymal stem cells ( BMSCs ) in vitro,the inhibition effects of M18 on cell proliferation were examined by MTT assay. Cell apoptosis was de-termined using Hoechst 33258 fluorescence staining and TUNEL method. Mitochondrial membrane poten-tial (△ψm ) was measured using a high content screening image system. Protein expression of caspase-3 , p53 and cytochrome C was detected with Western blot analysis. Results Treatment with M18 ( 4 ~32μmol·L-1 ) potently inhibited the proliferation of the cancer cells in time-and dose-dependent manners ( the IC50 value at 24 h in SMMC-7721 cells, MB-231cells, HCT-116 cells and HEPG-2 cells was 8. 65 μmol · L-1 , 9. 37 μmol · L-1 , 12. 74 μmol · L-1 and 9. 40μmol · L-1 , respectively ) . In contrast, M18 had weak cytotoxicity against BMSCs with IC50 value of 38. 96 μmol·L-1 . Levofloxacin had weak cytotoxicity against SMMC-7721 cells with IC50 value of 735. 10μmol·L-1 . Treatment of SMMC-7721cells with differ-ent concentrations of M18 for 24 h increased the per-centage of the apoptosis cells ( P <0. 05 ) and de-creased the mitochondrial membrane potential. In ad-dition, M18 increased protein expression of p53, caspase-3 and the cleaved activated forms of caspase-3 in SMMC-7721 cells. Treatment of SMMC-7721 cells with M18 significantly increased cytochrome C in the cytosol, and decreased cytochrome C in the mitochon-drial compartment. Conclusion The mitochondrial-dependent pathways are involved in M18 induction of apoptosis of SMMC-7721 cells.
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Objective To investigate the effect of Sufentainil on myocardial ischemia-reperfusion injury and caspase-3 to rat heart. Methods Ninety Wistar rats weighing 200-300g were randomly divided into 3 groups(n=30):sham group(group S), ischemia-reperfusion group (group I/R)and Sufentainil group (group SF). Each group was divided into 3 subgroups according to the time phases at 30, 60 and 120min(n=10).In group I/R and group S the animals were received normal saline intravenously. In group SF sufentainil 5μg/kg NS 20ml was given. After 24 h, all animals were anesthetized with intraperitioneal 20% urethane 1 mg/kg, intubated and mechanically ventilated. The chest was opened and heart exposed via thoracotomy.In group S , left artery anterior descending artery(LAD) was not ocluded. While in I/R and SF group myocardial ischemia was introduced by clamping LAD for40 min. The animals were killed at 30, 60 and 120 min of reperfusion respectively(n=10each). Cardiac tropoin I(cTnI), expression of caspase-3 and apoptosis of cell in heart tissues were measured at the same time.Ultrastructure of myocardium taking the from apex was examined by electron microscopy at the end of 120 min reperfusion. Results Compared with group S, the concentration of cTnI was increased in the other 2 groups(P<0.05).cTnI was significantly lower in group SF than in group I/R(P<0.05). Expression of caspase-3 and apoptosis index induced by myocardial reperfusion were attenuatated in group SF(P<0.05). The damage of myocardial ultrastructure caused by myocardial I/R were also significantly improved in group SF. Conclusion Sufentainil may relieve the heart cellular apoptosis by decreasing caspase-3expressing.
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Objective To observe the relationship between degree of venous injury and the indwelling time by injection of chemotherapy drugs with intravenous catheter system. Methods Totally 43 New Zealand rabbits were selected as the study sample. Among them, three rabbits were chosen by lot as a blank control, the others were evenly divided into two groups randomly. The veins at the edges of the two ears were taken out as the tested blood vessels for the infusion with intravenous catheter system. The two groups were injected respectively with physiological saline and chemotherapy drugs once daily, and then blocked with heparin salt water. After intraperitoneal anaesthesia, pathological sections were prepared by taking live samples from the ear vein where intravenous catheter system puncturing on the 2nd, 4th, 6th,8th and 10th day of transfusion. And inflammation and thrombosis in the vein had been observed under the light microscope. Results In the same indwelling time, the inflammatory response of the two groups was compared: no difference on the 2nd day; difference was seen on the 4th、6th and 8th day; but again no difference on the 10th day. Thrombosis compared: no difference on the 2nd, 4th day, but difference was seen on the 6th, 8th and 10th day. Conclusions Chemotherapy drugs has a strong irritant on blood vessels.The indwelling time should not be too long, generally advisable 2 days,even if no abnormal response is observed locally by the naked eye.
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Objective To evaluate the impact of HIV co-infection with HCV or HBV on the efficacy of highly active anti-retroviral therapy (HARRT). Methods The patients were divided into three groups: HIV + HBV + HCV co-infection group ( 23 patients), HIV + HCV co-infection group ( 166 patients), and HIV-only group (178 patients). HIV RNA, HCV RNA or HBV DNA were detected by real time PCR before treatment and 1,3,6,9 and 12 monthes after treatment, meanwhile the counts of CD4+ T lymphocyte and liver function including ALT, AST and TBil were tested. Results During one-year HAART, HIV RNA of HIV-only group, HIV + HBV + HCV co-infection group and HIV + HCV co-infection group decreased significantly from (6.78 ± 1.08), (6.23 ± 1.34), (6.54 ± 1.23) lg copies/ml to (0.53 ±0.15), (0.67 ±0.16),(0.43 ±0.11 ) lg copies/ml respectively (P＜.001 ). And CD4+ T lymphocyte counts of the three groups elevated significantly from ( 197 ± 127), (184 ± 113), (213 ± 143) cells/μl to (382 ±74), (383 ±70),(378 ±76) cells/μl respectively (P ＜0.001 ). However there were no differences among the three groups in HIV RNA and CD4+ T lymphocyte counts. There were no differences in liver functions including ALT,AST and TBil among the three groups. Conclusiom HIV co-infected with HBV and/or HCV does not impact on the efficacy of HAART. What more, HAART does not impact HCV replication.
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Matrix metalloproteinase 3 is one of matrix metalloproteinase family members, which degrades a wide range of components of the extracellular matrix and participates in tissue morphogenesis, wound healing and inflammation. In addition, matrix metalloproteinase 3 is involved in pathogenesis and progress of a spectrum of diseases and malignant tumors, such as rheumatic arthritis, arteriosclerosis, breast cancer, and so on. Recent studies have demonstrated that matrix metalloproteinase 3 may be a novel signaling proteinase from apoptotic neuronal cells to microglia, which results in degeneration of neurons in Alzheimer's disease and Parkinson's disease by activating microglia. There is also an association between genetic polymorphisms of matrix metalloproteinase 3 at promoter region 5A/6A and susceptibility of myocardial infarction. Decrease in serum concentration of matrix metalloproteinase 3 after myocardial infarction may be a useful parameter for diagnosing sudden death due to myocardial infarction in forensic practice. Expression of matrix metalloproteinase 3 varies with different types of brain injuries, suggesting that it may contribute to synaptic plasticity during functional recovery. To elucidate the time-dependent expression of matrix metalloproteinase 3 may provide a new way for wound age determination in the brain.