Objective To explore the application value of self-made visual teaching aids in gynecological and obstetrical nursing education. Methods A total of 240 nursing students in grade 2009 from Fujian Medical University and Fujian Health College were selected by cluster sampling and divided by simple randomization into 2 groups (the trial group and the control group). Besides the multimedia combined with traditional teaching adopted in both groups, the visual teaching aids for fetal intrauterine condition was also adopted in the trial group rather than the control group. Questionnaire survey and focus group interview were adopted to appraise the satisfactory degree of all nursing students and the teaching effects evaluation of students in the trial group. Results There were no significant differences between the two groups in education background, and intelligibility evaluation of theoretical study on both the fetal intrauterine condition and the complications in pregnancy and delivery periods (Pgt;0.05), while the difference was statistically significant in the satisfactory degree between different teaching methods (Plt;0.05). 85.0% of nursing students in the trial group thought that visual model could help them to better understand the complications in pregnancy and delivery periods, and the intrauterine condition, 99.17% of students thought that the teaching effect of visual model was better than traditional teaching, and 95.83% of students considered that visual model was favorable for course study. Conclusion The application of self-made visual teaching aids for fetal intrauterine condition makes gynecological and obstetrical nursing education more visual, facilitates students to better understand fetal intrauterine situation and part of the mechanism of pregnancy complications, arouses students’ learning interests, and lays a theory and practice foundation for follow-up internship, so as to enhance the quality of nursing teaching.
ObjectiveTo study the protective effects of ischemia preconditioning (IPC) on cryopreservation injury of rat liver.MethodsThe model of isolated nonrecirculated perfusion rat liver was established. The grafts were treated with IPC in different time (ischemia preconditioning time in IPC1 group was 5 min; the time in IPC2 group was 10 min; while the time in IPC3 group was 15 min). The cryopreservation injury of the grafts in each group was determined and compared. ResultsThe levels of aspartate transaminase (AST) and alanine transaminase (ALT) in the effluent solutions in IPC1 group were (40.1±6.3) U/L and （17.1±0.5） U/L respectively, and IPC2 group (53.6±3.7) U/L, （19.7±0.5） U/L, which were much lower than those of nonpreconditioning (NPC) group 〔(64.5±8.2) U/L, （23.8±3.9） U/L〕 (P＜0.05). Those in IPC1 group was much lower than those in IPC2 group and IPC3 group 〔(63.8±7.2) U/L,（22.8±2.5） U/L〕 (P＜0.05). The level of lactic acid dehydrogenase (LDH) in NPC group (104.3±20.6) U/L, IPC1 group (84.1±19.7) U/L, IPC2 group (90.5±21.1) U/L, and IPC3 group (103.1±18.5) U/L were of no significant difference (Pgt;0.05). The contents of bile product and the hepatocellular contents of ATP in IPC1 group were (53.5±10.2) μl and (6.15±0.65) μmol/g respectively, and IPC2 group (41.5±8.1) μl, (4.77±0.21) μmol/g, which were much higher than those NPC group 〔(22.8±9.7) μl, (2.62±0.34) μmol/g〕 (P＜0.05). Those in IPC1 group were much higher than those in IPC2 group and IPC3 group 〔(27.5±2.8) μl, (2.61±0.29) μmol/g〕 (P＜0.05). The contents of malondialdehyde (MDA) in liver tissue in IPC1 group was (4.36±0.26) nmol/gand IPC2 group (5.51±0.13)
Objective To investigate the protective effect of ischemic preconditioning (IP) on ischemicreperfusion injury of rat liver graft. MethodsMale Sprague Dawley rats were used as donors and recipients of orthotopic liver transplantation,the period of cold preservation and anhepatic phase were 100 min and 25 min respectively.Sixtyfour rats were randomly divided into 2 groups (n=32),control group: donor livers were flushed through the portal veins with physiological saline solution containing heparin only before harvested; IP group: before donor livers were harvested,the portal veins and hepatic arteries of them were interrupted for 10 min,and reflow was initiated for another 10 min,then did as control group.One half of each group were used to investigate 1 week survival rate of recipients,and another half of each group were used to take sample of blood and hepatic tissue after 2 hours of reperfusion of liver graft. ResultsOne week survival rate,amount of bile,serum NO and activity of antioxidase were higher in IP group than those in control group(P＜0.05),meanwhile,serum ALT,AST,LDH,TNF and superoxide in hepatic tissue were lower in IP group than those in control group (P＜0.05),and histological findings in IP group showed less injury than those in control group. Conclusion IP could increase production of serum NO,reduce the level of serum TNF and protect rat liver graft from ischemicreperfusion injury.
【Abstract】Objective To study the mechanisms of enhancing effect of mild hypothermia (MH) to ischemic preconditioning (IP) on hepatic ischemiareperfusion (I-R) injury. Methods To observe the content of the marker enzymes of liver damage (ALT,AST,LDH) and malondialdehyde (MDA), and activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSHPX), total antioxidase (TAX) in inferior vena cava blood above liver in nonischemic control group (n=6), I-R group (n=6), IP group (n=6) and mild hypothermic ischemic preconditioning (MHIP) group (n=6). Results After I-R the content of ALT,AST, LDH and MDA were significantly elevated (P＜0.01), SOD,CAT,GSH-PX,ACT activities were declined obviously (P＜0.01). The content of ALT,AST,LDH and MDA were significantly lower in IP group than those in I-R group, and in MHIP group than those in IP group (P＜0.01,P＜0.05), and the content of SOD, CAT,GSH-PX, ACT activities were significantly higher in IP group than those in I-R group, and in MHIP group than those in IP group (P＜0.01,P＜0.05). Conclusion Ischemic preconditioning may enhance the oxidation-resistance of liver, and reduce the oxygen free radical injury to liver after ischemia-reperfusion. Mild hypothermia may enhance the protective effect of IP on hepatic ischemiareperfusion injury.
Objective To investigate the influence of hypoxic preconditioning on pulmonary structure of rats exposed to simulated high altitude hypoxia and to explore the role of hypoxia inducible factor-1α（HIF-1α）.Methods Fifty-six Wistar rats were randomly divided into 7 groups(n=8 in each group),ie,a normal control group(N group)，an acute hypoxic control group(H0 group)，an acute hypoxic group(H1 group)，a 3 000 m hypoxic preconditioning group(C3.0 group)，a 3 000 m hypoxic preconditioning + acute hypoxic group (C3.1 group)，a 5 000 m hypoxic preconditioning group(C5.0 group)，and a 5 000 m hypoxic preconditioning + acute hypoxic group(C5.1 group).After treated with hypoxic preconditioning，the animals were exposed to simulated altitude of 6 000 m for 24 hours.Then the protein and mRNA expression of HIF-1α in lung of N，H0，C3.0 and C5.0 groups were assessed by Western blot and RT-PCR，respectively.The lung structure in N，H1，C3.1 and C5.1 groups was observed by light microscope and electron microscope.Results Pulmonary interstitial edema was apparently observed in H1 group，while significantly relieved in two hypoxic preconditioning groups.HIF-1α protein was not detected in rat lungs by Western blot analysis.Compared to N group，the levels of HIF-1α mRNA significantly increased in C3.0 group and C5.0 group(both Plt;0.01).Conclusions Hypoxic preconditioning can relieve hypoxic pulmonary interstitial edema and increase HIF-1α mRNA expression in rat lungs.HIF-1 may be involved in the process of hypoxic preconditioning in rat lungs.
Objective To investigate the effects of ischemic postconditioning （IPO） on inflammatory response inischemia-reperfusion （IR） injury of rat lungs in vivo. Methods Forty SD rats were randomly divided into 5 groups inclu-ding a sham surgery group （S group），a 30-minute IR group （I/R-30 group），a 120-minute IR group（IR-120 group），a 30-minute IPO group （IPO-30 group），and a 120-minute IPO group （IPO-120 group）. There were 8 rats in each group. All therats received left thoracotomy after anesthesia. In the sham surgery group，a line was only placed around the left hilum butnot fastened. In the I/R-30 group and I/R-120 group，a line was fastened to block the blood flow of the left lung for 1 hour，then loosened for reperfusion for 30 minutes and 120 minutes respectively. In the IPO-30 group and IPO-120 group，afterblocking the blood flow of the left lung for 1 hour，the left hilum was fastened for 10 seconds and loosened for 10 seconds（repeating 3 times for 1 minute），then the line was loosened for 30 minutes and 120 minutes respectively. The levels of interleukin-10 （IL-10） in lung tissues and soluble intercellular adhesion molecule-1 （sICAM-1） in plasma were measured. Histopathological changes of lung tissues were observed and diffuse alveolar damage （DAD） scores was calculated.Results The levels of plasma sICAM-1 in the I/R-30 group and I/R-120 group were significantly higher than that of S group ［（2.140±0.250）μg/L vs. （0.944±0.188）μg/L，P=0.003；（2.191±0.230）μg/L vs. （0.944±0.188）μg/L，P=0.003］. IL-10levels in lung tissues in the I/R-30group and I/R-120 group were also significantly higher than that of S group［（15.922±0.606）pg/mg pro vs. （7.261±0.877）pg/mg pro，P=0.037；（17.421±1.232）pg/mg pro vs. （7.261±0.877）pg/mg pro，P=0.042］. Pathologic lesions of lung tissues in the I/R-30 group and I/R-120 group were more severe than that of S group. After IPO, plasma sICAM-1 levels in the IPO-30 group and IPO-120 group were significantly lower than those in the I/R-30group and I/R-120 group respectively ［（1.501±0.188）μg/L vs.（2.140±0.250）μg/L，P=0.038；（1.350±0.295）μg/L vs.（2.191±0.230）μg/L，P=0.005］. IL-10 levels in lung tissues in the IPO-30 group and IPO-120 group were significantly higherthan those in the I/R-30 group and I/R-120 group respectively ［（20.950±1.673）pg/mg pro vs.（15.922±0.606）pg/mgpro，P=0.008；（25.334±1.173）pg/mg pro vs.（17.421±1.232）pg/mg pro，P=0.006］. DAD scores in the IPO-30 group andIPO-120 group were significantly lower than those in the I/R-30 group and I/R-120 group respectively ［6.8±1.4 vs. 11.5±1.9，P=0.007；7.5±1.6 vs. 13.2±1.7，P=0.005］. Pathological lesions of the lung tissues of IPO groups were less severe than those of I/R groups. Conclusion IPO can attenuate IR injury by inhibiting inflammatory response in rat lungs.
Objective To explore the impact of ischemic postconditioning on ischemia-reperfusion injury in isolatedelderly rat hearts and their relation with P-Akt. Methods A total of 30 healthy elderly SD rats (21-23 months old， male or female) with their body weight of 450-500 g were divided into 3 groups: control group， ischemia-reperfusion group， and postconditioning group， with 10 rats in each group. Coronary artery blood flow，myocardial infarction size， phosphorylatedAkt （p-Akt） expression， and changes in myocardium and mitochondria were detected. Results Coronary artery blood flow of the postconditioning group was significantly higher than that of the ischemia-reperfusion group （6.4±1.2 ml/min vs.3.1±1.2 ml/min， P＜0. 01）， and myocardial infarction size of the postconditioning group was significantly smaller thanthat of the ischemia-reperfusion group （35.0%±2.0% vs. 55.7%±3.6%， Plt;0. 05）. The expression of P-Akt was significantlyhigher， and myocardial fibers and mitochondria were preserved better in the postconditioning group than the ischemia-reperfusion group. Conclusion Ischemic postconditioning can protect isolated elderly rat hearts against ischemia-reperfusion injury， which may be related to P-Akt activation.
Abstract： Ischemia postconditioning is a new concept based on ischemic preconditioning. It has become a hot topic in protection of ischemic-reperfusion injury because of its effective protection, relative ease of application, and postconditioning. However, its precise mechanisms and most effective application methods are still unclear. This review covers recent progress in the understanding, developments (in remote postconditioning and pharmacological postconditioning), applications to the protection of heart, lung, liver, kidney, and brain, mechanisms and appropriate protocol of ischemic post-conditioning.
Abstract： Objective To observe the expression changes of microRNA 1 （miRNA-1） and microRNA 21（miRNA-21） after ischemic preconditioning （IPC）, ischemic postconditioning （IPO） and remote ischemic preconditioning （RIPC）in an ischemia-reperfusion rat heart model in vitro, as well as the expression of their target protein heat shock protein 70 （HSP70） and programmed cell death 4 （PDCD4）, and evaluate whether miRNA are involved in endogenous cardio-protective mechanism. Methods The Langendorff-perfused Sprague-Dawley rat hearts were randomly assigned into one of the four groups, control group （CON group, n=12）, ischemia preconditioning group （IPC group， n=12） , ischemia postconditioning group （IPO group， n=12） and remote ischemia preconditioning group （RIPC group，n=12）. Cardiac function was digitalized and analyzed. The expression of HSP70, PDCD4, B-cell lymphoma/leukemia-2 （Bcl-2） and Bax was detected by Western blotting. The expression of miRNA-1 and miRNA-21 was detected by real-time reverse transcriotion-polymerase chain reaction （RT-PCR）. Assessment of cardiac infarct size and myocardial apoptosis was determined using triphenyltetrazolium chloride （TTC） assay and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay （TUNEL） assay respectively. Results The expressions of miRNA-1 and miRNA-21 were up-regulated in IPC group, but the expression of miRNA-1 was down-regulated in RIPC group and IPO group （P＜0.05）. The expressionsof PDCD4, HSP70 and Bax were down-regulated in ‘conditioning’ groups compared with CON group （P＜0.05）. The expression of Bcl-2 was not statistically different among the four groups. The infarct size and the myocardial apoptosis in ‘conditioning’ hearts were significantly decreased compared with CON group （P＜0.05）. Conclusion The expressions of the miRNA-1 and miRNA-21 are different in IPC, RIPC and IPO groups, and their target proteins are not inversely correlated with the miRNAs in all the ‘conditioning’ groups.
Abstract： Objective To investigate the effects of calcium preconditioning (CP) on immature myocardial cell apoptosis and apoptosisregulated proteins. Methods The experiment was carried out from June 2000 to December 2001 in the Renmin Hospital of Wuhan University. Twelve rabbits with the age of 1421 d and the weight of 230300 g were divided into 2 groups with 6 in each group by random digital table. For rabbits in the ischemia/reperfusion group (I/R group), after Langendorff models were routinely set up, KrebsHenseleit (KH) solution was perfused for 20 minutes and reperfused for 120 minutes after 45 minutes of ischemia. For rabbits in the CP group, after Langendorff models were established, KH solution was perfused for20 minutes, and 45 seconds’ noncalcium KH solution perfusion and 5 minutes’ KH solution perfusion were repeated 3 times before 45 minutes of ischemia and 120 minutes of reperfusion of KH solution. In situ apoptosis identification and semiquantitative analysis were used to detect the myocardial cell apoptosis; agarose gel electrophoresis was used to detect the nucleosomal ladder of DNA fragments; and the expression of bcl-2, bax and fas were detected with Western blot method. Results The apoptosis rate for the CP group was lower than that of the I/R group (4.53%±1.22% vs. 12.30%±2.12%,t=7.780, P=0.000). Nucleosomal ladder of DNA fragments of the CP group was lower than that of the I/R group (OD value: 56 460±1 640 vs. 135 212±3 370,t=51.460,P=0.000). The expression of bcl-2 in the I/R group was lower than that of the CP group (OD value: 13 217±1 770 vs. 31 790±1 018,t=22.280, P=0.000). The expression of bax (OD value: 30 176±1 025 vs. 7 954±730, t=43.260, P=0.000) and fas (OD value: 29 197±1 233 vs. 8 140±867, t=34.220, P=0.000) in the I/R group was higher than that of the CP group. Conclusion CP can affect the expression of myocardial bcl-2, bax, and fas, and decrease immature myocardial cell apoptosis.