Spermine inhibits expression of Fas/FasL in simulated ischemia-reperfusion-injured cardiomyocytes of neonatal rat / 中国病理生理杂志

AIM: To explore the effects and possible mechanism of exogenous spermine on the apoptosis of primary cultured neonatal cardiomyocytes induced by simulated ischemia-reperfusion (I/R) injury. METHODS: To establish a model of simulated I/R, the primary cultured neonatal rat cardiomyocytes were incubated in ischemia-mimetic solution (under the conditions of hypoxia plus serum deprivation) for 2 h, and re-incubated the cells in normal culture medium for 24 h. The apoptotic cell death was assayed by flow cytometry. The morphological alterations of the cells were observed under transmission electron microscope. The transcription and expression of Fas and FasL were determined by the methods of RT-PCR, Western blotting and immunofluorescence. RESULTS: The cells exposed to I/R underwent significant apoptosis, and the percentage of apoptotic cells was 27.4%±1.8%, much higher than that in normal group (5.7%±0.3%). In I/R group the evident histopathological changes were observed and the myocardial transcription and expression of Fas and FasL were significantly upregulated. Compared to normal group, mRNA expression of Fas and FasL increased 2.2 folds and 2.4 folds, respectively, and their proteins increased 1.7 folds and 1.9 folds at 24 h of reperfusion respectively (P<0.01). Pretreatment with 10 μmol/L spermine significantly inhibited apoptosis of I/R injured cells, and the percentage of apoptotic cells was 21.7%±1.3% (P<0.01, as compared to I/P group). Spermine also suppressed the expression of Fas and FasL significantly (P<0.05 or P<0.01, as compared to I/P group). CONCLUSION: Spermine plays anti-apoptotic effect on the cultured neonatal myocardial cells under the condition of I/R injury by suppressing the expression of Fas/FasL.

Effects of the flurbiprofen axetil for postoperative patient-controlled intravenous analgesia on stress response after gynecological surgery / 中国医师进修杂志

Objective To observe the effects of flurbiprofen axetil postoperative patient-controlled intravenous analgesia (PCIA) on stress response in patients undergoing gynecological laparoscopy operation.Methods One hundred and twenty ASA Ⅰ - Ⅱ gynecological laparoscopy operation patients were randomized to two groups, 60 cases in each group.Group F received flurbiprofen axetil 4 mg/kg while group S were given sufentanil 1.5μ g/kg for postoperative PCIA.Tumor necrosis factor-α (TNF-α ) and interleukin (IL)-6, IL-8, IL- 10 were estimated preoperative(T_0), operation termination(T_1) and 48 h after operation(T_2).Results VAS scores were less than 4 scores and no significant difference between two groups.There was no significant difference in TNF- α intraclass and interclass between two groups(P > 0.05 ).IL-6, IL-8, IL- 10 in two groups were significantly higher at T_1 and T_2 than those at To (P< 0.05).IL-6, IL-8 at T_1 and T_2 were lower in group F than those in group S [T_1 and T_2: IL-6 was ( 18.39 ± 3.01 ), ( 13.43 ± 3.11 ) ng/L, IL-8 was (24.25 ± 2.75 ), ( 15.31 ± 2.65 ) ng/L in group F; IL-6 was (38.02 ± 2.95 ), (23.28 ± 2.43 ) ng/L, IL-8 was ( 37.56 ± 2.97 ), ( 24.86 ± 3.11 ) ng/L in group S]( P < 0.05 ).While IL- 10 was significantly higher and lasted longer in group F than that in group S [(26.72±4.41), (21.03±2.99) ng/L in group F; (22.18 ± 3.21), (16.89 ± 4.48) ng/L in group S](P < 0.05).Conclusion PCIA with flurbiprofen axetil in gynecological laparoscopy operation patients can alleviate inflammatory response.

The practice and discussion of"six processes"teaching methods in functional design experiments / 中华医学教育探索杂志

The functional experiment teaching is an inspection to students of their thinking methods and the operation abilities,and is also the summary and sublimation of this course theories teaching.To adapt to the demand for cultivation of the talented person by innovation education,we probe into the improvement of teaching methods of the functional design experiment,and practiced the new teaching system of "six processes"teaching methods such as speaking briefly,giving a demonstration,questioning,giving clue,study and discussion,evaluation,and push forward the biomedical science modes toward the development of "living creature-mental state-social medical science mode"direction.

Therapy of Hypertension Cerebral Hemorrhage with Micro-keyhole Craniotomy Double-channel Tube Lavage and Drainage / 医学研究杂志

0.05). Micro-keyhole craniotomy double-channel tube lavage and drainaging group had a significant lower rehemorrhagia rate and lower mortality.And the short-term effects,the long-term follow-up of patients with pathogenetic in key-hole group was significant better than that in the other groups.there was obvious difference(P

The effects of 17?-estradiol on cardiomyocyte hypertrophy induced by endothelin / 中国病理生理杂志

AIM: To investigate the effect of 17?-estradiol(E2) on myocardial hypertrophy induced by endothelin-1(ET-1) and the related mechanism.METHODS: Myocardial cells from neonate rats were cultured in vitro and myocardial hypertrophy model was established with ET-1.The effects of 17?-estradiol on myocardial hypertrophy were observed.The role of ERK1/2 in the effects of 17?-estradiol was also detected.RESULTS: Compared with control group,ET-1 increased cell protein content,cell surface area and -Leucine(-Leu) incorporation.Pretreatment with E2 for 24 h could inhibit the increase in cell protein content,cell surface area and -Leu incorporation induced by ET-1.ET-1 significantly stimulated ERK1/2 activity,which was prevented by pretreatment with E2.Tamoxifen,estradiol receptor antagonist,partially inhibited the effect of E2.The ability of ET-1 to stimulate -Leu incorporation was significantly blocked by PD98059,which could enhance the inhibitory effect of E2 on the increase of -Leu incorporation in cardiomyocytes induced by ET-1.CONCLUSION: E2 can inhibit cardiomyocyte hypertrophy induced by ET-1.This effect is mediated by estrogen receptor.ERK1/2 signal pathway is closely correlated with the inhibitory effect of E2 on cardiomyocyte hypertrophy induced by ET-1.