Amyloid beta-Peptides ; toxicity ; Animals ; Drugs, Chinese Herbal ; pharmacology ; Estradiol ; pharmacology ; PC12 Cells ; Peptide Fragments ; toxicity ; Rats

Purpose To observe the action time of parthenolide (PTN) as selective nuclear factor-κB(NF-κB) inhibitor in heart of rats.Methods Forty SD rats were randomly divided into control(CON) group,PTN group,dimethyl sulfoxide(DMSO) group,lipopolysaccharide(LPS) group and PTN+LPS group.The first day:PTN group,DMSO group and PTN+LPS group rats were respectively injected interapertoneally PTN(500 μg/kg) and DMSO; other groups rats were injected interapertoneally equivalent saline.The second day(in equivalent to 24 h after injecting PTN):in LPS group and PTN+LPS group LPS(12.5 mg/kg) was administered subcutaneously; other group rats were injected subcutaneously equivalent saline.Every heart was obtained in equivalentce to 1 h after injecting LPS to measure the expression of NF-κB p50 in nucleus,inhibitory kappaB(IκBα) and phosphorylation inhibitory kappaB(p-IκBα) in cytoplasm of cardiac myocytes through Western blotting.Results Compared with CON group,the expression of NF-κB p50,IκBα and p-IκBα had no difference in PTN and DMSO group.And in LPS group and PTN + LPS group,the expression of NF-κB p50 up-regulated significantly(P＜0.05),IκBα down-regulated(P＜0.05) and p-IκBα up-regulated significantly(P＜0.05).Conclusion LPS can activate NF-κB in 1 h and PTN in rats after 24 h has few effect.

Electroencephalogram (EEG) signals provide an objective physiological index for the identification of the driver's fatigue state. It is very important to choose appropriate channels and EEG signal features adaptively due to the features varying with different subjects and time. A support vector machine (SVM) based increasing feature selection algorithm for driving fatigue EEG classification is presented in this paper. The algorithm is a method to select EEG channels and features for driving fatigue adaptively in an ascending order. We can select the optimal feature each time from the remaining candidate features using the optimized SVM model minimum error rate as the index. The experimental calculation has characteristics of using 16 electrode channels which cover the whole head in the main area, of selecting 208 candidate features as the initial set, of selecting to the EEG data calculation recorded in 5 different time periods of a subject, and of choosing error rate of 2% as the algorithm termination condition. The selected features and models, therefore, can reach a high level of classification and generalization ability.
Algorithms ; Automobile Driving ; Electrodes ; Electroencephalography ; Fatigue ; Humans ; Support Vector Machine ; Time Factors

Animals ; Drugs, Chinese Herbal ; pharmacology ; PC12 Cells ; Patch-Clamp Techniques ; Potassium Channels, Voltage-Gated ; drug effects ; physiology ; Rats

This study is to explore the interventional effects of fluvastatin on anti-beta2GPI/beta2GPI-induced activation in THP-1 mononuclear cells. In vitro, human mononuclear cells THP-1 were treated with fluvastatin, LPS and anti-beta2GPI/beta2GPI, then the TF expression on THP-1 cells was detected by real-time quantitative PCR (RT-qPCR) or TF activity was detected by kit. TNF-alpha mRNA and its protein expression were investigated by RT-PCR and ELISA kit. The expression of phospho-NF-kappaB p65 and inhibitory protein of NF-kappaB (IkappaB-alpha) were measured by Western blotting. The results suggested that the expression of TF and TNF-alpha on THP-1 cells was significantly up-regulated with treatment of anti-beta2GPI/beta2GPI complex (100 mg x L(-1)), compared with that of untreated cells (P < 0.05). Fluvastatin (50 mg x L(-1)) could decrease TF (mRNA and activity) expression and the level of TNF-alpha (mRNA and protein) in THP-1 cells with anti-beta2GPI/beta2GPI complex. The expression of TF and TNF-alpha was shown in a concentration-dependent manner. Moreover, anti-beta2GPI/beta2GPI complex could downregulate IkappaB-alpha levels and increase the levels of phospho-NF-kappaB p65. And these effects of anti-beta2GPI/beta2GPI complex could be blocked by fluvastatin. In conclusion, fluvastatin may interfere the expression and regulation of NF-kappaB signal transduction pathway, thereby inhibit the effects of anti-beta2GPI/beta2GPI on activation of THP-1 cells, by decreasing the expression of TF and TNF-alpha.

With the advent of the modern medical mode,rehabilitation medicine teaching becomes an important part of the whole system of medical education.Theory on rehabilitation medicine education infiltrates clinical specialities and brings about a great advance in promoting subject development throughly during clinical education.

OBJECTIVETo study the effects of integrative medicine protocols on the neural function deficit and short-term disability outcomes in patients with acute ischemic cerebral stroke.

METHODS99 patients were randomly assigned to three groups, i.e., the Dengzhan Xixin (fleabane) group (Group A), the Kudiezi (sowthistle-leaf ixeris seedling) group (Group B), and the Western medicine control group (Group C). Dengzhan Xixin Injection was intravenously dripped to patients in Group A for 14 days. Chinese decoction was administered to them by pattern typing as well. Meanwhile, they took Dengzhan Shengmai Capsule for two months. Kudiezi Injection was intravenously dripped to patients in Group B for 14 days. Chinese decoction was administered to them by pattern typing as well. Meanwhile, they took Naoshuantong Capsule for two months. In addition to internal therapies, patients in Group A and B received acupuncture, massage, and external washing with Chinese medicine for 21 days. Patients in Group C also received modem rehabilitation therapy for 21 days, including rehabilitation training and electronic stimulus in addition to the internal medicine. The National Institute of Health Stroke Scale (NIHSS) and disability outcome (modified Rank Scale, mRS) were taken as main effect indices.

RESULTSThe NIHSS scores at each time point obviously decreased more than before treatment in all the three groups (P<0.01), but with no difference at each time point (P>0.05). The disability outcomes of all the three groups postponed as time went by. Significant difference existed among the three groups by log-lineal model (CATMOD) (P<0.05). The best effect was shown in Group B, with the markedly effective rate of 19. 35% and the total effective rate 54.84%.

CONCLUSIONSThe integrative medicine protocols could improve the nerve functions of ischemic stroke patients. Therefore, it could improve the disability outcomes. The comprehensive protocol (Kudiezi Injection + Naoshuantong Capsule + Chinese decoction according to pattern typing + acupuncture + massage + external washing with Chinese medicine) was better.

Aged ; Aged, 80 and over ; Brain Ischemia ; therapy ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Integrative Medicine ; Male ; Middle Aged ; Phytotherapy ; Stroke ; therapy ; Treatment Outcome

Objective To investigate the effects of sevoflurane delayed preconditioning on caspase recruitment domain (ARC) expression during myocardial ischemia-reperfusion (I/R) in rats. Methods Sixty-four adult male SD rats weighing 270-350 g were randomly divided into 4 groups ( n = 16 each): sham operation (group S); myocardial I/R group; sevoflurane + sham operation group (group S-S) and sevoflurane delayed preconditioning + myocardial I/R group (group S-I/R) . Myocardial I/R was induced by occlusion of anterior descending branch of left coronary artery for 30 min followed by 2 h of reperfusion in groups I/R and S-I/R. Group S-S inhaled 33% oxygen for 2 h, and sham operation was performed 24 h later. Group S-I/R inhaled 2.5% sevoflurane for 2 h, and then myocardial I/R was induced 24 h later. Eight animals were sacrificed at the end of 2 h reperfusion in each group and the hearts removed for determination of myocardial infarct size (IS) as a percentage of area at risk (AAR) by triphenyl tetrazolium chloride staining (IS/AAR) . Myocardial apoptosis was detected using TUNEL and apoptosis index was calculated. Another 4 animals were sacrificed immediately before ischemia and at the end of 2 h reperfusion to determine the expression of ARC and Caspase-8 in myocardium by Western blot. Results Compared with group S, the infarct size and apoptosis index were significantly increased in groups I/R and S-I/R, and ARC expression was up-regulated immediately before ischemia in groups S-S and S-I/R, and Caspase-8 expression was up-regulated at 2 h of reperfusion in group I/R ( P ＜ 0.05) . Compared with group I/R, the infarct size and apoptosis index were significantly decreased in group S-I/R, and ARC expression was up-regulated, while Caspase-8 expression was down-regulated at 2 h of reperfusion in groups S-S and S-I/R ( P ＜ 0.05) . Conclusion Sevoflurane delayed preconditioning can attenuate myocardial I/R injury through up-regulating the ARC expression and decreasing the myocardial apoptosis.

Objective To evaluate nuclear factor (NF)-κB signaling pathway and autophagy in inhaled sevoflurane-produced delayed myocardial protection in rats.Methods Ninety-six adult male Sprague-Dawley rats,weighing 270-350 g,were randomly assigned into 6 groups (n =16 each):sham operation group (group S),ischemia-reperfusion (I/R) group,sevoflurane group (SEVO group),specific NF-κB inhibitor parthenolide (PTN)group,dimethyl sulfoxide (DMSO) group and PTN + sevoflurane group (PTN + SEVO group).The animals were anesthetized with intraperitoneal pentobarbital 50 mg/kg,intubated and mechanically ventilated.Myocardial I/R was induced by 30 min of occlusion of the left anterior descending branch of coronary artery followed by 2 h of reperfusion.In group I/R,33％ oxygen was inhaled for 2 h.In group SEVO,2.5％ sevoflurane was inhaled for 2 h.In groups PTN and DMSO,PTN 500 μg/kg and DMSO were administered intraperitoneally 15 min before oxygen inhalation respectively.In group PTN + SEVO,PTN 500 μg/kg was administered intraperitoneally 15 min before exposure to sevoflurane.Myocardial I/R was induced 24 h after intraperitoneal administration.Eight animals in each group were sacrificed immediately before ischemia and the hearts were removed to detect the NF-κB activity and expression of LC3-Ⅱ and cathepsin B.The left animals in each group were sacrificed at 2 h of reperfusion and the hearts were removed to determine the myocardial infarct size (by TTC staining).Results Compared with group S,the myocardial infarct size was significantly increased at 2 h of reperfusion in the other groups,and the NF-κB activity was significantly increased and the expression of LC3-Ⅱ and cathepsin B was up-regulated immediately before ischemia in group SEVO (P ＜ 0.05).Compared with group I/R,the NF-κB activity was significantly increased and the expression of LC3-Ⅱ and cathepsin B was up-regulated immediately before ischemia,and the myocardial infarct size was significantly reduced at 2 h of reperfusion in group SEVO (P ＜ 0.05).Compared with group SEVO,the NF-κB activity was significantly decreased and the expression of LC3-Ⅱ and cathepsin B was down-regulated immediately before ischemia,and the myocardial infarct size was significantly increased at 2 h of reperfusion in DMSO,PTN and PTN + SEVO groups (P ＜ 0.05).Conclusion NF-κB signaling pathway and autophagy are involved in inhaled sevoflurane-produced delayed nyocardial protection in rats.

Objective To investigate the effect of sevoflurane (Sero) preconditioning (Precon) on cardiomyocyte apoptosis following myocardial ischemia-reperfusion (I/R) in rats. Methods Sixty-four adult male SD rats weighing 270-350 g were randomly divided into 4 groups ( n = 16 each): group Ⅰ sham operation (group S); group Ⅱ myocardial I/R; group Ⅲ Sero and group Ⅳ Sevo-Precon + myocardial I/R. The animals were anesthetized with intraperitoneal pentobarbital 50 mg/kg, intubated and mechanically ventilated. PET CO2 was maintained at 35-45 mm Hg. Myocardial I/R was induced by 30 min occlusion of the left anterior descending branch of coronary artery followed by 2 h reperfusion in group Ⅱ and Ⅳ . In group Ⅲ the animals inhaled 2.5 % sevoflurane for 30 min while in group Ⅳ the animals inhaled 2.5% sevoflurane for 30 min at 15 min before myocardial I/R. Eight animals were killed at the end of 2 h reperfusion in each group. The hearts were removed for determination of myocardial infarct size (IS) as a percentage of area at risk (AAR) (IS/AAR) by triphenyl tetrazolium chloride staining. Myocardial apoptosis was detected using TUNEL and apoptosis index (AI) was calculated. Another 4 animals were killed before ischemia and at the end of 2 h reperfusion for determining the expression of Bcl-2 and caspase-3 protein in myocardium by Western blot. Results Sevoflurane preconditioning significantly decreased infarct size and AI in group Ⅳ as compared with group Ⅱ (group I/R). Bcl-2 protein expression was significantly decreased and caspase-3 protein expression was significantly increased after 2 h reperfusion as compared with the expression before ischemia in group I/R (group Ⅱ ). Sevoflurane preconditioning significantly reversed the I/R-induced changes in Bcl-2 and caspase-3 protein expression. Conclusion Sevoflurane preconditioning can attenuate myocardial I/R injury by decreasing myocardial apoptosis.