Objective To evaluate the effects of biological rhythm disturbance on sedation induced by propofol in rats.Methods Thirty-two adult male Sprague-Dawley rats,weighing 180-220 g,were randomly divided into 4 groups (n =8 each) using a random number table:circadian rhythm + administration during night-time group (group CN),circadian rhythm + administration during day-time group (group CD),biological rhythm+administration during night-time group (group BN),and biological rhythm+administration during day-time group (group BD).In CN and CD groups,the rats were fed for 2 weeks in the experimental boxes in a 12 (7:00-19:00):12 h (19:00-7:00) light:dark cycle.While the rats were fed for 2 weeks in the experimental boxes in a 24 h light cycle.Propofol 75 mg/kg was intraperitoneally injected at 14:00 in CN and BN groups,or at 22:00 in CD and BD groups.The duration of loss of righting reflex was recorded.At 20 min after recovery of righting reflex,the cognitive function was assessed.The latency of passive avoidance was measured at 6,12,24 and 48 h after training.Results Compared with group CN,the duration of loss of righting reflex was significantly shortened,and the latency of passive avoidance was prolonged at 12 and 24 h after training in group CD,and the duration of loss of righting reflex and latency of passive avoidance at 12 and 24 h after training were shortened in group BN.Compared with group CD,no significant change was found in the duration of loss of righting reflex,and the latency of passive avoidance was significantly shortened at 24 h after training in group BD.There was no significant change between BN group and BD group in the duration of loss of righting reflex and latency of passive avoidance.Conclusion Biological rhythm disturbance can counteract circadian rhythmproduced effects on sedation induced by propofol in rats.

Objective:To observe the effect of sodium fluoride (NaF) on the expression of phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) signal and apoptosis in human osteosarcoma Saos-2 cells.Methods:Saos-2 cells were divided into 0 (control), 5, 10, 20 and 40 mg/L fluoride groups ( n= 3) according to the dose of NaF. The cells were collected after 24 and 48 h of culture in vitro. Western blotting was used to detect the expressions of PI3K/Akt signal and Forkhead transcription factor (FoxO) 1, and the apoptosis level of Saos-2 cells was detected by flow cytometry. Results:There were no significants differences in the expressions of PI3K and Akt in Saos-2 cells at 24 and 48 h ( P > 0.05). At 24 h, the expressions of phosphorylated PI3K (p-PI3K) in 5, 10, 20 and 40 mg/L fluoride groups (0.40 ± 0.06, 0.45 ± 0.02, 0.37 ± 0.06, 0.32 ± 0.06) were higher than that in the control group (0.28 ± 0.04, P < 0.05); at 48 h, the expressions of p-PI3K in 5 and 10 mg/L fluoride groups (0.46 ± 0.06, 0.58 ± 0.03) were higher than that in the control group (0.29 ± 0.04, P < 0.05), and that in the 40 mg/L fluoride group (0.21 ± 0.03) was lower than that in the control group ( P < 0.05). At 24 h, the expressions of phosphorylated Akt (p-Akt) in 5, 10 and 20 mg/L fluoride groups (0.27 ± 0.01, 0.30 ± 0.03, 0.27 ± 0.03) were higher than that in the control group (0.20 ± 0.02, P < 0.05); at 48 h, the expressions of p-Akt in 5 and 10 mg/L fluoride groups (0.42 ± 0.04, 0.60 ± 0.02) were higher than that in the control group (0.27 ± 0.01, P < 0.05), and that in the 40 mg/L fluoride group (0.18 ± 0.02) was lower than that in the control group ( P < 0.05). The expressions of FoxO1 in 10, 20 and 40 mg/L fluoride groups at 24 h (0.38 ± 0.07, 0.41 ± 0.06, 0.47 ± 0.08) were higher than that in the control group (0.34 ± 0.04, P < 0.05). At 48 h, the expressions of FoxO1 in 5, 10, 20 and 40 mg/L fluoride groups (0.36 ± 0.08, 0.37 ± 0.10, 0.54 ± 0.04, 0.73 ± 0.04) were higher than that in the control group (0.28 ± 0.04, P < 0.05). At 24 and 48 h, the apoptosis rates of control group and 5, 10, 20 and 40 mg/L fluoride groups were (2.867 ± 0.583)%, (3.647 ± 0.035)%, (3.773 ± 0.095)%, (5.440 ± 0.325)%, (7.203 ± 0.476)%; (3.707 ± 0.286)%, (4.023 ± 0.241)%, (4.970 ± 0.368)%, (12.473 ± 0.949)%, (19.387 ± 1.892)%, respectively. The apoptosis level of 40 mg/L fluoride group was higher than that of control group at 24 h ( P < 0.05), and that of 20 and 40 mg/L fluoride groups were higher than that of control group at 48 h ( P < 0.05). Conclusion:Fluoride can directly activate the PI3K/Akt signaling pathway in osteoblasts, and then has anti-apoptotic effect.

Objective: To observe the effects of He-Ne laser on the expression of extracellular matrix and its regulatory factors in degenerated temporomandibular joint(TMJ) of rabbits. Methods: 40 New Zealand adult white rabbits were randomly divided into normal group,sham model group,TMJOA model group and laser treatment group(n = 10),the rats in treatment group were treated by He-Ne laser irradination at acupoints. The rats in each group were divided into 1 d and 11 d groups(n = 5). The animals were respectively killed 1 d and 11 d after operation and HE staining was used to observe the histomorpholy. The protein expression of extracellular matrix and its regulatory factors were examined by Western blot. Results: After He-Ne laser treatment,the fiber layer of condylar cartilage was slightly loose,part of the fiber was newly produced. The level of Col-2,PRG-4,TIMP-1,BMP-2 was up-regulated and the of MMP-13 was down-regulated in the 11 d treatment group. Conclusion: He-Ne laser irradiation on acupoints may up-regulate the expression of extracellular matrix (Col-2 and PRG-4) and its regulatory factors (TIMP-1 and BMP-2),down-regulate the expression of MMP-13.

Neonatal hypoxic-ischemic encephalopathy often causes long-term adverse effect on neurological system or even death in near-term or full-term infants, but no effective treatment is available currently. Studies have shown that xenon can reduce brain injury caused by hypoxia-ischemia and is promising in clinical practice. The possible mechanisms include antagonism to glutamic acid receptors, anti-apoptosis, promotion of cell repair and xenon preconditioning. This article reviews the mechanism and research progress on neuroprotection effect of xenon in the treatment of neonatal hypoxic-ischemic encephalopathy.

OBJECTIVE: To investigate the mechanism by which epigallocatechin gallate (EGCG) induces gene demethylation and promotes the apoptosis of acute myeloid leukemia KG-1 and THP-1 cell lines. METHODS: KG-1 and THP-1 cells treated with 25, 50, 75, 100 or 150 μg/mL EGCG for 48 h were examined for gene methylation using MSP and for cell proliferation using MTT assay. The changes in cell cycle and apoptosis of the two cell lines after treatment with EGCG for 48 h were detected using flow cytometry. The mRNA and protein expressions of DNMT1, CHD5, p19, p53 and p21 in the cells were detected using RT-quantitative PCR and Western blot. RESULTS: EGCG dose-dependently reversed hypermethylation of gene and reduced the cell viability in both KG-1 and THP-1 cells ( < 0.05). EGCG treatment caused obvious cell cycle arrest in G1 phase, significantly increased cell apoptosis, downregulated the expression of DNMT1 and upregulated the expressions of CHD5, p19, p53 and p21 in KG-1 and THP-1 cells ( < 0.05). CONCLUSIONS EGCG reduces hypermethylation of gene in KG-1 and THP-1 cells by downregulating DNMT1 to restore its expression, which results in upregulated expressions of p19, p53 and p21 and induces cell apoptosis.

OBJECTIVE: Providing a risk assessment method for the implementation of radiotherapy to identify possible risks in the implementation of the treatment process, and proposing measures to reduce or prevent these risks. METHODS: A multidisciplinary expert evaluation team was developed and the radiotherapy treatment process flow was drawn. Through the expert team, the failure mode analysis is carried out in each step of the flow chart. The results were summarized and the (risk priority ordinal) score was obtained, and the quantitative evaluation results of the whole process risk were obtained. RESULTS: One hundred and six failure modes were obtained, risk assessment of (20%) high risk failure model are 22 and severity (≥ 8) high risk failure model are 27. The reasons for the failures were man-made errors or hardware and software failures. CONCLUSIONS Failure mode and effect analysis can be used to evaluate the risk assessment of radiotherapy, and it provides a new solution for risk control in radiotherapy field.
Healthcare Failure Mode and Effect Analysis ; Risk Assessment