Objective: To evaluate the proper sedative/hypnotic depth during total intravenous anesthesia (TIVA) with propofol,fentanyl and muscular relaxant. Method:Thirty ASA grade Ⅰ or Ⅱ patients were induced with propofol. The EEG values were monitored during loss of consciousness and period of no response to a transcutaneous electrical stimulation,and at the total propofol induction dosage of 6 mg?kg~(-1). After intubation,the patients were randomly allocated into two groups. The rate of propofol infusion was regulated to maintain bispectral index(BIS) values between the light sedative/hypnotic point and 5 below (group A),or to the values between the deep sedative/hypnotic point and 5 below (group B). Result: BIS values were 71?8 and 58?8 at the light and deep sedative/hypnotic points, respectively;The propofol infusion rate in group A was significantly lower than that in group B (4.2?0.9 vs 7.4?1.5mg?kg~(-1)?h~(-1)). Fentanyl, nimodipine and pancuronium dosages were not different between group A and B. Conclusion:During general anesthesia,the sedative/hypnotic depth titrated at the loss consciousness level,is proper with maintanence dose at 4.5-5mg?kg~(-1)?h~(-1)of propfol for the safe use even without montoring of EEG-BIS.

Objective To investigate the effect of propofol on the intracellular calcium ion concentration ([ Ca2+ ]i) in isolated rabbit tracheal smooth muscle cells (TSMCs).Methods The single rabbit TSMC was isolated by acute enzymatic isolation method as described by Cheng et al.The isolated TSMCs were randomly divided into 3 groups ( n =5 each):propofol group (group Ⅰ ),propofol + 2-aminoethoxy-diphenylborate (2-APB) group (group Ⅱ ) and propofol + the blocker ryanodine group (group Ⅲ).In group Ⅰ,the cells were incubated with propofol with the final concentration of 300 μmol/L for 15 min,followed by washing with calcium-free Hank's balanced salt solution (HBSS) for 3 times,acetylcholine 1 μmol/L was then added to the culture medium and [ Ca2+ ]i was recorded.In group Ⅱ,the cells were incubated with 2-APB with the final concentration of 40 μmol/L for 15 min,propofol with the final concentration of 300 μmol/L was then added,the cells were incubated with 2-APB and propofol for another 15 min,followed bywashing with calcium-free HBSS for 3 times,and acetylcholine 1 μmol/L was then added.In group Ⅲ,the cells were incubated with ryanodine with the final concentration of 10 μmol/L for 15 min,propofol with the final concentration of 300 μmol/L was then added,the cells were incubated with ryanodine and propofol for another 15 min,followed by washing with calcium-free HBSS for 3 times,and acetylcholine 1 μmol/L was then added.[ Ca2+ ]i in TSMCs was measured using the fluorescent Ca2+ indicator fluor-3/AM.Results Compared with group Ⅰ,no significant change was found in [Ca2+ ]i in group Ⅱ (P＞0.05),while [Ca2+ ]i was significantly decreased in group Ⅲ (P＜0.05).Conclusion Propofol can decrease the [Ca2+ ]i in isolated rabbit TSMCs,and the mechanism may be related to inhibition of inositol 1,4,5-trisphosphate pathway,but not ryanodine pathway.

Objective To investigate the effects of propofol on apoptosis following focal cerebral ischemia-reperfusion in a rat model of reversible middle cerebral artery occlusion(MCAO) .Methods Twenty-four male SD rats weighing 300-500 g were randomly divided into 3 groups: group I sham operation; group Ⅱ MCAO + normal saline; group Ⅲ MCAO + propofol. MACO was produced by insertion of a 2-0 nylon filament with rounded end into internal carotid artery toward brain until resistance was encountered. The depth of insertion was about 2 mm. The filament was withdrawn after 2 h for reperfusion. In group I (sham operation) carotid artery was exposed but no filament was inserted. In group Ⅲ (propofol) intraperitoneal propofol 100 mg?kg-1 was administered 20 min before reperfusion; while in groupⅡ(normal saline) normal saline was given instead of propofol 20 min before reperfusion. At the end of 2 h reperfusion the animals were decapitated and the brain was removed. Apoptosis was identified by TUNEL technique. Cellular structure was examined under light microscope. Results Propofol significantly inhibited neuronal apoptosis following focal cerebral ischemia-reperfusion. Swelling and necrosis of the neurons were significantly attenuated in group III . Conclusion Propofol protects neurons against focal cerebral ischemia-reperfusion in rats.

Objective To evaluate the role of P2X3 receptors in dorsal root ganglion in development of incisional pain in rats.Methods Twenty-four healthy male SD rats weighing 200-220 g were randomly divided into 3 groups(n = 8 each): control group(group C),incisional pain(group IP)and P2X3 receptor antagonist + IP group(group A).In group IP and A,a 1 cm longitudinal incision was made in the plantar surface of left hindpaw according to the method described by Brennan et al.in isoflurane-anesthetized rats.P2X3 receptor antagonist TNP-ATP 200 nmol was injected into the plantar surface of left hindpaw 30 min after plantar incision was made in group A,while equal volume of normal saline was given instead of TNP-ATP in group C and IP.The behavior of the hindpaw of the rats were assessed using cumulative pain score within 1 h after injection.The animals were sacri ficed 2 h after injection and the dorsal root ganglion was removed for determination of P2X3 receptor expression and intracellular Ca2+ concentrations.ResultsThe cumulative pain scores,P2X3 receptor expression and Ca2 + concentrations were significantly higher in group IP and A than in group C(P ＜ 0.05).The cumulative pain scores,P2X3 receptor expression and Ca2+ concentrations were significantly lower in group A than in group IP(P ＜0.05).Conclusion P2X3 receptors in dorsal root ganglion is involved in the development of incisional pain through increasing intracellular Ca2+ concentrations in rats.

Objective To investigate the antitumor activity of IL-24 delE5 in human leukemia cell line K562. Methods The expression of mda-7/IL-24 and its splice variant induced by TPA in leukemic cell lines, U937 and HL-60, was evaluated. The effects of IL-24 delE5 in K562 on cell proliferation, colony-forming ability, cell cycle, apoptosis, and tumor growth in vivo by using MTr assay, colony forming assay, flow cytometry, Annexin-V/PI and tumor xenograft models in nude mice were assessed. Meantime, the effects of IL-24 delE-5 and mda-7/IL-2A were compared. Results The expression of IL-24 dciE5 was detected in differentiated U937 and HL-60 cells. Transfection with IL-24 delE5 significantly reduced tumor cell viability, inhibited colony formation. Comparing with the control, G_0/G_1 stage add from (24.46±3.99) % to (42.69±3.04) %, caused cell cycle arrest in G_0/G_1 stage and significantly inhibited the growth of K562 transplantation tumor. No significant differences in the aforementioned antileukemia characteristics between IL-24 delE5 and mda-7/IL-24 was found. Conclusion Similar with mda-7/IL-24, IL-24 delE5 can efficiently inhibit the proliferation of K562 in vitro and in vivo, probably through induction of G_0/G_1 cell cycle arrest.

Objective To explore the mechanism of the cell-cycle arrest induced by human melanoma differentiation associated gene-7 (mda-7/IL-24) in chronic myelocytic leukemia cell line K562. Methods Microarray analysis was performed to determine the genes that were differentially regulated by mda-7/IL-24 in K562 cells, and was validated by realtime PCR. The phosphorylated pRb were detected by Western blotting analysis. Results A microarray analysis showed that G_0/G_1 phase-associated genes p21~(WAF-1) and BCCIP were up-egulated, while cdk6 and Smurf2 were down-regulated. The directional change in the expression of the four genes was successfully validated with real-time quantitative RT-PCR. pRb Set~(795) phosphorylation was observed with no modification of the pRb protein level. Conclusion These results suggest that IL-24/mda-7 may inhibit K562 proliferation and induce G_0/G_1 cell cycle angst by up-regulating p21~(WAF-1) and BCCIP, down-regulating cdk6 and Smurf2.

Objective:To analyze the features and clinical significance of damages to non pulmonary organs like the heart,kidney and peripheral blood in SARS patients.Methods:SPSS 11.0 and SDAS software packages were used to retrospectively analyze the damages to the heart,kidney and peripheral blood in 330 clinically confirmed SARS cases.Results:(1)The heart damage occurred within 1 week after SARS onset in mild cases; the rates of LDH,HBDH,CK and CK MB returning to normal were 74.2%,80.6%,100% and 100%,respectively.In severe cases,the heart damage usually occurred 1 week after SARS onset; the rates of LDH,HBDH,CK and CK MB returning to normal were 32.2%,29.5%,55.2% and 44.4%,respectively.Ten patients whose CK MB didnot return to normal died.(2) The changes of RBC count appeared after an average of 1 week (1 10 d) in 54.2% of the patients.It returned to normal in all the mild SARS cases after an average of 12.5(4 21) d but didnot in 18.4% of the severe cases ( P

Objective To explore the effects of intestinal trefoil factor ( ITF) on gastric mucosal epithelial cell proliferation and its possible molecular mechanism . Methods The cultured GES-1 cells were treated with ITF in the concentration of 100 ng/mL and 500 ng/mL in vitro, and then were observed using microscope for the morphological analysis .The Cell Counting Kit-8 ( CCK-8) was used to detect the proliferation activity of GES-1.The cultured GES-1 cells were treated with 100 ng/mL ITF and the specific inhibitor of PI3K/Akt signaling pathway LY294002 (15μmol/L) in vitro, and then were observed using microscope for the morphological analysis . The proliferation activity of treated GES-1cells was detected using CCK-8 and the expressions of p-Akt and Akt of PI3K/Akt signaling pathway were determined by Western blot . Results Compared with the control group , the proliferation activity of GES-1 cells in-creased after being treated with ITF and the higher concentration of ITF induced the higher proliferation activity .LY294002 inhibited the increased proliferation activity of GES-1induced by ITF.The data of Western blot indicated that ITF induced the expression of p -Akt and activated the P3IK/Akt signaling pathway to modulate the proliferation activity of GES -1 cells.However, LY294002 inhibited the PI3K/Akt signaling pathway and then decreased the proliferation activity of GES -1 cells. Conclusion ITF could promote the proliferation ac-tivity of GES-1 cells by activating PI3K/Akt signaling pathway .