Objective To investigate the effect of propofol on the activation of NF-?B and the expression of Bcl-2 and Caspase-3 gene in cerebral cortex after transient focal cerebral ischemia-reperfusion (I/R) and the possible mechanism. Methods Ninety healthy male Wistar rats aged 3-4 months weighing 250-300g were randomly divided into 3 groups (n=30 each) : group Ⅰ sham operation; group Ⅱ I/R and group Ⅲ propofol + I/R. The animals were anesthetized with intraperitoneal chloral hydrate 300 mg?kg-1. Left common, internal and external carotid arteries (CCA, ICA, ECA) were exposed. Middle cerebral artery occlusion (MCAO) was produced by inserting a nylon thread, 0.26-0.28 mm in diameter and 4.0 cm in length into ICA and advancing it cranially until resistance was felt. After 2 h MCAO the nylon thread was withdrawn to allow reperfusion. In propofol group propofol 100 mg?kg-1 was given IP 10 min before MCAO. The animals were decapitated at 2, 3, 6, 12, 24 and 72 h of reperfusion (n=5 at each time point in each group) . Their brains were immediately removed for determination of translocation of NF-?B in the neurons (by immuno-histochemistry) and expression of NF-?B in cerebral cortex (by Western blotting). The expression of Bcl-2 mRNA and Caspase-3 mRNA in cerebral cortex was determined by in situ hybridization. Neurological deficit was scored and microscopic examination of ischemic cerebral cortex was performed at 24 h of reperfusion. Results In I/R group (Ⅱ) NF-?B was significantly translocated from cytoplasm into the nucleus of the neurons in the ischemic cerebral cortex during 2-24 h of reperfusion while in non-ischemic cortex NF-?B was confined to the cytoplasm. The expression of NF-?B, Bcl-2 mRNA and Caspase-3 mRNA was significantly higher in ischemic cortex than in non-ischemic cortex. Neurologic deficit scores were higher in I/R group than in sham-operation group. Microscopic examination showed congestion and edema of ischemic cerebral cortex and degeneration and necrosis of the neurons in I/R group. In group Ⅲ propofol pretreatment significantly inhibited the translocation of NF-?B, decreased expression of NF-?B and Caspase-3 mRNA and increased Bcl-2 mRNA expression as compared with I/R group (Ⅱ) . Neurologic dificit and histologic damage induced by I/R were significantly ameliorated by propofol pretreatment. Conclusion Propofol pretreatment can inhibit apoptosis of neurons induced by I/R by inhibiting the activation of NF-B, up-regulating Bcl-2 gene and down-regulating Caspase-3 gene.

Objective To investigate the analgesic effect of adenosine A1 receptor agonist R( - )-N6-(2-phenylisopropyl)-adenosine (R-PIA) administered into the brainstem medial pontine reticular formation (mPRF) and the underlying mechanism. Methods Sixty male SD rats aged 8-10 weeks weighing 250-300 g were used in this study. The animals were anesthetized with intraperitoneal 10% chloral hydrate 300 mg?kg-1 .A 24-gauge stainless steel cannula was inserted into mPRF on one side using a stereotaxic apparatus. One week after operation the animals were randomly divided into 12 groups ( n=5 each) : groupⅠcontrol; groupⅡR-PIA 0.5?g; groupⅢR-PIA 1.0?g; groupⅣR-PIA 2.0?g; groupⅤtheophylline (an adenosine receptor antagonist) 5.0?g; groupⅥ8-cyclopentyl-1 ,3-dipropylxanthine (DPCPX, an adenosine A, receptor antagonist) 1.0?g; groupⅦglibenclamide (an ATP-sensitive K+ channel blocker) 5.0?g; groupⅧ4-aminopyridine (4-AP, a voltage dependent K+-channel blocker) 5.0?g; groupⅨtheophylline 5.0?g + R-PIA 2.0?g; groupⅩDPCPX 1.0?g + R-PIA 2.0?g; groupⅪglibenclamide 5.0?g + R-PIA 2.0?g and groupⅫ4-AP 5.0?g + R-PIA 2.0?g. All the drugs were injected into mPRF in 0.3?l of normal saline. In groupⅨ-ⅫR-PIA 2.0?g was administered 15 min after pretreatment with theophylline, DPCPX, glibenclamide or 4-AP. Analgesia was determined using the tailflick latency (TFL) (the time between the onset of the radiant heat stimulus and voluntary tail withdrawal) at 5, 15, 30, 45, 60 and 90 min after R-PIA injection into mPRF. The pain threshold was expressed as percentage of the maximal possible effect ( MPE) : MPE = (TFL after drug - baseline TFL)/( 10.0 -baseline TFL)?100% .Results R-PIA 0.5-2.0?g injected into mPRF produced significant analgesia in a dose-dependent manner. Pretreatment with theophylline or DPCPX completely reversed the analgesic effect of R-PIA while pretreatment with glibenclamide or 4-AP only partially reversed the analgesic effect of R-PIA.Conclusion R-PIA administered into mPRF produces analgesia through activation of both ATP-sensitive and voltage-dependent K+ -channel in mPRF.

Objective To investigate the effect of ketamine on the synaptic long-term potentiation(LTP) in the CA1 area of rat hippocampal slices,and to elucidate the mechanisms underlying the effect of ketamine on memory.Methods Hippocampal slices(400 ?m thick) were obtained from the brains of male Sprague-Dawley rats(2 months old) weighing 200-250 g that were decapitated.The slices were incubated in artificial cerebrospinal fluid(ACSF) at room temperature for at least 120 min before use.Forty-nine slices were randomly divided into 7 groups(n=7):control group,ketamine 1,5,10,30,50 and 100 ?mol?L-1 groups.All the slices in each group were perfused with ACSF,ketamine 1,5,10,30,50 or 100 ?mol?L-1,respectively.The slices in each group were performed to record evoked population spikes(PS) using extracellular microelectrode recording technique.Another forty-nine slices were randomly divided into 7 groups(n=7):LTP group,ketamine-LTP 1,5,10,30,50 and 100 ?mol?L-1 groups.All the slices in each group were perfused with ACSF,ketamine 1,5,10,30,50 or 100 ?mol?L-1,respectively.PSs were recorded for at least 30 min before LTP in each group.For LTP induction,high-frequency stimulation(HFS) conditioning pulses(100 Hz?s-1) were applied to the Schaffer collateral-commissural pathway of hippocampus using a bipolar stimulating electrode.The changes in PS amplitude after HFS were analyzed in each group.Results The PS amplitude of the rat hippocampal slices in ketamine 1,5,and 10 ?mol?L-1 groups had no significant difference compared with control group.The PS amplitude in ketamine 30,50 and 100 ?mol?L-1 groups decreased compared with control group(P

0.05),but it was significantly lower than that in LTP group (P

ObjectiveTo observe the effect of urethral stent implantation on detrusor-sphincter dyssynergia caused by neurogenic lower urinary tract dysfunction.Methods13 patients with detrusor-sphincter dyssynergia caused by neurogenic lower urinary tract dysfunction were treated with the operation of the urethral stent implantation. Voiding function, renal function, residual urine volume and hytronephrosis were examined before and after the operation to evaluate the effect of this procedure.ResultsAfter operation, 7 patients normally emptied their bladders and 6 patients had urinary incontinence. Urethral stents were removed from 2 patients in this group due to the irritation symptoms, the second implantation was performed in a patient due to the voiding difficulty. The renal function of patients after the operation had a non-significant improvement, but the residual urine volume and hytronephrosis improved significantly.Conclusion Urethral stent implantation can decrease residual urine volume and hytronephrosis in patients with detrusor-sphincter dyssynergia caused by neurogenic lower urinary tract dysfunction.

目的探讨系统功能训练对老年人工全膝关节置换(TKR)术后康复的效果观察。方法接受TKR老年患者21例36膝,入院后随机分A、B两组,A组实施系统功能训练,B组采用骨科常规护理。采用美国特种外科医院(HSS)膝关节评分标准在术前及术后3周末对A、B两组进行膝关节评分。结果两组患者TKR术后膝关节评分有显著差异(P<0.05)。结论系统功能训练有利于促进老年TKR术后康复。

Objective To investigate the time-dependent changes in glutamate (Glu) and 7-aminobutyric acid ( GABA) release in the rostral ventromedial medulla in a rat model of incisional pain. Methods Healthy male SD rats weighing 250-300 g were used in this study. Twelve rats in which microdialysis cannulae were implanted in the right rostral ventromedial medulla without neurological deficits were randomly divided into 2 groups ( n = 6 each): group A control and group B incisional pain. In group B an 1 cm long incision was made in the plantar surface of right hindpaw under 1.2% isoflurane anesthesia which was maintained for 5 min. Samples of dialysate were collected before incision (T_0 baseline) and at 3 h, 1 d, 2 d and 3 d after incision was made (T_(1-4)) in both groups for determination of Clu and GABA concentrations (by HPLC). Results In group B Glu and GABA concentrations in the dialysate were significantly increased at 1 d (T_2) and 3 h-3 d (T_(1-4)) respectively as compared with the baseline value at T_0 and were significantly higher than those in group A (control group). Conclusion Incisional pain increases the release of Glu and GABA in the rostral ventromedial medulla which might influence the function of descending pain modulation pathway.

cells, the expression of PTEN was up-regulated while pAkt down-regulated. Conclusions AS-miR-221 and AS-miR-222 may enhance the radiosensitivity of MCF-7 breast cancer cells by up-regulating the expression of PTEN.

Objective To investigate the effect of isoflurane on the levels of protein kinase A (PKA) and protein kinase C (PKC) in hippocampus in rats. Methods Thirty-six 3-month-old male SD rats weighing 180-220 g were randomly divided into 3 groups ( n = 12 each): group Ⅰ underwent the cognitive function test without being pretreated with isoflurane inhalation (group C); group Ⅱ and Ⅲ inhaled 1.2% isoflurane for 4 h and underwent the cognitive function test 2 days and 2 weeks later respectively (group Ⅰso1,Iso2). Morris water maze was used to assess the cognitive function and the escape latency was recorded. The animals were killed immediately after the test.The hippocampus was isolated for determination of the expression and activities of PKA and PKC.Results The escape latency was significantly longer in group Ⅲ than in group Ⅰ.The expression of PKA and PKC was significantly down-regulated and the activities of PKA and PKC were significantly decreased in group Ⅱand Ⅲ as compared with group Ⅰ . There was no significant difference in the expression and activities of PKA and PKC between group Ⅱ and Ⅲ . Conclusion Four hour 1.2% isoflurane inhalation can decrease cognitive function by inhibiting the levels of PKA and PKC in hippocampus.