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 After 2 h MCAO the nylon thread was withdrawn to allow reperfusion.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.

Cognition ; Cognition Disorders ; Humans ; Manganese ; Occupational Exposure

Medical genetics is one of the important basic courses in medical education. The teaching reform in course content, teaching method and experimental teaching was carried out to arouse their enthusiasm in study, cultivate their capabilities of analyzing of medical practice problem.

Angioplasty, Balloon, Coronary ; Coronary Artery Disease ; therapy ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; therapy ; Stents ; Vascular Malformations ; therapy

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

Objective To assess the effect and influencing factors on 131I treatment for cervical lymph node metastasis (LNM) after operation in patients with PTC.Methods PTC patients (n =117;45 males,72 females;average age (45.17± 15.50) years) with postoperative cervical LNM from January 2010 to December 2014 were analyzed retrospectively.LNM was diagnosed by surgical pathology,imaging results and clinical follow-up.Single factor analysis was performed in age,gender,operation mode,TNM stage,131I treatment time and other factors.The results for 131I treatment effect included CR,PR,NC.Two-sample t test and x2 test were used.Results Among the 117 PTC patients with postoperative LNM,53 (45.3％) cases had non-131 I-avid metastasis.Fifty of the 64 (54.7％) patients with 131I-avid metastasis were treated with 131I.Nineteen patients (38.0％) achieved CR,22 (44.0％) achieved PR,and 9 (18.0％) showed invalid results.Fourteen of the 64 patients underwent another cervical lymph node dissection.Nine patients achieved CR,5 patients achieved PR,and 4 PR patients were then treated with 131I and finally achieved CR.Single factor analysis showed that the influencing factors of non-131I-avid lymph node included patients' age (t =3.459),serum Tg level (x2 =6.698) and metastasis with 1s F-FDG uptake (x2 =26.928;all P＜0.05).The influencing factors of 131I treatment effect included lymph node dissection procedure (x2 =6.487),unilateral or bilateral lesion (x2=5.187) and LNM size (x2=8.099;all P＜0.05).Conclusions 131I treatment is ineffective for nearly 50％ of patients with non-131I-avid LNM.The influencing factors of 131I treatment effect include the lymph node dissection procedure,unilateral or bilateral lesions and LNM size.

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

The study is aimed to distinguish morphological characteristics of Dalbergiae Lignum collected from crude drug's markets and establish a identification methods and the quality standard for Dalbergiae Lignum. The macroscopic and microscopic features of Dalbergiae Lignum from crude drug's market were observed, analyzed and compared according to Hongmu specification issued by the People's Republic of China in 2000, and by the characteristics recorded in domestic monograph of Mucai Shibie (wood identification). The redwood of Dalbergiae Lignum cut into small pieces as medicinal material are dry heart wood of mahogany (trees from Dalbergia sp.), which characteristics of the small pieces as crude drug are different. There are differences in macroscopic and microscopic features about texture of wood and color, odor, taste, transverse section, radial section, tangential section. The results can provide basis for identification, application and improment of the quality standard of Dalbergiae Lignum as medicinal material.
China ; Dalbergia ; anatomy & histology ; chemistry ; classification ; Herbal Medicine ; economics ; Plants, Medicinal ; chemistry ; classification ; Quality Control ; Xylem ; anatomy & histology ; chemistry

Objective To evaluate the role of alpha4 beta2 neuronal nicotinic acetylcholine receptor in the inhibition of synaptic long-term potentiation (LTP) by isoflurane in the CA1 area of rat hippocampal slices.Methods Hippocampal slices (400 μm thick) were prepared from the brains of adult male SD rats, 2 months old, weighing 200-250 g, anesthetized with ether and decapitated. The slices were incubated in artificial cerebrospinal fluid (aCSF) at room temperature for at least 2 h before use. Seventy slices were randomly divided into 10 groups ( n = 7 each): Ⅰ LTP group in which the slices were perfused with aCSF; Ⅱ , Ⅲ and Ⅳ group in which the slices were perfused with aCSF containing isoflurane 0.125, 0.25 and 0.5 mmol/L respectively (group Ⅰ1-3 );Ⅴ and Ⅵ group in which the slices were perfused with aCSF containing epibatidine 0.1 and 1.0 μmol/L respectively (group E1.2 ); Ⅶ group epibatidine 0.1 μmol/L + isoflurane 0.25 mmol/L (group E1 + I2 ); Ⅷgroup epibatidine 1.0 μmol/L + isoflurane 0.25 mmol/L (group E2 + I2); Ⅸ group DHβE 0.1 μmol/L (group D); Ⅹ group DHβE 0.1 μmol/L + isoflurane 0.125 mmol/L (group D + I1 ). Population spikes (PS) were recorded for at least 30 min before LTP in each group. For LTP induction, high-frequency stimulation (HFS) was applied to the Schaffer collateral-commissural pathway of hippocampus and maintained for 15 min using a stimulating electrode.The changes in PS amplitude were analyzed at 5, 10, 15, 20, 25, 30, 40, 50 and 60 min after HFS in each group. Results Compared with group LTP, the PS amplitude was significantly decreased after HFS in group I1 ,I2, I3 , D, D + I1 and E1 + I2 ( P ＜ 0.05), while increased after HFS in group E1 .2 ( P ＜ 0.05 ), but no significant change was found after HFS in group E2 + I2 ( P ＞ 0.05). The PS amplitude was significantly decreased after HFS in group D + I1 compared with group I1 (P ＜ 0.05). The PS amplitude was significantly increased after HFS in group E1 + I2 and F2 + I2 compared with group I2 ( P ＜ 0.01 ). Conclusion Isoflurane inhibits LTP induction via inhibiting the activation of alpha4 beta2 nicotinic acetylcholine receptor in rat hippocampus.