Objective:To investigate the effects ofbody mass index on duration of non-hypoxic apnoea during induction and intubation of anesthesia.Methods:80 patients undergoing surgery with general anaesthesia aged 21～63 years old with ASA Ⅰ-Ⅱgrade and without special diseases were included.they were assigned to one of four groups according to body mass index:Group 1(normal,n=20),Group 2 (overweight,n=20),Group 3(Ⅰ? obesity,n=20)and Group 4(Ⅱ?obesity,n=20).Preoxygenation was achieved with an oxygen flowof10 litre/min within 4 minutes.After rapid sequence induction of anaesthesia,the trachea was intubated and the patient was left apneic with disconnected from the anaesthesia circuit until SpO2 decreased to 90%.The time taken for desaturation to 90%from the end of induction of anaesthesia was recorded.Arterial blood samples were drawn when patients to enter the operating room and the end of induction of anaesthesia and SpO2 decreased to 90%respectively for arterial blood ga(sABG)analysis.Results:Desaturation safety period(the time to desaturation to 90%)were significantly differences between four groups with different body mass index(P

OBJECTIVE To investigate and analyze the kinetics of serological marks and virus load of the follow-up blood donors. METHODS The quantitation of HBV DNA of 6 HBsAg negative and DNA positive blood donors was detected by Roche PCR Monitor,and the donors were genotyped and traced by serological tests. RESULTS(Three of 6 follow-up) donor samples were seroconverted after more than 40 days follow-up study.The viral loads were with range of(35-1.8)?10~4 copies/ml,1 of 6 donors had acute infection,the peak load was(1.8?10~4 copies/ml),3 of 6 were with lower level HBV carrier with fluctuating viral load ranged 100-500 copies/ml.One donor had decreasing viral load,when HBsAg converted to positive,virus wasn′t detected.The last one had fluctuating virus load below(100 copies/ml),intermittently falling below the threshold of the assay. CONCLUSIONS It is necessary to implement HBV DNA detection for blood screening,and further strengthen the safety of blood transfusion.

Objective To observe the therapeutic effect of folic acid on transient ischemic attack(TIA)patients with homocysteinaemia (Hcy ). Methods 129 patients of primary TIA with Hcy were divided into two groups randomly. The observation group ( n = 65 )was administered with conventional therapy and folic acid, and the control group ( n=64 ) was only given conventional therapy. The variances of the plasma HCA level three months later were compared, and remission rate of TIA and complete stroke incidence one year later were analyzed between two groups. Results The Hcy incidence rate of TIA patients was up to 41.4%. Three months later, the plasma HCA level of observation group was lower than control group( ( 14.27 ± 6. 13 ) μmol/L vs (24.99 ± 6.87 )μmol/L, t=2.799, P＜0. 01 ) ,and much lower than that of the control group post-treatment ( ( 14. 27 ±6. 13)μmol/L vs (24.68 ± 6.89) μmol/L, t = 2.735, P ＜ 0.01 ). One year later, the complete stroke incidence of TIA in observation group was lower than that of the control group(9.8% vs 25.0%, P＜0.05 ) ,and complete remission rate was higher than the latter(73.8% vs 50.0%, P ＜ 0. 01 ). Conclusion Folic acid can decrease the plasma HCA level of TIA patients with Hcy efficiently,and improve the prognosis of such patients.

Objective To investigate the risk factors for cerebral microbleeds (CMBs) and its correlation with the 24 h microalbuminuria (mALB) in patients with small artery occlusion (SAO).Methods The patients with SAO were enrolled.CMBs were detected with susceptibility-weighted imaging.The demographic and clinical characteristics and 24 h mALB of the patients were compared.Multivariate logistic regression analysis was used to identify the independent risk factors for CMB in patients with SAO.Spearman correlation analysis was used to investigate the correlation between the 24 h mALB and the degree of CMBs.Results A total of 90 patients with SAO were enrolled and 35 patients (38.89％) had CMBs.CMBs mainly distributed in basal ganglia/thalamus and infratentorial (62％) regions.The Age (70.8 ± 5.4 vs.67.3 ± 8.1; t =2.461,P =0.016),proportion of hypertension (80.0％ vs.52.7％ ;x2 =6.851,P =0.009),and 24 h mALB levels (16.257 ± 6.031 mg/24 h vs.11.910 ±5.458 mg/24 h; t =3.536,P =0.001) in the CBM group were significantly higher than those in the non-CMB group.Spearman rank correlation analysis showed that the 24 h mALB and the severity of CMB in patients with SAO showed a significant positive correlation (rs =0.795,P =0.000).The higher the 24 h mALB level was,the more severe the CMB degree would be.Multivariate logistic regression analysis showed that only 24 h mALB was the only independent risk factor for CMBs in patients with SAO (odds ratio,1.100,95％ confidence interval 1.031-1.176; P =0.002).Conclusions The 24 h mALB is an independent risk factor for CMB in patients with SAO.The 24 h mALB level is positively correlated with the severity of CMB,and it may be used as a marker for small vascular injury.

Objective To evaluate the effect of advanced age on sepsis-caused heterogeneity of nicotinic acetylcholine receptors (nAChR) in the cytomembrane of skeleton muscle in rats.Methods Twenty SPF adult rats (aged 4-5 months,weighing 250-280 g) and 20 aged male Sprague-Dawley rats (aged 18-20 months,weighing 550-600 g),were obtained from the Experimental Animal Centre of Chongqing Medical University.The adult rats were randomly divided into control group (CAd group,n =10) and sepsis group (SAd group,n =10).The aged rats were randomly divided into control group (CAg group,n =10) and sepsis group (SAg group,n =10).Sepsis was produced by cecal ligation and puncture.The specimens of anterior tibial muscle were obtained at 24 h after operation for determination of the expression of neuronal nAChR (α7-nAChR) and fetal nAChR (γ-nAChR) using immunohistochemistry and Western blot.Results The expression of γ-nAChR and α7-nAChR in the cytomembrane of anterior tibial muscle was significantly higher in CAg and SAd groups than in CAd group,and in SAg group than in CAg and SAd groups.Conclusion Advanced age can aggravate sepsis-induced heterogeneity of nAChR in the cytomembrane of skeleton muscle in rats.

We introduced the tutorial system in anesthesiology resident standardization training plan and management,and through the strict tutor qualification,strengthening tutor training mechanism,carrying out the tutor assessment mechanism and the cultivation of residents' comprehensive ability for medical treatment,scientific research and teaching,we improved the comprehensive quality of anesthesia resident physicians and the training quality.

Objective To investigate the effects of ketamine combined with electroconvulsive shock (ECS) on inflammation and amyloid-beta peptide in hippocampus of depressive rats.Methods Chronic unpredictable mild stress (CUMS) was used to generate animal models of depression.Forty-eight adult male Sprague-Dawley rats were randomly divided into 4 groups (n=12):depression model group (group D),electroconvulsive shock group (group DE),ketamine combined with electroconvulsive shock group (group DKE),and ketamine group (group DK).Rats in group D received sham ECS treatment;rats in group DE received ECS treatment;rats in group DKE were given intraper-itoneal injection of ketamine (100 mg/kg) and then received ECS treatment;rats in group DK were given intraperitoneal injection of ketamine (100 mg/kg) and then received sham ECS treatment.Morris water maze was used to assess the memory abilities of rats.The expression levels of IL-1β and TNF-α were measured by real-time PCR.Enzyme-linked immunosorbent assays were used to detect the levels of soluble Aβ.Results Before the administration of ECS or ketamine treatment,there was no significant difference in the escape latencies and space exploration time between the 4 groups (P>0.05).After the ECS and ketamine treatment,rats of group DKE exhibited a shorter escape latencies and a longer space exploration time,and the expression of IL-1β and TNF-α mRNA were down-regulated while the concentration of Aβ1-40 and Aβ1-42 were increased compared with group DE with significant difference (P<0.05).Conclusion Ketamine can alleviate ECS-induced learning and memory impairments in depressive rats.This cognition-protecting effect of ketamine may be attributed to its suppression of ECS-induced neuroinflammation and decrease of the levels of soluble Aβ in the hippocampus of depressive rats.

Aim To investigate the anti-apoptotic effect of NGF on H9 c2 cardiac myocytes in a hypoxia / reox-ygenation injury model and its mechanism. Methods The H9 c2 cardiac myocytes were randomly divided into five groups:control group ( C group) , hypoxia/reoxy-genation group ( H/R group) , NGF group ( N group) , NGF+LY294002 group ( N+L group) and LY294002 group( L group) . Each group received the correspond-ing treatment. Cell survival rate was tested by cell counter kit-8 methods. Apoptotic rate was evaluated by propidium iodide ( PI ) staining and flow cytometry (FCM). The levels of Caspase-12, p-Akt/Akt were e-valuated by Western blot. Results The NGF group could significantly protect the H9 c2 cardiac myocytes under the hypoxia / reoxygenation injury with increased cell survival rate. It also decreased the apoptotic per-centage, upregulated the level of p-Akt/Akt and inhib-ited the expression of Caspase-12 . As the specific in-hibitor of PI3k receptor, LY294002 decreased the level of p-Akt. Conclusion NGF has the effect of anti-ap-optosis on H9 c2 cardiac myocytes exposed to hypoxia /reoxygenation injury via PI3k-Akt signal pathway.

Objective To evaluate the effect of electroconvulsive therapy (ECT) on the expression of phosphorylated glutamate receptor 1 (p-GluR1) and Ca2+/calmodulin-dependent protein kinase Ⅱ α (p-CaMK Ⅱ α) under small dose ketamine combined with propofol anesthesia in the depressed rats.Methods Forty healthy adult male Sprague-Dawley rats,weighing 200-250 g,aged 2-3 months,were used in this study.Mental depression was induced by exposing the animals to chronic unpredictable mild stress (CUMS).Forty mentally depressed rats were divided randomly into 5 groups (n =8 each) using a random number table:M0-4 groups.Propofol 80 mg/kg and ketamine 10 mg/kg were injected intraperitoneally in M0-4 groups.After disappearance of righting reflex,M1-4 groups received ECT of 60,120,180 and 240 mC once a day for 7 consecutive days,respectively,by means of a current (frequency 50 Hz,sine-wave,pulse width 0.7 ms,1-s duration) delivered via ear-clip electrodes,while group M0 received ECT of no quantity of electric charge via ear-clip electrodes.Before CUMS,at 1 day after CUMS and at 1 day after ECT,sucrose preference test was applied to evaluate the depressive behavior.The sucrose preference percentage (SPP) was calculated.At 4 days after CUMS and 4 days after ECT,the learning and memory function was assessed using Morris water maze test.The rats were then sacrificed,and hippocampi were isolated to detect the expression of GluR1,p-GluRl,CaMK Ⅱ α and p-CaMK Ⅱ α by Western blot.Results The SPP was significantly lower after CUMS than before CUMS in M0-4 groups (P＜0.05).Compared with that after CUMS,the SPP was significantly increased,the escape latency was shortened,and the space exploration time was prolonged after ECT in M1-4 groups (P＜0.05).There was no significant difference in SPP after ECT between M1-4 groups (P＞0.05).Compared with group M0,the SPP was significantly increased,and the expression of pGluR1 and p-CaMK Ⅱ α was up-regulated in M1-4groups (P＜0.05).Compared with group M2,the escape latency was significantly prolonged,the space exploration time was shortened,and the expression of pGluR1 and p-CaMK Ⅱ α was down-regulated after ECT in the other groups (P＜0.05).There was no significant difference in GluR1 and CaMK Ⅱ α expression after ECT between the five groups (P＞ 0.05).Conclusion ECT can induce cognitive decline when applied for anti-depression under small dose ketamine combined with propofol anesthesia,and the mechanism is related to increased phosphorylation of GluR1 and CaMK Ⅱ α expression in rats.

Objective To explore the effect of low-dose ketamine combined with propofol anesthesia on expres?sion of glutamine receptor subunit 1 (GluR1) and 2 (GluR2) in the hippocampus of depressed rats after electroconvulsive therapy. Methods Healthy adult male Sprague-Dawley rats, weighing 200~250 g, were used in this study. Mental depres?sion was induced by chronic unpredictable mild stress. Thirty-two depressed rats were randomly divided into 4 groups (n=8): metal depression group (group A), ECT group (group B), ECT+propofol group (group C) and ECT+propofol+ket?amine group (group D). Eight normal rats served as control group. Control group received no treatment. Group A received intraperitoneal injection of normal saline 8 mL/kg plus sham ECT. Group B, C and D received ECT once a day for 7 con?secutive days following intraperitoneal injection of normal saline 8 mL/kg, propofol 80 mg/kg and propofol 80 mg/kg +ketamine 10mg/kg, respectively. Sucrose preference test and Morris water maze were performed to assess depressed be?havior and learning and memory function, respectively. RT-PCR and Western-blot assay were used to detect the expres?sion of GluR1 , GluR2 and their mRNA expression. Results After ECT, compared with control group and group A, changes of SPP in group B, C and D were obvious. The change of SPP in group D was much higher than all other groups (P<0.05). Rats in group B showed prolonged escape latency and shortened space exploration time, which were significantly different from all other groups (P<0.05). Rats in group D showed the most shortened escape latency and prolonged space exploration time (P<0.05). The expression of GluR1 was significantly increased in group B, C and D compared with group A (P<0.05). The expression of GluR2 and mRNA was significantly decreased in group B and C (P<0.05). The difference in GluR2 and mRNA expression was not significant among group A, D and control group (P>0.05). Conclusion Low-dose ketamine combined with propofol anesthesia exert effective antidepressive action and improve learning and memory function of depressed rats after electroconvulsive therapy. The beneficial effects of the ketamine combined with propofol anesthesia may be related to up-regulation expression of GluR1 and GluR2 in hippocampus.