Objective To investigate the effects of acute nicotine exposure on expression of Caspase-3 and apoptosis of neuron in adolescent rat's brain. Methods The Caspase-3 expression was detected with immunohistochemistry and Western blotting. Apoptosis cells were detected by TUNEL method. Results The Caspase-3 expression in cerebral cortex, hippocampal dentate gyrus, CA2 and CA3 of the experimental group was higher than that of the control group through immunohistiochemistry. The expression of Caspase-3 prototype and active fragments in cerebral cortex and hippocampus of the experimental group was higher than that of the control group with Western blotting. The TUNEL positive cells in cerebral cortex and hippocampal dentate gyrus of the experimental group were more than that of the control group.Conclusion Acute nicotine exposure can activate Caspase-3 and increase neuron apoptosis in cerebral cortex and hippocampal dentate gyrus of the adolescent rat's brain.

Objective To study the visual attention of mild cognitive impairment patients (MCI)by eyes movement training. Meathods 48 mild cognitive impairment patients were divided into eye movement training group,finger training group and untreated control group by single-blind randomized block method. Then they were trained respectively three months. Event-related potentials (ERPs) were used to measure the face recognition of them before and after training. The amplitude and latency of P3b elicited by target stimuli and P3a elicited by new stimuli of the three said groups were compared and contrasted. Results After training,the amplitude of P1 elicted by novelty stimulus were larger in eye movement training group( (6.78 ± 1.55 ) μV) and in finger training group ( ( 5.43 ± 1.47 ) μV) than untreated control group ( ( 3.09 ± 0.98 ) μV) significantly, especially in the frontal area. The amplitude of P1 elicted by target stimulus were larger in eye movement training group( (6.75 ±2.01 ) μV)than in finger training group( (4.12 ± 1.33 )μV)and untreated control group( (3.45 ± 1.01 )μV)significantly, especially in the frontal area. The amplitude of P3a were larger in eye movement training group( ( 10. 19 ± 3.09)μV ) than in finger training group ( ( 7.57 ± 2.66 ) μV ) and untreated control group ( ( 6.06 ± 2.03 ) μV ) (P ＜ 0.05,P＜0.05) significantly,especially in the frontal area. The latency of P3a were earlier in eye movement training group( (390.67 ±55.03 ) ms) compared to finger training group( (428.55 ± 48.68 ) ms) and untreated control group( (435.89 ± 59.21 )ms)significantly, especially in the frontal region and central parietal area. Conclusion Eyes movement can improve the MCI patients' non-selective attention function, especially in frontal area.The finger execrises have no significant effect on visual attention.

Objective To explore the effect of nicotine on the degeneration of dopaminergic neurons in PD rats. Methods Forty-five SD rats were randomly divided into three groups: PBS group (CON), normal saline + LPS ( NS ) group and nicotine +LPS ( NIC ) group. On 24 hours after LPS or PBS injection, inducible nitric oxide synthase ( iNOS ) protein expression was examined by immunoblotting. ON 14d after LPS or PBS injection, the numbers of tyrosine hydroxylase ( TH ) positive neurons and morphological changes of OX-42 positive cells in the substantia nigra(SN) were observed by immunohistochemistry. TH mRNA and TH protein expressions were examined by RT-PCR or immunoblotting. Results Compared with CON group, iNOS protein increased markedly 24 hours after LPS injection in NS group. TH positive neurons, TH mRNA and TH protein in the SN decreased remarkably 14 days after nigrainjiection. Most of microlglial showed big cell body with thicker and shorter processes. However, nicotine reversed the above changes, Compared with NS group, TH positive neurons, TH mRNA and TH protein in the SN increased remarkably in NIC. Besides, most microglia showed small cell body with slim and long processes. Conclusion Nicotine could prevent LPS-induced degeneration of DA neurons, probably because of that the pretreatment with nicotine blocks the activation of microglia and the expression iNOS protein.

Objective To study early face processing of mild cognitive impairment patients by using ERP method．Methods Sixteen healthy old man(normal group)and sixteen mild cognitive impairment patients(MCI group)served as subjects in experiment．Two runs of 300 stimuli(duration：50ms)of 3 facial and 3 non-facial pictures were randomly presented with equal probability(ISI：from 1000ms to 1500ms randomly)，and the subjects were asked to react to facial stimuli and non-facial stimuli by pressing the left button and risht button respectively as quickly as possible．Thirty-two channels electroencephalogram(EEG)Was recorded by Neuroscan Nuamps Systern．Results 1)Specific-face component N170 was found in both groups．Which was distributed at the temporal-occipital region．2)Compared with N170 in normal group，N170 amplitude Was significantly lower((-4．42±0．28)Μv vs(-7．00±0．28)Μv，F=41．52，P<0．01)at temporal-occipital region and delayed((158．91±2．17)ms vs(140．97±2．17)ms，F=34．09，P<0．01) in mild cognitive impairment group．Conclusion The early face processing mechanism of mild cognitive impairment patients may be different from normal people．

ObjectiveTo explore the influence of mental abacus calculation (MAC) training on children's form recognition.Methods 28 children ( 14 children with MAC training and 14 children with non-MAC traning)were investigated by using event-related potential(ERP) technology.The event-related potentials were recorded when subjects were in the different form shape recognition.Results ( 1 ) The amplitudes of the posterior P1 evoked by the children with MAC training ( (9.59 ± 3.58) μV) were significantly greater than that of the children without MAC training ( (7.06 ± 2.84) μV) ( P ＜ 0.05 ).(2) The amplitudes of right temporal-posterior N170 of children with MAC( ( -9.83 ±2.97) μV) were markedly less than that of children with non-MAC( ( - 12.45 ±2.51 ) μV) ( P ＜ 0.05 ).( 3 ) The amplitudes of prefrontal P3 of children with MAC ( (7.65 ± 2.25 ) μV) were remarkably greater than that of children with non-MAC ( (4.89 ± 3.35 ) μV) ( P ＜ 0.05 ).ConclusionThe brain function of form recognition in children is influenced by mental abacus calculation training.

Objective To observe the effect of nicotine(NIC) on the activation and resultant death of microglia induced by LPS. Methods The animal model that exposed to chronic nicotine treatment was established and LPS was injected intraperitoneally to induce the activation of microglia. Furthermore, the CD11b-positive microglia in cerebral cortex, hippocampal and substantia ngra were observed through immunohistochemical staining. BV2 cells(Microglial cell line of mouse) were subcultured, simultaneously the following kits were used including CCK-8 kit assay for cell activity, Nitric oxide assay kit assay for NO release, RT-PCR assay for the iNOS,TNF-α,IL-1β,IL-6,COX-2,IRF-1,Caspase-11 mRNA expression, Western blotting assay for the protein expression of P-I-κB and Caspase-3. Results Nicotine suppressed the CD11b-positive microglia expression in cerebral cortex,hippocampal and substantia ngra induced by LPS;Nicotine inhibited the activation-induced cell death (AICD), attenuated NO release, reduced iNOS,TNF-α,IL-1β,IL-6,COX-2,IRF-1,Caspase-11 mRNA expression, decreased the protein expression including P-I-κB and Caspase-3 of BV2 cells. Conclusion Nicotine pretreatment can suppress the activation and resultant death of microglial cells induced by LPS, which suggests that nicotine may play a neuroprotective role on inflammatory reaction of brain.;

Objective To investigate the radioprotective function and its mechanism of Sulforaphane (SF) in mice acute radiation-induced lung injury.Methods Totally 40 female C57BL/6J mice were equally divided into 5 groups randomly.Group A,treated by SF 3 mg/kg plus radiation;group B,treated by SF 5 mg/kg plus radiation;group C,treated by SF 10 mg/kg plus radiation;radiation group with a single dose of 12 Gy in 6 MV X-ray by a linear accelerator,and control group with sham radiation.The mice in drug group were administered intraperitoneally with different concentration of SF every other day from 7 d before irradiation to 7 d after irradiation,while the same volume of DMSO plus physiological saline solvent was given in the control and radiation groups.After being sacrificed at 14 d of SF administration,the pathomorphological changes of mice were observed in trauma lung tissue,the positioning and expression of NLRP3 was observed by immunohistochemical staining,the levels of IL-6,TNF-α and TGF-β1 in bronchoalveolar lavage fluid (BALF) were measured by ELISA,the expressions of NLRP3 and IL-1β mRNA in lung tissue were assayed by qRT-PCR,the expressions of NF-κB p65,NLRP3 and IL-1β proteins in lung tissue were assayed by Western blot,the activity of NF-κB was detected by EMSA.Results In comparison with radiation group,there was an obvious amelioration in pathological injury of lung tissue in the treatment groups:the expression of NLRP3 in lung tissue decreased;the concentration of NLRP3 in the drug intervention group (SF 10 mg / kg) markedly decreased (F =42.750,P ＜ 0.05).the IL-6,TNF-a and TGF-β1 levels in BALF decreased (tIL-6 =-62.65-21.00;tTNF-α =-32.18-16.57;tTGF-β1 =-58.22-46.11,P ＜ 0.05);the expressions of NLRP3 and IL-1β mRNA markedly decreased (tNLRP3 =-6.56-5.68;tIL-1β =-29.75--21.20,P ＜ 0.05),and the expressions of NF-κB p65,NLRP3 and IL-1β proteins decreased (tNF-κB p65 =-34.00--1.71,tNLRP3 =-25.01--16.91,tIL-1β =-73.70--55.14,P ＜ 0.05);the relative expressions of NF-κB p65 and NLRP3 were reduced in a dose-dependent manner (r =0.945,0.926);and the activity of NF-κB were obviously reduced (tNF-κB =-38.68,-614.82,-2 831.40,P ＜ 0.05).Conclusions Sulforaphane effectively alleviates the RILI in lung of mice by downregulating the expressions of inflammatory factor NLRP3.

Objective:To explore diagnostic value of soluble tumor necrosis factor - like weak inducer of apoptosis (sTWEAK) and interleukin (IL) -6 concentrations in patients with acute coronary syndrome (ACS) .Methods:A total of 170 ACS patients hospitalized in our hospital from Jan 1st ,2014 to Jun 31st ,2014 were selected as ACS group ,mean‐while ,80 inpatients with stable angina pectoris (SAP) confirmed by coronary angiography (CAG) or coronary CT were se‐lected as SAP group ,and another 80 patients excluded for coronary heart disease (CHD) by CAG were regarded as normal control group .ACS group was further divided into ST elevation myocardial infarction (STEMI) group (n=45) ,non -STEMI (NSTEMI) group (n=52) and unstable angina pectoris (UAP) group (n=73) .Plasma sTWEAK and serum IL‐6 concentrations were compared among all groups .Results:Compared with normal control group and SAP group ,there were significant rise in concentrations of plasma sTWEAK [ (120.32 ± 10.15) ng/L vs .(123.86 ± 15.23) ng/L vs .(140.05 ± 17.51) ng/L] and serum IL‐6 [ (110.34 ± 26.01) pg/ml vs .(112.38 ± 25.74) pg/ml vs .(245.23 ± 68.58) pg/ml] (P<0.01 all) ,but there were no significant difference between normal control group and SAP group , P>0.05. There were no significant difference in plasma sTWEAK and serum IL‐6 concentrations among UAP group ,NSTEMI group and STEMI group , P>0.05 all .Conclusion:Plasma sTWEAK and serum IL‐6 concentrations significantly rise in ACS patients ,which possesses certain diagnostic value for ACS .

It had some advantages when microwave induced hyperthermia were used to treat inferior femora and superior shinbone tumor.The device of circulation water,which could induce hypothermia during the treatment procedure needed to be used.Large amount of normal saline at the room temperature was perfused through this device,so the temperature of surrounding normal tissues and organs was reducd and the functions of nerve,vessel and knee were protected.It is safe and convenient measure that keep the operation go on smoothly.Summarized 54 cases of superior shinbone tumor that were used this device in the operation and experienced that it provided an effectiveness support for the operation.

Objective:To investigate the induction of apoptosis by isoalantolactone in human cervical cancer Hela cells is mediated through ROS generation and Mitochondrial dysfunction. Methods: Cells were treated with isoalantolactone in a dose-dependent manner in the presence or absence of NAC for 24 h as the experimental group,and the normal cells were used as control group. Cell viabilities were determined by the MTT assay;the nuclear morphology of Hela cells were observed under fluorescence microscope using the Hoechst 33258 staining;apoptosiscell cycle and reactive oxygen species ( ROS ) and mitochondrial membrane potential(MMP) were measured by flow cytometry;the protein expression levels of cytochrome C,Bcl-2,Bax and Caspase-3 were detected by Western blot. Results:In the present study,we found that isoalantolactone inhibits growth in a dose-dependent manner in Hela cells. Further studies revealed that Hela cells were treated with 20 and 40 μmol/L isoalantolactone for 24 h,after which we could observe the fragmented nuclei and the increased apoptosis rate. And we also found that isoalantolactone arrested the cell cycle at S phase and increased generation of reactive oxygen species and dissipation of mitochondrial membrane potential (△ψm) in Hela cells. While pretreatment with NAC obviously blocked the apoptotic and inhibition effect of isoalantolactone indicating that induction of apoptosis is ROS-dependent,Western blot study showed that isoalantolactone increased the expression of Bax and cleaved Caspase-3 and decreased the expression of Bcl-2 with concomitant release of cytochrome C from mitochondria into cytosol. Conclusion: Isoalantolactone could inhibit the proliferation and induce the apoptosis of human cervical cancer Hela cells in vitro through mediating ROS generation and Mi-tochondrial dysfunction, the mechanism of which is also accompanied by up-regulation of Bax expression, down-regulation of Bcl-2 expression,activation of Caspase-3 and release of cytochrome C.