Background The high rate of long-term relapse is a major cause of smoking cessation failure.Recently,neurofeedback training has been widely used in the treatment of nicotine addiction;however,approximately 30%of subje...Background The high rate of long-term relapse is a major cause of smoking cessation failure.Recently,neurofeedback training has been widely used in the treatment of nicotine addiction;however,approximately 30%of subjects fail to benefit from this intervention.Our previous randomised clinical trial(RCT)examined cognition-guided neurofeedback and demonstrated a significant decrease in daily cigarette consumption at the 4-month follow-up.However,significant individual differences were observed in the 4-month follow-up effects of decreased cigarette consumption.Therefore,it is critical to identify who will benefit from pre-neurofeedback.Aims We examined whether the resting-state electroencephalography(EEG)characteristics from pre-neurofeedback predicted the 4-month follow-up effects and explored the possible mechanisms.Methods This was a double-blind RCT.A total of 60 participants with nicotine dependence were randomly assigned to either the real-feedback or yoked-feedback group.They underwent 6 min closed-eye resting EEG recordings both before and after two neurofeedback sessions.A follow-up assessment was conducted after 4 months.Results The frontal resting-state theta power spectral density(PSD)was significantly altered in the real-feedback group after two neurofeedback visits.Higher theta PSD in the real-feedback group before neurofeedback was the only predictor of decreased cigarette consumption at the 4-month follow-up.Further reliability analysis revealed a significant positive correlation between theta PSD pre-neurofeedback and post-neurofeedback.A leave-one-out cross-validated linear regression of the theta PSD pre-neurofeedback demonstrated a significant correlation between the predicted and observed reductions in cigarette consumption at the 4-month follow-up.Finally,source analysis revealed that the brain mechanisms of the theta PSD predictor were located in the orbital frontal cortex.Conclusions Our study demonstrated changes in the resting-state theta PSD following neurofeedback training.Moreover,the resting-state theta PSD may serve as a prognostic marker of neurofeedback effects.A higher resting-state theta PSD predicts a better long-term response to neurofeedback treatment,which may facilitate the selection of individualised interventions.展开更多
Background Smoking is a serious public health problem. Patients with schizophrenia usually have a higher prevalence of smoking than the general population, but the level of nicotine dependence is seldom studied, espec...Background Smoking is a serious public health problem. Patients with schizophrenia usually have a higher prevalence of smoking than the general population, but the level of nicotine dependence is seldom studied, especially for patients living in the communities. Aims This study aimed to examine the level of nicotine dependence in Chinese community-dwelling patients with schizophrenia and explored its associated sociodemographic and clinical factors. Methods A total of 621 patients with schizophrenia treated in the primary care centres of Guangzhou were consecutively recruited. The level of nicotine dependence was assessed with the Chinese version of the Fagerstrom Test for Nicotine Dependence (FTND). Results 148 patients with schizophrenia were current smokers, and the mean (SD) score of FTND was 5.06 (2.55) for all the current smokers. The prevalence of nicotine addiction was 48.0%(95% Cl: 40.0%-56.0%) in patients with current smoking. The patients with schizophrenia had a significantly higher level of nicotine dependence than the Chinese general population. Multiple linear regression analysis revealed that male gender, being unemployed, having a family history of psychiatric disorders, having major medical conditions, first illness episode and less severe positive symptoms were significantly associated with a higher level of nicotine dependence. Conclusion Community-dwelling patients with schizophrenia in China, especially male patients, had a higher level of nicotine dependence than the general population.展开更多
Since 1989,numerous scientific studies have been conducted todetermine whether smoking is a danger to health.The trend of theevidence has been consistent and indicates that there is a serious
BACKGROUND: Our group previously reported that right-sided vagus nerve stimulation(RVNS) significantly improved outcomes after cardiopulmonary resuscitation(CPR) in a rat model of cardiac arrest(CA). However, whether ...BACKGROUND: Our group previously reported that right-sided vagus nerve stimulation(RVNS) significantly improved outcomes after cardiopulmonary resuscitation(CPR) in a rat model of cardiac arrest(CA). However, whether left-sided vagus nerve stimulation(LVNS) could achieve the same effect as RVNS in CPR outcomes remains unknown.METHODS: A rat model of CA was established using modified percutaneous epicardial electrical stimulation to induce ventricular fibrillation(VF). Rats were treated with LVNS or RVNS for 30 minutes before the induction of VF. All animals were observed closely within 72 hours after return of spontaneous circulation(ROSC), and their health and behavior were evaluated every 24 hours.RESULTS: Compared with those in the RVNS group, the hemodynamic measurements in the LVNS group decreased more notably. Vagus nerve stimulation(VNS) decreased the serum levels of tumor necrosis factor-alpha(TNF-α) and the arrhythmia score, and attenuated inflammatory infiltration in myocardial tissue after ROSC, regardless of the side of stimulation, compared with findings in the CPR group. Both LVNS and RVNS ameliorated myocardial function and increased the expression of α-7 nicotinic acetylcholine receptor in the myocardium after ROSC. Moreover, a clear improvement in 72-hour survival was shown with VNS pre-treatment, with no significant difference in efficacy when comparing the laterality of stimulation. CONCLUSIONS: LVNS may have similar effects as RVNS on improving outcomes after CPR.展开更多
BACKGROUND: Our previous research proved that vagus nerve stimulation(VNS) improved the neurological outcome after cardiopulmonary resuscitation(CPR) by activating α7 nicotinic acetylcholine receptor(α7nAChR) in a r...BACKGROUND: Our previous research proved that vagus nerve stimulation(VNS) improved the neurological outcome after cardiopulmonary resuscitation(CPR) by activating α7 nicotinic acetylcholine receptor(α7nAChR) in a rat model, but the underlying mechanism of VNS in neuroprotection after CPR remains unclear.METHODS: In vivo, we established a mouse model of cardiac arrest(CA)/CPR to observe the survival rate, and the changes in inflammatory factors and brain tissue after VNS treatment. In vitro, we examined the effects of α7nAChR agonist on ischemia/reperfusion(I/R)-induced inflammation in BV2 cells under oxygen-glucose deprivation/reoxygenation(OGD/R) conditions. We observed the changes in cell survival rate, the levels of inflammatory factors, and the expressions of α7nAChR/Janus kinase 2(JAK2) and toll-like receptor 4(TLR4)/nuclear factor-κB(NF-κB).RESULTS: In vivo, VNS preconditioning enhanced functional recovery, improved the survival rate, and reduced hippocampal CA1 cell damage, and the levels of inflammatory mediators after CA/CPR. The application of α7nAChR agonists provided similar effects against cerebral injury after the return of spontaneous circulation(ROSC), while α7nAChR antagonists reversed these neuroprotective impacts. The in vitro results mostly matched the findings in vivo. OGD/R increased the expression of tumor necrosis factor-alpha(TNF-α), TLR4 and NF-κB p65. When nicotine was added to the OGD/R model, the expression of TLR4, NF-κB p65, and TNF-α decreased, while the phosphorylation of JAK2 increased, which was prevented by preconditioning with α7nAChR or JAK2 antagonists.CONCLUSION: The neuroprotective effect of VNS correlated with the activation of α7nAChR. VNS may alleviate cerebral IR injury by inhibiting TLR4/NF-κB and activating the α7nAChR/JAK2 signaling pathway.展开更多
The highly specific ligand of the N-acetylcholine receptor（N-AChR）,alpha-bungarotoxin,was used to determine the effect of soman,sarin and VX onN-AChR of the diaphragm and extensor digitorum Iongus muscle of mice and...The highly specific ligand of the N-acetylcholine receptor（N-AChR）,alpha-bungarotoxin,was used to determine the effect of soman,sarin and VX onN-AChR of the diaphragm and extensor digitorum Iongus muscle of mice andrats.The effects of the three anti-cholinesterase agents on N-AChR weredifferent.Sarin did not act directly on N-AChR and cause a change in the numberof N-AChR.VX decreased the binding sites of the receptor by binding with N-AChRdirectly.The LD<sub>50</sub>was 0.054mg/kg in mousse.Soman increased the binding sites,e.g.1～1.5 LD<sub>50</sub>soman increased the number of N-AChR of mouse diaphragm by 25%.The peak increaseof N-AChR was reached 0.5 h after poisoning and could last 96h.The receptornumber was still 22% higher than that of the control on the fourth day aftersoman poisoning in rats.Soman mainly increased the number of extrasynapticN-AChR,leading to the enhancement of sensitivity of cholinergic effectors toacetylcholine（ACh）,which is similar to the hypersensitiveness resulting fromdenervation.These findings are of significance in probing the receptor mecha-nisms and treatment of soman poisoning.展开更多
Anti-bungarotoxin anti-serum,which has the internal image of nicotinicacetylcholine receptor,was used as a tool to measure anti-idiotypic antibodies toantibodies to Iigand of nicotinic acctylcholine receptor in scra f...Anti-bungarotoxin anti-serum,which has the internal image of nicotinicacetylcholine receptor,was used as a tool to measure anti-idiotypic antibodies toantibodies to Iigand of nicotinic acctylcholine receptor in scra from 81 patients withmyasthenia gravis.Enzyme-linked immunosorbcnt assay was adopted.Thc positive ratewas 46.9%(38/81).The specific cross inhibitory test with nicotinic acetylcholinereceptor was positive.Anti-idiotype antibodies to antibodies to ligand of nicotinicacetylcholine receptor in sera of different types of myasthenia gravis patients classified ac-cording to modified Osserman’s standard and myasthenia gravis patients with or withoutthymoma were comparcd in this study and the role of anti-idiotype antibodies toantibodies to Iigand of nicotinic acctylcholinc receptor in the immunity of myasthcniagravis and the possibility of thcrapeutic use of anti-idiotype antibodies arc discussed.展开更多
基金This work was supported by the National Natural Science Foundation of China(32000750,32171080,71942003,and 32161143022)Grants for Scientific Research of BSKY(XJ201907)from Anhui Medical University+4 种基金Scientific Research Improvement Project of Anhui Medical University(2021xkjT018)Research Fund of Anhui Institute of Translational Medicine(2022zhyx-C02)Basic and Clinical Collaborative Research Improvement Project of Anhui Medical University(2020xkjT020)The Chinese National Programs for Brain Science and Brain-like Intelligence Technology(2021ZD0202101)CAS-VPST Silk Road Science Fund 2021(GLHZ202128).The numerical calculations in this paper have been done on the Medical Big Data Supercomputing Center System of Anhui Medical University and Bioinformatics Center of the University of Science and Technology of China.
文摘Background The high rate of long-term relapse is a major cause of smoking cessation failure.Recently,neurofeedback training has been widely used in the treatment of nicotine addiction;however,approximately 30%of subjects fail to benefit from this intervention.Our previous randomised clinical trial(RCT)examined cognition-guided neurofeedback and demonstrated a significant decrease in daily cigarette consumption at the 4-month follow-up.However,significant individual differences were observed in the 4-month follow-up effects of decreased cigarette consumption.Therefore,it is critical to identify who will benefit from pre-neurofeedback.Aims We examined whether the resting-state electroencephalography(EEG)characteristics from pre-neurofeedback predicted the 4-month follow-up effects and explored the possible mechanisms.Methods This was a double-blind RCT.A total of 60 participants with nicotine dependence were randomly assigned to either the real-feedback or yoked-feedback group.They underwent 6 min closed-eye resting EEG recordings both before and after two neurofeedback sessions.A follow-up assessment was conducted after 4 months.Results The frontal resting-state theta power spectral density(PSD)was significantly altered in the real-feedback group after two neurofeedback visits.Higher theta PSD in the real-feedback group before neurofeedback was the only predictor of decreased cigarette consumption at the 4-month follow-up.Further reliability analysis revealed a significant positive correlation between theta PSD pre-neurofeedback and post-neurofeedback.A leave-one-out cross-validated linear regression of the theta PSD pre-neurofeedback demonstrated a significant correlation between the predicted and observed reductions in cigarette consumption at the 4-month follow-up.Finally,source analysis revealed that the brain mechanisms of the theta PSD predictor were located in the orbital frontal cortex.Conclusions Our study demonstrated changes in the resting-state theta PSD following neurofeedback training.Moreover,the resting-state theta PSD may serve as a prognostic marker of neurofeedback effects.A higher resting-state theta PSD predicts a better long-term response to neurofeedback treatment,which may facilitate the selection of individualised interventions.
文摘Background Smoking is a serious public health problem. Patients with schizophrenia usually have a higher prevalence of smoking than the general population, but the level of nicotine dependence is seldom studied, especially for patients living in the communities. Aims This study aimed to examine the level of nicotine dependence in Chinese community-dwelling patients with schizophrenia and explored its associated sociodemographic and clinical factors. Methods A total of 621 patients with schizophrenia treated in the primary care centres of Guangzhou were consecutively recruited. The level of nicotine dependence was assessed with the Chinese version of the Fagerstrom Test for Nicotine Dependence (FTND). Results 148 patients with schizophrenia were current smokers, and the mean (SD) score of FTND was 5.06 (2.55) for all the current smokers. The prevalence of nicotine addiction was 48.0%(95% Cl: 40.0%-56.0%) in patients with current smoking. The patients with schizophrenia had a significantly higher level of nicotine dependence than the Chinese general population. Multiple linear regression analysis revealed that male gender, being unemployed, having a family history of psychiatric disorders, having major medical conditions, first illness episode and less severe positive symptoms were significantly associated with a higher level of nicotine dependence. Conclusion Community-dwelling patients with schizophrenia in China, especially male patients, had a higher level of nicotine dependence than the general population.
文摘Since 1989,numerous scientific studies have been conducted todetermine whether smoking is a danger to health.The trend of theevidence has been consistent and indicates that there is a serious
基金supported by research grants from the National Natural Science Foundation of China (81571866, 82072137)。
文摘BACKGROUND: Our group previously reported that right-sided vagus nerve stimulation(RVNS) significantly improved outcomes after cardiopulmonary resuscitation(CPR) in a rat model of cardiac arrest(CA). However, whether left-sided vagus nerve stimulation(LVNS) could achieve the same effect as RVNS in CPR outcomes remains unknown.METHODS: A rat model of CA was established using modified percutaneous epicardial electrical stimulation to induce ventricular fibrillation(VF). Rats were treated with LVNS or RVNS for 30 minutes before the induction of VF. All animals were observed closely within 72 hours after return of spontaneous circulation(ROSC), and their health and behavior were evaluated every 24 hours.RESULTS: Compared with those in the RVNS group, the hemodynamic measurements in the LVNS group decreased more notably. Vagus nerve stimulation(VNS) decreased the serum levels of tumor necrosis factor-alpha(TNF-α) and the arrhythmia score, and attenuated inflammatory infiltration in myocardial tissue after ROSC, regardless of the side of stimulation, compared with findings in the CPR group. Both LVNS and RVNS ameliorated myocardial function and increased the expression of α-7 nicotinic acetylcholine receptor in the myocardium after ROSC. Moreover, a clear improvement in 72-hour survival was shown with VNS pre-treatment, with no significant difference in efficacy when comparing the laterality of stimulation. CONCLUSIONS: LVNS may have similar effects as RVNS on improving outcomes after CPR.
基金supported by research grants from the National Natural Science Foundation of China (grant no. 81571866 and grant no. 82072137)。
文摘BACKGROUND: Our previous research proved that vagus nerve stimulation(VNS) improved the neurological outcome after cardiopulmonary resuscitation(CPR) by activating α7 nicotinic acetylcholine receptor(α7nAChR) in a rat model, but the underlying mechanism of VNS in neuroprotection after CPR remains unclear.METHODS: In vivo, we established a mouse model of cardiac arrest(CA)/CPR to observe the survival rate, and the changes in inflammatory factors and brain tissue after VNS treatment. In vitro, we examined the effects of α7nAChR agonist on ischemia/reperfusion(I/R)-induced inflammation in BV2 cells under oxygen-glucose deprivation/reoxygenation(OGD/R) conditions. We observed the changes in cell survival rate, the levels of inflammatory factors, and the expressions of α7nAChR/Janus kinase 2(JAK2) and toll-like receptor 4(TLR4)/nuclear factor-κB(NF-κB).RESULTS: In vivo, VNS preconditioning enhanced functional recovery, improved the survival rate, and reduced hippocampal CA1 cell damage, and the levels of inflammatory mediators after CA/CPR. The application of α7nAChR agonists provided similar effects against cerebral injury after the return of spontaneous circulation(ROSC), while α7nAChR antagonists reversed these neuroprotective impacts. The in vitro results mostly matched the findings in vivo. OGD/R increased the expression of tumor necrosis factor-alpha(TNF-α), TLR4 and NF-κB p65. When nicotine was added to the OGD/R model, the expression of TLR4, NF-κB p65, and TNF-α decreased, while the phosphorylation of JAK2 increased, which was prevented by preconditioning with α7nAChR or JAK2 antagonists.CONCLUSION: The neuroprotective effect of VNS correlated with the activation of α7nAChR. VNS may alleviate cerebral IR injury by inhibiting TLR4/NF-κB and activating the α7nAChR/JAK2 signaling pathway.
文摘The highly specific ligand of the N-acetylcholine receptor（N-AChR）,alpha-bungarotoxin,was used to determine the effect of soman,sarin and VX onN-AChR of the diaphragm and extensor digitorum Iongus muscle of mice andrats.The effects of the three anti-cholinesterase agents on N-AChR weredifferent.Sarin did not act directly on N-AChR and cause a change in the numberof N-AChR.VX decreased the binding sites of the receptor by binding with N-AChRdirectly.The LD<sub>50</sub>was 0.054mg/kg in mousse.Soman increased the binding sites,e.g.1～1.5 LD<sub>50</sub>soman increased the number of N-AChR of mouse diaphragm by 25%.The peak increaseof N-AChR was reached 0.5 h after poisoning and could last 96h.The receptornumber was still 22% higher than that of the control on the fourth day aftersoman poisoning in rats.Soman mainly increased the number of extrasynapticN-AChR,leading to the enhancement of sensitivity of cholinergic effectors toacetylcholine（ACh）,which is similar to the hypersensitiveness resulting fromdenervation.These findings are of significance in probing the receptor mecha-nisms and treatment of soman poisoning.
文摘Anti-bungarotoxin anti-serum,which has the internal image of nicotinicacetylcholine receptor,was used as a tool to measure anti-idiotypic antibodies toantibodies to Iigand of nicotinic acctylcholine receptor in scra from 81 patients withmyasthenia gravis.Enzyme-linked immunosorbcnt assay was adopted.Thc positive ratewas 46.9%(38/81).The specific cross inhibitory test with nicotinic acetylcholinereceptor was positive.Anti-idiotype antibodies to antibodies to ligand of nicotinicacetylcholine receptor in sera of different types of myasthenia gravis patients classified ac-cording to modified Osserman’s standard and myasthenia gravis patients with or withoutthymoma were comparcd in this study and the role of anti-idiotype antibodies toantibodies to Iigand of nicotinic acctylcholinc receptor in the immunity of myasthcniagravis and the possibility of thcrapeutic use of anti-idiotype antibodies arc discussed.
