Psychoactive substances abusing may induce neuron-specific adaptation and lead to physical and psychological dependence.Moreover,psychoactive substances have toxicological actions to cause physical damages.It has been reported that DNA methylation,acting as an epigenetic modification,may be one of the mechanisms involved in these adaptive changes and physical damages.This review shows a general introduction to the molecular mechanism of DNA methylation,and expounds the pharmacological and toxicological effects of some psychoactive substances on DNA methylation,including ethanol,methamphetamine,morphine,and cocaine.

Research into methamphetamine-induced neurotoxicity has experienced a resurgence in recent years. This is due to an increased abuse of the substance internationally. The long-term abuse of methamphetamine will result in neurochemical, neuropathological and behavioral changes. Recent data implicate that dopamine oxidation, glutamate-induced excitotoxicity, disruption of mitochondria, and apoptosis are involved in the injury of methamphetamine to central nervous system. Further, Involvement of cell death-related genes in the neurotoxic effects of methamphetamine is also discussed.

Drug abuse and addiction are increasingly severe, which is both a serious social problem and an important medical research work. It is very significant to evaluate dependence potential of centrally acting drugs. Several lines of evidence have shown that there is a close relationship between drug sensitization and drug abuse and addiction. More attention has been directed to sensitization of abused drugs. We introduce the establishment of behavioral sensitization animal model, review neurobiological mechanisms underlying development and expression of behavioral sensitization, and further discuss the role of behavioral sensitization animal model in evaluation of drug dependence.

Alcohol is widely abused in contemporary social life, which has become a serious medical and social problem because it hurts human health and endangers public safety. Recent re-search has developed several active substances that can effective-ly improve or treat this syndrome via affecting the mesolimbic do-pamine nervous pathway to dampen rewarding effectiveness in-duced by ethanol. This paper reviews the progress in near-term studies of alcoholism-intervening agents, aiming at providing ref-erences for related mechanism exploration and drug development.

Objective:To construct and evaluate a Salmeterol lungs-specific liposomal delivery system.Methods:①Liposome were prepared by the reverse-phase evaporation method and instilled into the tracheas of SD strain rats.The influence of Salmeterol on the uptakes of liposome was evaluated.②pEGFPC1(25 ?g/rodent) encapsulated in lungs-specific liposome were administered intravenously into Guinea pigs,GFP expression were observed by means of fluorescent microscopy 24h and 48h after administration.Results:①2,4,8,12,16 hours after instillation,lungs-specific liposome uptake were significantly higher than nonspecific liposome uptake(P

0.05).Conclusion The MVD and micrometastasis of regional lymph nodes,which act as the supplement parameter of TNM stages of esophageal cancer for T and N factors,are the important prognosis factors for esophageal cancer.

Objective: To investigate the role of anti-inflammatory cytokine IL-10 in the pathogenesis of asthma.Methods:IL-10 internal standards was constructed by restriction digest.The expression levels of IL-10 mRNA were determined in peripheral blood and induced sputum of 23 asthmatic patients by(RT-PCR) with this competitive internal standards. Results:There was no IL-10 mRNA expression in most of the asthmatics.IL-10 mRNA was detected in some catabatic patients.But IL-10 mRNA was readily detected in 29 normal subjects. Conclusion:Airway inflammation of asthma was related to the expression of IL-10 gene.Asthmatic patients may have difficulty in IL-10 synthesis with transcript.

Aim To investigate the effects of L-type calcium channel blockers on tramadol-induced analgesia.Methods Hot-plate test and writhing test were used to measure the analgesia induced by tramadol. Verapamil, nimodipine or nifedipine was co-administrated with tramadol to determine its effects on tramadol analgesia.Results Tramadol (10, 20, 40 mg?kg -1 in hot-plate test or 2, 5,10 mg?kg -1 in writhing test) produced significantly analgesia in hot-plate test and writhing test. Co-administration of verapamil and tramadol prolonged the latency of pain response of mice in hot-plate test.In writhing test, verapamil, nimodipine and nifedipine could potentiate the analgesic effect of tramadol in a dose-dependent manner.Conclusion L-type calcium channel blockers can potentiate tramadol-induced analgesia. Calcium influx mediated by L-type calcium channels may be involved in tramadol-induced analgesia.

It is traditionally thought that interleukins are produced by immunocytes. However, abundant evidence indicates that neuron and neuroglia also produce and excrete interleukins. Brain derived interleukins have reciprocal action with multiple neurotransmitters, and influence animal's behavior, learning and memory. Moreover, brain derived interleukins are involved in Alzheimers disease, depression and so on. Further investigation on brain derived interleukins may improve in understanding the pathophysiology of some related diseases.