Nitric oxide, an intracellular messenger molecule linked to activation of N Methyl D aspartate(NMDA) receptor, plays a role in morphine tolerance and dependence. Nitric Oxide Synthase (NOS) inhibitors attenuate or block morphine actions. NO/NOS system has an effect on morphine induced place preference. Actions of NO/NOS system are involved in the activation of opioid receptors. The effect of NO/NOS system on the expression of morphine withdrawal symptoms may be partially mediated by noradrenergic neuron system. Thus reviews on interactions between NO/NOS system and opioid system are very important towards applications of opioid analgesic as well as treatment against opioid tolerance and withdrawal.

Opioids were widely applied to analgesia and treatment of coughing, diarrhea, anxiety and sleepless. Opioids had toxic effects while playing pharmaceutical roles with oxidative injury as one of the most important toxic effects. Multi-organ or systems in our body were more liable to be damaged either by opioids reduced concentration of glutathione, the reductant or antioxidant, or by increased concentration of reactive oxidative species. To further clarify the research progress in opioids induced oxidative injury is very important towards opioids applications as well as prevention and cure of drug abuse.

Objective To study the effect of morphine on gene expression of enzymes involved in salvage and catabolism pathways of purine nucleotides metabolism in nerve cells.Methods PC12 cells were cultivated and divided into morphine treated groups which were treated with morphine(10 mg?L~(-1) culture) for 12,24,48, 72 h,and control groups which were treated with normal saline for 12,24,48 and 72 h.Total RNA of PC12 cells was isolated.HGPRT,AK,ADK mRNA levels were determined by using the reverse transcription polymerase chain reaction(RT-PCR); the ?-actin mRNA expression was used as an internal control.Results As compared with corresponding control groups,HGPRT mRNA levels in PC12 cells were increased significantly after 12 and 24 h treatment with morphine(P

Objective To investigate relationship of microalbuminuria (MAU) and insulin resistance (IR) to severity of coronary lesions in patients with acute coronary syndrome (ACS), and its predictive value for short-term prognosis in then.Methods In total, 162 ACS patients admitted to the department of cardiology, Guangzhou First People's Hospital, Guangzhou, Guangdong province during January 2008 to June 2009 were selected and divided into three groups according to their urine albumin excretion rate (UAER): 54 cases in normal group with UAER less than 20 μg/min, 62 cases in microalbuminuria group with UAER of (20-200)μg/min, and 46 cases in mass-albuminuria group with UAER more than 200 μg/min.Difference in IR (by homeostasis model assessment, HOMA ) and severity of coronary lesions among the three groups was assessed.Effects of baseline MAU and IR on main adverse cardiac events within the recent six months were observed in ACS patients after percutaneous coronary intervention (PCI).Results IR increased and coronary lesions aggravated as UAER increasing in all the three groups of ACS patients (P＜0.05 or P＜0.01).MAU associated with IR, with a coefficient of correlation of 0.366 (P＜0.01).Results of multivariate logistic regression analysis showed that both MAU and IR were strong independent predictors for main adverse cardiac events in ACS patients within six months after PCI.Conclusions MAU and IR associate with severity of coronary lesions in ACS patients, suggesting certain predictive value for main adverse cardiac events in short-term after PCI.

Issues on basic medical English teaching,curriculum and the construction ne-cessity for teaching material were analyzed and discussed.The corresponding strategy toward these issues in our university and the progress we have made were reported.

BACKGROUND: Many studies have suggested that angiotensin-converting enzyme inhibitors(ACEI) protect blood vessels through anti-atherosclerosis independent of lowering blood pressure, but its mechanism is still unclear.OBJECTIVE: To investigate the anti-atherosclerotic mechanism of ACEI by observing the effects of Enalapril on lipoprotein(a) and oxygen free radicals in patients with acute myocardial infarction (AMI) .DESIGN: A controlled study based on the observation of the patients with AMI.SETTING: Second Department of the South Building, General Hospital of Chinese PLAPARTICIPANTS: Thirty-five inpatients with AMI(19 males and 16 females, aged 42 -75 years old, and averaged (62 ± 9) years old and hospitalized at the Department of Cardiology of Tianjin Harbor Hospital from April 2001 to August 2002 were chosen. These patients were randomly divided into 2 groups: the therapeutic group(20 cases) and the control group(15cases). Inclusion criteria: the diagnosis of patients with AMI was confirmed by WHO criteria. Exclusion criteria: patients with renal dysfunction, shock,hypotension, a history of allergy to ACEI, and a history of severe cough induced by ACEI. All patients had not taken ACEI in the past 2 weeks and agreed to participate in this study.METHODS: On early morning of the third day after AMI, patients in the treatment group took 5 mg of Enalapril one time. If they had no first-dose reaction of hypotension, on the fourth day after AMI, the patients of the treatment group were given a dose of 5 mg twice per day for the following 2 weeks. Then, they were given the drug at a dose of 10 mg twice per day for 2 weeks. The patients in the control group were not given Enalapril. Blood samples were taken respectvely prior to the administration and 2 weeks and 4 weeks after the administration in the two groups. Serum content of lipoprotein(a), oxygen free radicals, triglyceride, total cholesterol, high density lipoprotein(HDL) cholesterol, Apo(a) were measured.MAIN OUTCOME MEASURES: We compared the level of serum of lipoprotein (a), oxygen free radicals (OFR), triglyceride, total cholesterol,HDL cholesterol, Apo(a) pre-treatment and post-treatment respectively in patients of the two groups.RESULTS: Serum levels of OFR were significantly lowered in the treatment group, which were(1 423.14±216.23), (1 076.62±287.12) and (566.57 ± 138.02) U/mL respectively 2 weeks and 4 weeks before and after the treatment(t =2. 937, 3. 571, P ＜0. 01), but there were no significant changes in serum concentrations of lipoprotein(a) and lipids( P ＞ 0.05) .CONCLUSION: Enalapril improved the prognosis of patients with AMI by antioxidation, but not by lowering the serum levels of lipoprotein(a) and lipids. The study can serve as a theoretical reference that the mechanism of Enalapril might inhibit atherosclerosis in patients with AMI.

Objective To investigate the effect of acidic serine protease ASPNJ on the expression of heat shock protein HSP90, 60 and 27 in human chronic myeloid leukemia K562 cells, in order to reveal the related mechanism of anti leukemic effects of ASPNJ. Methods K562 leukemia cell lines were cultured in vitro and treated with ASPNJ alone or in combination with chemotherapeutic agents. Western blot and RT-PCR were used to detect the changes of HSP90, 60 and 27 gene expressions in levels of total protein and membrane protein, as well as in mRNA levels. Results ASPNJ showed different effects on the expression of HSPs in total protein and membrane protein levels and had some modified effect on HSPs in total protein or membrane protein levels. Effects of ASPNJon expression of HSPs mRNA were not apparent, but HSPs mRNA were apparently lower in the ASPNJ and doxorubicin combination group than that in the ASPNJ alone or doxorubicin alone groups. Conclusion The mechanism of ASPNJ on the inhibitory effect of leukemia cells proliferation and the promoting effects on chemotherapeutic drugs may involve some complicated correlations with the effect of ASPNJ on the expression of HSPs and the modification of HSPs proteins.