Objective To investigate the effect of warm needling on learning and memory abilities and the calmodulin kinaseⅡ (CaMKⅡ) content of prefrontal cortex area in morphine withdrawal rats andexplore the mechanism of its action. Methods Forty clean-grade male SD rats were randomly allocated to control, model, manual needling and warm needling groups, 10rats each. A SD rat model of morphine addiction and withdrawal was made by dorsal subcutaneous injection of day-by-day incremental morphine and rapid withdrawal with Naloxone after addiction. Learning and memory abilities were tested using a Morris water maze and the CaMKⅡ content of prefrontal cortex area was measured by an immunohistochemical method in every group of rats.Results There were statistically significant differences in mean platform escape latency, the number of platform crossing and the CaMKⅡ content of PFC area between the control, manual needling or warm needling group of rats and the model group (P<0.01). There were statistically significant differences in mean platform escape latency, the number of platform crossing and the CaMKⅡ content of PFC area between the warm needling and manual needling groups (P<0.05).Conclusions Warm needling treatment can restore learning and memory abilities in morphine withdrawal rats. The mechanism of its action may be related to an increase in the CaMKⅡ content of prefrontal cortex area.

Objective To investigate the joint action of CXCL16 G1850A and TNF-α T1031C genes polymorphisms in patients with atherosclerotic cerebral infarction (ACI). Methods CXCL16 gene, G1850A and TNF-α gene T1031C mononucleotide polymorphism were tested with polymerase chain reaction followed by restriction fragment length polymorphism (PCR-RFLP) in 120 ACI patients and 75 healthy controls. Results The CXCL16 gene 1850 site AA genotype (35.8% vs 20.0%), A allele frequency (59.6% vs 44.0%), the TNF-αgene 1031 site CC genotype(2.5% vs 1.3%), C allele frequency(21.3% vs 11.3%)in ACI group were significantly higher than in the control group(P < 0.05). There was a positive correlation between the joint action of CXCL16 G1850A and TNF-α T1031C genes polymorphisms and ACI (χ2= 7.502,df = 2,P = 0.023). Conclusion The CXCL16 gene 1850, A allele and TNF-α gene 1031 C allele were risk factors for ACI. There is a positive correlation between the joint action of CXCL16 G1850A and TNF-α T1031C genes polymorphisms on ACI.

OBJECTIVE:To establish capillary GC method for the determination of residual organic solvents in artesunate,such as methanol and ethyl acetate.METHODS:Capillary GC was adopted and the temperature of flame ionization detector was 250℃.RESULTS:The linear range were 0.03～0.605 mg?mL-1 for methanol(r=0.999 8) and 0.05～1.002 mg?mL-1 for ethyl acetate(r=0.999 7).The average recovery rates were 98.7% for methanol(RSD=3.0%) and 99.1% for ethyl acetate(RSD=2.1%).Only the ethyl acetate was detected in samples.CONCLUSION:Established method is simple and accurate for the content determination of residual organic solvents in artesunate.

Objective To evaluate the effect of clonidine added to ropivacaine for epidural anesthesia. Methods Sixty ASA Ⅰ - Ⅱ patients aged 24-62 yr, weighing 50-76 kg, scheduled for elective gynecological surgery under epidural anesthesia were randomly assigned to one of four equal groups of 15 patients each, according to the dose of clonidine added to ropivacaine solution: group 1 (R) received no clonidine and served as control; group 2-4 in which clonidine 50, 100 or 150 ug was added to 0.75% ropivacaine 25 ml (R-C 50, R-C 100, R-C 150). Epidural anesthesia was performed at L2-3. Epidural catheter was inserted into epidural space and advanced in cephalad direction for 3.5 cm. Ropivacaine solution was prepared and provided by a specially designated person. A test dose of 5 ml of ropivacaine was given. 5 min later when epidural placement of catheter was confirmed, the rest 20 ml of ropivacaine was given in fractions of 5 ml every 2-3 min. At the beginning of operation midazolam 2.5-3.5 mg was given iv. During operation if the patient felt uncomfortable when viscera were being pulled, ketamine 0.5 mg? kg-1 was given iv. The onset and duration of analgesia, the height of black, the degree of motor block as well as adverse effects were recorded. Results The onset time of motor block was significantly shorter, the duration of analgesia was significantly longer, the incidences of visceral pain and shivering were significantly lower and ketamine requirement was significantly reduced in group R-C 100 and R-C 150 as compared with group R. However the incidence of hypotension, the amount of fluid infused and epinedrine requirement were significantly increased in group R-C 150. Conclusion The addition of clonidine 100 ug to 0.75 % ropivacaine 25 ml improves the effect of epidural block without increasing adverse effects.

Objective To explore the relationship between angiotensin I-converting enzyme(ACE)gene I/D and angiotensin Ⅱ type 1 receptor(AT1R)gene A1166C polymorphisms and cereral infarction(CI).Methods ACE and AT1R genotypes were investigated with the method of PCR-RLFP in 88 patients with CI and compared with 90 age-matched population controls.Results AC genotypic frequency(31.8%)and C allele frequency(15.9%)of AT1R gene in CI group were significently higher than those in control group(11.1%,5.6%)(all P0.05).Conclusions The polymorphism of AT1R A1166C is related to the incidence of CI.There are synergistic effects of ACE DD genotype and AT1R gene A1166C polymorphisms on the risk of CI.

Objective To investigate the relationship between polymorphisms of angiotensinogen(AGT) gene T704C and cerebrovascular disease(CVD).Methods AGT T704C genotype and allele were examined by PCR-RLFP in 82 patients with cerebral infarction(CI group),70 patients with intracerebral hemorrhage(ICH group) and 89 age-matched normal controls(NC group).The AGT T704C genotype and allele frequencies among the 3 groups were compared and analyzed.The effectes of AGT T704C genotype and the risk factors of stroke to induce CI snd ICH were analyzed by Logistic regression. Results The frequencies of AGT 704CC genotype and C allelic in CI group(63.4%,79.9%) were significantly higher than those in NC group(34.8%,61.2%)(allP

With the constant deepening of the study in the genetic factors of eardio-cerebrovascular diseases, the relation between the renin-angiotensin system (RAS) gene polymorphisms and hypertension is increasingly receiving attention. As an important component of RAS, renin has received much concern in the genetic research of cardio-cerebrovascular diseases and its gene polymorphisrns have become the candidate genes of hypertension, coronary heart disease and stroke, etc.

AIM:Toinvestigatewhetherandhowhumanchorionicgonadotropin(HCG)treatmentameliorates endometriosis in the endometriotic rat model .METHODS:The rat model of endometriosis was established and the model rats were divided into 4 groups.The rats in HCG groups were treated with 19.4, 25.8 and 51.6 IU/100 g of HCG every day (low-dose HCG, medium-dose HCG and high-dose HCG, respectively).The rats in control group were treated with 0.9%NaCl.After 15 days (3 estrous cycles), the ectopic lesion volume and ultrastructural characteristics in eutopic and ectopic endometria were investigated .RESULTS: After HCG treatment , the volume of endometriotic lesions was signifi-cantly smaller than that before treatment .Numerous and mitochondrial , endoplasmic reticulum and ribosomes were ob-served in the cytoplasm of eutopic and ectopic endometrium before treatment .After treatment , some cell structures were not clear , and mitochondrial cristae decreased or disappeared partly .Some cells were densed and shrinkage , autophagosome in cytoplasm increased , and mitochondria and endoplasmic reticulum swelt .CONCLUSION:HCG therapy appears to be an effective treatment for endometriosis in rats attributed to its influence on cell metabolism dysfunction of eutopic and ectopic endometria .

The pharmacokinetics of 16-dehydropregnenolone (16-DHP),a sterols compound isolated from Solanum lyratum Thunb.,was investigated in rats following a single intramuscular administration (40 mg/kg).The concentration of 16-DHP in rat plasma was determined by a high performance liquid chromatography (HPLC) method with UV detection.Levonorgestrel was used as the internal standard (IS).The pharmacokinetic parameters of 16-DHP were derived by non-compartmental method.After a single intramuscular administration,the maximum plasma concentration (Cmax,) was (289 ±25)ng/mL,time to reach Cmax(tmax) was (0.38±0.14) h,the elimination half-life (t1/2) was (2.5±1.1)h,the area under the plasma concentration-time curve from time zero to the time of the last measurable concentration (AUC10-t)) was (544 ± 73 )ng· h/mL.The results indicated that 16-DHP was alsorbed quickly and eliminated rapidly in rats after the intramuscular injection.