Objective To investigate the clinical effect of acupuncture therapy for ascending and descending Qi for the treatment of insomnia with the syndrome of liver stagnation. Methods Sixty quantified patients were randomized into 2 groups, 30 cases in each group. The patients in the treatment group were treated by acupuncture therapy for ascending and descending Qi, and the control group was given conventional acupuncture therapy. The polysomnography ( PSG) results and Pittsburgh sleep quality index ( PSQI) were compared before and after treatment, and the clinical efficacy was evaluated after treatment in the two groups. Results ( 1) The parameters of total sleep time, deep sleep time and rapid eye movement ( REM) time were prolonged, and the sleep latency and waking-up frequency in both groups were reduced after treatment (P<0.05 compared with those before treatment), and the improvement of total sleep time, deep sleep time and REM time in the treatment group was significantly superior to that in the control group (P<0.05). (2) PSQI scores in both groups were reduced after treatment ( P<0.01 compared with those before treatment) , and the reduction in the treatment group was more significant than that in the control group (P<0.01). (3) The total effective rate in the treatment group was 93.33%and was 76.67%in the control group. The efficacy in the treatment group was better than that in the control group (P<0.01). Conclusion Acupuncture therapy for ascending and descending Qi has better effect on insomnia with liver stagnation than conventional acupuncture therapy, being practical and innovative.

Aged ; Aging ; drug effects ; Arteriosclerosis ; drug therapy ; Dementia ; drug therapy ; Drugs, Chinese Herbal ; therapeutic use ; Humans ; Hyperlipidemias ; drug therapy ; Medicine, Chinese Traditional ; Phytotherapy ; Yang Deficiency ; drug therapy ; Yin Deficiency ; drug therapy

Objective To survey the relationship between myocardial damage of chronic and latent Keshan disease with A360P missense mutation in desmin gene exon6. Methods By clinical epidemiology method,30 cases had been collected randomly among chronic Keshan disease patients and 30 cases equally among healthy adults (inner control groups) in Diantou town,Huangling county,Shaanxi province,a Keshan disease area,and 30 cases among health adults(outer control group) in Chang'an district,Xian city,a normal area. Genome DNA had been extracted from 90 blood samples. Different restriction sites had been analyzed by the methods of PCR,digested by restriction endonuclease and electrophoresis. By virtue of Bsp1286 Ⅰ enzyme,122 bp and 60 bp strap could be found in control group from exnn4,showing that Bsp1286 Ⅰ enzyme was active. By virtue of Bsp1286 Ⅰ enzyme,desmin gene exon6 was digested to 184 bp and 66 bp strip when A360P missense mutation site exited in exon6. Results One hundred and twenty two bp and 60 bp strap could be found in control group from exon4 digested by Bsp1286 Ⅰ ,which showed Bsp1286 Ⅰ enzyme was active. Two hundred and fifty bp strips can only be found in digest products of exon6. One hundred and eighty-four and 66 bp strips which were the products of DNA digested by Bsp1286 Ⅰ could not be found. A360P missense mutation site of desmin gene exon6 had not been found among chronic and latent Keshan disease patients and tow control groups in Keshan disease area and in normal area. Conclusions A360P missense mutation site of desmin gene exon6 has not been found among chronic and latent Keshan disease patients. A360P missense mutation of desmin gene exon6 probably is not predisposing genes of chronic Keshan disease.

ObjectiveTo establish a method of isolation and culture of neural stem cells(NSCs). MethodsTissues of ventral midbrain were isolated from a rat embryo,and the NSCs were cultured stimulated with basic fibroblast growth factor(bFGF)in vitro.The cells were identified by immunocytochemistry.ResultsNSCs proliferated into neurosphere in symmetric and non-symmetric cleavage ways,and differentiated into neuron, astroglia and oligodendrosyte. ConclusionsThe method has been established to isolate and culture the neural stem cells.

Objective To investigate the correlation between body mass index ( BMI) , type Ⅱ diabetes and colorectal neoplastic lesions including adenoma and adenocarcinoma. Methods A total of 971 subjects, aged 20-86, who underwent colonoscopy from July 2008 to July 2009 were included. The body height and weight were measured, and history of type Ⅱ diabetes was recorded. Based on the results of colonoscopy and pathology, the subjects were divided into study group (with confirmed adenoma or adenocarcinoma; n =471) and normal control group (n = 500). All data were analyzed by using logistic multi-factors regression. Results With adjustment for some potential mixed factors, obesity group run 2. 55 times of risk of colorectal adenoma or adencarcinoma compared with the normal weight group (OR = 2.55, 95% CI: 1.26-3.05, P =0.027), among which obese male's risk was 3. 32 (OR =3.32, 95% CI: 1. 50-6. 86, P = 0.007) times of that in normal weight males. There was no correlation between female's BMI and incidence of colorectal adenoma & adencarcinoma. Patients with type Ⅱ diabetes ran 2. 10 times of risk of developing colorectal neoplastic lesions compared with those without ( OR = 2.10, 95% CI: 1. 25 - 3. 57, P = 0.010). Incidence of colorectal adenoma & adencarcinoma was 3 times higher in those with type II diabetes less than 6 years, compared with those with history more than 6 years ( OR = 3.00, 95% CI: 1.05 - 10. 86, P =0. 040), which was not correlated with gender of diabetic patients. Those with both type Ⅱ diabetes and obesity had 3.05 times of risk of colorectal adenoma & adencarcinoma, compared with non-obese diabetic patients (OR = 3.05,95% CI: 1.08 - 18.41, P - 0.041). Conclusion Obesity is positively correlated with colorectal adenoma and adencarcinoma, and obese males run higher risk than females. Type Ⅱ diabetes also leads to a higher incidence of colorectal neoplastic lesions, which will run even higher when combined with o-besity.

Objective To provide an approach to research of peroxisome proliferator activated receptor (PPAR) ? 2 function, mouse PPAR? 2 (mPPAR? 2) gene was cloned and its transient expression in eukaryotic cells was carried out. Methods mPPAR? 2 mRNA from epididymis fat pad of Chinese Kunming mice was amplified by RT PCR and subcloned into plasmid pcDNA3 to generate the recombinant plasmid pcDNA3/mPPAR? 2 which was confirmed to contain the amplified target gene segments with fluorescence sequencing. The recombinant plasmid pcDNA3/mPPAR? 2 was used to transfect COS 7 with lipofectamine and the expressing product was detected with immune fluorescence assay and Western blot. Results The sequencing results for amplified target gene showed that the sequence of mPPAR? 2 from epididymis fat pad of Chinese Kunming mice is similar to that of mouse PPAR? 2 in Genbank, only at the site of 383 amino acid where Ser (AGC) substitutes Asn (AAC). pcDNA3/mPPAR? 2 was efficiently expressed in eukaryotic cells in vitro. Conclusion This work is the experimental basis for further researching on PPAR? 2 function.

Objective To express the mouse peroxisome proliferator activated receptor ? 2 (mPPAR? 2) in NIH3T3 cells induced by the recombinant retrovirus vector. Methods mPPAR? 2 gene digested from the recombinant plasmid pcDNA3/mPPAR? 2 containing the target gene segment was subcloned into retrovirus vector pGCEN to generate the recombinant retrovirus pGCEN/mPPAR? 2. The recombinant retrovirus pGCEN/mPPAR? 2 and pGCEN were used to transfect PA317 cells with LipofectAMINE, and anti G418 clones of PA317 cells were selected and viral supernatants were harvested and used to infect NIH3T3 cells. The expressing products were identified with immune flurescence assay (IFA) and Western Blot. Results The recombinant retrovirus pGCEN/mPPAR? 2 was constructed, and 5?10 4 CFU/ml and 6?10 5 CFU/ml of pGCEN/mPPAR? 2 containing and pGCEN containing viral supernatants were obtained respectively. mPPAR? 2 was expressed in NIH3T3 cells mediated by the recombinant retrovirus vector. Conclusion This work is the basis for the foundation of adipocyte differentiation model in vitro and further researching on the molecular mechanism of adipocyte differentiation induced by PPAR? 2.

Many researches have focused on the wnt-frizzled cascade in the recent years, while much work has been done in neoplastic diseases and embryology, the role of the wnt-frizzled signal transduction pathway in cardiovascular diseases has only recently begun to be explored. It plays a very important role in many physiological and pathophysiological processes, such as its transduction pathway, the healing after myocardial infarction, the proliferation, differentiation and orientation of cardiomyocytes, angiogenesis/neovascularization, cardiac hypertrophy and heart failure, the deposition of the extracellular matrix and so on. This article is aimed at its relation with myocardial infarction and the role of this pathway in cardiovascular diseases.[

Objective To construct eukaryotic expression vector of antisense MBD1 gene fragment and to provide a tool for studying MBD1 gene function. Methods PCR primers were designed according to the coding sequence of MBD1 gene. Xba I and Kpn I recognition sequences and cutting sites were added to the 5' end of the sense and antisense primer respectively. The 342 bp specific PCR fragment was obtained from the cDNA of biliary tract carcinoma cell line QBC-939 using RT-PCR, the purified PCR fragment was then inserted reversely into the multiple cloning site of eukaryotic expression vector pcDNA3. 1 ( + ). The constructed recombinant plasmid was identified by PCR confirmation, Xba I and Kpn I double enzyme digestion and DNA sequencing. Results The 322 bp specific DNA band was obtained by PCR, Xba I and Kpn I double digestion produced a 327 bp and a 5. 4 kb DNA band which represent the inserted target gene fragment and the vector respectively. The sequencing result confirmed that the sequence of inserted fragment was correct. Conclusion The eukaryotic expression vector of antisense MBD1 gene fragment was constructed successfully by using gene cloning technique. It will be a useful tool for studying MBD1 gene function in DNA methylation and tumorigenesis.