Single-nucleotide polymorphisms of the MyoG gene were tested using PCR-SSCP from 73 Landrace pigs, 68 Large White pigs, 57 Yimeng pigs and 83 Laiwu pigs. The effects of the MyoG gene on the birth weight, the average daily gain, the meat tenderness, and the backfat thickness were also analyzed. On the basis of the DNA sequence (M14331) of the porcine MyoG gene, primers were designed to amplify MyoG gene. One polymorphism was found in the amplified region of intron 1, in which two alleles ( A, and B) and three genotypes (AA, AB, and BB ) were examined. A G→ C transition was detected at 2 943 locus by sequencing the homozygotes. The results show that: ( 1 ) The Large White breed differed significantly ( P ＜0.05) in genotype distribution from the Landrace, the Laiwu and the Yimeng breeds;and the Laiwu breed differed significantly( P ＜ 0.05) in genotype distribution from the Landrace and the Yimeng breeds; whereas no significant differences( P ＞ 0.05) were found in genotype distribution between the Landrace and the Yimeng breeds. (2) On the basis of the fixed effect model, significant differences ( P ＜ 0.05) were found in the birth weight and the tenderness among the different MyoG genotypes, whereas no significant differences ( P ＞ 0.05)existed in the average daily gain and the backfat thickness. (3) Using least square analysis, it was seen that significant differences ( P ＜ 0.05) exist in the meat tenderness between the individuals of the BB genotypes and those of the AA genotypes; and significant differences ( P ＜ 0.05 ) were found in the backfat thickness compared the pigs of the AA genotypes with the pigs of the AB, BB genotypes. These results suggest that the MyoG genotype has significant effects on the meat quality, the growth rate, and the backfat thickness,therefore MyoG gene can be used in marker-assisted selection to improve meat quality and growth rate, and to accelerate the breeding progress.

Objective To investigate the activation of β-sheet breaker peptide H102 on ERK signal transduction pathway in brain of PAP double transgenic mice. Methods PAP double transgenic mice were randomly divided into model group and H102 treatment group (n=10 for each group). A group of C57BL/6J mice with the same genetic background was served as controls. H102 (5.8 mg/kg) 5 μL was infused by intranasal administration to mice in H102 treatment group, and equal volume of blank solution of H102 (chitosan, BSA) was given to mice in control group and model group. The ability of spatial reference memory was tested by Morris water maze after 30 days of treatment. Then immunohistochemistry tests and Western blot technique were used to detect the content of RAS, P-MEK and P-ERK proteins in mouse brain. Results (1) The ability of learning and memory was significantly lower in model group than that of control group. The ability of learning and memory was significantly improved in treatment group than that in model group (P<0.05). (2) The contents of RAS, P-MEK and P-ERK in mouse brain were significantly lower in model group than those of control group, and these protein ex-pressions were significantly increased in treatment group than those in model group (P<0.01). Conclusion β-sheet break-er peptide H102 can activate ERK signal transduction pathway in brain of PAP double transgenic mice, increase PAS, P-MEK and P-ERK levels in nerve cells, and improve the ability of learning and memory in PAP mice.

Objective To achieve the fusion expression of the entire human beta-defensin-3(hBD-3) gene. Method We synthesized two oligonucleotide primers accor ding to the codon preference of Escherichia coli. The gene was cloned into p GEX -4T-2 to establish the pGEX-4T-2-hBD-3 as the fusion expression vector by PCR. Transformed into E.coli strain DH5α, the express vector was induced an d ex pressed by IPTG. The fusion protein GST-hBD-3 was obtained by repeated cycles of freezing and thawing, cut by thrombin to attain the recombinant hBD-3 protei n. Result The result of the antibacterial peptide agarose diffu sion assay shows the antibacterial activity of the rhBD-3 against the S.aureu s exists, and it reaches 0.843U. Conclusion The fusion expr ession of the hBD-3 gene is successful.

Objective: To investigate the effect of long-term deep slow-wave sleep deprivation on the gonad axis, sperm abnormality rate, and structure of the testis in male rats and possible mechanisms. Methods: A total of 30 specific pathogen-free male Wistar rats aged 5 weeks were randomly divided into slow-wave sleep deprivation group 1 (SD1 group) , slow-wave sleep and sleep time deprivation group 2 (SD2 group) , and control group, with 10 rats in each group. The flower pot method was used to establish a model of sleep deprivation. In addition to 12-hour sleep deprivation at night, the rats in the SD1 group were given interference once every 24 minutes, and those in the SD2 group were deprived of sleep for 8 minutes every 24 minutes; the rats in the control group were given 12-hour light illumination and then placed in dark environment for 12 hours. All rats were sacrificed by exsanguination from the femoral artery, and the testis, the epididymis, and blood were collected for analysis. Sperm abnormality rate and sperm motility rate were measured, and cauda epididymal sperm counting was performed. ELISA was used to measure the serum levels of testosterone (T) , follicle-stimulating hormone (FSH) , and luteinizing hormone (LH) . Results: Compared with the control group, the SD2 group had a significant increase in organ coefficient of the epididymis (P<0.05) and a significant reduction in sperm motility rate (P<0.05) . There were significant differences between the SD1 group and the SD2 group in the increase in sperm abnormality rate (P<0.05) and the reduction in cauda epididymal sperm count (P<0.05) . The levels of FSH and T tended to increase, and the level of LH tended to decrease. Pathological examination showed degeneration and vacuolization of a small amount of spermatogenic cells in the SD1 group; in the SD2 group, there were significant degeneration, edema, and vacuolization of most spermatogenic cells, some spermatogenic cells were observed in the lumen, and there were no sperms in the lumen. Conclusion Long-term deep slow-wave sleep deprivation impairs the structure of the testis, affects sperm motility rate and sex hormones, and increases the risk of sperm abnormality.