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Sponsored by the Center for Science and Technology Development of the Ministry of Education
Supervised by Ministry of Education of the People's Republic of China
Abstract:The reproductive performance of female hen mainly depends on ovarian and follicular development. Therefore the complete insight of the mechanisms leading to the development of ovary is very important. In this respect we have studied early ovarian development until the formation of primordial follicles in the chicken. Our study was based on on the early ovarian development and then post hatching development of ovary. We have noticed asymmetric ovarian developmental phenomenon after E7.5 of embryonic chicken sex differentiation. The size of the right side ovary was not distinct and cortex disappeared. The right ovarian germ cell proliferation rate gradually decreased from E5.5 to E7.5 and some of them were crowded into the medullary lacunae by programmed cell death. In our another study we have noticed that the primordial follicle formation started to commence after the third day after hatching and it became rapid after first week of post hatching to two weeks of post hatching in the female chicken. In addition to this, we have observed an abnormal phenomenon during the formation of primordial follicle when a low number of the multiple oocyte follicles that were thought to be oocyte cysts and did not completely break apart during cyst breakdown due to the unknown reason. This underlying mechanisms needs further research. Therefore, our study of early ovarian development in the chicken will make a theoretical base for further understanding of the regulation of reproduction function and improving the laying performance in poultry.
Abstract:The multi-resistance gene cfr has been widely disseminated among the livestock in China. A total of 444 Staphylococcus isolates recovered from pigs, workers, and the environment of a slaughterhouse and a hog market in Guangzhou, China, to investigate the prevalence and dissemination of cfr among staphylococci from different sources. 20 (4.5%) staphylococcal isolates, including one Staphylococcus cohnii, one Staphylococcus aureus, and 18 Staphylococcus simulans, harboured the cfr gene. The cfr-carrying S. aureus strain BKED isolated from the ground surface swab in hog market, exhibits spa type t889 and belongs to the clonal lineage ST9. SmaI pulsed-field gel electrophoresis (PFGE) analysis of 26 staphylococcal strains (22 S. simulans and 4 S. cohnii ), including previously reported cfr-carrying staphylococci of animal food origin, exhibited 19 major PFGE patterns A-S. Clonal spread of cfr between porcine strains and strains of human, the environment, food origins occurred. The genetic contexts of the cfr gene in plasmids pHNKF3, pHNZT2 and pHNCR35 from S. simulans of swine or human origin were very similar to that observed in other Staphylococcus species isolated from animal, human clinics, and animal food. In summary, clone spread and horizontal transmission via mobile elements were the two main ways leading to the dissemination of the multi-resistance gene cfr among staphylococcal isolates from different sources. Given the possibility that the cfr gene is transferred from animals to humans via the food chain, close contact and the environment, continued surveillance of this gene in pigs and workers in close contact with them is warranted.
TO cite this article:LIN Dachuan,WANG Jing,WEI Hongkun, et al. Distribution of the Multidrug Resistance Gene cfr in Staphylococcus Isolates from Pigs, Workers, and the Environment of a Hog market and a Slaughterhouse in Guangzhou, China[OL].[17 December 2014] http://en.paper.edu.cn/en_releasepaper/content/4623852
Abstract:The CIDEC protein is located in lipid droplets (LDs) and the endoplasmic reticulum (ER), and is induced in fatty liver. However, the binding domain, the functional domain and the underlying mechanism of CIDEC in stimulating fat accumulation remain unclear. Here, we investigated the subcellular localization and function of pig CIDEC and confirmed CIDEC promotes unilocular development of LDs, reduces the specific surface area (SSA) of LDs and stimulates fat accumulation in HepG2 cells. By analyzing a series of CIDEC mutants, we revealed the N-domain (1-173 aa) is involved in LD localization and the C-domain (174-238 aa) is necessary for LD fusion. Further analysis indicated that the 106-173 aa region includes an ER-binding domain. Moreover, CIDEC stayed in the ER under lipid deficient conditions and translocated to LDs under fatty acid stimulation suggesting that localization of CIDEC in the ER is prior to the LD. Conclusions: Our data indicated excessive nutrition stimulated hepatic CIDEC expression and an increasing level of CIDEC induced hepatic LD fusion and fat accumulation. Our work suggests that CIDEC protects LDs by decreasing the SSA of LDs and is involved in the development of fatty liver.
Abstract:miRNAs are a large family of small regulatory elements that direct messenger RNA degradation or disrupt mRNA translation. High-throughput Solexa sequencing approa
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