Objective:The mouse mammary cancer cell line IL-23/MA-891 expressing IL-23 protein was set up and the effect of IL-23 on growth and other biological character of the cells was studied.Methods:The IL-23 gene was sequencely transfected into two packing cell lines (ecotropic ?2 and amphotropic PA317) by a retrovirus vector (LXSN),and the positive cellular clones were screened by G418.After infection to MA-891 cells with the culture supernatant of IL-23/PA317 cells and selected with G418,the IL-23/MA-891 cells to express IL-23 mRNA and protein was detected with RT-PCR,ELISA and immunocytochemical stairing,respectively.The expression of H-2Kb(MHCⅠ),I-Ab(MHC Ⅱ),CD80,CD86 and FAS was examined with flow cytometry.The ability to secrete IFN-? by mouse splenocytes stimulated with the culture supernatant of IL-23/MA-891 cells was detected with ELISA.The proliferation of MA-891,LXSN/MA-891 and IL-23/MA-891 cells was detected by MTT colorimetry and flow cytometry in vitro.Results:IL-23/MA-891 cells express IL-23 stably in mRNA and protein level.The expressing of H-2Kb(MHCⅠ),I-Ab( MHCⅡ),CD80,CD86 and FAS protein by flow cytometry were showing no difference in three kinds of cells.The proliferation rate of IL-23/MA-891 cells were showing little decresed,but statistically showing no difference with parental cells.The culture supernatant of IL-23/MA-891 cells induced secretion of IFN-? by mouse splenocytes were increased compared to parental cells.Conclusion:The cellular clone IL-23/MA-891 with high level expression of IL-23 was produced.

Objective To investigate laparoscopic management in patients of posttraumatic acute acaleulous cholecystitis (AAC).Methods In this study,laparoscopic exploration was performed in 14 AAC cases during the past 5 years.Results Nine patients were treated with laparoscopic cholecystectomy,three by laparoscopic subtotal cholecystectomy,two were converted to open surgery.All patients were cured without major complications.Conclusions Laparoscopic cholecystectomy in the treatment of AAC is safe,less traumatic and quickly recovery in carefully selected AAC patients.

Many people affected by fragile X syndrome (FXS) and autism spectrum disorders have sensory processing deficits, such as hypersensitivity to auditory, tactile, and visual stimuli. Like FXS in humans, loss of Fmr1 in rodents also cause sensory, behavioral, and cognitive deficits. However, the neural mechanisms underlying sensory impairment, especially vision impairment, remain unclear. It remains elusive whether the visual processing deficits originate from corrupted inputs, impaired perception in the primary sensory cortex, or altered integration in the higher cortex, and there is no effective treatment. In this study, we used a genetic knockout mouse model (Fmr1^KO), in vivo imaging, and behavioral measurements to show that the loss of Fmr1 impaired signal processing in the primary visual cortex (V1). Specifically, Fmr1^KO mice showed enhanced responses to low-intensity stimuli but normal responses to high-intensity stimuli. This abnormality was accompanied by enhancements in local network connectivity in V1 microcircuits and increased dendritic complexity of V1 neurons. These effects were ameliorated by the acute application of GABA_A receptor activators, which enhanced the activity of inhibitory neurons, or by reintroducing Fmr1 gene expression in knockout V1 neurons in both juvenile and young-adult mice. Overall, V1 plays an important role in the visual abnormalities of Fmr1^KO mice and it could be possible to rescue the sensory disturbances in developed FXS and autism patients.
Animals ; Disease Models, Animal ; Fragile X Mental Retardation Protein/metabolism* ; Fragile X Syndrome/metabolism* ; Humans ; Mice ; Mice, Knockout ; Neurons/metabolism*