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Zhen Q.,Jilin University | Lu Y.,Centers for Disease Control and Prevention | Yuan X.,Academy of Military Medical science | Qiu Y.,Institute of Jingfeng Medical Laboratory Animal | And 7 more authors.
Clinical Microbiology and Infection | Year: 2013

Human brucellosis is mainly caused by contact with Brucella-infected animals and their secretions and carcasses. Individuals who are continuously in contact with animals are considered to be at a high risk but only some show symptoms and are diagnosed as cases of brucellosis. Here, we showed that asymptomatic brucellosis infections occur among humans. Asymptomatic infections mainly result from less frequent contact with Brucella and/or contact with low-virulence Brucella. In our study, patients with asymptomatic infection had low antibody titres and different contact patterns. Awareness of asymptomatic infection is important for early diagnosis of brucellosis and prevention of chronic infection. © 2013 European Society of Clinical Microbiology and Infectious Diseases.


Yang L.,Beijing Institute of Radiation Medicine | Li W.,Institute of JingFeng Medical Laboratory Animal | Liu B.,Centers for Disease Control and Prevention | Wang S.,Beijing Institute of Radiation Medicine | And 3 more authors.
Archives of Dermatological Research | Year: 2016

iRhom2 is necessary for maturation of TNFα-converting enzyme, which is required for the release of tumor necrosis factor. In the previous study, we found that the iRhom2Uncv mutation in N-terminal cytoplasmic domain-encoding region (iRhom2Uncv) leads to aberrant hair shaft and inner root sheath differentiation, thus results in a hairless phenotype in homozygous iRhom2Uncv/Uncv BALB/c mice. In this study, we found iRhom2 mutation decreased hair matrix proliferation, however, iRhom2Uncv/Uncv mice displayed hyperproliferation and hyperkeratosis in the interfollicular epidermis along with hypertrophy in the sebaceous glands. The number of bulge SCs was not altered and the hair follicle cycle is normal in iRhom2Uncv/Uncv mice. The decreased proliferation in hair matrix but increased proliferation in epidermis and sebaceous glands in iRhom2Uncv/Uncv mice may implying that iRhom2Uncv mutation blocks bugle stem cells assuming the fate of hair follicle. This study identifies iRhom2 as a novel regulator for determination of keratinocyte lineages. © 2016 Springer-Verlag Berlin Heidelberg


Liu B.,Institute of JingFeng Medical Laboratory Animal | Xu Y.,Institute of JingFeng Medical Laboratory Animal | Li W.-L.,Institute of JingFeng Medical Laboratory Animal | Zeng L.,Institute of JingFeng Medical Laboratory Animal
BMB Reports | Year: 2015

A mouse homozygous for the spontaneous mutation uncovered (Uncv) has a hairless phenotype. A 309-bp non-frameshift deletion mutation in the N-terminal cytoplasmic domain of iRhom2 was identified in Uncv mice (iRhom2Uncv) using target region sequencing. The detailed molecular basis for how the iRhom2 mutation causes the hairless phenotype observed in the homozygous iRhom2Uncv mouse remains unknown. To identify differentially expressed proteins in the skin of wild-type and homozygous iRhom2Uncv littermates at postnatal day 5, proteomic approaches, including two-dimensional gel electrophoresis and mass spectrometry were used. Twelve proteins were differentially expressed in the skin in a comparison between wild-type and homozygous iRhom2Uncv mice. A selection of the proteomic results were tested and verified using qRT-PCR, western blot and immunohistochemistry. These data indicate that differentially expressed proteins, especially KRT73, MEMO1 and Coro-1, might participate in the mechanism by which iRhom2 regulates the development of murine skin. © 2015 by The Korean Society for Biochemistry and Molecular Biology.


Wenlong L.,Institute of JingFeng Medical Laboratory Animal | Leilei Y.,Beijing Institute of Radiation Medicine | Wei F.,Institute of JingFeng Medical Laboratory Animal | Yi C.,Beijing Institute of Biotechnology | And 8 more authors.
Biotechnology Letters | Year: 2015

Objectives: We used optical imaging of live animals and transgenic technology to develop a pulmonary fibrosis model in mice that can non-invasively and in real-time trace the pulmonary fibrosis process. Results: Fibroblast activation protein-α (FAPα) is selectively expressed in fibrotic foci of human pulmonary fibrosis. It is not expressed in normal tissue. We confirmed that FAPα is upregulated in fibroblasts of murine pulmonary fibrosis. Moreover, TGF-β1, a central pathological mediator of fibrotic diseases, could promote FAPα expression in mouse embryonic fibroblasts. Luciferase reporter assays showed that 5.4 kb FAPα promoter response activities to TGF-β1 was stronger than of the 2.1 kb promoter. We generated a transgenic mouse line expressing firefly luciferase under the control of the 5.4 kb FAPα gene promoter (FAPα-p-luc). After experimentally inducing murine pulmonary fibrosis, there luminescence appeared in the chests and excised lungs of FAPα-p-luc mice. The intensity of luminescence became stronger with the exacerbation of pulmonary fibrosis. Conclusion: Fluorescence intensity reflects the degree of pulmonary fibrosis in FAPα-p-luc mice. and this mouse model may be used to investigate molecular mechanisms and drug screening of pulmonary fibrosis. © 2015, Springer Science+Business Media Dordrecht.


Leilei Y.,Beijing Institute of Radiation Medicine | Bing L.,Institute of JingFeng Medical Laboratory Animal | Yang L.,Beijing Institute of Radiation Medicine | Shaoxia W.,Beijing Institute of Radiation Medicine | And 8 more authors.
PLoS ONE | Year: 2014

iRhom1 and iRhom2 are inactive homologues of rhomboid intramembrane serine proteases lacking essential catalytic residues, which are necessary for the maturation of TNFα-converting enzyme (TACE). In addition, iRhoms regulate epidermal growth factor family secretion. The functional significance of iRhom2 during mammalian development is largely unclear. We have identified a spontaneous single gene deletion mutation of iRhom2 in Uncv mice. The iRhom2Uncv/Uncv mice exhibit hairless phenotype in a BALB/c genetic background. In this study, we observed dysplasia hair follicles in iRhom2Uncv/Uncv mice from postnatal day 3. Further examination found decreased hair matrix proliferation and aberrant hair shaft and inner root sheath differentiation in iRhom2Uncv/Uncv mutant hair follicles. iRhom2 is required for the maturation of TACE. Our data demonstrate that iRhom2Uncv cannot induce the maturation of TACE in vitro and the level of mature TACE is also significantly reduced in the skin of iRhom2Uncv/Uncv mice. The activation of Notch1, a substrate of TACE, is disturbed, associated with dramatically down-regulation of Lef1 in iRhom2Uncv/Uncv hair follicle matrix. This study identifies iRhom2 as a novel regulator of hair shaft and inner root sheath differentiation. © 2014 Leilei et al.


PubMed | Institute of JingFeng Medical Laboratory Animal
Type: Journal Article | Journal: Biotechnology letters | Year: 2015

We used optical imaging of live animals and transgenic technology to develop a pulmonary fibrosis model in mice that can non-invasively and in real-time trace the pulmonary fibrosis process.Fibroblast activation protein- (FAP) is selectively expressed in fibrotic foci of human pulmonary fibrosis. It is not expressed in normal tissue. We confirmed that FAP is upregulated in fibroblasts of murine pulmonary fibrosis. Moreover, TGF-1, a central pathological mediator of fibrotic diseases, could promote FAP expression in mouse embryonic fibroblasts. Luciferase reporter assays showed that 5.4kb FAP promoter response activities to TGF-1 was stronger than of the 2.1kb promoter. We generated a transgenic mouse line expressing firefly luciferase under the control of the 5.4kb FAP gene promoter (FAP-p-luc). After experimentally inducing murine pulmonary fibrosis, there luminescence appeared in the chests and excised lungs of FAP-p-luc mice. The intensity of luminescence became stronger with the exacerbation of pulmonary fibrosis.Fluorescence intensity reflects the degree of pulmonary fibrosis in FAP-p-luc mice. and this mouse model may be used to investigate molecular mechanisms and drug screening of pulmonary fibrosis.

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