Ji Liu

Harbin Medical University, Charbin, Heilongjiang Sheng, China

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Publications (4)10.42 Total impact

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    ABSTRACT: Type VI secretion system (T6SS) has increasingly been believed to participate in the infection process for many bacterial pathogens, but its role in the virulence of Salmonella typhimurium remains unclear. To look into this, we deleted the T6SS cluster from the genome of S. typhimurium 14028s and analyzed the phenotype of the resulting T6SS knockout mutant (T6SSKO mutant) in vitro and in vivo. We found that the T6SSKO mutant exhibited reduced capability in colonizing the spleen and liver in an in vivo colonization competition model in BALB/c mice infected by the oral route. Additionally, infection via intraperitoneal administration also showed that the T6SSKO mutant was less capable of colonizing the mouse spleen and liver than the wild-type strain. We did not detect significant differences between the T6SSKO and wild-type strains in epithelial cell invasion tests. However, in the macrophage RAW264.7 cell line, the T6SSKO mutant survived and proliferated significantly more poorly than the wild-type strain. These findings indicate that T6SS gene cluster is required for full virulence of S. typhimurium 14028s in BALB/c mice, possibly due to its roles in bacterial survival and proliferation in macrophages. (© 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim).
    No preview · Article · Jul 2013 · Journal of Basic Microbiology
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    ABSTRACT: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited disease leading to recurrent ischemic stroke and vascular dementia. Numerous mutations in the 23 exons of the NOTCH3 gene have been reported to cause CADASIL in Caucasian populations, but the full spectrum of genetic changes leading to this disease is yet to be known and, especially, very few reports are available on CADASIL in Asian populations. We genotyped members of a 5-generational Han Chinese family with CADASIL patients and identified an R133C mutation in the NOTCH3 gene. Clinical analysis demonstrated that the penetrance of the mutation was not complete. Five of the mutation carriers, not exposed to the known vascular risk factors, did not show any clinical feature of CADASIL, suggesting the importance of environmental factors to the development of this disease. Members of a 5-generational Han Chinese family with CADASIL patients had an R133C mutation in the NOTCH3 gene but only individuals exposed to known vascular risk factors developed CADASIL.
    Full-text · Article · May 2012 · PLoS ONE
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    ABSTRACT: Salmonella virulence plasmids (VPs) contribute to pathogenesis during the systemic phase of infection. Only eight serovars have been found to contain VP, and the size of VP is unique to the host serovar, suggesting VPs are mainly transmitted vertically. According to this hypothesis, VPs should have the same phylogenetic relationships as the chromosomes among the bacteria that carry the VPs. To test this hypothesis, we sequenced VPs from the serovar Enteritidis and Pullorum, named pSENV and pSPUV, respectively, and compared them with VPs from other Salmonella serovars. The overall results supported our hypothesis with the exception of pSENV, which was more similar to VPs from the more distantly related serovars Typhimuirum, Choleraesuis and Paratyphi C than to those from the very closely related serovars Dublin and Gallinarum/Pullorum with regard to either gene content or nucleotide similarity. These findings demonstrate that Enteritidis acquired pSENV by horizontal transfer.
    Full-text · Article · Mar 2012 · Infection, genetics and evolution: journal of molecular epidemiology and evolutionary genetics in infectious diseases
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    ABSTRACT: Hypokalemic periodic paralysis (HypoPP) is an autosomal dominant disorder characterized by periodic attacks of muscle weakness associated with a decrease in the serum potassium level. Several mutations in the skeletal muscle calcium channel α-subunit gene CACNA1S have been documented to be causative for HypoPP, but mutations in other genes have also been implicated in HypoPP. To further reveal the genetic causes of HypoPP, we genotyped members of a five-generational Chinese family with HypoPP patients and identified a novel His916Gln mutation in all male HypoPP patients of the family. Clinical analysis demonstrated that the penetrance of the mutation was complete in male carriers, but we did not find evident clinical features in female carriers. This study expanded the spectrum of CACNA1S mutations associated with HypoPP and demonstrated a gender difference in the penetrance of the disease.
    Full-text · Article · Aug 2011 · Journal of Molecular Neuroscience