Central Hospital of Taizhou City

Taizhou, China

Central Hospital of Taizhou City

Taizhou, China
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Zhang L.,Fudan University | Zhang L.,Central Hospital of Taizhou City | Zhu C.,Fudan University | Guo Y.,Shenyang University | And 10 more authors.
Journal of Virology | Year: 2014

Hypoxia-inducible factor 1α (HIF-1α) has been frequently implicated in many cancers as well as viral pathogenesis. Kaposi's sarcoma-associated herpesvirus (KSHV) is linked to several human malignancies. It can stabilize HIF-1α during latent infection and undergoes lytic replication in response to hypoxic stress. However, the mechanism by which KSHV controls its latent and lytic life cycle through the deregulation of HIF-1α is not fully understood. Our previous studies showed that the hypoxia-sensitive chromatin remodeler KAP1 was targeted by the KSHV-encoded latency-associated nuclear antigen (LANA) to repress expression of the major lytic replication and transcriptional activator (RTA). Here we further report that an RNA interferencebased knockdown of KAP1 in KSHV-infected primary effusion lymphoma (PEL) cells disrupted viral episome stability and abrogated sub-G1/G1 arrest of the cell cycle while increasing the efficiency of KSHV lytic reactivation by hypoxia or using the chemical 12-O-tetradecanoylphorbol-13-acetate (TPA) or sodium butyrate (NaB). Moreover, KSHV genome-wide screening revealed that four hypoxia-responsive clusters have a high concurrence of both RBP-Jk and HIF-1α binding sites (RBS+HRE) within the same gene promoter and are tightly associated with KAP1. Inhibition of KAP1 greatly enhanced the association of RBP-Jk with the HIF-1α complex for driving RTA expression not only in normoxia but also in hypoxia. These results suggest that both KAP1 and the concurrence of RBS+HRE within the RTA promoter are essential for KSHV latency and hypoxia-induced lytic reactivation. © 2014, American Society for Microbiology.


Yuehua X.,Central Hospital of Taizhou City | Shen W.,Disease Control Centerof Taizhou City | Zhou H.,Zhejiang University | Zhou L.,Shanghai Ruijin Hospital | Li Z.,Central Hospital of Taizhou City
Molecular Medicine Reports | Year: 2013

Four clinical isolates of imipenem-resistant Klebsiella pneumoniae were isolated from clinical patient specimens and from samples obtained from hygienic surveillance in our hospital. We examined their minimum inhibitory concentration (MIC) to various types of antibiotics, detected the carbapenemases by a modified Hodge test and analyzed the genotype and homogeneity. The enzyme, Klebsiella pneumoniae carbapenemase (KPC)-2, was detected in all four isolates and this was the main cause of their imipenem resistance. In addition, these four isolates also contained the extended-spectrum β-lactamase (ESBL) gene blaCTX-M-9 and the cephalosporinase (AmpC) gene blaDHA-1, which resulted in multidrug resistance. © 2013 Spandidos Publications Ltd.


Li Z.,Central Hospital of Taizhou City | Chen H.,Central Hospital of Taizhou City | Chen X.,Central Hospital of Taizhou City | Zhou T.,Wenzhou Medical College | And 3 more authors.
Journal of Bacteriology | Year: 2012

Vibrio vulnificus, which is the causative agent of cholera, is a Gram-negative, curved, motile, and rod-shaped bacterium. Here, we present the draft genome sequence of the type strain, ATCC 27562, which was the first isolated Vibrio vulnificus strain. © 2012, American Society for Microbiology.


Liang X.-D.,Nanjing Medical University | Dai Y.-C.,Central Hospital of Taizhou City | Li Z.-Y.,Central Hospital of Taizhou City | Gan M.-F.,Taizhou University | And 9 more authors.
PLoS ONE | Year: 2014

The mitotic spindle checkpoint (SAC) genes have been considered targets of anticancer therapies. Here, we sought to identify the attractive mitotic spindle checkpoint genes appropriate for human hepatocellular carcinoma (HCC) therapies. Through expression profile analysis of 137 selected mitotic spindle checkpoint genes in the publicly available microarray datasets, we showed that 13 genes were dramatically up-regulated in HCC tissues compared to normal livers and adjacent non-tumor tissues. A role of the 13 genes in proliferation was evaluated by knocking them down via small interfering RNA (siRNA) in HCC cells. As a result, several mitotic spindle checkpoint genes were required for maintaining the proliferation of HCC cells, demonstrated by cell viability assay and soft agar colony formation assay. Then we established sorafenib-resistant sublines of HCC cell lines Huh7 and HepG2. Intriguingly, increased TTK expression was significantly associated with acquired sorafenib-resistance in Huh7, HepG2 cells. More importantly, TTK was observably up-regulated in 46 (86.8%) of 53 HCC specimens. A series of in vitro and in vivo functional experiment assays showed that TTK overexpression promoted cell proliferation, anchor-dependent colony formation and resistance to sorafenib of HCC cells; TTK knockdown restrained cell growth, soft agar colony formation and resistance to sorafenib of HCC cells. Collectively, TTK plays an important role in proliferation and sorafenib resistance and could act as a potential therapeutic target for human hepatocellular carcinoma. © 2014 Liang et al.


PubMed | Central Hospital of Taizhou City
Type: Journal Article | Journal: Molecular medicine reports | Year: 2013

Four clinical isolates of imipenem-resistant Klebsiella pneumoniae were isolated from clinical patient specimens and from samples obtained from hygienic surveillance in our hospital. We examined their minimum inhibitory concentration (MIC) to various types of antibiotics, detected the carbapenemases by a modified Hodge test and analyzed the genotype and homogeneity. The enzyme, Klebsiella pneumoniae carbapenemase (KPC)-2, was detected in all four isolates and this was the main cause of their imipenem resistance. In addition, these four isolates also contained the extended-spectrum -lactamase (ESBL) gene blaCTX-M-9 and the cephalosporinase (AmpC) gene blaDHA-1, which resulted in multidrug resistance.

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