ABSTRACT
To investigate the role of the transcription factor p53 in the course of the dengue virus (DV) infection. The human hepatocellular carcinoma cell strain HepG2 with a low expression level of p53 was built by using the retroviral-mediated RNA interference technology, and was detected by Western blot. The wild group and the interference group were respectively infected by the type 2 DV. The viral titration was detected by the Vero plaque assay, the viral multiplication was detected by the immunofluorescence, the cell apoptosis after virus infection was detected by FCM and the level of IFN-ß was analyzed by ELISA. Compared to the wild group, the expression level of p53 in the interference group decreased significantly, which indicated that the HepG2 cell strain with the low expression level of p53 was successfully built. 24h after DV infection, the virus titration in the interference group was 100 times higher than that in the wild group. The result of the immunofluorescence showed that, the amount of green fluorescent cells in the interference group was significant higher than that in the wild group. It was indicated that the DV infection was inhibited by p53. However, 24h after DV infection, there was no significant difference in the amount of apoptotic cells in both groups. And the amount of IFN-ß in the wild group increased 6 times. The DV infection was inhibited by the transcription factor p53 by activating type I interferon pathway other than promoting the cell apoptosis.
Subject(s)
Dengue Virus/physiology , Dengue/metabolism , Dengue/virology , Interferon Type I/biosynthesis , Transcription Factors/metabolism , Tumor Suppressor Protein p53/metabolism , Apoptosis , Dengue/genetics , Enzyme-Linked Immunosorbent Assay , Gene Expression , Hep G2 Cells , Humans , Signal Transduction , Transcription Factors/genetics , Tumor Suppressor Protein p53/genetics , Viral LoadABSTRACT
Acquisition of the staphylococcal chromosome cassette mec (SCCmec) is one of the key reasons for the resistance of methicillin-resistant Staphylococcus aureus (MRSA). SCCmec is composed of a mec gene complex encoding the PBP2a determinant that is responsible for the ß-lactam resistance of MRSA, and a ccr gene complex encoding recombinases that mediate the integration of SCCmec into and its excision from the recipient chromosome, and so-called three junkyard (J) regions of different sizes. The SCCmec elements carried by MRSA from different geographic locations are diverse, and each type contains characteristic DNA fragments in size. These characteristics of SCCmec element may facilitate the usage of SCCmec in the molecular typing of MRSA strains. In this review, we summarize the structure and function of SCCmec elecments, and discuss the application of SCCmec elements in the molecular typing of MRSA.
Subject(s)
DNA Transposable Elements , Methicillin-Resistant Staphylococcus aureus/isolation & purification , Staphylococcal Infections/microbiology , Animals , Bacterial Proteins/genetics , Bacterial Proteins/metabolism , Humans , Methicillin-Resistant Staphylococcus aureus/classification , Methicillin-Resistant Staphylococcus aureus/enzymology , Methicillin-Resistant Staphylococcus aureus/genetics , Molecular Typing , Recombinases/genetics , Recombinases/metabolismSubject(s)
Behavior , Education, Nursing/methods , Health Knowledge, Attitudes, Practice , Hygiene , Awareness , China , Humans , Students, NursingABSTRACT
Our previous study showed that dengue virus 2 (DENV2) infection induces rearrangement of vimentin into dense structures at the perinuclear area. However, the underlying mechanism of this phenomenon is poorly characterized. In the present work, we found that vimentin and Ser71 phosphorylated vimentin display similar distributions in DENV2-infected cells. DENV2 infection also induced ROCK activation and phosphorylation of vimentin at Ser71 as the DENV2 infection progressed. Furthermore, Ser71 phosphorylation and vimentin rearrangement induced by DENV2 infection were blocked by the ROCK inhibitor Y-27632. In addition, DENV2 led to endoplasmic reticulum (ER) redistribution in the perinuclear region of the host cells, which was partially blocked by pretreatment with Y-27632. Together, these data support indicate that ROCK may have a role in governing regulating vimentin and ER rearrangement during DENV2 infection. We hypothesize that DENV2 infection, via ROCK activation, induces both vimentin rearrangement and ER redistribution around the perinuclear region, which may play a structural role in anchoring DENV2 to replication sites.
Subject(s)
Dengue Virus/physiology , Vimentin/metabolism , rho-Associated Kinases/metabolism , Amides/pharmacology , Cell Line , Endoplasmic Reticulum/drug effects , Endoplasmic Reticulum/metabolism , Endoplasmic Reticulum/virology , Humans , Phosphorylation/drug effects , Pyridines/pharmacology , Virus Replication , rho-Associated Kinases/antagonists & inhibitorsABSTRACT
A series of novel amine-derived bis-azole compounds were designed by the systematical structural modification of Fluconazole and synthesized by a convenient and efficient method, and the antimicrobial activities for all prepared compounds were evaluated in vitro against six representative bacterial strains and two fungal strains. Bioactive results indicated that some synthesized compounds exhibited moderate or even better activities in comparison with the reference drugs. Especially, bis-imidazole 5b and its salts gave significant antibacterial efficacy against all tested bacteria strains including MRSA, while bis-triazoles 4b-c and their corresponding salts exhibited better activities against Candida albicans, Bacillus proteus than standard drugs Fluconazole and Norfloxacin respectively. Unexpectedly, bis-bromides 3a-f presented excellent activities against all tested microbial strains.
