Mechanism underlying the bio-effects of an electromagnetic field based on the Huang-Ferrell model.

To understand the beneficial and harmful bio-effects of extremely low frequency electromagnetic fields, we studied the MAPK/ERK signaling pathway based on the Huang-Ferrell model. The sensitivity analysis method was used to study the influence of the model parameters on the activity of ERK, and to further investigate the key biochemical reactions and proteins. The results of the simulation show that an increase in the reaction rate of MAPK/ERK kinase had little effect on ERK activation and the steady-state molecular number. However, a decrease in the reaction rate of MAPK/ERK kinase significantly affected the trigger time of ERK activation and decreased the steady-state molecular number. Together with the biological significance of ERK activity, our findings indicate that the effects of electromagnetic fields are a result of the decrease in the reaction rate of MAPK/ERK kinase, which eventually determines whether these effects cause physical damage or are beneficial in treatment.

Effect of RNAi-mediated silencing of Livin gene on biological properties of colon cancer cell line LoVo.

This study aimed to investigate the effect of RNAi-mediated silencing of the Livin gene on biological properties of the colon cancer cell line LoVo. Interference vectors pSilencer4.1-Ll and pSilencer4.1-L2 targeting the Livin gene were constructed and transfected into LoVo cells. The expression of the Livin gene was determined by RT-PCR and Western blotting. The apoptosis, cell cycle, colony formation, proliferation of LoVo cells, as well as their sensitivity to cisplatin, were detected by flow cytometry, colony formation assay and MTT. Livin mRNA and protein expression in LoVo cells could be effectively silenced by pSilencer4.1-Ll but not pSilencer4.1-L2. In the pSilencer4.1-Ll transfection group, the apoptosis rate of LoVo cells was significantly higher than in the control group (24.2 ± 3.2 vs 8.1 ± 1.4%, P < 0.01), and after 72 h, cell proliferation was clearly decreased (about 70% inhibition). Compared with the control group, the colony formation rate in pSilencer4.1-Ll transfection group was obviously decreased (15 ± 4.6 vs 85 ± 5.8%, P < 0.01), with increased proportion of S phase cells (45.7 ± 4.9 vs 28.0 ± 3.0%, P < 0.01), decreased proportion of G1 phase cells (43.0 ± 5.2 vs 62.8 ± 5.1%, P < 0.01), and increased sensitivity to cisplatin (apoptosis rate increased from 43.4 ± 6.9 to 65.3 ± 6.2%, P < 0.01). pSilencer4.1-Ll can effectively silence Livin gene expression in LoVo colon cancer cells, inhibit cell proliferation and colony formation, induce apoptosis, and enhance sensitivity to cisplatin.

Molecular analysis and frequency of Staphylococcus aureus virulence genes isolated from bloodstream infections in a teaching hospital in Tianjin, China.

Staphylococcus aureus is an important cause of bloodstream infections worldwide. We examined the prevalence of genes that encode erythromycin ribosome methylase and bacterial toxins in S. aureus collected from bloodstream infections. Sixty different S. aureus isolates were obtained from blood cultures of patients who were admitted to a Teaching Hospital in Tianjin from January 2006 to August 2011. The susceptibility of the isolates to 16 antibiotics was tested. Methicillin-resistant S. aureus (MRSA) was identified using the disk diffusion method with cefoxitin. PCR was used to detect genes that encode the staphylococcal enterotoxins, Panton-Valentine leukocidin, toxic shock syndrome toxin 1 and erythromycin ribosome methylase. Molecular analysis of the MRSA strains was done using pulsed-field gel electrophoresis (PFGE) and staphylococcal cassette chromosome mec (SCCmec) typing. The positivity rates of mecA, ermA, ermB, and ermC in the isolates were 13/60, 10/60, 18/60, and 18/60, respectively. Among the 60 isolates, 30 harbored enterotoxin genes, with sea as the most frequent toxin gene (33%), followed by sec (15%), sed (12%), and seb (5%). The see and tst genes were not found in any of the isolates. The pvl gene was detected in four strains. Eleven MRSA isolates were of the SCCmec type III; two MRSA isolates could not be determined through SCCmec typing. PFGE analysis of the 13 MRSA isolates produced 8 distinct pulsotypes. Virulence genes and erythromycin ribosome methylase genes were highly prevalent in these isolates. The PFGE results demonstrated that the MRSA spread through cloning, mainly involving SCCmec type III.