Influenza virus H1N1 induced apoptosis of mouse astrocytes and the effect on protein expression.

OBJECTIVE: To investigate the effects of influenza A virus H1N1 infection on the proliferation and apoptosis of mouse astrocytes cells and its protein expression. METHODS: After mouse astrocytes was infected with purified influenza A virus H1N1 in vitro, viral integration and replication status of the cells were detected by RT-PCR assay, cell proliferation and apoptosis was determined by MTT method and flow cytometry, respectively. Associated protein expression was detected by Western blotting. RESULTS: Agarose gel electrophoresis showed H1N1 virus can infect astrocytes and can be copied. MTT staining showed H1N1 virus infection can inhibit the proliferation of mouse astrocytes, which makes cell viability decreased significantly. Flow cytometry showed that the proportion of Annein V staining positive vascular endothelial cells in the influenza A virus group was significantly higher than that in the control group. Western blot analysis showed after 24 h and 32 h of infection, there were cells caspase-3 protein and the expression of its active form (lysed caspase-3 protein) increased. The proportion of Bax/Bcl-2 also increased. CONCLUSIONS: Influenza A virus can infect human vascular endothelial cells and proliferation and it can induce apoptosis of endothelial cells.

[Effects of simvastatin on homocysteine-induced endothelial dysfunction and inflammatory response].

OBJECTIVE: To investigate the effects of simvastatin (SIM) on homocysteine (HCY)-induced endothelial dysfunction and inflammatory response. METHODS: Human umbilical vein endothelial cells (HUVECs) were isolated from the umbilical cords from healthy lying-in women and cultured and added with HCY of the concentrations of 0.1, 0.25, 0.5, and 1 mmol/L respectively, or HCY 0.25 mmol/L + SIM of the concentrations of 1, 10 and 20 micromol/L respectively for 1 hour. ELISA was used to detect the cell viability with MTT method. Western blotting was used to examine the protein expression of the cell inflammatory factors, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, macrophage chemoattractant protein (MCP)-1, and intercellular adhesion molecule (ICAM)-1, ELISA was used to detect the contents of the cell inflammatory factors. RESULTS: HCY of different doses inhibited the viability of HUVECs dose-dependently (all P < 0. 01). The survival rates of the HCY-induced HUVECs pretreatment by SIM of the concentrations of 1, 10 and 20 micromol/L for 1 hour were 1.72 +/- 0.03 times, 2.54 +/- 0.09 times, and 3.14 +/- 0.11 times respectively that of the control group (all P < 0. 01). HCY of different concentration of 0.25 mmol/L increased the protein expression of TNF-alpha, IL-6, MCP-1, and ICAM-1 significantly; however, the expression levels of TNF-alpha, IL-6, MCP-1, and ICAM-1 of the 0.25 mmol/L HCY-treated HUVECs that were pretreated by SIM of the concentration of 10 micromol/L for 1 hour were, 0.23 +/- 0.05, 0.14 +/- 0.03, 0.13 +/- 0.04, and 0.21 +/- 0.07 respectively, not significantly different from those at the time of 0 hour (all P > 0.05). CONCLUSION: Simvastatin inhibits the homocysteine-induced endothelial impairment and inflammatory response.

[Optical-fiber Fourier transform spectrometer].

A novel Fourier transform spectrum analyzer based on a single mode fiber Mach-Zehnder interferometer is reported. An optical fiber Fourier transform spectrometer, with bulk optics components replaced by fiber optical components and with the moving mirror replaced by a piezoelectric element fiber stretcher was constructed. The output spectrum of a LD below threshold was measured. Experiment result agrees with that by using grating spectrum analyzer, showing the feasibility of the optic fiber Fourier transform spectrometer for practical spectrum measurement. Spectrum resolution -7 cm(-1) was obtained in our experiment. The resolution can be further improved by increasing the maximum optical path difference.

Molecular modeling of the bacterial outer membrane receptor energizer, ExbBD/TonB, based on homology with the flagellar motor, MotAB.

The MotA/MotB proteins serve as the motor that drives bacterial flagellar rotation in response to the proton motive force (pmf). They have been shown to comprise a transmembrane proton pathway. The ExbB/ExbD/TonB protein complex serves to energize transport of iron siderophores and vitamin B12 across the outer membrane of the Gram-negative bacterial cell using the pmf. These two protein complexes have the same topology and are homologous. Based on molecular data for the MotA/MotB proteins, we propose simple three-dimensional channel structures for both MotA/MotB and ExbB/ExbD/TonB using modeling methods. Features of the derived channels are discussed, and two possible proton transfer pathways for the ExbBD/TonB system are proposed. These analyses provide a guide for molecular studies aimed at elucidating the mechanism by which chemiosmotic energy can be transferred either between two adjacent membranes to energize outer membrane transport or to the bacterial flagellum to generate torque.