Growth curve and cell cycle analysis Cells were seeded into 24 well plate and cultured as described above. Cells were dissociated from the plate and cell number counted every 24 hrs. For cell cycle analysis, cells were fixed in 70% ethanol for 1hr at 4 C after washing in PBS1% Glu cose and pelleted. Cells were then re suspended in 1ml of propidium selleck chem iodide solution and incubated at 37 C for 1hr. Cells were filtered through 40 70 um mesh and cell cycle pro file was analyzed with the FACSCalibur flow cytometer. Data represents mean SD from three independent experiments. Tumor formation assay The study was conducted in accordance with the guide lines for the Care and Use of Laboratory Animals in Guangzhou Institutes of Biomedicine and Health.

Before transplantation, MCF 7 cells stably ex pressing SNX16, SNX2 or a control vector were re suspended in cell culture medium and cell number was counted. Six week old SCID mice were inoculated subcutaneously with the MCF 7 cells. Tumors were dissected and weighed 27 days post implantation. Background Brain inflammation accompanied by brain injury Inhibitors,Modulators,Libraries has been a focus of research efforts because of its possible roles in the onset and progression of a number of neurodegenera tive diseases. However, most brain inflammation studies have focused on neurons, and little information on how brain inflammation affects other brain cells, Inhibitors,Modulators,Libraries including astrocytes and oligodendrocytes, is available. Astrocytes function to maintain the homeostasis of the brain micro environment by taking up potassium, glutamate, and water from the extracellular space, and supplying nutri ents and growth factors to neurons.

Oligodendrocytes myelinate axons, allowing for rapid propagation of action potentials to axon terminals. Inhibitors,Modulators,Libraries Therefore, it is important to know how these cells respond to brain injury. Studies of systemic inflammation showed that inflam mation has dual functions a cytotoxic function to kill infected microbes and a repair function to regenerate damaged tissues. In the presence of proinflammatory stimulators Inhibitors,Modulators,Libraries such as IFN, monocytesmacrophages are classically activated and protect the tissue from infection by producing cytotoxic inflammatory molecules. On the other hand, in the presence of IL 4 and IL 13, monocytesmacrophages are alternatively activated, and produce several molecules that are involved in anti inflammation and repairregeneration.

Therefore, in myocardial injury, monocytesmacrophages rapidly remo ve cell debris and lead to myofibroblast infiltration and collagen deposition through production of high levels of TGF B and VEGF A. In injured skin, macrophage depletion causes delays in healing processes. Previously, we reported that in lipopolysaccharide Inhibitors,Modulators,Libraries or ATP injected brain and contusion induced spinal cord, resident microglia as well as neurons die in the damage core and monocytes appear and fill the damage core. In the ischemic http://www.selleckchem.com/products/Rapamycin.html brain, infiltration of blood monocytes has been reported.