Objective To screen the optimum conditions carrying murine melanoma B16 cells in spaceflights without cares.MethodsMurine melanoma cells were cultured on micocarriers and grouped depending on cells concentration, serum concentration, microcarrier number and temperature.After 33 days, B16 cells were stained by Giemsa, observed with phase-contrast microscope and counted for surviving percentage.ResultsThe optimum conditions,in which the surviving percentages were 8% and 10%, were obtained in the experiments.B16 cells were carried in the 20th recoverable satellite orbiting 18 days under the optimum conditions. After recovering, 110 strain monocloned cells were survived and the surviving percentage was 1.1%.ConclusionThe optimum conditions carrying murine melanoma B16 cells in spaceflights without cares seems to be obtained,and it did improve the surviving time and percentage of cells in spaceflights without cares.

ObjectiveTo search for a new method of anti-tumor immunity,using mutated tumor cells by spaceflight.MethodsTumor cells were carried in the Shenzhou 4 and the recoverable satellite No.18.After 7 days and 18 days spaceflight respectively,the effects of spaceflight were investigated primarily.Results2382 and 1 strains of mutated tumor cells from the airship No.4 and the recoverable satellite No.18 had been obtained respectively. Comparing with the control group, the growth rate of mutated cells decreased, moreover, the secretion of cytokines also changed.ConclusionSpaceflight may affect physiological characteristics of tumor cells, and that, there was a negative correlation between the ratio of surviving cells and carrying time.

BACKGROUND: Epidemiological studies have suggested that noise exposure may increase the risk of type 2 diabetes mellitus (T2DM), and experimental studies have demonstrated that noise exposure can induce insulin resistance in rodents. The aim of the present study was to explore noise-induced processes underlying impaired insulin sensitivity in mice. METHODS: Male ICR mice were randomly divided into four groups: a control group without noise exposure and three noise groups exposed to white noise at a 95-dB sound pressure level for 4 h/day for 1, 10, or 20 days (N1D, N10D, and N20D, respectively). Systemic insulin sensitivity was evaluated at 1 day, 1 week, and 1 month post-noise exposure (1DPN, 1WPN, and 1MPN) via insulin tolerance tests (ITTs). Several insulin-related processes, including the phosphorylation of Akt, IRS1, and JNK in the animals' skeletal muscles, were examined using standard immunoblots. Biomarkers of inflammation (circulating levels of TNF-α and IL-6) and oxidative stress (SOD and CAT activities and MDA levels in skeletal muscles) were measured via chemical analyses. RESULTS: The data obtained in this study showed the following: (1) The impairment of systemic insulin sensitivity was transient in the N1D group but prolonged in the N10D and N20D groups. (2) Noise exposure led to enhanced JNK phosphorylation and IRS1 serine phosphorylation as well as reduced Akt phosphorylation in skeletal muscles in response to exogenous insulin stimulation. (3) Plasma levels of TNF-α and IL-6, CAT activity, and MDA concentrations in skeletal muscles were elevated after 20 days of noise exposure. CONCLUSIONS Impaired insulin sensitivity in noise-exposed mice might be mediated by an enhancement of the JNK/IRS1 pathway. Inflammation and oxidative stress might contribute to insulin resistance after chronic noise exposure.
Animals ; Biomarkers ; metabolism ; Inflammation ; physiopathology ; Insulin Receptor Substrate Proteins ; genetics ; metabolism ; Insulin Resistance ; genetics ; immunology ; MAP Kinase Signaling System ; physiology ; Male ; Mice ; Mice, Inbred ICR ; Mitogen-Activated Protein Kinase 8 ; genetics ; metabolism ; Noise ; adverse effects ; Oxidative Stress ; physiology ; Proto-Oncogene Proteins c-akt ; genetics ; metabolism ; Random Allocation ; Time Factors