The role of residence time in diagnostic models of global carbon storage capacity: model decomposition based on a traceable scheme.

As a key factor that determines carbon storage capacity, residence time (τE) is not well constrained in terrestrial biosphere models. This factor is recognized as an important source of model uncertainty. In this study, to understand how τE influences terrestrial carbon storage prediction in diagnostic models, we introduced a model decomposition scheme in the Boreal Ecosystem Productivity Simulator (BEPS) and then compared it with a prognostic model. The result showed that τE ranged from 32.7 to 158.2 years. The baseline residence time (τ'E) was stable for each biome, ranging from 12 to 53.7 years for forest biomes and 4.2 to 5.3 years for non-forest biomes. The spatiotemporal variations in τE were mainly determined by the environmental scalar (ξ). By comparing models, we found that the BEPS uses a more detailed pool construction but rougher parameterization for carbon allocation and decomposition. With respect to ξ comparison, the global difference in the temperature scalar (ξt) averaged 0.045, whereas the moisture scalar (ξw) had a much larger variation, with an average of 0.312. We propose that further evaluations and improvements in τ'E and ξw predictions are essential to reduce the uncertainties in predicting carbon storage by the BEPS and similar diagnostic models.

Effect of hyperthermia on tight junctions of endothelial cells in the in vitro blood-brain barrier model and its molecular mechanism / 中华创伤杂志

Objective To discuss the effect of hyperthermia on tight junctions of the endothelial cells in the blood-brain barrier and explore the molecular mechanism. Methods An in vitro blood-brain barrier model was established by coculture of ECV304 and astrocytes. Transendothelial resistance (TER) of in vitro blood-brain barrier was determined by Millicell-ERS system. The morphological change of tight junctions of the endothelial cells in the in vitro blood-brain barrier was determined by the method of silver staining. The expression levels of zonula occluden 1 (ZO-1) and occludin were analyzed by means of semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and Western bloting. Results After two hours at 43℃, the mean value of TER was decreased from (321.30? 58.59) ??cm2 to (65.67?6.02) ??cm2. The integrity of tight junctions was destroyed and the expressions of ZO-1 and occludin decreased significantly. Conclusions Hyperthermia can destroy the tight junctions of the endothelial cells in the in vitro blood-brain barrier. The expression decrease of ZO-1 and occludin induced by hyperthermia is one of the most important molecular mechanisms.

Changes of aquaporin expression in blood-brain barrier induced by glioma cells / 中国病理生理杂志

AIM: To investigate the effects of glioma cells on aquaporin expression in blood-brain barrier and their importance in pathophysiology. METHODS: A blood-brain barrier model was established by coculture of ECV304 and astrocytes in vitro . HPLC was used to determine the change of water transport of in vitro blood-brain barrier model after the influence of glioma cells. The expression levels of AQP1 and AQP4 were analyzed by semiquatitative RT-PCR. RESULTS: Glioma cells decreased expression level of AQP4 of astrocytes and induced abnormal expression of aquaporin-1 in endothelial cell line. The water transport of in vitro blood-brain barrier model from luminal side to abluminal side was increased after coculture with glioma cells. CONCLUSION: The vasogenic brain edema induced by glioma cells may not be the result of hyperpermeability of blood-brain barrier to macromolecules in plasma. The changes of aquaporin expression may be the molecular basis of brain edema induced by glioma cells.