Plant uptake of CO2 outpaces losses from permafrost and plant respiration on the Tibetan Plateau.

High-latitude and high-altitude regions contain vast stores of permafrost carbon. Climate warming may result in the release of CO2 from both the thawing of permafrost and accelerated autotrophic respiration, but it may also increase the fixation of CO2 by plants, which could relieve or even offset the CO2 losses. The Tibetan Plateau contains the largest area of alpine permafrost on Earth. However, the current status of the net CO2 balance and feedbacks to warming remain unclear, given that the region has recently experienced an atmospheric warming rate of over 0.3 °C decade-1 We examined 32 eddy covariance sites and found an unexpected net CO2 sink during 2002 to 2020 (26 of the sites yielded a net CO2 sink) that was four times the amount previously estimated. The CO2 sink peaked at an altitude of roughly 4,000 m, with the sink at lower and higher altitudes limited by a low carbon use efficiency and a cold, dry climate, respectively. The fixation of CO2 in summer is more dependent on temperature than the loss of CO2 than it is in the winter months, especially at higher altitudes. Consistently, 16 manipulative experiments and 18 model simulations showed that the fixation of CO2 by plants will outpace the loss of CO2 under a wetting-warming climate until the 2090s (178 to 318 Tg C y-1). We therefore suggest that there is a plant-dominated negative feedback to climate warming on the Tibetan Plateau.

Human activities alter response of alpine grasslands on Tibetan Plateau to climate change.

The world's largest alpine pastures are found on the Tibetan Plateau, where considerable climate changes and human impacts have been experienced. Identifying their contributions to terrestrial productivity is essential if we are to adapt to, or mitigate the effects of, climate change. In this work, we begin by showing how the current warming and wetting of the climate over the last three decades has favored plant growth, as consistently captured by satellite observations and 15 models. However, the interactions between climate factors explain less of the variation in greenness observed by satellites after the 2000s, implying non-climatic influences. Next, we show that there is a significant negative impact of livestock grazing on pasture greenness, especially in peak summer. Official statistics across 72 counties verify these negative impacts, especially in poorer pastures with a higher density of grazing livestock. The variation in grazing density has a stronger negative effect on vegetation growth during the early part of the growing season after the 2000s, as compared with that before the 2000s. We found a compensatory effect of grazing and climate on alpine grassland growth, and the grazing regulates the response of vegetation greenness to climate change by modulating the dependency of vegetation growth on temperature. Thus, we suggest there is a weakening influence of climate on the greenness of alpine pastures, largely due to a strengthening influence of management, which should be considered by both the scientific community and policymakers.

[Construction of VEGF recombinant plasmid pcDNA/V and its expression in model rats with acute myocardial ischemia].

The cDNA encoding human Vascular Endothelial Growth Factor 165 (VEGF165) was amplified using RT-PCR from human tonsil tissue and cloned into eukaryotic expression vector pcDNA3.1 (+). The recombinant plasmid pcDNA/V was transferred into 293 cells mediated by liposome and the cells stably expressing VEGF were selected under the pressure of G418. ELISA and Western blotting demonstrated that the eukaryotic expression vector pcDNA/V was successfully constructed and its corresponding protein could be expressed efficiently in vitro. Chick Charioallantoic Membrane (CAM) bioassay showed that recombinant protein has biological activity of hVEGF. Model rats with acute myocardial ischemia were used to further study the expression of VEGFin vivo. The model rats were divided randomly into three groups: control group, pcDNA3.1 (+) group and pcDNA/V group. 50microL naked plasmid DNA or saline was intramyocardially injected at three sites into the border zone of infarction. The hearts of rats were excised and fixed histologically, then the infarction sizes were studied by immunohistochemical staining and electron microscope after four weeks. Immunohistochemical staining for VEGF appeared to be negative in control and pcDNA3.1 (+) groups. In pcDNA/V group, myocardial cells in infarction border zone showed positive staining for VEGF in cytoplasm. Ultrastructural anaylsis showed that there were visible hyperplasia of vascular endothilium in pcDNA/V group. The control and pcDNA3.1 (+) groups showed less capillary hyperplasia. In this study, VEGF165 gene was successfully cloned and its protein expressed in vitro and in vivo was of bioactivity, which provides a basis for the further study of biological functions of human VEGF.