Spatial distribution patterns of annual soil carbon accumulation and carbon storage in the Jiuduansha wetland of the Yangtze River estuary.

Wetlands are important carbon (C) pools for terrestrial ecosystems, and C stored in different types of wetlands accounts for about 30% of total terrestrial C. As one of the most important ecological barriers in Shanghai, with functions of climate regulation, interception, and purification, and as a C sink, the Jiuduansha wetland has received research attention. However, little research has been done on the spatial differences in amount of average annual net C accumulation and C storage of each shoal: Jiangya Nansha, Shangsha, and Zhongxiasha. In this study, plant biomass, plant organic C, soil respiration, soil organic C content, and soil bulk density of different vegetation zones in the three shoals were analyzed to determine the spatial variability of annual net C accumulation capability and soil organic C storage of the Jiuduansha wetland. The results showed that the Zhongxiasha shoal played the most important role as a C sink, and it accumulated 77,839.44 t organic C per year. Regarding the annual C accumulation capacity per unit area, the Phragmites communis zone was higher than for all other vegetation zones, indicating that P. communis had the greatest C accumulation capacity. 7835.38 t, 46,827.41 t, and 173,623.1 t of organic C were stored in the Jiangya Nansha, Shangsha, and Zhongxiasha shoals, respectively. The C storage in soil was closely related to annual C accumulation, and there were two main reasons for the difference of spatial pattern of annual C accumulation: biomass and properties of plants and the properties of tidal water.

Preliminary manifestation of the Yangtze River Protection Strategy in improving the carbon sink function of estuary wetlands.

In 2016, the Yangtze River Protection Strategy was proposed and a series of measures were applied to restore the health and function of the Yangtze River ecosystem. However, the impact of these measures on the carbon (C) sink capacity of the Yangtze River estuary wetlands has not been exhaustively studied. In this work, the effects of these measures on the C sink capacity of Yangtze River estuary wetlands were examined through the long-term monitoring of C fluxes, soil respiration, plant growth and water quality. The C flux of the Yangtze River estuary wetlands has become increasingly negative after the implementation of these measures, mainly owing to reduction in soil CO2 emission. The decrease in the chemical fertilizer release and returning farmland to wetland had led to the improvement of water quality in the estuary area, which further reduced soil heterotrophic microbial activity, and ultimately decreasing soil CO2 emissions of estuary wetlands.

Identification of T cell-signaling pathways that stimulate latent HIV in primary cells.

Eradication of HIV infection depends on the elimination of a small, but stable population of latently infected T cells. After the discontinuation of therapy, activation of latent virus can rekindle infection. To purge this reservoir, it is necessary to define cellular signaling pathways that lead to activation of latent HIV. We used the SCID-hu (Thy/Liv) mouse model of HIV latency to analyze a broad array of T cell-signaling pathways and show in primary, quiescent cells that viral induction depends on the activation of two primary intracellular signaling pathways, protein kinase C or nuclear factor of activated T cells (NF-AT). In contrast, inhibition or activation of other important T cell stimulatory pathways (such as mitogen-activated protein kinase, calcium flux, or histone deacetylation) do not significantly induce virus expression. We found that the activation of NF-kappaB is critical to viral reactivation; however, all pathways that stimulate NF-kappaBdonot reactivate latent virus. Our studies further show that inhibition of NF-kappaB does not prevent activation of HIV by NF-AT, indicating that these pathways can function independently to activate the HIV LTR. Thus, we define several molecular pathways that trigger HIV reactivation from latency and provide evidence that latent HIV infection is maintained by the functional lack of particular transcription factors in quiescent cells.

Molecular characterization, reactivation, and depletion of latent HIV.

Antiretroviral therapy is unable to eliminate HIV infection in a small, long-lived population of latently infected T cells, providing a source for renewed viral replication following cessation of therapy. Analysis of individual latently infected cells generated in the SCID-hu (Thy/Liv) mouse demonstrated no functional viral RNA produced in the latent state. Following reactivation viral expression was dramatically increased, rendering the infected cells susceptible to an anti-HIV immunotoxin. Treatment with the immunotoxin in conjunction with agents that activate virus expression without inducing cell division (IL-7 or the non-tumor-promoting phorbol ester prostratin) depleted the bulk of the latent reservoir and left uninfected cells able to respond to subsequent costimulation. We demonstrate that activation of latent virus is required for targeting by antiviral agents and provide the basis for future therapeutic strategies to eradicate the latent reservoir.