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Drained wetlands are thought to be carbon (C) source hotspots, and rewetting is advocated to restore C storage in drained wetlands for climate change mitigation. However, current assessments of wetland C balance mainly focus on vertical fluxes between the land and atmosphere, frequently neglecting lateral carbon fluxes and land‐use effects. Here, we conduct a global synthesis of 893 annual net ecosystem C balance (NECB) measures that include net ecosystem exchange of CO2, along with C input via manure fertilization, and C removal through biomass harvest or hydrological exports of dissolved organic and inorganic carbon, across wetlands of different status and land uses. We find that elevating water table substantially reduces net ecosystem C losses, with the annual NECB decreasing from 2579 (95% interval: 1976 to 3214) kg C ha−1 year−1 in drained wetlands to −422 (−658 to −176) kg C ha−1 year−1 in natural wetlands, and to −934 (−1532 to −399) kg C ha−1 year−1 in rewetted wetlands globally. Climate, land‐use history, and time since water table changes introduce variabilities, with drainage for (sub)tropical agriculture or forestry uses showing high annual C losses, while the net C losses from drained wetlands can continue to affect soil C pools for several decades. Rewetting all types of drained wetlands is needed, particularly for those formerly agriculture‐used (sub)tropical wetlands where net ecosystem C losses can be largely reduced. Our findings suggest that elevating water table is an important initiative to reduce C losses in degraded wetlands, which could contribute to policy decisions for managing wetlands to enhance their C sequestration. [ABSTRACT FROM AUTHOR]

Determination of tipping points in nitrogen (N) isotope (δ15N) natural abundance, especially soil δ15N, with increasing aridity, is critical for estimating N‐cycling dynamics and N limitation in terrestrial ecosystems. However, whether there are linear or nonlinear responses of soil δ15N to increases in aridity and if these responses correspond well with soil N cycling remains largely unknown. In this study, we investigated soil δ15N and soil N‐cycling characteristics in both topsoil and subsoil layers along a drought gradient across a 3000‐km transect of drylands on the Qinghai–Tibetan Plateau. We found that the effect of increasing aridity on soil δ15N values shifted from negative to positive with thresholds at aridity index (AI) = 0.27 and 0.29 for the topsoil and subsoil, respectively, although soil N pools and N transformation rates linearly decreased with increasing aridity in both soil layers. Furthermore, we identified markedly different correlations between soil δ15N and soil N‐cycling traits above and below the AI thresholds (0.27 and 0.29 for topsoil and subsoil, respectively). Specifically, in wetter regions, soil δ15N positively correlated with most soil N‐cycling traits, suggesting that high soil δ15N may result from the "openness" of soil N cycling. Conversely, in drier regions, soil δ15N showed insignificant relationships with soil N‐cycling traits and correlated well with factors, such as soil‐available phosphorus and foliage δ15N, demonstrating that pathways other than typical soil N cycling may dominate soil δ15N under drier conditions. Overall, these results highlight that different ecosystem N‐cycling processes may drive soil δ15N along the aridity gradient, broadening our understanding of N cycling as indicated by soil δ15N under changing drought regimes. The aridity threshold of soil δ15N should be considered in terrestrial N‐cycling models when incorporating 15N isotope signals to predict N cycling and availability under climatic dryness. [ABSTRACT FROM AUTHOR]

Background: In vivo pig liver xenotransplantation preclinical trials appear to have poor efficiency compared to heart or kidney xenotransplantation because of xenogeneic rejection, including coagulopathy, and particularly thrombocytopenia. In contrast, ex vivo pig liver (wild type) perfusion systems have been proven to be effective in "bridging" liver failure patients until subsequent liver allotransplantation, and transgenic (human CD55/CD59) modifications have even prolonged the duration of pig liver perfusion. Despite the fact that hepatocyte cell lines have also been proposed for extracorporeal blood circulation in conditions of acute liver failure, porcine hepatocyte cell lines, and the GalT‐KO background in particular, have not been developed and applied in this field. Herein, we established immortalized wild‐type and GalT‐KO porcine hepatocyte cell lines, which can be used for artificial liver support systems, cell transplantation, and even in vitro studies of xenotransplantation. Methods: Primary hepatocytes extracted from GalT‐KO and wild‐type pigs were transfected with SV40 LT lentivirus to establish immortalized GalT‐KO porcine hepatocytes (GalT‐KO‐hep) and wild‐type porcine hepatocytes (WT). Hepatocyte biomarkers and function‐related genes were assessed by immunofluorescence, periodic acid‐Schiff staining, indocyanine green (ICG) uptake, biochemical analysis, ELISA, and RT‐PCR. Furthermore, the tumorigenicity of immortalized cells was detected. In addition, a complement‐dependent cytotoxicity (CDC) assay was performed with GalT‐KO‐hep and WT cells. Cell death and viability rates were assessed by flow cytometry and CCK‐8 assay. Results: GalT‐KO and wild‐type porcine hepatocytes were successfully immortalized and maintained the characteristics of primary porcine hepatocytes, including albumin secretion, ICG uptake, urea and glycogen production, and expression of hepatocyte marker proteins and specific metabolic enzymes. GalT‐KO‐hep and WT cells were confirmed as having no tumorigenicity. In addition, GalT‐KO‐hep cells showed less apoptosis and more viability than WT cells when exposed to complement and xenogeneic serum. Conclusions: Two types of immortalized cell lines of porcine hepatocytes with GalT‐KO and wild‐type backgrounds were successfully established. GalT‐KO‐hep cells exhibited higher viability and injury resistance against a xenogeneic immune response. [ABSTRACT FROM AUTHOR]

Hepatic macrophages play pivotal roles in tolerance induction after liver transplantation (LT). However, macrophages possess functional heterogeneities, and the protective role of M2c macrophages, a macrophage subtype characterized by the surface marker CD163 that secretes interleukin-10 (IL-10) and transforming growth factor-β1 (TGF-β1), in acute rejection following LT, has not been addressed. The aim of this study was to determine whether polarized macrophages of the M2c subtype could improve outcomes after LT for rats, including survival rate, liver function, and inflammatory infiltration. In our study, the numbers of CD163-positive cells were found to be increased in tolerant liver grafts. Immediately following the surgery, M2c macrophages induced from rat bone marrow-derived cells were infused into recipients; this significantly improved survival rate and liver function. The expression levels of IL-10 and TGF-β1 were markedly increased in these rats compared to those in the control group. Furthermore, CD8 + T-cell infiltration was reduced, whereas the numbers of apoptotic cells increased, in rats treated with M2c. To explore the mechanisms of the protective role of M2c, the numbers of major histocompatibility complex (MHC) class II positive cells were found to be decreased and the expression of N-acetylglucosaminyltransferase V (MGAT5) was up-regulated in M2c infusion groups. Together, these findings demonstrate that polarization of macrophages towards the M2c phenotype ameliorated acute rejection in a rat LT model and may provide a novel and effective therapeutic approach for AR after transplantation., Competing Interests: None., (AJTR Copyright © 2020.)

Introduction: Glutamine metabolism is essential for the proliferation of cancer cells. Transported by SLC1A5, a Na + dependent transporter, glutamine is absorbed for further use. Recent studies have revealed the anti-tumor effect of berberine. The present study aimed to evaluate the effect of berberine on cancer cell glutamine metabolism., Materials and Methods: The inhibitory effect of berberine on liver cancer cells was analyzed by CCK-8 and EdU assay. The glutamine concentrations were detected by ELISA and UHPLC-MRM-MS analysis. Glutamine metabolism-related proteins were determined by Western blot, immunofluorescent analysis and immunohistochemistry., Results: Berberine inhibited the proliferation of Hep3B and BEL-7404 cell in vitro. Berberine suppressed the glutamine uptake by inhibiting SLC1A5. The upregulation of SLC1A5 led to an increased glutamine uptake and improved tolerance to berberine. Berberine suppresses SLC1A5 expression by inhibiting c-Myc. Furthermore, berberine suppresses the growth of tumor xenografts, and the expression of SLC1A5 and c-Myc in vivo. The high expression of SLC1A5 in hepatocellular carcinoma (HCC) tissues is associated with poor prognosis., Conclusion: Berberine can suppress the proliferation of liver cancer cells by reducing SLC1A5 expression., Competing Interests: The authors report no conflicts of interest in this work, (© 2019 Zhang et al.)