Evaluation of the HadISST1 and NSIDC 1850 onward sea ice datasets with a focus on the Barents-Kara seas

In recent years,long-term continuous sea-ice datasets have been developed,and they cover the periods before and after the satellite era.How these datasets differ from one another before the satellite era,and whether one is more reliable than the other,is important but unclear because the sea-ice record before 1979 is sparse and not continuous.In this letter,two sets of sea-ice datasets are evaluated:one is the HadISST1 dataset from the Hadley Centre,and the other is the SIBT1850(Gridded Monthly Sea Ice Extent and Concentration,from 1850 Onward)dataset from the National Snow and Ice Data Center(NSIDC).In view of its substantial importance for climate,the winter sea ice in the Barents and Kara seas(BKS)is of particular focus.A reconstructed BKS sea-ice extent(SIE)is developed using linear regression from the mean of observed surface air temperature at two adjacent islands,Novaya Zemlya and Franz Josef Land(proxy).One validation illustrates that the proxy is substantially coherent with the BKS sea-ice anomaly in the observations and the CMIP5(phase 5 of the Coupled Model Intercomparison Project)historical experiments.This result indicates that the proxy is reasonable.Therefore,the establishment of the reconstructed BKS SIE is also reasonable.The evaluation results based on the proxy suggest that the sea-ice concentration prior to the satellite era in the NSIDC dataset is more realistic and reliable than that in the Hadley Centre dataset,and thus is more appropriate for use.

Phosphatidylserine released from apoptotic cells in tumor induces M2-like macrophage polarization through the PSR-STAT3-JMJD3 axis

Background:Understanding how the tumor microenvironment is shaped by various factors is important for the development of new therapeutic strategies.Tumor cells often undergo spontaneous apoptotic cell death in tumor microen-vironment,these apoptotic cells are histologically co-localized with immunosup-pressive macrophages.However,the mechanism by which tumor cell apoptosis modulates macrophage polarization is not fully understood.In this study,we aimed to explore the tumor promoting effects of apoptotic tumor cells and the signal pathways involved.Methods:Apoptotic cells and macrophages in tumors were detected by immunohistochemical staining.Morphological analysis was performed with Giemsa staining.Lipids generated from apoptotic cells were detected by liq-uid chromatography-mass spectrometry.Phosphatidylserine-containing lipo-somes were prepared to mimic apoptotic cells.The expression of protein was determined by real-time PCR,immunohistochemistry enzyme-linked immunosorbent assay and Western blotting.Mouse malignant ascites and subcu-taneous tumor models were designed for in vivo analysis.Transgenic mice with specific genes knocked out and inhibitors specific to certain proteins were used for the mechanistic studies.Results:The location and the number of apoptotic cells were correlated with that of macrophages in several types of carcinomas.Phosphatidylserine,a lipid molecule generated in apoptotic cells,induced polarization and accumulation of M2-like macrophages in vivo and in vitro.Moreover,sustained administration of phosphoserine promoted tumor growth in the malignant ascites and subcuta-neous tumor models.Further analyses suggested that phosphoserine induced a M2-like phenotype in macrophages,which was related to the activation of phosphoserine receptors including T-cell immunoglobin mucin 4(TIM4)and the FAK-SRC-STAT3 signaling pathway as well as elevated the expression of the histone demethylase Jumonji domain-containing protein 3(JMJD3).Adminis-tration of specific inhibitors of these pathways could reduce tumor progression.Conclusions:This study suggest that apoptotic cell-generated phosphoserine might be a notable signal for immunosuppressive macrophages in tumors,and the related pathways might be potential therapeutic targets for cancer therapy.