Abstract. Sea ice loss is proposed as a primary reason for the Arctic amplification, although the physical mechanism of the Arctic amplification and its connection with sea ice melting is still in debate. In the present study, monthly ERA-Interim reanalysis data are analyzed via cyclostationary empirical orthogonal function analysis to understand the seasonal mechanism of sea ice loss in the Arctic Ocean and the Arctic amplification. While sea ice loss is widespread over much of the perimeter of the Arctic Ocean in summer, sea ice remains thin in winter only in the Barents–Kara seas. Excessive turbulent heat flux through the sea surface exposed to air due to sea ice reduction warms the atmospheric column. Warmer air increases the downward longwave radiation and subsequently surface air temperature, which facilitates sea surface remains to be free of ice. This positive feedback mechanism is not clearly observed in the Laptev, East Siberian, Chukchi, and Beaufort seas, since sea ice refreezes in late fall (November) before excessive turbulent heat flux is available for warming the atmospheric column in winter. A detailed seasonal heat budget is presented in order to understand specific differences between the Barents–Kara seas and Laptev, East Siberian, Chukchi, and Beaufort seas.

Sea ice reduction is accelerating in the Barents and Kara Seas. Several mechanisms are proposed to explain the accelerated loss of Arctic sea ice, which remains to be controversial. In the present study, detailed physical mechanism of sea ice reduction in winter (December–February) is identified from the daily ERA interim reanalysis data. Downward longwave radiation is an essential element for sea ice reduction, but can primarily be sustained by excessive upward heat flux from the sea surface exposed to air in the region of sea ice loss. The increased turbulent heat flux is used to increase air temperature and specific humidity in the lower troposphere, which in turn increases downward longwave radiation. This feedback process is clearly observed in the Barents and Kara Seas in the reanalysis data. A quantitative assessment reveals that this feedback process is being amplified at the rate of ~8.9% every year during 1979–2016. Availability of excessive heat flux is necessary for the maintenance of this feedback process; a similar mechanism of sea ice loss is expected to take place over the sea-ice covered polar region, when sea ice is not fully recovered in winter.

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CD4+CD25+ regulatory T (Treg) cells play crucial roles in the host response to tumors. Increasing evidence supports the existence of elevated numbers of Treg cells in solid tumors and hematologic malignancies. In this study, the effects of methyl gallate on Treg cells were examined. Methyl gallate inhibited Treg cell-suppressive effects on effector CD4+ T cells and Treg migration toward tumor environment. The expression of Treg surface markers including CTLA-4, CCR4, CXCR4, and glucocorticoid-induced TNFR was significantly suppressed upon methyl gallate treatment. Furthermore, forkhead box P3 (Foxp3) expression was also significantly decreased by methyl gallate, suggesting that the suppressive effects of methyl gallate on Treg were medicated by decrease of Treg-specific transcription factor Foxp3. In tumor-bearing hosts, methyl gallate treatment substantially reduced tumor growth and prolonged the survival rate. In contrast, nu/nu mice did not show decreased tumor progression in response to methyl gallate. In addition, in tumor-bearing Treg-depleted mice, tumor growth and the survival rates were not changed by methyl gallate treatment, strongly suggesting that the main therapeutic target of methyl gallate in tumor suppression was related to modulation of the CD4+CD25+ Treg cell functions. In the spleen of tumor-bearing mice, methyl gallate treatment induced a significant decrease in the CD4+CD25+Foxp3high Treg cell population. Especially, the number of tumor-infiltrating CD25+Foxp3high Treg cells was significantly lower in methyl gallate-treated mice. These results suggest that methyl gallate can be used to reverse immune suppression and as a potentially useful adjunct for enhancing the efficacy of immune-based cancer therapy.

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Our proposed model is able to accurately predict subtle cortisol excess and its chronic manifestations in AI patients.