Factors contributing to rapid decline of Arctic sea ice in autumn

Autumn Arctic sea ice has been declining since the beginning of the era of satellite sea ice observations. In this study, we examined the factors contributing to the decline of autumn sea ice concentration. From the Beaufort Sea to the Barents Sea, autumn sea ice concentration has decreased considerably between 1982 and 2020, and the rates of decline were the highest around the Beaufort Sea. We calculated the correlation coefficients between sea ice extent (SIE) anomalies and anomalies of sea surface temperature (SST), surface air temperature (SAT) and specific humidity (SH). Among these coefficients, the largest absolute value was found in the coefficient between SIE and SAT anomalies for August to October, which has a value of −0.9446. The second largest absolute value was found in the coefficient between SIE and SH anomalies for September to November, which has a value of −0.9436. Among the correlation coefficients between SIE and SST anomalies, the largest absolute value was found in the coefficient for August to October, which has a value of −0.9410. We conducted empirical orthogonal function (EOF) analyses of sea ice, SST, SAT, SH, sea level pressure (SLP) and the wind field for the months where the absolute values of the correlation coefficient were the largest. The first EOFs of SST, SAT and SH account for 39.07%, 63.54% and 47.60% of the total variances, respectively, and are mainly concentrated in the area between the Beaufort Sea and the East Siberian Sea. The corresponding principal component time series also indicate positive trends. The first EOF of SLP explains 41.57% of the total variance. It is mostly negative in the central Arctic. Over the Beaufort, Chukchi and East Siberian seas, the zonal wind weakened while the meridional wind strengthened. Results from the correlation and EOF analyses further verified the effects of the ice–temperature, ice–SH and ice–SLP feedback mechanisms in the Arctic. These mechanisms accelerate melting and decrease the rate of formation of sea ice. In addition, stronger meridional winds favor the flow of warm air from lower latitudes towards the polar region, further promoting Arctic sea ice decline

hBcl2 overexpression in BMSCs enhances resistance to myelin debris-induced apoptosis and facilitates neuroprotection after spinal cord injury in rats

Abstract After spinal cord injury (SCI), the accumulation of myelin debris at the lesion exacerbates cell death and hinders axonal regeneration. Transplanted bone marrow mesenchymal stem cells (BMSCs) have been proven to be beneficial for SCI repair, but they are susceptible to apoptosis. It remains unclear whether this apoptotic process is influenced by myelin debris. Here, we constructed rat BMSCs overexpressing human B-cell lymphoma 2 (hBcl2) alone (hBcl2 group), BMSCs overexpressing hBcl2 with an endoplasmic reticulum-anchored segment (hBcl2-cb) (cb group), and a negative control group (NC group) for transplantation in this study. Immunocytochemistry staining validated the successful expression of hBcl2 in BMSCs within the hBcl2 group and cb group. All BMSCs from each group exhibited the ability to phagocytize myelin debris. Nevertheless, only BMSCs derived from the hBcl2 group exhibited heightened resistance to apoptosis and maintained prolonged viability for up to 5 days when exposed to myelin debris. Notably, overexpression of hBcl2 protein, rather than its endoplasmic reticulum-anchored counterpart, significantly enhanced the resistance of BMSCs against myelin debris-induced apoptosis. This process appeared to be associated with the efficient degradation of myelin debris through the Lamp1+ lysosomal pathway in the hBcl2 group. In vivo, the hBcl2 group exhibited significantly higher numbers of surviving cells and fewer apoptotic BMSCs compared to the cb and NC groups following transplantation. Furthermore, the hBcl2 group displayed reduced GFAP+ glial scarring and greater preservation of NF200+ axons in the lesions of SCI rats. Our results suggest that myelin debris triggers apoptosis in transplanted BMSCs, potentially elucidating the low survival rate of these cells after SCI. Consequently, the survival rate of transplanted BMSCs is improved by hBcl2 overexpression, leading to enhanced preservation of axons within the injured spinal cord