As one of the most vulnerable sectors exposed to the COVID-19 pandemic, transport sectors have been severely affected. However, the shocks and impact mechanisms of infectious diseases on transport sectors are not fully understood. This paper employs a multi-sectoral computable general equilibrium model of China, CHINAGEM, with highly disaggregated transport sectors to examine the impacts of the COVID-19 pandemic on China’s transport sectors and reveal the impact mechanisms of the pandemic shocks with the decomposition analysis approach. This study suggests that, first, multiple shocks of the COVID-19 pandemic to transport sectors are specified, including the supply-side shocks that raised the protective cost and reduced the production efficiency of transport sectors, and the demand-side shocks that reduced the demand of households and production sectors for transportation. Second, the outputs of all transport sectors in China have been severely affected by the COVID-19 pandemic, and passenger transport sectors have larger output decreases than freight transport sectors. While the outputs of freight transport sectors are expected to decline by 1.03–2.85%, the outputs of passenger transport sectors would decline by 3.08–11.44%. Third, with the decomposition analysis, the impacts of various exogenous shocks are quite different, while the changes in the output of different transport sectors are dominated by different exogenous shocks. Lastly, while the supply-side shocks of the pandemic would drive output decline in railway, waterway, and aviation transport sectors, the demand-side shocks would drive so in the road, pipeline, and other transport sectors. Moreover, the COVID-19 pandemic has negative impacts on the output of most non-transport sectors and the macro-economy in China. Three policy implications are recommended to mitigate the damages caused by the COVID-19 pandemic to the transport sectors.

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Atherosclerosis-associated cardiovascular disease is one of the main causes of death and disability among patients with diabetes mellitus. However, little is known about the impact of S-nitrosylation in diabetes-accelerated atherosclerosis. Here, we show increased levels of S-nitrosylation of guanine nucleotide-binding protein G(i) subunit alpha-2 (SNO-GNAI2) at Cysteine 66 in coronary artery samples from diabetic patients with atherosclerosis, consistently with results from mice. Mechanistically, SNO-GNAI2 acted by coupling with CXCR5 to dephosphorylate the Hippo pathway kinase LATS1, thereby leading to nuclear translocation of YAP and promoting an inflammatory response in endothelial cells. Furthermore, Cys-mutant GNAI2 refractory to S-nitrosylation abrogated GNAI2-CXCR5 coupling, alleviated atherosclerosis in diabetic mice, restored Hippo activity, and reduced endothelial inflammation. In addition, we showed that melatonin treatment restored endothelial function and protected against diabetes-accelerated atherosclerosis by preventing GNAI2 S-nitrosylation. In conclusion, SNO-GNAI2 drives diabetes-accelerated atherosclerosis by coupling with CXCR5 and activating YAP-dependent endothelial inflammation, and reducing SNO-GNAI2 is an efficient strategy for alleviating diabetes-accelerated atherosclerosis.

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Objectives: The mechanism and immunoregulatory role of human natural killer (NK) cells in acute graft-vs.-host-disease (aGVHD) remains unclear. This study quantitatively analyzed the cytotoxicity of donor NK cells toward allo-reactive T cells, and investigated their relationship with acute GVHD (aGVHD). Methods: We evaluated NK dose, subgroup, and receptor expression in allografts from 98 patients who underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT). A CD107a degranulating assay was used as a quantitative detection method for the cytotoxic function of donor NK cells to allo-reactive T cells. In antibody-blocking assay, NK cells were pre-treated with anti-DNAM-1(CD226), anti-NKG2D, anti-NKP46, or anti-NKG-2A monoclonal antibodies (mAbs) before the degranulating assay. Results: NK cells in allografts effectively inhibited auto-T cell proliferation following alloantigen stimulation, selectively killing alloantigen activated T cells. NKG2A − NK cell subgroups showed higher levels of CD107a degranulation toward activated T cells, when compared with NKG2A − subgroups. Blocking NKG2D or CD226 (DNAM-1) led to significant reductions in degranulation, whereas NKG2A block resulted in increased NK degranulation. Donor NK cells in the aGVHD group expressed lower levels of NKG2D and CD226, higher levels of NKG2A, and showed higher CD107a degranulation levels when compared with NK cells in the non-aGVHD group. Using univariate analysis, higher NK degranulation activities in allografts (CD107a high) were correlated with a decreased risk in grade I-IV aGVHD (hazard risk [HR] = 0.294; P < 0.0001), grade III-IV aGVHD (HR = 0.102; P < 0.0001), and relapse (HR = 0.157; P = 0.015), and improved overall survival (HR = 0.355; P = 0.028) after allo-HSCT. Multivariate analyses showed that higher NK degranulation activities (CD107a high) in allografts were independent risk factors for grades, I-IV aGVHD (HR = 0.357; P = 0.002), and grades III-IV aGVHD (HR = 0.13; P = 0.009). Sheng et al. NK Cytotoxicity Against Activated-T Predict GVHD Conclusions: These findings reveal that the degranulation activity of NK in allografts toward allo-activated T cells was associated with the occurrence and the severity of aGVHD, after allogeneic stem cell transplantation. This suggested that cytotoxicity of donor NK cells to allo-reactive T cells have important roles in aGVHD regulation.