PUBLIC SPENDING AS A NEW DETERMINATE OF SUSTAINABLE DEVELOPMENT GOAL AND GREEN ECONOMIC RECOVERY: POLICY PERSPECTIVE ANALYSIS IN THE POST-COVID ERA

Green economy talks about combing final mechanisms that have ecological and macroeconomic system gains. Likewise, this research piece examined the effects of increased spending on fiscal policies and tightening fiscal policies concerning greening the economic activity as the globe reclaims itself from the COVID-19 in China. Analysis was done applying the China longitudinal data for the period 2008–2018. We utilized the ordinary least square as well as the quantile regression equation to meticulously approximate the influences of increased fiscal spending policies in addition to tightening fiscal policies has on greening the economic system acts as the countries reclaim themselves from the pandemic via a formulated green performance indicator of China nations. The findings indicate a rather exciting pattern by saying a percentage growth in fiscal policy led to nearly 6.5% growth, that is, less than 0.5 growth in the minimum carbon dioxide polluting vaporous from energy suppliers, such as natural gas, and a 0.2% less than 0.01 cuts in the midway carbon dioxide polluting liquefied energy suppliers, that is, hydrocarbon byproducts and a nonsignificant expansion of 0.2%, more significant than 0.5 in the entire case scenario coming from polluting dense energy suppliers, that is, from coal byproduct sources. At the same time, a 1% expansion in fiscal policy reduces cumulative carbon dioxide pollution to 0.2%, less than 0.05%. On this score, the presence of the environmental hypothesis was authenticated in all scenarios analyzed. Furthermore, the causality test indicated a dual movement causative correlation between fiscal policy and carbon dioxide pollution and one-way movement concerning the fiscal policy to energy use. The findings demonstrated that China witnessed a rising switch to green advancement in China;their Green Economic Efficiency increased steadily.

Distinct immune signatures discriminate between asymptomatic and presymptomatic SARS-CoV-2pos subjects.

Increasing numbers of SARS-CoV-2-positive (SARS-CoV-2pos) subjects are detected at silent SARS-CoV-2 infection stage (SSIS). Yet, SSIS represents a poorly examined time-window wherein unknown immunity patterns may contribute to the fate determination towards persistently asymptomatic or overt disease. Here, we retrieved blood samples from 19 asymptomatic and 12 presymptomatic SARS-CoV-2pos subjects, 47 age/gender-matched patients with mild or moderate COVID-19 and 27 normal subjects, and interrogated them with combined assays of 44-plex CyTOF, RNA-seq and Olink. Notably, both asymptomatic and presymptomatic subjects exhibited numerous readily detectable immunological alterations, while certain parameters including more severely decreased frequencies of CD107alow classical monocytes, intermediate monocytes, non-classical monocytes and CD62Lhi CD8+ Tnaïve cells, reduced plasma STC1 level but an increased frequency of CD4+ NKT cells combined to distinguish the latter. Intercorrelation analyses revealed a particular presymptomatic immunotype mainly manifesting as monocytic overactivation and differentiation blockage, a likely lymphocyte exhaustion and immunosuppression, yielding mechanistic insights into SSIS fate determination, which could potentially improve SARS-CoV-2 management.

ACE2 and Innate Immunity in the Regulation of SARS-CoV-2-Induced Acute Lung Injury: A Review.

Despite the protracted battle against coronavirus acute respiratory infection (COVID-19) and the rapid evolution of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), no specific and effective drugs have to date been reported. Angiotensin-converting enzyme 2 (ACE2) is a zinc metalloproteinase and a critical modulator of the renin-angiotensin system (RAS). In addition, ACE2 has anti-inflammatory and antifibrosis functions. ACE has become widely known in the past decade as it has been identified as the primary receptor for SARS-CoV and SARS-CoV-2, being closely associated with their infection. SARS-CoV-2 primarily targets the lung, which induces a cytokine storm by infecting alveolar cells, resulting in tissue damage and eventually severe acute respiratory syndrome. In the lung, innate immunity acts as a critical line of defense against pathogens, including SARS-CoV-2. This review aims to summarize the regulation of ACE2, and lung host cells resist SARS-CoV-2 invasion by activating innate immunity response. Finally, we discuss ACE2 as a therapeutic target, providing reference and enlightenment for the clinical treatment of COVID-19.

Integrating longitudinal clinical laboratory tests with targeted proteomic and transcriptomic analyses reveal the landscape of host responses in COVID-19.

The pathophysiology of coronavirus disease 19 (COVID-19) involves a multitude of host responses, yet how they unfold during the course of disease progression remains unclear. Here, through integrative analysis of clinical laboratory tests, targeted proteomes, and transcriptomes of 963 patients in Shanghai, we delineate the dynamics of multiple circulatory factors within the first 30 days post-illness onset and during convalescence. We show that hypercortisolemia represents one of the probable causes of acute lymphocytopenia at the onset of severe/critical conditions. Comparison of the transcriptomes of the bronchoalveolar microenvironment and peripheral blood indicates alveolar macrophages, alveolar epithelial cells, and monocytes in lungs as the potential main sources of elevated cytokines mediating systemic immune responses and organ damages. In addition, the transcriptomes of patient blood cells are characterized by distinct gene regulatory networks and alternative splicing events. Our study provides a panorama of the host responses in COVID-19, which may serve as the basis for developing further diagnostics and therapy.