has affected the global economy like no other crisis in the history of mankind. It forced worldwide lockdown and economic shutdown to the point from where the recovery process has been very difficult. It has affected demand, supply, production and consumption in such a way that the entire economic development cycle has gone to its lowest levels. COVID-19 has also affected the social and economic sustainability structure which has led from one crisis to another and the developing countries have been the worst hit. Economic crisis resulted in unemployment leading to labour migrations, inevitable casualties and rising poverty etc. However, at a certain level, a few industries and organizations have shown resilience with better anticipation and survivability which may lead them to a quicker recovery. The current study aims at presenting a holistic view of organizational resilience which leads to the overall sustainable development. The study considers three aspects of organizational resilience as crisis anticipation, organizational robustness and recoverability. It assesses the impact of the aspects of resilience on social sustainability and economic sustainability. The study uses empirical analysis of primary data which is analysed to verify the hypothesized relationships by using a structural equation modelling approach. The study finds out that predicting the crisis and disruptions, building robustness and recoverability have a positive effect on both the social and economic aspects of sustainability. Findings of the study have their practical implications for industry, researchers and society.

This article reports metabolic consequences of JAK2-mutant myeloproliferative neoplasms (MPNs) with a therapeutic translational impact: expression of mutant JAK2 induces abnormal metabolic activity of MPN cells, resulting in hypoglycemia, adipose tissue atrophy, and early mortality.

Interleukin-1β (IL-1β) is a master regulator of inflammation. Increased activity of IL-1β has been implicated in various pathological conditions including myeloproliferative neoplasms (MPNs). Here we show that IL-1β serum levels and expression of IL-1 receptors on hematopoietic progenitors and stem cells correlate with JAK2-V617F mutant allele fraction in peripheral blood of patients with MPN. We show that the source of IL-1β overproduction in a mouse model of MPN are JAK2-V617F expressing hematopoietic cells. Knockout of IL-1β in hematopoietic cells of JAK2-V617F mice reduces inflammatory cytokines, prevents damage to nestin-positive niche cells and reduces megakaryopoiesis, resulting in decrease of myelofibrosis and osteosclerosis. Inhibition of IL-1β in JAK2-V617F mutant mice by anti-IL-1β antibody also reduces myelofibrosis and osteosclerosis and shows additive effects with ruxolitinib. These results suggest that inhibition of IL-1β with anti-IL-1β antibody alone or in combination with ruxolitinib could have beneficial effects on the clinical course in patients with myelofibrosis.