Bridging Systems and People-Centred Approaches in Urban Vulnerability Research: Insights for Resilience from Dawei, Myanmar

Dawei, a coastal secondary city in southeastern Myanmar, is poised to face significant social and environmental change. Dawei’s location at the head of the Dawei River estuary, just 30 kilometres from the Andaman Sea and 350 kilometres to the west of Bangkok, has attracted increasing attention from foreign investors. Namely, to develop a Special Economic Zone, build the largest deep-sea port in the region, and connect Dawei by road to the southern economic corridor of mainland Southeast Asia. Little is known about how these developments will affect Dawei, nor how climate change will interact with such changes to shape urban vulnerability. In this chapter, we examine how Dawei’s urban systems are exposed to various climatic and non-climatic stresses and investigate how this plays out through people’s everyday livelihoods. Our analysis then turns to how people cope and adapt to social and environmental change, illuminating how social capital and the ways that people relate are fundamental to shaping resilience. We situate this analysis within the larger context of Myanmar’s political and economic transition, highlighting both the challenges that this transition poses to vulnerability and the possibility of shaping a resilient future

The cyclin-dependent kinase inhibitor SNS-032 has single agent activity in AML cells and is highly synergistic with cytarabine

SNS-032 (BMS-387032) is a selective cyclin-dependent kinase (CDK) inhibitor. In this study, we evaluated its effects on primary acute myeloid leukemia (AML) samples (n=87). In vitro exposure to SNS-032 for 48 h resulted in a mean LD50 of 139±203 nM; Cytarabine (Ara-C) was more than 35 times less potent in the same cohort. SNS-032-induced a dose-dependent increase in annexin V staining and caspase-3 activation. At the molecular level, SNS-032 induced a marked dephosphorylation of serine 2 and 5 of RNA polymerase (RNA Pol) II and inhibited the expression of CDK2 and CDK9 and dephosphorylated CDK7. Furthermore, the combination of SNS-032 and Ara-C showed remarkable synergy that was associated with reduced mRNA levels of the antiapoptotic genes XIAP, BCL2 and MCL1. In conclusion, SNS-032 is effective as a single agent and in combination with Ara-C in primary AML blasts. Treatment with Ara-C alone significantly induced the transcription of the antiapoptotic genes BCL2 and XIAP. In contrast, the combination of SNS-032 and Ara-C suppressed the transcription of BCL2, XIAP and MCL1. Therefore, the combination of SNS-032 and Ara-C may increase the sensitivity of AML cells to the cytotoxic effects of Ara-C by inhibiting the transcription of antiapoptotic genes