Livelihood and vulnerability in the wake of Typhoon Yolanda: lessons of community and resilience

Livelihood strategies that are crafted in ‘extra-ordinary’ post-disaster conditions should also be able to function once some semblance of normalcy has resumed. This article aims to show that the vulnerability experienced in relation to Typhoon Yolanda was, and continues to be, directly linked to inadequate livelihood assets and opportunities. We examine the extent to which various livelihood strategies lessened vulnerability post-Typhoon Yolanda and argue that creating conditions under which disaster survivors have the freedom to pursue sustainable livelihood is essential in order to foster resilience and reduce vulnerability against future disasters. We offer suggestions to improve future relief efforts, including suggestions made by the survivors themselves. We caution against rehabilitation strategies that knowingly or unknowingly, resurrect pre-disaster vulnerability. Strategies that foster dependency, fail to appreciate local political or ecological conditions or undermine cooperation and cohesion in already vulnerable communities will be bound to fail. Some of the livelihood strategies that we observed post-Typhoon Yolanda failed on some or all of these points. It is important for future policy that these failings are addressed

Sarcoplasmic reticulum calcium mishandling central tenet in heart failure?

Excitation-contraction coupling links excitation of the sarcolemmal surface membrane to mechanical contraction. In the heart this link is established via a Ca-induced Ca release process, which, following sarcolemmal depolarisation, prompts Ca release from the sarcoplasmic reticulum (SR)\ua0though the ryanodine receptor (RyR2). This substantially raises the cytoplasmic Ca concentration to trigger systole. In diastole, Ca is removed from the cytoplasm, primarily via the sarcoplasmic-endoplasmic reticulum Ca-dependent ATPase (SERCA) pump on the SR\ua0membrane, returning Ca to the SR store. Ca movement across the SR is thus fundamental to the systole/diastole cycle and plays an essential role in maintaining cardiac contractile function. Altered SR Ca homeostasis (due to disrupted Ca release, storage, and reuptake pathways) is a central tenet of heart failure and contributes to depressed contractility, impaired relaxation, and propensity to arrhythmia. This review will focus on the molecular mechanisms that underlie asynchronous Ca cycling around the SR in the failing heart. Further, this review will illustrate that the combined effects of expression changes and disruptions to RyR2 and SERCA2a regulatory pathways are critical to the pathogenesis of heart failure