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Numerous studies highlight the pivotal role of Citizen Initiatives (CIs) in urban sustainability, yet existing methodologies often fall short in capturing their comprehensive neighborhood impact. This article validates the Multi-criteria tool for Assessing the Sustainability of CIs (MASCIs), specifically designed for the nuanced assessment of CIs on neighborhood sustainability. The primary objective is to thoroughly assess and validate MASCIs through a mixed-method approach, including interviews with fifteen experts surveyed on the system's suitability and application to six CIs in Barcelona. Results show that 53.33% of experts found current indicators suitable, with valuable suggestions for improvement. The implementation of the system in CIs validates the usefulness of the tool to quantify the impact of these initiatives in the community. The study reveals the nuanced nature of these initiatives, emphasizing context, stakeholder participation, and adaptability. This research enriches discussions on citizen-driven sustainability by addressing gaps in evaluation systems, deepening our understanding of their broader implications for urban development.

BACKGROUND: Rapid pacing rates induce alternations in the cytosolic calcium concentration caused by fluctuations in calcium released from the sarcoplasmic reticulum (SR). However, the relationship between calcium alternans and refractoriness of the SR calcium release channel (RyR2) remains elusive. METHODOLOGY/PRINCIPAL FINDINGS: To investigate how ryanodine receptor (RyR2) refractoriness modulates calcium handling on a beat-to-beat basis using a numerical rabbit cardiomyocyte model. We used a mathematical rabbit cardiomyocyte model to study the beat-to-beat calcium response as a function of RyR2 activation and inactivation. Bi-dimensional maps were constructed depicting the beat-to-beat response. When alternans was observed, a novel numerical clamping protocol was used to determine whether alternans was caused by oscillations in SR calcium loading or by RyR2 refractoriness. Using this protocol, we identified regions of RyR2 gating parameters where SR calcium loading or RyR2 refractoriness underlie the induction of calcium alternans, and we found that at the onset of alternans both mechanisms contribute. At low inactivation rates of the RyR2, calcium alternans was caused by alternation in SR calcium loading, while at low activation rates it was caused by alternation in the level of available RyR2s. CONCLUSIONS/SIGNIFICANCE: We have mapped cardiomyocyte beat-to-beat responses as a function of RyR2 activation and inactivation, identifying domains where SR calcium load or RyR2 refractoriness underlie the induction of calcium alternans. A corollary of this work is that RyR2 refractoriness due to slow recovery from inactivation can be the cause of calcium alternans even when alternation in SR calcium load is present.