Objectives: To qualitatively compare the influence of different ownership which is considered as a kind of institutional environment in public hospitals, private hospitals, and mixed-ownership hospitals on hospital governance structure and organizational behavior. Design: Qualitative descriptive study, using semi-structured, in-depth interviews and thematic template analysis, theoretically informed by critical realism. Participants: 27 key informants including national policymakers in charge of the health sector, influential researchers, local administrators responsible for implementing policies, and hospital managers who are experienced in institutional change. Results: Hospital ownership has a significant influence on hospitals in terms of decision-making power allocation, residual ownership allocation, market entry level, accountability, and social functions. These five aspects in hospital organizational structure incentivize hospitals to adapt to the internal and external environment of the hospital organization—such as market environment, governance, and financing arrangements—affect the behavior of the hospital organization, and ultimately affect the efficiency of hospital operation and quality of service. The incentives under the public system are relatively distorted. Private hospitals have poor performance in failing their social functions due to their insufficient development ability. Compared to them, mixed ownership hospitals have a better performance in terms of incentive mechanism and organizational development. Conclusion: Public hospitals should improve the governance environment and decision-making structure, so as to balance their implementation of social functions and achieve favorable organizational development. For private hospitals, in addition to the optimization of the policy environment, attempts should be made to strengthen their supervision. The development of mixed-ownership hospitals should be oriented towards socialized governance.
For shade‐intolerant plants, changes in light quality through competition from neighbors trigger shade avoidance syndrome (SAS): a series of morphological and physiological adaptations that are ultimately detrimental to plant health and crop yield. Phytochrome‐interacting factor 7 (PIF7) is a major transcriptional regulator of SAS in Arabidopsis; however, how it regulates gene expression is not fully understood. Here, we show that PIF7 directly interacts with the histone chaperone anti‐silencing factor 1 (ASF1). The ASF1‐deprived asf1ab mutant showed defective shade‐induced hypocotyl elongation. Histone regulator homolog A (HIRA), which mediates deposition of the H3.3 variant into chromatin, is also involved in SAS. RNA/ChIP‐sequencing analyses identified the role of ASF1 in the direct regulation of a subset of PIF7 target genes. Furthermore, shade‐elicited gene activation is accompanied by H3.3 enrichment, which is mediated by the PIF7‐ASF1‐HIRA regulatory module. Collectively, our data reveal that PIF7 recruits ASF1‐HIRA to increase H3.3 incorporation into chromatin to promote gene transcription, thus enabling plants to effectively respond to environmental shade.
Light and temperature are two key environmental signals that share several molecular components that, in turn, regulate plant growth. Darkness and high ambient temperatures promote skoto-and thermomorphogenesis, including stem elongation. Heat shock proteins 90 (HSP90s) facilitate the adaptation of organisms to various adverse environmental stimuli.Here, we showed that HSP90s are required for hypocotyl elongation during both skotoand thermomorphogenesis.When HSP90s activities are impaired by the knockdown of HSP90s expression or the application of HSP90 inhibitors, the expression levels and protein abundance of PHYTOCHROME-INTERACTING FACTOR 4 (PIF4) markedly decreased. EARLY FLOWERING 3 (ELF3) deficiency was resistant to the inhibition of HSP90s activities. Furthermore, HSP90s interacted with and destabilized ELF3. In the CONSTITUTIVE PHOTOMORPHOGENIC 1 (COP1) mutant, the changes in endogenous PIF4 and ELF3 protein levels caused by the inhibition of HSP90s activities were abolished. HSP90s enhanced the interaction between COP1 and ELF3, reduced ELF3 functional effects on PIF4 and modulated hypocotyl elongation during skotoand thermomorphogenesis.Our results indicated that HSP90s participate in light and temperature signalling via the COP1-ELF3-PIF4 module to regulate hypocotyl growth in changing environments.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.