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Purpose Methods Findings Conclusions Implications for nursing practice The purpose of this study was to examine knowledge, attitude, and barriers toward care planning documentation practices with standardized nursing languages (SNLs) of nurses and nursing students at a midwestern healthcare system, comparing student and nurse responses.Cross‐sectional surveys were given over a 2‐month period with nurses and nursing students at different sites in a midwestern healthcare system, using convenience sampling. The Knowledge, Attitude, and Barriers to Using Standardized Nursing Languages and Current Practices Survey was adapted for use and re‐tested for validity/reliability (Content Validity Index 0.81–1.00; Cronbach alpha = 0.82–0.99) with 28 Likert scale items measuring knowledge, attitude, and barriers. Descriptive statistics, composite scores, correlations, t‐tests, and multiple regression were used to analyze the concepts of the tool.134/400 RNs responded (34%); 109/116 students responded (93.9%). Data analyses indicate adequate to superior levels of knowledge related to SNLs and NANDA International, Nursing Interventions Classification (NIC), and Nursing Outcomes Classification (NOC), collectively referred to as NNN (NANDA, NIC, & NOC), positive attitudes toward SNLs/NNN and for adopting SNLs/NNN into documentation practices, but moderate to great barriers for implementation in practice. Barriers included lack of financial resources for change, lack of mentors, and lack of mandates to use SNLs. Students scored significantly higher than nurses in attitude only.Perceptions of nurses and student nurses for current documentation indicate awareness of inadequacy in existing systems and willingness to change existing systems for standardized languages, with perceived barriers to change/implementation of SNLs. Students were more positive about SNLs than nurses.Major implications for nursing are to reevaluate electronic documentation systems and determine how to insert and easily apply SNLs in these systems, such that nursing care documentation is standardized, interoperable, effective, time‐saving, and attainable. [ABSTRACT FROM AUTHOR]

Near the tropical‐temperate transition zone, warming winter temperatures are expected to facilitate the poleward range expansion of freeze‐sensitive tropical organisms. In coastal wetlands of eastern and central North America, freeze‐sensitive woody plants (mangroves) are expected to expand northward into regions currently dominated by freeze‐tolerant herbaceous salt marsh plants. To advance understanding of mangrove range expansion, there is a need to refine temperature thresholds for mangrove freeze damage, mortality and recovery.We integrated data from 38 sites spread across the mangrove range edge in the Gulf of Mexico and Atlantic coasts of North America, including data from a regional collaborative network – the Mangrove Migration Network. In 2018, an extreme freeze event affected 60% of these sites, with minimum temperatures ranging from 0 to −7°C.We used temperature and vegetation data from before and after the freeze to quantify temperature thresholds for leaf damage, mortality and biomass recovery of the black mangrove (Avicennia germinans) – the most freeze‐tolerant mangrove species in North America.For A. germinans individuals near their northern range limit, our results indicate that temperature thresholds for leaf damage are close to −4°C, but temperature thresholds for mortality are closer to −7°C. Thresholds are expected to be warmer for more southern A. germinans individuals and for the other two common mangrove species in the region (Laguncularia racemosa and Rhizophora mangle). Regenerative buds allowed A. germinans to resprout and recover quickly from above‐ground freeze damage. Hence, biomass recovery levels during the first post‐freeze growing season were 90%, 78%, 62% and 45% for temperatures of −4, −5, −6 and −7°C, respectively. Due to a combination of vigorous resprouting and new recruitment from propagules, we expect full recovery at most sites within 1–3 years, assuming no further freeze events.Synthesis. To improve predictions of tropical range expansion in response to climate change, there is a need to better understand tropical species' responses to winter temperature extremes. Collectively, our results refine temperature thresholds for A. germinans freeze damage, mortality and recovery, which can improve predictions of mangrove range expansion and coastal wetland ecological transformations in a warming climate. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Transected axons of the central nervous system fail to regenerate and instead die back away from the lesion site, resulting in permanent disability. Although both intrinsic (eg, microtubule instability, calpain activation) and extrinsic (ie, macrophages) processes are implicated in axonal dieback, the underlying mechanisms remain uncertain. Furthermore, the precise mechanisms that cause delayed 'bystander' loss of spinal axons, that is, ones that were not directly damaged by the initial insult, but succumbed to secondary degeneration, remain unclear. Our goal was to evaluate the role of intra-axonal Ca(2+) stores in secondary axonal degeneration following spinal cord injury. METHODS: We developed a 2-photon laser-induced spinal cord injury model to follow morphological and Ca(2+) changes in live myelinated spinal axons acutely following injury. RESULTS: Transected axons 'died back' within swollen myelin or underwent synchronous pan-fragmentation associated with robust Ca(2+) increases. Spared fibers underwent delayed secondary bystander degeneration. Reducing Ca(2+) release from axonal stores mediated by ryanodine and inositol triphosphate receptors significantly decreased axonal dieback and bystander injury. Conversely, a gain-of-function ryanodine receptor 2 mutant or pharmacological treatments that promote axonal store Ca(2+) release worsened these events. INTERPRETATION: Ca(2+) release from intra-axonal Ca(2+) stores, distributed along the length of the axon, contributes significantly to secondary degeneration of axons. This refocuses our approach to protecting spinal white matter tracts, where emphasis has been placed on limiting Ca(2+) entry from the extracellular space across cell membranes, and emphasizes that modulation of axonal Ca(2+) stores may be a key pharmacotherapeutic goal in spinal cord injury. Ann Neurol 2014;75:220-229. [ABSTRACT FROM AUTHOR]

Objective Transected axons of the central nervous system fail to regenerate and instead die back away from the lesion site, resulting in permanent disability. Although both intrinsic (eg, microtubule instability, calpain activation) and extrinsic (ie, macrophages) processes are implicated in axonal dieback, the underlying mechanisms remain uncertain. Furthermore, the precise mechanisms that cause delayed 'bystander' loss of spinal axons, that is, ones that were not directly damaged by the initial insult, but succumbed to secondary degeneration, remain unclear. Our goal was to evaluate the role of intra-axonal Ca2+ stores in secondary axonal degeneration following spinal cord injury. Methods We developed a 2-photon laser-induced spinal cord injury model to follow morphological and Ca2+ changes in live myelinated spinal axons acutely following injury. Results Transected axons 'died back' within swollen myelin or underwent synchronous pan-fragmentation associated with robust Ca2+ increases. Spared fibers underwent delayed secondary bystander degeneration. Reducing Ca2+ release from axonal stores mediated by ryanodine and inositol triphosphate receptors significantly decreased axonal dieback and bystander injury. Conversely, a gain-of-function ryanodine receptor 2 mutant or pharmacological treatments that promote axonal store Ca2+ release worsened these events. Interpretation Ca2+ release from intra-axonal Ca2+ stores, distributed along the length of the axon, contributes significantly to secondary degeneration of axons. This refocuses our approach to protecting spinal white matter tracts, where emphasis has been placed on limiting Ca2+ entry from the extracellular space across cell membranes, and emphasizes that modulation of axonal Ca2+ stores may be a key pharmacotherapeutic goal in spinal cord injury. Ann Neurol 2014;75:220-229 [ABSTRACT FROM AUTHOR]