Exploring the turbulent nature of nurses' workflow.

Turbulence is a central feature of nurses' workflow, yet it has received insufficient attention regarding how it affects nurses' work conditions. To enhance understanding of turbulence, we expanded upon and added refinements to an early conceptualization that included communication and workload as major sources of turbulence. For communication, the contributions of interruptions and handoffs are further explored. For workload, patient turnover and supplies/equipment are further explored; human resources and the built environment were added. Potential consequences of turbulence are also identified including increased cognitive work, increased workarounds, and diminished nurse well-being. Actions to address turbulent workflow include teaching students and nurses strategies to manage turbulence; attending to the practice environment such as staffing composition, remedying longstanding issues with supplies and equipment, and developing technology platforms with nurse input; and suggesting investigations to advance understanding of how turbulence influences nurses and to devise effective interventions.

The Influence of Time and Place on the Experiences of US Military Nurses in Vietnam.

BACKGROUND: Although the conflict in Vietnam (usually referred to as the Vietnam War) ended almost 50 years ago, few research-based publications of nurses' experiences in Vietnam exist. PURPOSE: The purpose of this study was to expand what is known about the experiences of US military nurses who served in Vietnam. METHODS: This secondary analysis used qualitative description to examine interview data from 15 nurses who served in-country (within Vietnam) and in-theater supporting Vietnam (e.g., Guam, the Philippines) between 1965 and 1972. FINDINGS: We found that nurses' experiences varied based on time deployed and place deployed (land, sea, or air; in-country or in-theater). The influence of time and place on US military nurses' experiences in Vietnam are illustrated through findings pertaining to danger, daily life, and work. The most prominent differences were between nurses assigned in-country and those assigned in-theater. DISCUSSION: The findings illustrate ways research of more recent and future conflicts might be strengthened.

Developing an instrument to assess empowering nurse leader communication behaviours.

AIM: The overall purpose of the study was to develop an instrument to assess empowering nurse leader communication behaviours. BACKGROUND: Effective communication by nurse leaders promotes empowerment, yet communication assessments are often broad in nature without specifying precise behaviours. METHODS: An instrument development process was used to identify empowering nurse leader communication behaviours. Nurses working in United States military health care facilities (n = 240) provided responses to 47 pilot items, along with a 12-item psychological empowerment instrument to test for concurrent criterion validity. RESULTS: After review of item performance, 12 items were deleted. An exploratory factor analysis supported either a 2- or 3-factor model, with confirmatory factor analyses conducted to validate the underlying latent variables of empowering and limiting behaviours. The final nurse leader communication assessment consists of 2 factors consisting of 20 positive items (empowering subscale) and 15 negative items (limiting subscale). CONCLUSION: The final 2-factor assessment supports the theoretical premise of the empowering and limiting behaviours. Further testing may provide further dimensional clarity. IMPLICATIONS FOR NURSING MANAGEMENT: Use of the assessment can provide a basis for the development of training for individual nurse leaders or for facility nurse leaders as a collective.

Loss of ß-PIX inhibits focal adhesion disassembly and promotes keratinocyte motility via myosin light chain activation.

During healing of the skin, the cytoskeleton of keratinocytes and their matrix adhesions, including focal adhesions (FAs), undergo reorganization. These changes are coordinated by small GTPases and their regulators, including the guanine nucleotide exchange factor ß-PIX (also known as ARHGEF7). In fibroblasts, ß-PIX activates small GTPases, thereby enhancing migration. In keratinocytes in vitro, ß-PIX localizes to FAs. To study ß-PIX functions, we generated ß-PIX knockdown keratinocytes. During wound closure of ß-PIX knockdown cell monolayers, disassembly of FAs is impaired, and their number and size are increased. In addition, in the ß-PIX knockdown cells, phosphorylated myosin light chain (MLC; also known as MYL2) is present not only in the leading edge of cells at the wound front, but also in the cells following the front, while p21-activated kinase 2 (PAK2), a regulator of MLC kinase (MYLK), is mislocalized. Inhibition or depletion of MYLK restores FA distribution in ß-PIX knockdown cells. Traction forces generated by ß-PIX knockdown cells are increased relative to those in control cells, a result consistent with an unexpected enhancement in the migration of single ß-PIX knockdown cells and monolayers of such cells. We propose that targeting ß-PIX might be a means of promoting epithelialization of wounds in vivo.

The 3'UTR of the α6 integrin message regulates localization of α6ß4 integrin heterodimers.

The α6ß4 integrin heterodimer is an essential component of hemidesmosomes (HDs) and HD-related structures, which adhere epithelial cells to the underlying extracellular matrix. In this study, we focused on the importance of the α6 integrin 3' untranslated region (UTR) in α6ß4 integrin localization. To do so, A549 cells (a type II lung alveolar cell line) and immortalized human epidermal keratinocytes (iHEK) were infected with adenovirus encoding the entire α6 integrin protein with or without portions of its 3'UTR. In infected A549 cells, we detected α6ß4 integrin heterodimers containing the product of the adenovirus, regardless of whether the α6 integrin 3'UTR was present. However, only those α6 integrin proteins whose messages contained bases 4770-5633 of the α6 integrin 3'UTR were targeted to matrix adhesion sites. Moreover, overexpression of the full length α6 integrin 3'UTR, minus the coding sequence, in A549 cells disrupts the localization of endogenous α6ß4 integrin heterodimers. Following infection of iHEKs with the same adenovirus, the induced α6 integrin protein localizes to HDs regardless of whether its message possessed a 3'UTR. In sharp contrast, in α6 integrin depleted iHEKs, restoring α6 integrin expression using the coding sequence alone via adenoviral transduction resulted in α6 integrin preferentially forming α6ß1 rather than α6ß4 integrin heterodimers. α6ß4 integrin was only observed in knocked down cells following infection of adenovirus encoding the α6 integrin coding sequence with its 3'UTR. In summary, our data indicate that the α6 integrin 3'UTR is a key regulator of α6ß4 integrin heterodimer assembly and incorporation at sites of cell-matrix adhesion.

Usability of and Satisfaction With Vocera Wireless Communication.

Qualitative reports of hands-free communication devices highlight numerous improvements in communication. The purpose of this study was to assess both usability and satisfaction scores at approximately 1 year after the implementation of a hands-free communication device at two different large military facilities. To do this, a survey that included the System Usability Scale and questions to assess satisfaction with regard to use, quality, and user satisfaction was provided to staff at both of these facilities. System usability scores indicated moderate satisfaction (61.7 at facility A, 63.8 at facility B). User satisfaction rated highest levels of agreement with the hands-free devices as an important system and being useful (35%-37% at facility A, 46% at facility B). Scores regarding improving the quality of work (A = 12%, B = 16%); safety of patients (A = 23%, B = 29%); and ability to do their job in a timely manner (A = 23%, B = 29%) were the lowest. The results highlight the potential benefits of Vocera for improving communication within the healthcare team. Given the large percentage of staff turnover at both of these facilities, the sustained benefit of hands-free devices will require ongoing training and continued evaluation of workflow processes.

Identifying the constructs of empowering nurse leader communication through an instrument development process.

AIM: The purpose of this article was to describe the constructs of empowering front-line nurse leader communication behaviours. BACKGROUND: Leaders' communication behaviours are instrumental in establishing a positive work environment. Nurse empowerment, a characteristic of a positive work environment, is influenced by communication behaviours. However, characteristics of empowering nurse leader communication behaviours have not been well-defined. METHODS: The constructs of empowering nurse leader communication behaviours were identified and refined during the instrument development process. A priori constructs were identified through a literature search, presented to focus groups of military nurses (N = 16), and refined during the procedures of item development. RESULTS: Eight final constructs emerged as a result of the iterative methods of item development: comprehensibility, listening, openness, feedback, empathy, nonverbal, paralanguage and manner. CONCLUSION: The constructs that describe empowering nurse leader communication behaviours are based on theoretical tenets of empowering communication and leadership, as well as the perspectives of military nurses. IMPLICATIONS FOR NURSING MANAGEMENT: Nurse managers can use the findings to implement innovative leadership assessments and training that focuses on Nurse Leader communication to enhance the nursing workplace environment.

The culture contributing to interruptions in the nursing work environment: An ethnography.

AIMS AND OBJECTIVES: To understand the occurrence of interruptions within the culture of the medical nursing unit work environment. BACKGROUND: Interruptions may lead to errors in nursing work. Little is known about how the culture of the nursing work environment contributes to interruptions. DESIGN: A micro-focused ethnographic study was conducted. METHOD: Data collection involved extensive observation of a nursing unit, 1:1 observations of nurses and follow-up interviews with the nurses. Data were analysed from unstructured field notes and interview transcripts. The definitions of interruption and culture guided coding, categorising and identification of themes. RESULTS: A framework was developed that describes the medical nursing unit as a complex culture full of unpredictable, nonlinear changes that affect the entire interconnected system, often in the form of an interruption. The cultural elements contributing to interruptions included (i) the value placed on excellence in patient care and meeting personal needs, (ii) the beliefs that the nurses had to do everything by themselves and that every phone call was important, (iii) the patterns of changing patients, patient transport and coordination of resources and (iv) the normative practices of communicating and adapting. CONCLUSIONS: Interruptions are an integral part of the culture of a medical nursing unit. Uniformly decreasing interruptions may disrupt current practices, such as communication to coordinate care, that are central to nursing work. In future research, the nursing work environment must be looked at through the lens of a complex system. RELEVANCE TO CLINICAL PRACTICE: Interventions to minimise the negative impact of interruptions must take into account the culture of the nursing as a complex adaptive system. Nurses should be educated on their own contribution to interruptions and issues addressed at a system level, rather than isolating the interruption as the central issue.

Lung-specific loss of α3 laminin worsens bleomycin-induced pulmonary fibrosis.

Laminins are heterotrimeric proteins that are secreted by the alveolar epithelium into the basement membrane, and their expression is altered in extracellular matrices from patients with pulmonary fibrosis. In a small number of patients with pulmonary fibrosis, we found that the normal basement membrane distribution of the α3 laminin subunit was lost in fibrotic regions of the lung. To determine if these changes play a causal role in the development of fibrosis, we generated mice lacking the α3 laminin subunit specifically in the lung epithelium by crossing mice expressing Cre recombinase driven by the surfactant protein C promoter (SPC-Cre) with mice expressing floxed alleles encoding the α3 laminin gene (Lama3(fl/fl)). These mice exhibited no developmental abnormalities in the lungs up to 6 months of age, but, compared with control mice, had worsened mortality, increased inflammation, and increased fibrosis after the intratracheal administration of bleomycin. Similarly, the severity of fibrosis induced by an adenovirus encoding an active form of transforming growth factor-ß was worse in mice deficient in α3 laminin in the lung. Taken together, our results suggest that the loss of α3 laminin in the lung epithelium does not affect lung development, but plays a causal role in the development of fibrosis in response to bleomycin or adenovirally delivered transforming growth factor-ß. Thus, we speculate that the loss of the normal basement membrane organization of α3 laminin that we observe in fibrotic regions from the lungs of patients with pulmonary fibrosis contributes to their disease progression.

Plectin-containing, centrally localized focal adhesions exert traction forces in primary lung epithelial cells.

Receptor clustering upon cell attachment to the substrate induces assembly of cytoplasmic protein complexes termed focal adhesions (FAs), which connect, albeit indirectly, the extracellular matrix to the cytoskeleton. A subset of cultured primary alveolar epithelial cells (AEC) display a unique pattern of vinculin/paxillin/talin-rich FAs in two concentric circles when cultured on glass and micropatterned substrates: one ring of FAs located at the cell periphery (pFAs), and another FA ring located centrally in the cell (cFAs). Unusually, cFAs associate with an aster-like actin array as well as keratin bundles. Moreover, cFAs show rapid paxillin turnover rates following fluorescence recovery after photobleaching and exert traction forces similar to those generated by FAs at the cell periphery. The plakin protein plectin localizes to cFAs and is normally absent from pFAs, whereas tensin, a marker of mature/fibrillar adhesions, is found in both cFAs and pFAs. In primary AEC in which plectin expression is depleted, cFAs are largely absent, with an attendant reorganization of both the keratin and actin cytoskeletons. We suggest that the mechanical environment in the lung gives rise to the assembly of unconventional FAs in AEC. These FAs not only show a distinctive arrangement, but also possess unique compositional and functional properties.

Actinin-4 in keratinocytes regulates motility via an effect on lamellipodia stability and matrix adhesions.

During wound repair, epidermal cells at the edge of an injury establish front-rear polarity through orchestrated changes in their cytoskeleton and adhesion structures. The polarity and directed migration of such cells is determined by the assembly, extension, and stabilization of a lamellipodium. Actinin-4 associates with lamellipodia and has been implicated in regulating lamellipodial structure, function and assembly. To study the functions of actinin-4 in human keratinocytes, we used shRNA to generate knockdown cells and compared their motility behavior and matrix adhesion assembly to scrambled shRNA treated control keratinocytes. Actinin-4 knockdown keratinocytes lack polarity, assemble multiple lamellipodia with a 2× increased area over controls, display reduced activity of the actin remodeling protein cofilin, and fail to migrate in a directional manner. This motility defect is rescued by plating knockdown cells on preformed laminin-332 matrix. In actinin-4-knockdown keratinocytes, focal contact area is increased by 25%, and hemidesmosome proteins are mislocalized. Specifically, α6ß4 integrin localizes to large lamellipodial extensions, displays reduced dynamics, and fails to recruit its bullous pemphigoid antigen binding partners. Together, our data indicate a role for actinin-4 in regulating the steering mechanism of keratinocytes via profound effects on their matrix adhesion sites.

Laminin-332 and α3ß1 integrin-supported migration of bronchial epithelial cells is modulated by fibronectin.

The repair of the bronchiolar epithelium damaged by cell-mediated, physical, or chemical insult requires epithelial cell migration over a provisional matrix composed of complexes of extracellular matrix molecules, including fibronectin and laminin. These matrix molecules support migration and enhance cell adhesion. When cells adhere too tightly to their matrix they fail to move; but if they adhere too little, they are unable to develop the traction force necessary for motility. Thus, we investigated the relative contributions of laminin and fibronectin to bronchiolar cell adhesion and migration using the immortalized bronchial lung epithelial cell line (BEP2D) and normal human bronchial epithelial (NHBE) cells, both of which assemble a laminin α3ß3γ2 (LM332)/fibronectin-rich matrix. Intriguingly, BEP2D and NHBE cells migrate significantly faster on an LM332-rich matrix than on fibronectin. Moreover, addition of fibronectin to LM332 matrix suppresses motility of both cell types. Finally, fibronectin enhances the adhesion of both BEP2D and NHBE cells to LM332-coated surfaces. These results suggest that fibronectin fine tunes LM332-mediated migration by boosting bronchiolar cell adhesion to substrate. We suggest that, during epithelial wound healing of the injured airway, fibronectin plays an important adhesive role for laminin-driven epithelial cell motility by promoting a stable cellular interaction with the provisional matrix.

α6ß4 integrin, a master regulator of expression of integrins in human keratinocytes.

Three major laminin and collagen-binding integrins in skin (α6ß4, α3ß1, and α2ß1) are involved in keratinocyte adhesion to the dermis and dissemination of skin cells during wound healing and/or tumorigenesis. Knockdown of α6 integrin in keratinocytes not only results in motility defects but also leads to decreased surface expression of the α2, α3, and ß4 integrin subunits. Whereas α2 integrin mRNA levels are decreased in α6 integrin knockdown cells, α3 and ß4 integrin mRNAs levels are unaffected. Expression of either α6 or α3 integrin in α6 integrin knockdown cells restores α2 integrin mRNA levels. Moreover, re-expression of α6 integrin increases ß4 integrin protein at the cell surface, which results in an increase in α3 integrin expression via activation of initiation factor 4E-binding protein 1. Our data indicate that the α6ß4 integrin is a master regulator of transcription and translation of other integrin subunits and underscore its pivotal role in wound healing and cancer.

Lung-specific loss of the laminin α3 subunit confers resistance to mechanical injury.

Laminins are heterotrimeric glycoproteins of the extracellular matrix that are secreted by epithelial cells and which are crucial for the normal structure and function of the basement membrane. We have generated a mouse harboring a conditional knockout of α3 laminin (Lama3(fl/fl)), one of the main laminin subunits in the lung basement membrane. At 60 days after intratracheal treatment of adult Lama3(fl/fl) mice with an adenovirus encoding Cre recombinase (Ad-Cre), the protein abundance of α3 laminin in whole lung homogenates was more than 50% lower than that in control-treated mice, suggesting a relatively long half-life for the protein in the lung. Upon exposure to an injurious ventilation strategy (tidal volume of 35 ml per kg of body weight for 2 hours), the mice with a knockdown of the α3 laminin subunit had less severe injury, as shown by lung mechanics, histology, alveolar capillary permeability and survival when compared with Ad-Null-treated mice. Knockdown of the α3 laminin subunit resulted in evidence of lung inflammation. However, this did not account for their resistance to mechanical ventilation. Rather, the loss of α3 laminin was associated with a significant increase in the collagen content of the lungs. We conclude that the loss of α3 laminin in the alveolar epithelium results in an increase in lung collagen, which confers resistance to mechanical injury.

Interruptions during nurses' work: A state-of-the-science review.

The purpose of this state-of-the-science review was to examine empirical evidence from studies of interruptions conducted in acute care nurses' work environments. A total of 791 articles published from 2001 through 2011 were reviewed; 31 met the criteria to be included in the sample. Despite sustained multinational and multidisciplinary attention to interruptions during nurses' work, the current findings suggest that beliefs about the ill effects of interruptions remain more conjecture than evidence-based. Pre-existing beliefs and biases may interfere with deriving a more accurate grasp of interruptions and their effects. Future research would benefit from examinations of interruptions that better capture their complexity, to include their relationships to both positive and negative outcomes for both patients and health care workers.

Type XVII collagen regulates lamellipod stability, cell motility, and signaling to Rac1 by targeting bullous pemphigoid antigen 1e to alpha6beta4 integrin.

Rac1 activity, polarity, lamellipodial dynamics, and directed motility are defective in keratinocytes exhibiting deficiency in ß4 integrin or knockdown of the plakin protein Bullous Pemphigoid Antigen 1e (BPAG1e). The activity of Rac, formation of stable lamellipodia, and directed migration are restored in ß4 integrin-deficient cells by inducing expression of a truncated form of ß4 integrin, which lacks binding sites for BPAG1e and plectin. In these same cells, BPAG1e, the truncated ß4 integrin, and type XVII collagen (Col XVII), a transmembrane BPAG1e-binding protein, but not plectin, colocalize along the substratum-attached surface. This finding suggested to us that Col XVII mediates the association of BPAG1e and α6ß4 integrin containing the truncated ß4 subunit and supports directed migration. To test these possibilities, we knocked down Col XVII expression in keratinocytes expressing both full-length and truncated ß4 integrin proteins. Col XVII-knockdown keratinocytes exhibit a loss in BPAG1e-α6ß4 integrin interaction, a reduction in lamellipodial stability, an impairment in directional motility, and a decrease in Rac1 activity. These defects are rescued by a mutant Col XVII protein truncated at its carboxyl terminus. In summary, our results suggest that in motile cells Col XVII recruits BPAG1e to α6ß4 integrin and is necessary for activation of signaling pathways, motile behavior, and lamellipodial stability.

A dystroglycan/plectin scaffold mediates mechanical pathway bifurcation in lung epithelial cells.

In alveolar epithelial cells (AECs), the membrane-anchored proteoglycan dystroglycan (DG) is a mechanoreceptor that transmits mechanical stretch forces to activate independently the ERK1/2 and the adenosine 5'-monophosphate-activated protein kinase (AMPK) signaling cascades in a process called pathway bifurcation. We tested the hypothesis that the cytoskeleton cross-linker plectin, known to bind both DG and AMPK in muscle cells, acts as a scaffold to regulate DG-mediated mechanical stimulation and pathway bifurcation. We demonstrate that plectin and DG form a complex in AECs and that this complex interacts with ERK1/2 and AMPK. Plectin knockdown reduces DG interaction with AMPK but not with ERK1/2. Despite this, mechanoactivation of both signaling pathways is significantly attenuated in AECs deficient in plectin. Thus, DG has the dual role of mechanical receptor and scaffold for ERK1/2, whereas plectin acts as a scaffold for AMPK signaling but is also required for DG-mediated ERK1/2 activation. We conclude that the DG-plectin complex plays a central role in transmitting mechanical stress from the extracellular matrix to the cytoplasm.

Laminin deposition in the extracellular matrix: a complex picture emerges.

Laminins are structural components of basement membranes. In addition, they are key extracellular-matrix regulators of cell adhesion, migration, differentiation and proliferation. This Commentary focuses on a relatively understudied aspect of laminin biology: how is laminin deposited into the extracellular matrix? This topic has fascinated researchers for some time, particularly considering the diversity of patterns of laminin that can be visualized in the matrix of cultured cells. We discuss current ideas of how laminin matrices are assembled, the role of matrix receptors in this process and how laminin-associated proteins modulate matrix deposition. We speculate on the role of signaling pathways that are involved in laminin-matrix deposition and on how laminin patterns might play an important role in specifying cell behaviors, especially directed migration. We conclude with a description of new developments in the way that laminin deposition is being studied, including the use of tagged laminin subunits that should allow the visualization of laminin-matrix deposition and assembly by living cells.

Nurse Leader Expertise for Pandemic Management: Highlighting the Essentials.

The COVID-19 pandemic requires military nurse leaders in various patient care settings to engage in disaster response. Evidence supports essential leadership attributes for nurses that include skilled communication, organizational influence, and personnel management. Yet, nursing expertise that shapes nurse leader responsibilities during disaster management remains unclear. A description of how military nurse leaders contributed their nursing expertise during the COVID-19 pandemic response at one U.S. Military health care facility is provided to begin to delineate disaster management responsibilities.

A comparison of working conditions among nurses in Magnet and non-Magnet hospitals.

OBJECTIVES: To compare working conditions (ie, schedule, job demands, and practice environment) of nurses working in American Nurses Credentialing Center-designated Magnet and non-Magnet hospitals. BACKGROUND: Although nurse retention has been reported as more favorable among Magnet hospitals, controversy still exists on whether Magnet hospitals have better working conditions. METHOD: A secondary data analysis was conducted of the Nurses Worklife and Health Study using responses from the 837 nurses working in 171 hospitals: 14 Magnet and 157 non-Magnet facilities in the Wave 3 follow-up survey. Contingency tables and t tests compared working conditions by Magnet status. To accommodate clustering of nurses in hospitals, the Huber-White sandwich estimator was used to obtain robust SEs and variance estimates. RESULT: Nurses in Magnet hospitals were significantly less likely to report jobs that included mandatory overtime (P =.04) or on-call (P =.01), yet hours worked did not differ. They also reported significantly lower physical demands (P =.03), although the means for Magnet hospital nurses and non-Magnet nurses were quite similar (30.1 vs 31.0). Furthermore, comparison of the groups on nursing practice environment and perceived patient safety found no significant differences. CONCLUSION: Working conditions reported by nurses working in Magnet and non-Magnet hospitals varied little.