Digital nursing practice theory: a scoping review and thematic analysis

AimsThis scoping review aims to identify existing theories associated with digital nursing practice toadd a lens on the future use of digital technologies by nurses.DesignA review of theories related to digital technology in nursing practice was conducted followingthe framework described by Arksey and O’Malley. All published literature up until 12th May2022 was included.Data sourcesSeven databases were utilised including Medline, Scopus, CINAHL, ACM Digital Library, IEEEXplore, BNI and Web of Science. A Google Scholar search was also performed.Review methodsThe search terms included (nurs* AND (digital OR technol* OR e-health or ehealth or digitalhealth or telemedicine or telehealth) AND theory).ResultsThe database searches yielded 282 citations. After screening, 9 papers were included in thereview. These described 8 distinct nursing theories.ConclusionThe focuses of the theories included the role of technology in society and nursing. Howtechnology should be developed to support nursing practice. Health consumers’ use of nursinginformatics. The use of technology as an expression of caring and the preservation ofhumanness. The relationship between human persons and non-human actants and the creationof nursing technologies as caring in addition to existing technologies.Three themes were identified including the role of technology as an agent within the patientenvironment; nurse interactions with technology to achieve ‘knowing’ of patients and thenecessity of technological competence among nurses. Then, using Actor Network Theory (ANT)a zoom-out lens to map the concepts was propose

Influence of Thoracic Fluid Compartments on Pulmonary Congestion in Chronic Heart Failure

Introduction: Pulmonary congestion is a common finding of heart failure (HF), but it remains unclear how pulmonary and heart blood volumes (Vp and Vh, respectively) and extravascular lung water (EVLW) change in stable HF and affect lung function. Methods: Fourteen patients with HF (age 68 ± 11 y, LVEF 33 ± 8%) and 12 control subjects (age 65 ± 9 y) were recruited. A pulmonary function test, thoracic computerized tomographic (CT) scan, and contrast perfusion scan were performed. From the thoracic scan, a histogram of CT attenuation of lung tissue was generated and skew, kurtosis, and full-width half-max (FWHM) calculated as surrogates of EVLW. Blood volumes were calculated from the transit time of the contrast through the great vessels of the heart. Results: Patients with HF had greater Vp and Vh (Vp 0.55 ± 0.21 L vs 0.41 ± 0.13 L; Vh 0.53 ± 0.33 L vs 0.40 ± 0.15 L) and EVLW (skew 3.2 ± 0.5 vs 3.7 ± 0.7; kurtosis 19.4 ± 6.6 vs 25.9 ± 9.4; FWHM 73 ± 13 HU vs 59 ± 9 HU). Spirometric measures were decreased in HF (percentage of predicted: forced vital capacity 86 ± 17% vs 104 ± 9%; forced expiratory volume in 1 second 83 ± 20% vs 105 ± 11%; maximal mid-expiratory flow 82 ± 42% vs 115 ± 43%). Vp was associated with decreased expiratory flows, and EVLW was associated with decreased lung volumes. Conclusions: Congestion in stable patients with HF includes expanded Vp and Vh and increased EVLW associated with reductions in lung volumes and expiratory flows

Keratinocyte growth factor for the treatment of the acute respiratory distress syndrome (KARE): a randomised, double-blind, placebo-controlled phase 2 trial

<p>(<b>A</b>) Immunofluorescence signal for dystrophin is significantly reduced in the SSI heart (bottom left panel) compared with the immunofluorescent signal in the SHAM heart (upper left panel), and the SHAM+ALLN (upper right panel) and SSI+ALLN (bottom right panel) myocardium. (<b>B</b>) Protein levels of dystrophin in the SHAM, SSI, SHAM+ALLN and SSI+ALLN hearts were measured 24 h after the CLP procedure and were expressed in arbitrary units (AUs). α-Tubulin was used to determine equivalent loading conditions. The results (n = 6 per group) are representative of three different experiments. Scale bars indicate 50 μm.</p

COVID sex lives : survey 1 report

This report presents initial findings from the first survey of Covid Sex Lives project. Public health measures to mitigate the spread of coronavirus are translated into media messaging by organisations that target the health of different groups. This research studies the experiences of Men who have Sex with Men (MSM), during the COVID-19 pandemic in the United Kingdom. Our focus is on uses of dating and hook up apps, sexual activity and how and how this has changed during the pandemic as restrictions such as social distancing and lockdowns have been introduced. We are conducting this research with a view to help improve policy and practice around MSM sexual wellbeing and public health messaging, shed light on what to look for where MSM are concerned, and provide learning about COVID public health messaging that will benefit MSM and the general population. The research is a collaboration between the University of Salford, Kings College London, Birmingham City University and Newcastle University and is funded by UKRI. You can find out more here: https://hub.salford.ac.uk/health-and-society-research/public-healthmessaging- during-the-covid-pandemic-dating-app-usage-and-sexual-wellbeing-among-menwho- have-sex-with-men

COVID sex lives : survey 2 report

This report presents initial findings from the second survey of Covid Sex Lives project. Public health measures to mitigate the spread of coronavirus are translated into media messaging by organisations that target the health of different groups. This research studies the experiences of Men who have Sex with Men (MSM), during the COVID-19 pandemic in the United Kingdom. Our focus is on uses of dating and hook up apps, sexual activity and how this has changed during the pandemic as restrictions such as social distancing and lockdowns have been introduced. We are conducting this research with a view to help improve policy and practice around MSM sexual wellbeing and public health messaging, shed light on what to look for where MSM are concerned, and provide learning about COVID public health messaging that will benefit MSM and the general population. The research is a collaboration between the University of Salford, Kings College London, Birmingham City University and Newcastle University and is funded by UKRI. You can find out more and view our past reports here: https://hub.salford.ac.uk/health-and-society-research/public-health-messaging-during-the-covid-pandemic-dating-app-usage-and-sexual-wellbeing-among-men-who-have-sex-with-men

Identifying divergent design thinking through the observable behavior of service design novices

© 2018, Springer Nature B.V. Design thinking holds the key to innovation processes, but is often difficult to detect because of its implicit nature. We undertook a study of novice designers engaged in team-based design exercises in order to explore the correlation between design thinking and designers’ physical (observable) behavior and to identify new, objective, design thinking identification methods. Our study addresses the topic by using data collection method of “think aloud” and data analysis method of “protocol analysis” along with the unconstrained concept generation environment. Collected data from the participants without service design experience were analyzed by open and selective coding. Through the research, we found correlations between physical activity and divergent thinking, and also identified physical behaviors that predict a designer’s transition to divergent thinking. We conclude that there are significant relations between designers’ design thinking and the behavioral features of their body and face. This approach opens possible new ways to undertake design process research and also design capability evaluation

Airway mucins promote immunopathology in virus-exacerbated chronic obstructive pulmonary disease.

The respiratory tract surface is protected from inhaled pathogens by a secreted layer of mucus rich in mucin glycoproteins. Abnormal mucus accumulation is a cardinal feature of chronic respiratory diseases but the relationship between mucus and pathogens during exacerbations is poorly understood. We identified elevations in airway MUC5AC and MUC5B concentrations during spontaneous and experimentally-induced chronic obstructive pulmonary disease (COPD) exacerbations. MUC5AC was more sensitive to changes in expression during exacerbation and was therefore more predictably associated with virus load, inflammation, symptom severity, decrements in lung function, and secondary bacterial infections. MUC5AC was functionally related to inflammation as Muc5ac-deficient (Muc5ac-/-) mice had attenuated rhinovirus (RV)-induced airway inflammation and exogenous MUC5AC glycoprotein administration augmented inflammatory responses and increased release of extracellular adenosine triphosphate (ATP) in mice and human airway epithelial cell cultures. Hydrolysis of ATP suppressed MUC5AC augmentation of rhinovirus-induced inflammation in mice. Therapeutic suppression of mucin production using an epidermal growth factor receptor (EGFR) antagonist ameliorated immunopathology in a mouse COPD exacerbation model. The coordinated virus induction of MUC5AC and MUC5B suggests that non-Th2 mechanisms trigger mucin hypersecretion during exacerbations. Our data identifies a pro-inflammatory role for MUC5AC during viral infection and suggest that MUC5AC inhibition may ameliorate COPD exacerbations

The degradation of p53 and its major E3 ligase Mdm2 is differentially dependent on the proteasomal ubiquitin receptor S5a.

p53 and its major E3 ligase Mdm2 are both ubiquitinated and targeted to the proteasome for degradation. Despite the importance of this in regulating the p53 pathway, little is known about the mechanisms of proteasomal recognition of ubiquitinated p53 and Mdm2. In this study, we show that knockdown of the proteasomal ubiquitin receptor S5a/PSMD4/Rpn10 inhibits p53 protein degradation and results in the accumulation of ubiquitinated p53. Overexpression of a dominant-negative deletion of S5a lacking its ubiquitin-interacting motifs (UIM)s, but which can be incorporated into the proteasome, also causes the stabilization of p53. Furthermore, small-interferring RNA (siRNA) rescue experiments confirm that the UIMs of S5a are required for the maintenance of low p53 levels. These observations indicate that S5a participates in the recognition of ubiquitinated p53 by the proteasome. In contrast, targeting S5a has no effect on the rate of degradation of Mdm2, indicating that proteasomal recognition of Mdm2 can be mediated by an S5a-independent pathway. S5a knockdown results in an increase in the transcriptional activity of p53. The selective stabilization of p53 and not Mdm2 provides a mechanism for p53 activation. Depletion of S5a causes a p53-dependent decrease in cell proliferation, demonstrating that p53 can have a dominant role in the response to targeting S5a. This study provides evidence for alternative pathways of proteasomal recognition of p53 and Mdm2. Differences in recognition by the proteasome could provide a means to modulate the relative stability of p53 and Mdm2 in response to cellular signals. In addition, they could be exploited for p53-activating therapies. This work shows that the degradation of proteins by the proteasome can be selectively dependent on S5a in human cells, and that this selectivity can extend to an E3 ubiquitin ligase and its substrate

The isothiocyanate class of bioactive nutrients covalently inhibit the MEKK1 protein kinase

<p>Abstract</p> <p>Background</p> <p>Dietary isothiocyanates (ITCs) are electrophilic compounds that have diverse biological activities including induction of apoptosis and effects on cell cycle. They protect against experimental carcinogenesis in animals, an activity believed to result from the transcriptional induction of "Phase 2" enzymes. The molecular mechanism of action of ITCs is unknown. Since ITCs are electrophiles capable of reacting with sulfhydryl groups on amino acids, we hypothesized that ITCs induce their biological effects through covalent modification of proteins, leading to changes in cell regulatory events. We previously demonstrated that stress-signaling kinase pathways are inhibited by other electrophilic compounds such as menadione. We therefore tested the effects of nutritional ITCs on MEKK1, an upstream regulator of the SAPK/JNK signal transduction pathway.</p> <p>Methods</p> <p>The activity of MEKK1 expressed in cells was monitored using in vitro kinase assays to measure changes in catalytic activity. The activity of endogenous MEKK1, immunopurified from ITC treated and untreated LnCAP cells was also measured by in vitro kinase assay. A novel labeling and affinity reagent for detection of protein modification by ITCs was synthesized and used in competition assays to monitor direct modification of MEKK1 by ITC. Finally, immunoblots with phospho-specific antibodies were used to measure the activity of MAPK protein kinases.</p> <p>Results</p> <p>ITCs inhibited the MEKK1 protein kinase in a manner dependent on a specific cysteine residue in the ATP binding pocket. Inhibition of MEKK1 catalytic activity was due to direct, covalent and irreversible modification of the MEKK1 protein itself. In addition, ITCs inhibited the catalytic activity of endogenous MEKK1. This correlated with inhibition of the downstream target of MEKK1 activity, i.e. the SAPK/JNK kinase. This inhibition was specific to SAPK, as parallel MAPK pathways were unaffected.</p> <p>Conclusion</p> <p>These results demonstrate that MEKK1 is directly modified and inhibited by ITCs, and that this correlates with inhibition of downstream activation of SAPK. These results support the conclusion that ITCs may carry out many of their actions by directly targeting important cell regulatory proteins.</p