Nursing and Conflict Communication: A Review

The study of conflict and nursing has generated a complex set of literatures. Communication scholars prioritize interactive dynamics, offering well-developed theory. Nurse researchers prioritize dynamics of a clinical environment. This review offers a background in organizational conflict studies, summarizing social scientific advances to provide a conceptual foundation for nursing conflict research. Nursing literature frames conflict as a feature of the workplace environment, equated with emotion—particularly incivility. Communication literature frames conflict as natural and functional, focusing on issues but neglecting emotion. The most fruitful approach would rely on a communication-grounded view of conflict processes and a nursing-grounded view of workplace context. Together, communication and nursing researchers can create an approach to nursing conflict superior to either body of literature on its own. This review supports that end. First, it summarizes organizational conflict research. Next, nursing conflict research is reviewed and critiqued in light of conflict communication theory, highlighting research well-grounded in social science. The scope of this review is conflict among persons and interactive processes of conflict management, concentrating on nurses but also including other healthcare professionals (usually physicians)

A Template Analysis of Intimate Partner Violence Survivors’ Experiences of Animal Maltreatment: Implications for Safety Planning and Intervention

This study explores the intersection of intimate partner violence (IPV) and animal cruelty in an ethnically diverse sample of 103 pet-owning IPV survivors recruited from community-based domestic violence programs. Template analysis revealed five themes: (a) Animal Maltreatment by Partner as a Tactic of Coercive Power and Control, (b) Animal Maltreatment by Partner as Discipline or Punishment of Pet, (c) Animal Maltreatment by Children, (d) Emotional and Psychological Impact of Animal Maltreatment Exposure, and (e) Pets as an Obstacle to Effective Safety Planning. Results demonstrate the potential impact of animal maltreatment exposure on women and child IPV survivors’ health and safety

Nutritional risk index is a better predictor of early mortality than conventional nutritional markers after transcatheter aortic valve replacement: A prospective cohort study

Background: Nutritional risk index (NRI) has been shown to better predict survival than body mass index (BMI) or albumin after several cardiovascular interventions. Under assessment herein is whether NRI can have higher predictive value than conventional parameters for short-term survival after transcatheter aortic valve replacement (TAVR).Methods: A prospective cohort study was performed. In-hospital, 1-month and 3-month survival was evaluated. Since most patients undergoing TAVR are over 65, the NRI definition for a geriatric population (GNRI) was used. The impact of baseline BMI, albumin levels, and GNRI on in-hospital and short-term survival was assessed.Results: One hundred fifty two patients aged 82 ± 5.4 were included. In-hospital, 1-month, and 3-month mortality was 5.3%, 5.9%, and 9.2%, respectively. Mean GNRI was 112.7 ± 11.9, and was significantly lower in patients who died in-hospital (101.0 ± 8.8 vs. 113.3 ± 11.7), at 30 days (103.4 ± 10.9 vs. 113.3 ± 11.7), and at 90 days (104.0 ± 9.6 vs. 113.6 ± 11.8) than in survivors (all, p < 0.05). Three-month mortality in patients with no nutritional risk was 6.8% (9/132) vs. 25% (5/20) in patients with malnutrition (p = 0.022). In univariate analysis, GNRI predicted in-hospital, 30-day, and 90-day mortality (all, p < 0.05). Predictive value remained significant after adjusting for age, EuroSCORE II, and STS-Score (p < 0.05). Based on receiver operating curves, GNRI (AUC: 0.73) showed a betterdiscrimination for 3-month mortality than albumin (0.69), weight (0.67) or BMI (0.62). The optimal cut-off value was 109.8.Conclusions: The geriatric nutritional risk index predicts short-term mortality after TAVR and has a higher discriminating ability than other commonly used nutritional variables. It is a simple parameter that identifies those patients who could benefit from pre-procedural nutritional therapy

De novo mutation in SLC25A22 gene: expansion of the clinical and electroencephalographic phenotype

The SLC25A22 (Solute Carrier Family 25, Member 22) gene encodes for a mitochondrial glutamate/H+ symporter and is involved in the mitochondrial transport of metabolites across the mitochondrial membrane. We hereby report a 12-year-old girl presenting with early-onset epileptic encephalopathy, hypotonia, and global developmental delay. Whole exome sequencing identified a novel homozygous missense mutation in SLC25A22 gene (c.97A>G; p.Lys33Glu), as the likely cause of the disease. The phenotype of our patient and EEG recordings do not completely overlap with the phenotypes previously described, leading to a new and more complex form of disease associated with SLC25A22 variants, characterized by dyskinetic movements and oculogyric crisis

Pain and agitation treatment in severe dementia patients: The need for Italian Mobilization-Observation-Behavior-Intensity-Dementia (I-MOBID2) pain scale translation, adaptation and validation with psychometric testing

The 97% of dementia patients develops fluctuant neuropsychiatric symptoms often related to under-diagnosed and unrelieved pain. Up to 80% severe demented nursing home residents experiences chronic pain due to age-related comorbidities. Patients lacking self-report skills risk not to be appropriately treated for pain. Mobilization-Observation-Behavior-Intensity-Dementia (MOBID2) is the sole pain scale to consider the frequent co-occurrence of musculoskeletal and visceral pain and to unravel concealed pain through active guided movements. Accordingly, the Italian real-world setting can benefit from its translation and validation. This clinical study provides a translated, adapted and validated version of the MOBID2, the Italian I-MOBID2. The translation, adaptation and validation of the scale for non-verbal, severe demented patients was conducted according to current guidelines in a cohort of 11 patients over 65 with mini-mental state examination ≤ 12. The I-MOBID2 proves: good face and scale content validity index (0.89); reliable internal consistency (Cronbach's α = 0.751); good to excellent inter-rater (Intraclass correlation coefficient, and test-retest (ICC = 0.902) reliability. The construct validity is high (Rho = 0.748 p < 0.05 for 11 patients, Spearman rank order correlation of the overall pain intensity score with the maximum item score of I-MOBID2 Part 1; rho=0.895 p < 0.01 for 11 patients, for the overall pain intensity score with the maximum item score of I-MOBID2 Part 2) and a good rate of inter-rater and test-retest agreement was demonstrated by Cohen's K = 0.744. The average execution time is of 5.8 min, thus making I-MOBID2 a useful tool suitable also for future development in community setting with administration by caregivers

Inorganic mercury modifies Ca2+ signals, triggers apoptosis and potentiates NMDA toxicity in cerebellar granule neurons

Hg2+ (0.1 microM-0.5 microM) modified the Ca2+ signals elicited by either KCl or the glutamate-receptor agonist, N-methyl-D-aspartate (NMDA), in cerebellar granule cells (CGCs). Hg2+ enhanced the intracellular Ca2+ transient elicited by high K+ and prevented a complete recovery of the resting intracellular Ca2+ concentration ([Ca2+]i) after either KCl or NMDA stimulation. Higher Hg2+ concentrations (up to 1 microM) increased [Ca2+]i directly. Following the short-term exposure to Hg2+, CGCs underwent apoptosis, which was identified by the cleavage of DNA into large (700-50 kbp) and oligonucleosomal DNA fragments, and by the appearance of typical apoptotic nuclei. Combined treatment with 0.1-0.3 microM Hg2+ and a sublethal NMDA concentration (50 microM) potentiated DNA fragmentation and apoptotic cell death. When the exposure to Hg2+ was carried out in Ca2+-free media or in the presence of Ca2+ channel blockers (L-type or NMDA-R antagonists), the effects on signalling and apoptosis were prevented. Our results suggest that very low Hg2+ concentrations can trigger apoptosis in CGCs by facilitating Ca2+ entry through membrane channels

Longer telomere length in peripheral white blood cells is associated with risk of lung cancer and the rs2736100 (CLPTM1L-TERT) polymorphism in a prospective cohort study among women in China.

A recent genome-wide association study of lung cancer among never-smoking females in Asia demonstrated that the rs2736100 polymorphism in the TERT-CLPTM1L locus on chromosome 5p15.33 was strongly and significantly associated with risk of adenocarcinoma of the lung. The telomerase gene TERT is a reverse transcriptase that is critical for telomere replication and stabilization by controlling telomere length. We previously found that longer telomere length measured in peripheral white blood cell DNA was associated with increased risk of lung cancer in a prospective cohort study of smoking males in Finland. To follow up on this finding, we carried out a nested case-control study of 215 female lung cancer cases and 215 female controls, 94% of whom were never-smokers, in the prospective Shanghai Women's Health Study cohort. There was a dose-response relationship between tertiles of telomere length and risk of lung cancer (odds ratio (OR), 95% confidence interval [CI]: 1.0, 1.4 [0.8-2.5], and 2.2 [1.2-4.0], respectively; P trend = 0.003). Further, the association was unchanged by the length of time from blood collection to case diagnosis. In addition, the rs2736100 G allele, which we previously have shown to be associated with risk of lung cancer in this cohort, was significantly associated with longer telomere length in these same study subjects (P trend = 0.030). Our findings suggest that individuals with longer telomere length in peripheral white blood cells may have an increased risk of lung cancer, but require replication in additional prospective cohorts and populations

Value of minimum intensity projections for chest CT in COVID-19 patients

Purpose: To investigate whether minimum intensity projection (MinIP) reconstructions enable more accurate depiction of pulmonary ground-glass opacity (GGO) compared to standard transverse sections and multiplanar reformat (MPR) series in patients with suspected coronavirus disease 2019 (COVID-19). Method: In this multinational study, chest CT scans of 185 patients were retrospectively analyzed. Diagnostic accuracy, diagnostic confidence, image quality regarding the assessment of GGO, as well as subjective time-efficiency of MinIP and standard MPR series were analyzed based on the assessment of six radiologists. In addition, the suitability for COVID-19 evaluation, image quality regarding GGO and subjective time-efficiency in clinical routine was assessed by five clinicians. Results: The reference standard revealed a total of 149 CT scans with pulmonary GGO. MinIP reconstructions yielded significantly higher sensitivity (99.9 % vs 95.6 %), specificity (95.8 % vs 86.1 %) and accuracy (99.1 % vs 93.8 %) for assessing of GGO compared with standard MPR series. MinIP reconstructions achieved significantly higher ratings by radiologists concerning diagnostic confidence (medians, 5.00 vs 4.00), image quality (medians, 4.00 vs 4.00), contrast between GGO and unaffected lung parenchyma (medians, 5.00 vs 4.00) as well as subjective time-efficiency (medians, 5.00 vs 4.00) compared with MPR-series (all P <.001). Clinicians preferred MinIP reconstructions for COVID-19 assessment (medians, 5.00 vs 3.00), image quality regarding GGO (medians, 5.00 vs 3.00) and subjective time-efficiency in clinical routine (medians, 5.00 vs 3.00). Conclusions: MinIP reconstructions improve the assessment of COVID-19 in chest CT compared to standard images and may be suitable for routine application

Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ‘accidental cell death’ (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. ‘Regulated cell death’ (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death

Is complexity leadership theory complex enough? A critical appraisal, some modifications and suggestions for further research

Scholars are increasingly seeking to develop theories that explain the underlying processes whereby leadership is enacted. This shifts attention away from the actions of ‘heroic’ individuals and towards the social contexts in which people with greater or lesser power influence each other. A number of researchers have embraced complexity theory, with its emphasis on non-linearity and unpredictability. However, some complexity scholars still depict the theory and practice of leadership in relatively non-complex terms. They continue to assume that leaders can exercise rational, extensive and purposeful influence on other actors to a greater extent than is possible. In effect, they offer a theory of complex organizations led by non-complex leaders who establish themselves by relatively non-complex means. This testifies to the enduring power of ‘heroic’ images of leader agency. Without greater care, the terminology offered by complexity leadership theory could become little more than a new mask for old theories that legitimize imbalanced power relationships in the workplace. This paper explores how these problems are evident in complexity leadership theory, suggests that communication and process perspectives help to overcome them, and outlines an agenda for further research on these issues