Advocacy and policy in action: Developing a financial and healthcare safety net for nurses.

INTRODUCTION: The COVID-19 pandemic has opened a dialogue regarding advocacy and policy changes that need to occur at the federal, state, and local levels to ensure provisions for the financial and healthcare well-being of nurses. Often nurses struggle as the "breadwinners" in their families caring for multiple generations, thus leading them to live paycheck to paycheck. DESIGN: A review of current and proposed policy changes. The pandemic demonstrated clearly through governmental executive orders that laws and regulations could be changed more rapidly than the traditional routes, illustrating an ability to enact change in nursing practice. At the federal level, provisions are not made to ensure that nurses who risk their lives during pandemic times are adequately compensated monetarily and through extended healthcare benefits, often provided for police, fire, and other emergency personnel. RESULTS/CONCLUSIONS: Suggestions for new policy and advocacy agendas are proposed based on the gap in coverage noted during and after this pandemic. CLINICAL RELEVANCE: COVID-19 has brought to the forefront gaps in the financial and healthcare safety nets for nurses in the United States. Opportunities exist to inform via advocacy and policy reform at the federal, state, and local governmental agencies regarding the need for extended financial and healthcare provisions for nurses.

A cross-hospital exploration of nurses' experiences with horizontal violence.

AIM: To explore nurses' experiences of horizontal violence (HV) in three diverse non-affiliated organisations within a single city in the USA. BACKGROUND: Horizontal violence, also called workplace bullying or lateral violence, is a long-standing nursing issue. METHOD: Content analysis was used to analyse open-format textual responses from 126 registered nurses. RESULTS: A powerful collective story emerged from nurses' shared experiences with HV, describing the characters and the setting in which HV and its consequences exist. Nurses' depictions of HV were consistent despite the different organisational structures of their workplaces suggesting that hospital type is not the explanation for HV, rather the culture of acute care nursing. Nurses want change and asked for tactics to resolve HV within their institutions; some provided specific solutions. CONCLUSION: Nurse managers must continue to address HV by using a variety of known tactics, as well as adopting new evidence-based interventions as they are identified. The anti-bullying message should be disseminated through professional nursing organisations as well as in local health-care establishments. IMPLICATIONS FOR NURSING MANAGEMENT: Nurse managers need to be the culture champions who hold individuals accountable for HV and foster professionalism through their leadership.

The degree of horizontal violence in RNs practicing in New York State.

This study examined the degree of horizontal violence (HV) among RNs practicing in New York State (NYS). The objective was to determine the knowledge of HV and the degree of being a victim among practicing RNs. A descriptive survey using Briles' Sabotage Savvy Questionnaire, measuring occurrences of HV and nurses' knowledge of HV, was conducted among 2659 RNs in NYS hospitals. Findings demonstrate a significantly greater (P < .05) degree of HV in union versus nonunion cultures and less HV in Magnet® organizations. Gender and RN education significantly impacted HV. Developing organizational, leadership, and individual interventions to address HV helps create a culture of safety.

The prevalence of horizontal violence in New York State registered nurses.

The purpose of this descriptive study was to examine the knowledge of nursing administrators about horizontal violence (HV) among New York Organization of Nurse Executive members and to ascertain if they used evidence-based leadership in their roles. In this paper the authors describe the research conducted and examine evidence-based leadership with regard to HV The authors discuss what HV is, the theories that explain HV, and the impact of HV on the nurse, the nursing profession, and patient care. Research findings were consistent with the theoretical literature, which suggests that HV is so ingrained in nursing's organizational culture that it is not recognized. Until a phenomenon is recognized and named little can be done to alter it.

NAD(P)H oxidase inhibition attenuates neuronal chronotropic actions of angiotensin II.

It is well established that the central cardiovascular effects of angiotensin II (Ang II) involve superoxide production. However, the intracellular mechanism by which reactive oxygen species (ROS) signaling regulates neuronal Ang II actions remains to be elucidated. In the present study, we have used neuronal cells in primary cultures from the hypothalamus and brain stem areas to study the role of ROS on the cellular actions of Ang II. Ang II increases neuronal firing rate, an effect mediated by the AT(1) receptor subtype and involving inhibition of the delayed rectifier potassium current (I(Kv)). This increase in neuronal activity was associated with increases in NADPH oxidase activity and ROS levels within neurons, the latter evidenced by an increase in ethidium fluorescence. The increases in NADPH oxidase activity and ethidium fluorescence were blocked by either the AT(1) receptor antagonist losartan or by the selective NAD(P)H oxidase inhibitor gp91ds-tat. Extracellular application of the ROS scavenger, Tempol, attenuated the Ang II-induced increase in neuronal firing rate by 70%. In addition, gp91ds-tat treatment resulted in a 50% inhibition of Ang II-induced increase in firing rate. In contrast, the ROS generator Xanthine-Xanthine oxidase significantly increased neuronal firing rate. Finally, Ang II inhibited neuronal I(Kv,) and this inhibition was abolished by gp91ds-tat treatment. These observations demonstrate, for the first time, that Ang II regulates neuronal activity via a series of events that includes ROS generation and inhibition of I(Kv). This signaling seems to be a critical cellular event in central Ang II regulation of cardiovascular function.

Novel mechanism of brain soluble epoxide hydrolase-mediated blood pressure regulation in the spontaneously hypertensive rat.

The role of soluble epoxide hydrolase (sEH) in the central control of blood pressure (BP) has not been elucidated in spite of peripheral sEH overexpression being linked to hypertension. Thus, our objective was to investigate the involvement of brain sEH in BP control. sEH expression in the hypothalamus and brain stem, two cardioregulatory brain areas, was increased in the spontaneously hypertensive rat (SHR) compared to the Wistar Kyoto (WKY) rat. Inhibition of the enzyme by intracerebroventricular (icv) delivery of AUDA further increased both BP and heart rate (HR) by 32 +/- 6 mmHg and 54 +/- 10 bpm, respectively, (P<0.05) in the SHR. Analysis of waveform telemetry data revealed a decrease in spontaneous baroreceptor reflex gain following sEH inhibition, indicating the sustained increase in BP may be due to a decrease in baroreceptor reflex function. The hypertensive effect of sEH inhibition is likely a result of an increase in epoxyeicosatrienoic acid (EET)-mediated generation of ROS. This view is supported by the following: 1) Inhibition of EET formation attenuates AUDA-induced increase in BP; 2) delivery of an EET agonist increases BP and HR in the WKY rat, and 3) inhibition of NAD(P)H oxidase by gp91ds-tat prevents AUDA-induced increases in BP and HR. Finally, electrophysiological studies demonstrate that AUDA increased neuronal firing rate exclusively in the SHR, an effect completely abolished by gp91ds-tat. These observations suggest that EETs and sEH inhibition are involved in increasing BP in the SHR. We suggest that an increased expression of sEH is a futile central nervous system response in protection against hypertension.

Hypertension-linked decrease in the expression of brain gamma-adducin.

Gene profiling data coupled with adducin polymorphism studies led us to hypothesize that decreased expression of this cytosolic protein in the brain could be a key event in the central control of hypertension. Thus, our objectives in the present study were to (1) determine which adducin subunit gene demonstrates altered expression in the hypothalamus and brainstem (two cardioregulatory-relevant brain areas) in two genetic strains of hypertensive rats and (2) analyze the role of adducins in neurotransmission at the cellular level. All three adducin subunits (alpha, beta, and gamma) were present in the hypothalamus and brainstem of Wistar Kyoto (WKY) and spontaneously hypertensive (SH) rats. However, only the gamma-adducin subunit expression was 40% to 60% lower in the SH rat compared with WKY rat. A similar decrease in gamma-adducin expression was observed in the hypothalamus and brainstem of the renin transgenic rat compared with its normotensive control. Losartan treatment of the SH rat failed to normalize gamma-adducin gene expression. A hypertension-linked decrease of gamma-adducin was confirmed by demonstrating a decrease in gamma-adducin expression in hypothalamic/brainstem neuronal cultures from prehypertensive SH rats. Neuronal firing rate was evaluated to analyze the role of this protein in neurotransmission. Perfusion of a gamma-adducin-specific antibody caused a 2-fold increase in the neuronal firing rate, an effect similar to that observed with angiotensin II. Finally, we observed that preincubation of neuronal cultures for 8 hours with 100 nmol/L angiotensin II caused a 60% decrease in endogenous gamma-adducin and was associated with a 2-fold increase in basal firing rate. These observations support our hypothesis that a decrease in gamma-adducin expression in cardioregulatory-relevant brain areas is linked to hypertension possibly by regulating the release of neurotransmitters.

Creating a Nurse-Led Culture to Minimize Horizontal Violence in the Acute Care Setting: A Multi-Interventional Approach.

Horizontal violence (HV) is prevalent in nursing. However, few strategies are identified to address this phenomenon that undermines communication and patient safety. Nurses at an acute care hospital implemented multiple interventions to address HV resulting in increased knowledge of hospital policies regarding HV, and significantly (p < .05) less HV prevalence than was reported by nurses in other organizations throughout New York State. With the aid and oversight of nursing professional development specialists, evidence-based interventions to address HV were developed including policies, behavioral performance reviews, and staff/manager educational programs.

Functional genomics as an emerging strategy for the investigation of central mechanisms in experimental hypertension.

Centrally mediated increases in sympathetic nerve activity and attenuated arterial baroreflexes contribute to the pathogenesis of hypertension. Despite the characterization of cellular and physiological mechanisms that regulate blood pressure and alterations that contribute to hypertension, the genetic and molecular basis of this pathophysiology remains poorly understood. Strategies to identify genes that contribute to central pathophysiologic mechanisms in hypertension include integrative biochemistry and physiology as well as functional genomics. This article summarizes recent progress in applying functional genomics to elucidate the genetic basis of altered central blood pressure regulatory mechanisms in hypertension. We describe approaches others and we have undertaken to investigate gene expression profiles in hypertensive models in order to identify genes that contribute to the pathogenesis of hypertension. Finally, we provide the readers a roadmap for negotiating the route from experimental findings of gene expression profiling to translating their therapeutic potential. The combination of gene expression profiling and the phenotypic characterization of in vitro and in vivo loss or gain of function experiments for candidate genes have the potential to identify genes involved in the pathogenesis of hypertension and may present novel targets for therapy.

An asset-based community initiative to reduce television viewing in New York state.

BACKGROUND: Childhood obesity is an epidemic. Addressing this problem will require the input of many sectors and change in many behaviors. The "community" must be part of the solution, and the solution must be constructed on existing assets that lend strength to positive environmental change. OBJECTIVE: To catalyze an established asset-based community partnership to support efforts to reduce television viewing time by developing and providing alternative activities as part of a broader, 3-year study to reduce childhood obesity among preschool-aged children in rural, upstate New York. METHOD: Asset mapping was utilized to compile an inventory of individual and community strengths upon which a partnership could be established. Facilitated focus group sessions were conducted to better understand childcare environmental policies and practices, and to guide changes conducive to health and fitness. Planning meetings and targeted outreach brought key stakeholders together for a community-participatory initiative to support positive environmental change. RESULTS.: The partnership planned and initiated an array of after-school and weekend community activities for preschool-aged children and their families in the weeks preceding, during, and following a designated 'TV Turn-off' week in April, 2004 and March, 2005. CONCLUSION: Methods of asset-based community development are an effective way to engage community participation in public health initiatives.