The Role of Early Life Gut Mycobiome on Child Health.

The human gut microbiota is composed of bacteria (microbiota or microbiome), fungi (mycobiome), viruses, and archaea, but most of the research is primarily focused on the bacterial component of this ecosystem. Besides bacteria, fungi have been shown to play a role in host health and physiologic functions. However, studies on mycobiota composition during infancy, the factors that might shape infant gut mycobiota, and implications to child health and development are limited. In this review, we discuss the factors likely shaping gut mycobiota, interkingdom interactions, and associations with child health outcomes and highlight the gaps in our current knowledge of this ecosystem.

Impact of psychosocial factors on the success of neuromodulation treatment for patients with persistent pain.

INTRODUCTION: Significant interindividual variability in spinal cord stimulation (SCS) outcomes exists. Due to its high cost and risks of complications, criteria to guide patient selection for SCS trials and their outcomes would be helpful. With increased focus on the use of patient-reported outcomes to improve care, we aim to evaluate the National Institute of Health Patient Reported Outcome Measurement Information System measures for an association with successful SCS trials in patients with persistent pain. METHODS: Our prospective, observational study enrolled 60 patients with persistent pain who underwent an SCS trial. Patients completed demographic and Patient Reported Outcome Measurement Information System computer adaptive test (PROMIS CAT) assessments to measure self-reported pain interference, depression, anxiety, physical functioning, and sleep disturbance at the time they presented for placement of their trial device. RESULTS: Of the 58 patients who underwent successful electrode placement, 11 had an unsuccessful trial. There were no differences in patient demographics between patients with a successful and an unsuccessful trial. Patients who had a successful SCS trial reported lower pre-trial levels of anxiety, depression, and sleep disturbance and decreased post-trial levels of depression, sleep disturbance, and pain interference. CONCLUSIONS: We found that patients with high levels of depression, anxiety, and sleep disturbance using the PROMIS CAT were predictive of unsuccessful trials. In addition, we found that patients with successful SCS trials reported lower levels of these domains on PROMIS CAT administered at the end of the trial.

Enhancer-activated RET confers protection against oxidative stress to KMT2A-rearranged acute myeloid leukemia.

Ectopic activation of rearranged during transfection (RET) has been reported to facilitate lineage differentiation and cell proliferation in different cytogenetic subtypes of acute myeloid leukemia (AML). Herein, we demonstrate that RET is significantly (p < 0.01) upregulated in AML subtypes containing rearrangements of the lysine methyltransferase 2A gene (KMT2A), commonly referred to as KMT2A-rearranged (KMT2A-r) AML. Integrating multi-epigenomics data, we show that the KMT2A-MLLT3 fusion induces the development of CCCTC-binding (CTCF)-guided de novo extrusion enhancer loop to upregulate RET expression in KMT2A-r AML. Based on the finding that RET expression is tightly correlated with the selective chromatin remodeler and mediator (MED) proteins, we used a small-molecule inhibitor having dual inhibition against RET and MED12-associated cyclin-dependent kinase 8 (CDK8) in KMT2A-r AML cells. Dual inhibition of RET and CDK8 restricted cell proliferation by producing multimodal oxidative stress responses in treated cells. Our data suggest that epigenetically enhanced RET protects KMT2A-r AML cells from oxidative stresses, which could be exploited as a potential therapeutic strategy.

Identification of Regulatory Elements in Primary Sensory Neurons Involved in Trauma-Induced Neuropathic Pain.

Chronic pain is a significant public health issue that is often refractory to existing therapies. Here we use a multiomic approach to identify cis-regulatory elements that show differential chromatin accessibility and reveal transcription factor (TF) binding motifs with functional regulation in the rat dorsal root ganglion (DRG), which contain cell bodies of primary sensory neurons, after nerve injury. We integrated RNA-seq to understand how differential chromatin accessibility after nerve injury may influence gene expression. Using TF protein arrays and chromatin immunoprecipitation-qPCR, we confirmed C/EBPγ binding to a differentially accessible sequence and used RNA-seq to identify processes in which C/EBPγ plays an important role. Our findings offer insights into TF motifs that are associated with chronic pain. These data show how interactions between chromatin landscapes and TF expression patterns may work together to determine gene expression programs in rat DRG neurons after nerve injury.

Spinal Cord Stimulation Increases Chemoefficacy and Prevents Paclitaxel-Induced Pain via CX3CL1.

INTRODUCTION: Despite increasing utilization of spinal cord stimulation (SCS), its effects on chemoefficacy, cancer progression, and chemotherapy-induced peripheral neuropathy (CIPN) pain remain unclear. Up to 30% of adults who are cancer survivors may suffer from CIPN, and there are currently no effective preventative treatments. MATERIALS AND METHODS: Through a combination of bioluminescent imaging, behavioral, biochemical, and immunohistochemical approaches, we investigated the role of SCS and paclitaxel (PTX) on tumor growth and PTX-induced peripheral neuropathy (PIPN) pain development in T-cell-deficient male rats (Crl:NIH-Foxn1rnu) with xenograft human non-small cell lung cancer. We hypothesized that SCS can prevent CIPN pain and enhance chemoefficacy partially by modulating macrophages, fractalkine (CX3CL1), and inflammatory cytokines. RESULTS: We show that preemptive SCS enhanced the antitumor efficacy of PTX and prevented PIPN pain. Without SCS, rats with and without tumors developed robust PIPN pain-related mechanical hypersensitivity, but only those with tumors developed cold hypersensitivity, suggesting T-cell dependence for different PIPN pain modalities. SCS increased soluble CX3CL1 and macrophages and decreased neuronal and nonneuronal insoluble CX3CL1 expression and inflammation in dorsal root ganglia. CONCLUSION: Collectively, our findings suggest that preemptive SCS is a promising strategy to increase chemoefficacy and prevent PIPN pain via CX3CL1-macrophage modulation.

De novo methylation of histone H3K23 by the methyltransferases EHMT1/GLP and EHMT2/G9a.

Epigenetic modifications to histone proteins serve an important role in regulating permissive and repressive chromatin states, but despite the identification of many histone PTMs and their perceived role, the epigenetic writers responsible for generating these chromatin signatures are not fully characterized. Here, we report that the canonical histone H3K9 methyltransferases EHMT1/GLP and EHMT2/G9a are capable of catalyzing methylation of histone H3 lysine 23 (H3K23). Our data show that while both enzymes can mono- and di-methylate H3K23, only EHMT1/GLP can tri-methylate H3K23. We also show that pharmacologic inhibition or genetic ablation of EHMT1/GLP and/or EHMT2/G9a leads to decreased H3K23 methylation in mammalian cells. Taken together, this work identifies H3K23 as a new direct methylation target of EHMT1/GLP and EHMT2/G9a, and highlights the differential activity of these enzymes on H3K23 as a substrate.

CCAAT enhancer binding protein gamma (C/EBP-γ): An understudied transcription factor.

The CCAAT enhancer binding protein (C/EBP) family of transcription factors are important transcriptional mediators of a wide range of physiologic processes. C/EBP-γ is the shortest C/EBP protein and lacks a canonical activation domain for the recruitment of transcriptional machinery. Despite its ubiquitous expression and ability to dimerize with other C/EBP proteins, C/EBP-γ has been studied far less than other C/EBP proteins, and, to our knowledge, no review of its functions has been written. This review seeks to integrate the current knowledge about C/EBP-γ and its physiologic roles, especially in cell proliferation, the integrated stress response, oncogenesis, hematopoietic and nervous system development, and metabolism, as well as to identify areas for future research.

Global gene expression and chromatin accessibility of the peripheral nervous system in animal models of persistent pain.

BACKGROUND: Efforts to understand genetic variability involved in an individual's susceptibility to chronic pain support a role for upstream regulation by epigenetic mechanisms. METHODS: To examine the transcriptomic and epigenetic basis of chronic pain that resides in the peripheral nervous system, we used RNA-seq and ATAC-seq of the rat dorsal root ganglion (DRG) to identify novel molecular pathways associated with pain hypersensitivity in two well-studied persistent pain models induced by chronic constriction injury (CCI) of the sciatic nerve and intra-plantar injection of complete Freund's adjuvant (CFA) in rats. RESULTS: Our RNA-seq studies identify a variety of biological process related to synapse organization, membrane potential, transmembrane transport, and ion binding. Interestingly, genes that encode transcriptional regulators were disproportionately downregulated in both models. Our ATAC-seq data provide a comprehensive map of chromatin accessibility changes in the DRG. A total of 1123 regions showed changes in chromatin accessibility in one or both models when compared to the naïve and 31 shared differentially accessible regions (DAR)s. Functional annotation of the DARs identified disparate molecular functions enriched for each pain model which suggests that chromatin structure may be altered differently following sciatic nerve injury and hind paw inflammation. Motif analysis identified 17 DNA sequences known to bind transcription factors in the CCI DARs and 33 in the CFA DARs. Two motifs were significantly enriched in both models. CONCLUSIONS: Our improved understanding of the changes in chromatin accessibility that occur in chronic pain states may identify regulatory genomic elements that play essential roles in modulating gene expression in the DRG.

Human brain region-specific variably methylated regions are enriched for heritability of distinct neuropsychiatric traits.

BACKGROUND: DNA methylation dynamics in the brain are associated with normal development and neuropsychiatric disease and differ across functionally distinct brain regions. Previous studies of genome-wide methylation differences among human brain regions focus on limited numbers of individuals and one to two brain regions. RESULTS: Using GTEx samples, we generate a resource of DNA methylation in purified neuronal nuclei from 8 brain regions as well as lung and thyroid tissues from 12 to 23 donors. We identify differentially methylated regions between brain regions among neuronal nuclei in both CpG (181,146) and non-CpG (264,868) contexts, few of which were unique to a single pairwise comparison. This significantly expands the knowledge of differential methylation across the brain by 10-fold. In addition, we present the first differential methylation analysis among neuronal nuclei from basal ganglia tissues and identify unique CpG differentially methylated regions, many associated with ion transport. We also identify 81,130 regions of variably CpG methylated regions, i.e., variable methylation among individuals in the same brain region, which are enriched in regulatory regions and in CpG differentially methylated regions. Many variably methylated regions are unique to a specific brain region, with only 202 common across all brain regions, as well as lung and thyroid. Variably methylated regions identified in the amygdala, anterior cingulate cortex, and hippocampus are enriched for heritability of schizophrenia. CONCLUSIONS: These data suggest that epigenetic variation in these particular human brain regions could be associated with the risk for this neuropsychiatric disorder.

Spinal cord stimulation prevents paclitaxel-induced mechanical and cold hypersensitivity and modulates spinal gene expression in rats.

INTRODUCTION: Paclitaxel-induced peripheral neuropathy (PIPN) is a common dose-limiting side effect of this cancer treatment drug. Spinal cord stimulation (SCS) has demonstrated efficacy for attenuating some neuropathic pain conditions. OBJECTIVE: We aim to examine the inhibitory effect of SCS on the development of PIPN pain and changes of gene expression in the spinal cord in male rats after SCS. METHODS: We examined whether traditional SCS (50 Hz, 6-8 h/session daily for 14 consecutive days) administered during paclitaxel treatment (1.5 mg/kg, i.p.) attenuates PIPN-related pain behavior. After SCS treatment, we performed RNA-seq of the lumbar spinal cord to examine which genes are differentially expressed after PIPN with and without SCS. RESULTS: Compared to rats treated with paclitaxel alone (n = 7) or sham SCS (n = 6), SCS treatment (n = 11) significantly inhibited the development of paclitaxel-induced mechanical and cold hypersensitivity, without altering open-field exploratory behavior. RNA-seq showed that SCS induced upregulation of 836 genes and downregulation of 230 genes in the spinal cord of paclitaxel-treated rats (n = 3) as compared to sham SCS (n = 5). Spinal cord stimulation upregulated immune responses in paclitaxel-treated rats, including transcription of astrocyte- and microglial-related genes, but repressed transcription of multiple gene networks associated with synapse transmission, neuron projection development, γ-aminobutyric acid reuptake, and neuronal plasticity. CONCLUSION: Our findings suggest that traditional SCS may attenuate the development of pain-related behaviors in PIPN rats, possibly by causing aggregate inhibition of synaptic plasticity through upregulation and downregulation of gene networks in the spinal cord.

Sex differences in gene regulation in the dorsal root ganglion after nerve injury.

BACKGROUND: Pain is a subjective experience derived from complex interactions among biological, environmental, and psychosocial pathways. Sex differences in pain sensitivity and chronic pain prevalence are well established. However, the molecular basis underlying these sex dimorphisms are poorly understood particularly with regard to the role of the peripheral nervous system. Here we sought to identify shared and distinct gene networks functioning in the peripheral nervous systems that may contribute to sex differences of pain in rats after nerve injury. RESULTS: We performed RNA-seq on dorsal root ganglia following chronic constriction injury of the sciatic nerve in male and female rats. Analysis from paired naive and injured tissues showed that 1513 genes were differentially expressed between sexes. Genes which facilitated synaptic transmission in naïve and injured females did not show increased expression in males. CONCLUSIONS: Appreciating sex-related gene expression differences and similarities in neuropathic pain models may help to improve the translational relevance to clinical populations and efficacy of clinical trials of this major health issue.

RNA-seq of spinal cord from nerve-injured rats after spinal cord stimulation.

Spinal cord stimulation has become an important modality in pain treatment especially for neuropathic pain conditions refractory to pharmacotherapy. However, the molecular control of inhibitory and excitatory mechanisms observed after spinal cord stimulation are poorly understood. Here, we used RNA-seq to identify differences in the expression of genes and gene networks in spinal cord tissue from nerve-injured rats with and without repetitive conventional spinal cord stimulation treatment. Five weeks after chronic constrictive injury to the left sciatic nerve, male and female rats were randomized to receive repetitive spinal cord stimulation or no treatment. Rats receiving spinal cord stimulation underwent epidural placement of a miniature stimulating electrode and received seven sessions of spinal cord stimulation (50 Hz, 80% motor threshold, 0.2 ms, constant current bipolar stimulation, 120 min/session) over four consecutive days. Within 2 h after the last spinal cord stimulation treatment, the L4-L6 spinal segments ipsilateral to the side of nerve injury were harvested and used to generate libraries for RNA-seq. Our RNA-seq data suggest further increases of many existing upregulated immune responses in chronic constrictive injury rats after repetitive spinal cord stimulation, including transcription of cell surface receptors and activation of non-neuronal cells. We also demonstrate that repetitive spinal cord stimulation represses transcription of several key synaptic signaling genes that encode scaffold proteins in the post-synaptic density. Our transcriptional studies suggest a potential relationship between specific genes and the therapeutic effects observed in patients undergoing conventional spinal cord stimulation after nerve injury. Furthermore, our results may help identify new therapeutic targets for improving the efficacy of conventional spinal cord stimulation and other chronic pain treatments.

Peripherally Acting µ-Opioid Receptor Agonists Attenuate Ongoing Pain-associated Behavior and Spontaneous Neuronal Activity after Nerve Injury in Rats.

BACKGROUND: Ongoing neuropathic pain is difficult to treat. The authors examined whether dermorphin [D-Arg2, Lys4] (1-4) amide, a peripherally acting µ-opioid receptor agonist, attenuates ongoing pain-associated manifestations after nerve injury in rats and mice. METHODS: Using conditioned place preference assay, the authors tested whether animals show a preference to the environment associated with drug treatment. Wide-dynamic range and dorsal root ganglion neuronal activities were measured by electrophysiology recording and calcium imaging. RESULTS: Nerve-injured animals stayed longer in dermorphin [D-Arg2, Lys4] (1-4) amide-paired chamber after conditioning than during preconditioning (rats: 402.4 ± 61.3 vs. 322.1 ± 45.0 s, 10 mg/kg, n = 9, P = 0.009; mice: 437.8 ± 59.4 vs. 351.3 ± 95.9 s, 2 mg/kg, n = 8, P = 0.047). Topical ganglionic application of dermorphin [D-Arg2, Lys4] (1-4) amide (5 µM, 1 µl, n = 5) reduced the numbers of small-diameter dorsal root ganglion neurons that showed spontaneous activity (1.1 ± 0.4 vs. 1.5 ± 0.3, P = 0.044) and that were activated by test stimulation (15.5 ± 5.5 vs. 28.2 ± 8.2, P = 0.009) after injury. In neuropathic rats, dermorphin [D-Arg2, Lys4] (1-4) amide (10 mg/kg, n = 8) decreased spontaneous firing rates in wide-dynamic range neurons to 53.2 ± 46.6% of predrug level, and methylnaltrexone (5 mg/kg, n = 9) blocked dermorphin [D-Arg2, Lys4] (1-4) amide-induced place preference and inhibition of wide-dynamic range neurons. Dermorphin [D-Arg2, Lys4] (1-4) amide increased paw withdrawal threshold (17.5 ± 2.2 g) from baseline (3.5 ± 0.7 g, 10 mg/kg, n = 8, P = 0.002) in nerve-injured rats, but the effect diminished after repeated administrations. CONCLUSIONS: Peripherally acting µ-opioids may attenuate ongoing pain-related behavior and its neurophysiologic correlates. Yet, repeated administrations cause antiallodynic tolerance.

Associations between genetic and epigenetic variations in cytokine genes and mild persistent breast pain in women following breast cancer surgery.

Persistent pain following breast cancer surgery is a significant problem. Both inherited and acquired mechanisms of inflammation appear to play a role in the development and maintenance of persistent pain. In this longitudinal study, growth mixture modeling was used to identify persistent breast pain phenotypes based on pain assessments obtained prior to and monthly for 6months following breast cancer surgery. Associations between the "no pain" and "mild pain" phenotypes and single nucleotide polymorphisms (SNPs) spanning 15 cytokine genes were evaluated. The methylation status of the CpG sites found in the promoters of genes associated with pain group membership was determined using bisulfite sequencing. In the multivariate analysis, three SNPs (i.e., interleukin 6 (IL6) rs2069840, C-X-C motif chemokine ligand 8 (CXCL8) rs4073, tumor necrosis factor (TNF) rs1800610) and two TNF CpG sites (i.e., c.-350C, c.-344C) were associated with pain group membership. These findings suggest that variations in IL6, CXCL8, and TNF are associated with the development and maintenance of mild persistent breast pain. CpG methylation within the TNF promoter may provide an additional mechanism through which TNF alters the risk for mild persistent breast pain after breast cancer surgery. These genetic and epigenetic variations may help to identify individuals who are predisposed to the development of mild levels of persistent breast pain following breast cancer surgery.

Association of Implementation of Practice Standards for Electrocardiographic Monitoring With Nurses' Knowledge, Quality of Care, and Patient Outcomes: Findings From the Practical Use of the Latest Standards of Electrocardiography (PULSE) Trial.

BACKGROUND: Although continuous electrocardiographic (ECG) monitoring is ubiquitous in hospitals, monitoring practices are inconsistent. We evaluated implementation of American Heart Association practice standards for ECG monitoring on nurses' knowledge, quality of care, and patient outcomes. METHODS AND RESULTS: The PULSE (Practical Use of the Latest Standards of Electrocardiography) Trial was a 6-year multisite randomized clinical trial with crossover that took place in 65 cardiac units in 17 hospitals. We measured outcomes at baseline, time 2 after group 1 hospitals received the intervention, and time 3 after group 2 hospitals received the intervention. Measurement periods were 15 months apart. The 2-part intervention consisted of an online ECG monitoring education program and strategies to implement and sustain change in practice. Nurses' knowledge (N=3013 nurses) was measured by a validated 20-item online test, quality of care related to ECG monitoring (N=4587 patients) by on-site observation, and patient outcomes (mortality, in-hospital myocardial infarction, and not surviving a cardiac arrest; N=95 884 hospital admissions) by review of administrative, laboratory, and medical record data. Nurses' knowledge improved significantly immediately after the intervention in both groups but was not sustained 15 months later. For most measures of quality of care (accurate electrode placement, accurate rhythm interpretation, appropriate monitoring, and ST-segment monitoring when indicated), the intervention was associated with significant improvement, which was sustained 15 months later. Of the 3 patient outcomes, only in-hospital myocardial infarction declined significantly after the intervention and was sustained. CONCLUSIONS: Online ECG monitoring education and strategies to change practice can lead to improved nurses' knowledge, quality of care, and patient outcomes. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01269736.

Reader domain specificity and lysine demethylase-4 family function.

The KDM4 histone demethylases are conserved epigenetic regulators linked to development, spermatogenesis and tumorigenesis. However, how the KDM4 family targets specific chromatin regions is largely unknown. Here, an extensive histone peptide microarray analysis uncovers trimethyl-lysine histone-binding preferences among the closely related KDM4 double tudor domains (DTDs). KDM4A/B DTDs bind strongly to H3K23me3, a poorly understood histone modification recently shown to be enriched in meiotic chromatin of ciliates and nematodes. The 2.28 Å co-crystal structure of KDM4A-DTD in complex with H3K23me3 peptide reveals key intermolecular interactions for H3K23me3 recognition. Furthermore, analysis of the 2.56 Å KDM4B-DTD crystal structure pinpoints the underlying residues required for exclusive H3K23me3 specificity, an interaction supported by in vivo co-localization of KDM4B and H3K23me3 at heterochromatin in mammalian meiotic and newly postmeiotic spermatocytes. In vitro demethylation assays suggest H3K23me3 binding by KDM4B stimulates H3K36 demethylation. Together, these results provide a possible mechanism whereby H3K23me3-binding by KDM4B directs localized H3K36 demethylation during meiosis and spermatogenesis.

Epigenetic regulation and measurement of epigenetic changes.

Epigenetic mechanisms provide an adaptive layer of control in the regulation of gene expression that enables an organism to adjust to a changing environment. Epigenetic regulation increases the functional complexity of deoxyribonucleic acid (DNA) by altering chromatin structure, nuclear organization, and transcript stability. These changes may additively or synergistically influence gene expression and result in long-term molecular and functional consequences independent of the DNA sequence that may ultimately define an individual's phenotype. This article (1) describes histone modification, DNA methylation, and expression of small noncoding RNA species; (2) reviews the most common methods used to measure these epigenetic changes; and (3) presents factors that need to be considered when choosing a specific tissue to evaluate for epigenetic changes.

The success of enteral nutrition and ICU-acquired infections: a multicenter observational study.

BACKGROUND AND AIMS: The objective of this study was to evaluate the relationship between increasing success with enteral nutrition (EN) and acquired infection in the Intensive Care Unit (ICU). METHODS: We conducted a prospective, multicenter, observational study in 3 Medical/Surgical ICUs. We included patients mechanically ventilated in ICU more than 72 h and who received enteral nutrition only. Charts were reviewed to determine success with EN delivery and clinical outcomes. Suspected infections were adjudicated by 2 or more clinicians to determine the presence or absence of infection (rated as either probable or possible infection). RESULTS: Of the 207 patients included in this analysis, the average age was 62.0 years; APACHE II score was 23.3; BMI: 28.5; and 73% were medical. Overall, patients received 48.9% (range 0-120%) of their energy and 45.1% (range 0-120%) of their protein requirements from EN. Overall, 25.1% developed an infection after 72 h from admission, 21.7% developed an infection after 96 h from admission, and the 28-day mortality was 29.0%. In a regression model, greater amounts of energy and protein were consistently associated with a reduction in infection. However, estimates only achieved levels near statistical significance for risk of at least 1 probable infection after >96 h (Odds Ratio [0R]: 0.32, 95% Confidence Interval [CI]: 0.10-1.02, p=0.054 and OR: 0.40, 95% CI: 0.18-0.89, p=0.024 per 1000 kcal/day energy and 30 grams/day protein, respectively). In all cases, the OR was lower when considering infections that developed after 96 h compared to infections that developed after 72 h and when considering 'Probable' infections compared to all infections which included 'Possible' infections. CONCLUSIONS: Successful EN may be associated with a reduction in infectious complications, particularly after 96 h of ICU admission.

Improving nurses' ability to identify anatomic location and leads on 12-lead electrocardiograms with ST elevation myocardial infarction.

BACKGROUND: ST segment elevation on the electrocardiogram (ECG) signifies complete occlusion of a coronary artery. Nurses play a significant role in obtaining, interpreting, and communicating 12-lead ECG findings. AIMS: We evaluate a hand held paper tool to determine if it assists nurses; (1) identify the presence of ST elevation myocardial infarction (STEMI), (2) location, and (3) leads. METHODS: A pre-test/post-test design was used. At pre-test, nurses from the emergency department (ED), coronary care unit (CCU), and the progressive care (PC) were given 6 patient scenarios (3 STEMI and 3 non-STEMI) and a corresponding 12-lead ECG. This was followed by a brief in-service on how to use the hand held tool. The nurse then interpret the same six ECGs (in a different order) using the hand held tool. RESULTS: Seventy-five nurses participated. Identification of STEMI location improved when the tool was used. Lead identification improved in 2 of the 3 STEMI scenarios. Overall, nurses' ability to correctly identify the 3 non-ischemic ECGs was low, and in one ECG was lower when the tool was used. CONCLUSION: For ECGs with a STEMI pattern an easy-to-learn tool improves nurses' ability to identify STEMI location. Nurses require education for identifying ECG leads, and non-ischemic ECG patterns.

Evaluation of a device to facilitate female urethral catheterization.

Urethral catheterization is a skilled procedure that nurses in hospital settings perform routinely. The opening of the female urethra is located within the vulvar vestibule, making insertion of urinary catheters into females a greater technical challenge than in males. Researchers evaluated whether a new device might decrease the time required for catheter insertion, increase the likelihood of inserting the catheter on the first attempt (improved accuracy), and reduce patient discomfort. Comments about the device from both patients and nurses also are reported.