Miracle-dz/UniFAR-FTUs huggingface dataset:
Effects of Rounding on Patient Satisfaction and Patient Safety on a Medical-Surgical Unit

Purpose: This project examines an intervention developed to decrease patient uncertainty regarding nurse availability for response to immediate needs, leading to higher patient satisfaction scores and improved patient safety. Background/Rationale: Research supports the premise that frequent patient rounding has a positive impact on patient satisfaction and safety. Rounding has been noted to elevate patients' certainty for their needs. When a rounding model is practiced, patients become more certain that a nurse will be available for immediate needs (assistance to the bathroom, pain interventions, or addressing questions about care). Description of the Innovation: Rounds are completed by the charge nurse every 2 hours and include addressing the "4 P's. " The 4 P's encompass the assessment of pain, potty, position, and presence. Using Mishel's Uncertainty of Illness model as a basis, the concept of help uncertainty is defined for this clinical project. Outcomes: A marked increase in patient satisfaction and decrease in call-light frequency have been revealed. The unit's rate of falls has declined since the initiation of the rounding model. Conclusion: A routine presence of a registered nurse has promoted patient safety as seen by the declining falls scores. Patient certainty of nurse presence and the trust in the nursing care have flourished since the implementation of this model and are evidenced in the increasing patient satisfaction scores and patient surveys. Implications: The implications to nursing practice based on these outcomes are that a routine rounding practice by the charge nurse will serve to improve patient safety and satisfaction.
Hierarchical and Redundant Roles of Activating FcγRs in Protection against Influenza Disease by M2e-Specific IgG1 and IgG2a Antibodies

ABSTRACT The ectodomain of matrix protein 2 is a universal influenza A virus vaccine candidate that provides protection through antibody-dependent effector mechanisms. Here we compared the functional engagement of Fcγ receptor (FcγR) family members by two M2e-specific monoclonal antibodies (MAbs), MAb 37 (IgG1) and MAb 65 (IgG2a), which recognize a similar epitope in M2e with similar affinities. The binding of MAb 65 to influenza A virus-infected cells triggered all three activating mouse Fcγ receptors in vitro, whereas MAb 37 activated only FcγRIII. The passive transfer of MAb 37 or MAb 65 in wild-type, Fcer1g−/−, Fcgr3 −/−, and Fcgr1 −/− Fcgr3 −/− BALB/c mice revealed the importance of these receptors for protection against influenza A virus challenge, with a clear requirement of FcγRIII for IgG1 MAb 37 being found. We also report that FcγRIV contributes to protection by M2e-specific IgG2a antibodies. IMPORTANCE There is increased awareness that protection by antibodies directed against viral antigens is also mediated by the Fc domain of these antibodies. These Fc-mediated effector functions are often missed in clinical assays, which are used, for example, to define correlates of protection induced by vaccines. The use of antibodies to prevent and treat infectious diseases is on the rise and has proven to be a promising approach in our battle against newly emerging viral infections. It is now also realized that Fcγ receptors significantly enhance the in vivo protective effect of broadly neutralizing antibodies directed against the conserved parts of the influenza virus hemagglutinin. We show here that two M2e-specific monoclonal antibodies with close to identical antigen-binding specificities and affinities have a very different in vivo protective potential that is controlled by their capacity to interact with activating Fcγ receptors.
Genome Sequence of a Monoreassortant H1N1 Swine Influenza Virus Isolated from a Pig in Hungary

ABSTRACT The genome of a porcine H1N1 influenza A strain is reported in this study. The strain proved to be a monoreassortant strain with a typical porcine N1 gene on the genetic backbone of the pandemic H1N1 influenza A virus strain. Monitoring of descendants of the pandemic 2009 H1N1 strain is needed because of concerns that more-virulent strains may emerge in forthcoming epidemic seasons.
Proviruses Selected for High and Stable Expression of Transduced Genes Accumulate in Broadly Transcribed Genome Areas

ABSTRACT Retroviruses and retrovirus-derived vectors integrate nonrandomly into the genomes of host cells with specific preferences for transcribed genes, gene-rich regions, and CpG islands. However, the genomic features that influence the transcriptional activities of integrated retroviruses or retroviral vectors are poorly understood. We report here the cloning and characterization of avian sarcoma virus integration sites from chicken tumors. Growing progressively, dependent on high and stable expression of the transduced v-src oncogene, these tumors represent clonal expansions of cells bearing transcriptionally active replication-defective proviruses. Therefore, integration sites in our study distinguished genomic loci favorable for the expression of integrated retroviruses and gene transfer vectors. Analysis of integration sites from avian sarcoma virus-induced tumors showed strikingly nonrandom distribution, with proviruses found prevalently within or close to transcription units, particularly in genes broadly expressed in multiple tissues but not in tissue-specifically expressed genes. We infer that proviruses integrated in these genomic areas efficiently avoid transcriptional silencing and remain active for a long time during the growth of tumors. Defining the differences between unselected retroviral integration sites and sites selected for long-terminal-repeat-driven gene expression is relevant for retrovirus-mediated gene transfer and has ramifications for gene therapy.
FATORES DE (IN)SATISFAÇÃO NO TRABALHO DA EQUIPE DE ENFERMAGEM EM UTI PEDIÁTRICA

Estudio de abordaje cualitativo del tipo exploratorio descriptivo. Tuvo como objetivos investigar los factores que contribuyen para la satisfaccion y para la insatisfaccion en el trabajo del equipo de enfermeria en Unidad de Terapia Pediatrica, asi como proponer estrategias de abordaje que favorezcan la satisfaccion en en trabajo, de acuerdo con la percepcion de los propios miembros del equipo. Los datos f ueron obtenidos con 18 profesionales actuantes en UTI Pediatr ica de dos hospitales del mu nicipio de Curitiba - Parana, de febrero a mayo de 2011, utilizandose la entrevista semiestructurada. Los resultados fueron examinados por medio de la tecnica de analisis de contenido y muestran la percepcion de la complejidad de ser profesional de enfermeria actuante en terapia intensiva, apuntando y promoviendo la reflexion sobre la relacion de dialogo entre cuidar y ser cuidado.
Herd Immunity to GII.4 Noroviruses Is Supported by Outbreak Patient Sera

ABSTRACT Noroviruses (NoVs) of genogroup II, cluster 4 (GII.4), are the most common cause of outbreaks of acute gastroenteritis worldwide. During the past 13 years, GII.4 NoVs caused four seasons of widespread activity globally, each associated with the emergence of a new strain. In this report, we characterized the most recent epidemic strain, GII.4-2006 Minerva, by comparing virus-like particle (VLP) antigenic relationships and histo-blood group antigen (HBGA) binding profiles with strains isolated earlier. We also investigated the seroprevalence and specificity of GII.4 antibody in the years prior to, during, and following the GII.4 pandemic of 1995 and 1996 using a large collection of acute- and convalescent-phase serum pairs (n = 298) collected from 34 outbreaks. In a surrogate neutralization assay, we measured the blockade of HBGA binding using a panel of GII.4 VLPs representing strains isolated in 1987, 1997, 2002, and 2006 and a GII.3 VLP representing a strain isolated in the mid-1990s. Serum titers required for 50% HBGA blockade were compared between populations. In general, blockade of GII.4 VLP-HBGA binding was greater with convalescent-phase outbreak sera collected near the time of origin of the VLP strain. Heterotypic genotypes did not contribute to herd immunity against GII.4 NoVs based on their inability to block GII.4 VLP binding to HBGA. However, previous exposure to GII.4 NoV followed by infection by GII.3 NoV appeared to evoke an immune response to GII.4 NoV. These results support the hypothesis that herd immunity is a driving force for GII.4 evolution in the U.S. population. The data also suggest that complex patterns of cross-protection may exist across NoV genotypes in humans.
The Effects of Top Management Professional Development on Administrator Turnover

This study examines how characteristics associated with professional development of the top management team in 406 nursing homes can affect administrator turnover. Tenure, education, and membership in a professional association are the characteristics investigated. Data used in this investigation came from a survey of nursing facilities and the 1999 On-line Survey, Certification, and Reporting system. Using logistic regression analyses, the effects of the professional development characteristics of the top management team on the turnover of administrators were examined. The average annual turnover rate of administrators was 43%. Controlling for seven organizational factors, the results are generally significant for tenure and membership in a professional association. This study shows that both aggregate and dissimilarity measures of tenure and professional association membership are important influences on administrator turnover. These results suggest that nursing home owners may want to hire top managers with strong professional membership ties or should encourage top managers to make these ties.
Effect of Two Different Doses of Gabapentin on the Intraocular Pressure and Hemodynamic Stress Responses to Laryngoscopy and Tracheal Intubation

Background. The stress response to laryngoscopy and intubation causes an undesirable increase in heart rate, blood pressure, and intraocular pressure. This study was designed to compare the effect of two doses of gabapentin on the stress response to laryngoscopy and intubation. Patients and Methods. (ASA I and II) 60 patients, aged from 18 to 60 years undergoing elective eye surgery requiring endotracheal intubation, were randomly allocated into 3 groups, 20 patients each. 2 hours before the surgery, group I received oral placebo, and groups II and III received oral gabapentin 800 mg and 1200 mg, respectively. Heart rate (HR), mean arterial pressure (MAP), and intraocular pressure (IOP) were measured before and after induction of anesthesia, immediately after, 5 minutes, and 10 minutes after intubation. Results. Gabapentin 1200 mg prevented the increase in HR, MAP, and IOP, secondary to laryngoscopy and intubation, and kept them below the baseline till 10 minutes after intubation (), while with gabapentin 800 mg, the increase in HR, MAP, and IOP was nonsignificant () and returned to levels below the baseline at 5 and 10 minutes after intubation. Conclusion. Preoperative gabapentin 1200 mg effectively prevented the stress response to laryngoscopy and intubation; meanwhile, gabapentin 800 mg only prevented significant stress response.
Proliferation Capacity and Cytotoxic Activity Are Mediated by Functionally and Phenotypically Distinct Virus-Specific CD8 T Cells Defined by Interleukin-7Rα (CD127) and Perforin Expression

ABSTRACT Cytotoxicity and proliferation capacity are key functions of antiviral CD8 T cells. In the present study, we investigated a series of markers to define these functions in virus-specific CD8 T cells. We provide evidence that there is a lack of coexpression of perforin and CD127 in human CD8 T cells. CD127 expression on virus-specific CD8 T cells correlated positively with proliferation capacity and negatively with perforin expression and cytotoxicity. Influenza virus-, cytomegalovirus-, and Epstein-Barr virus/human immunodeficiency virus type 1-specific CD8 T cells were predominantly composed of CD127+ perforin−/CD127− perforin+, and CD127−/perforin− CD8 T cells, respectively. CD127−/perforin− and CD127−/perforin+ cells expressed significantly more PD-1 and CD57, respectively. Consistently, intracellular cytokine (gamma interferon, tumor necrosis factor alpha, and interleukin-2 [IL-2]) responses combined to perforin detection confirmed that virus-specific CD8 T cells were mostly composed of either perforin+/IL-2− or perforin−/IL-2+ cells. In addition, perforin expression and IL-2 secretion were negatively correlated in virus-specific CD8 T cells (P < 0.01). As previously shown for perforin, changes in antigen exposure modulated also CD127 expression. Based on the above results, proliferating (CD127+/IL-2-secreting) and cytotoxic (perforin+) CD8 T cells were contained within phenotypically distinct T-cell populations at different stages of activation or differentiation and showed different levels of exhaustion and senescence. Furthermore, the composition of proliferating and cytotoxic CD8 T cells for a given antiviral CD8 T-cell population appeared to be influenced by antigen exposure. These results advance our understanding of the relationship between cytotoxicity, proliferation capacity, the levels of senescence and exhaustion, and antigen exposure of antiviral memory CD8 T cells.
Immediate Activation Fails To Rescue Efficient Human Immunodeficiency Virus Replication in Quiescent CD4+ T Cells

ABSTRACT Unlike activated T cells, quiescent CD4+ T cells have shown resistance to human immunodeficiency virus (HIV) infection due to a block in the early events of the viral life cycle. To further investigate the nature of this block, we infected quiescent CD4+ T cells with HIV-1NL4-3 and immediately stimulated them. Compared to activated (prestimulated) cells, these poststimulated cells showed slightly decreased viral entry and delays in the completion of reverse transcription. However, the relative efficiency of integration was similar to that of prestimulated cells. Together, this resulted in decreased expression of tat/rev mRNA and synthesis of viral protein. Furthermore, based on cell cycle staining and BrdU incorporation, poststimulated cells expressing viral protein failed to initiate a second round of their cell cycle, independently of Vpr-mediated arrest. Together, these data demonstrate that the early stages of the HIV life cycle are inefficient in these poststimulated cells and that efficient replication cannot be induced by subsequent activation.
The Augmentation of a Collagen/Glycosaminoglycan Biphasic Osteochondral Scaffold with Platelet-Rich Plasma and Concentrated Bone Marrow Aspirate for Osteochondral Defect Repair in Sheep

Objective: This study investigates the combination of platelet-rich plasma (PRP) or concentrated bone marrow aspirate (CBMA) with a biphasic collagen/glycosaminoglycan (GAG) osteochondral scaffold for the treatment of osteochondral defects in sheep. Design: Acute osteochondral defects were created in the medial femoral condyle (MFC) and the lateral trochlea sulcus (LTS) of 24 sheep (n = 6). Defects were left empty or filled with a 6 × 6-mm scaffold, either on its own or in combination with PRP or CBMA. Outcome measures at 6 months included mechanical testing, International Cartilage Repair Society (ICRS) repair score, modified O’Driscoll histology score, qualitative histology, and immunohistochemistry for type I, II, and VI collagen. Results: No differences in mechanical properties, ICRS repair score, or modified O’Driscoll score were detected between the 4 groups. However, qualitative assessments of the histological architecture, Safranin O content, and collagen immunohistochemistry indicated that in the PRP/scaffold groups, there was a more hyaline cartilage–like tissue repair. In addition, the addition of CBMA and PRP to the scaffold reduced cyst formation in the subchondral bone of healed lesions. Conclusion: There was more hyaline cartilage–like tissue formed in the PRP/scaffold group and less subchondral cystic lesion formation in the CBMA and PRP/scaffold groups, although there were no quantitative differences in the repair tissue formed.
The Chondroprotective Role of Erythromycin in a Murine Joint Destruction Model

Objective Inflammation is a major player in the joint destruction process. Macrolide antibiotics have recently been found to have a novel anti-inflammatory function, but their effects on the joint are unknown. Our objective was to investigate the effect of macrolide antibiotic erythromycin on cartilage gene expression under inflammatory conditions as well as on joint pathology in an in vivo inflammatory joint destruction model. Design In our in vivo studies, mouse knee joints were injected with monosodium iodoacetate (MIA), a chemical that inhibits glycolysis and causes joint inflammation and matrix loss. Erythromycin was administered by daily intraperitoneal injection. Changes in joint cartilage and synovium were evaluated by histological analysis. In our in vitro studies, primary bovine articular chondrocytes were treated with erythromycin in the presence of pro-inflammatory cytokine IL-1β or lipopolysaccharide (LPS), and cartilage gene expression analysis was performed. Results Regional differences in cartilage matrix destruction along the medial-lateral axis were observed in joints of MIA-injected mice. Erythromycin treatment inhibited cartilage matrix loss and synovitis in these joints. In addition, erythromycin inhibited IL-1β and LPS-induced expression of MMPs and iNOS, as well as the positive regulatory loop between IL-1β and Toll-like receptor 4 (TLR4) in articular chondrocytes. Furthermore, erythromycin prevented LPS-induced NF-κB activation, a key mediator of TLR4-mediated cartilage destruction process. Conclusions Erythromycin has the ability to inhibit catabolic gene expression mediated by IL-1β and TLR4 in chondrocytes in vitro and maintains cartilage matrix levels in experimental inflammatory joint destruction in vivo, suggesting that it possesses a chondroprotective activity.
Signal Detection in a Space–Frequency Coded Cooperative Communication System With Multiple Carrier Frequency Offsets by Exploiting Specific Properties of the Code Structure

In cooperative communications, carrier frequency offsets (CFOs) between pairs of nodes may be different, making CFO compensation difficult, if not impossible. These multiple CFOs may drastically degrade the performance of a space-frequency (SF)-coded cooperative system. In this paper, we consider the signal-detection problem in an SF-coded cooperative communication system with multiple CFOs, where the SF codes are rotational based and can achieve both full spatial and full multipath diversity orders in a multiantenna system. By exploiting the structure of the SF codes, we propose three signal detection methods to deal with the multiple CFOs problem in the SF-coded orthogonal frequency-division multiplexing (OFDM) system - the minimum mean-squared error (MMSE) filtering method, the two-stage simple frequency-shift Q taps method, and the multiple fast Fourier transform (M-FFT) method - all of which offer different tradeoffs between performance and computational complexity. Simulation results indicate that our proposed detection methods work well, as long as the carrier frequency offsets between nodes are not unreasonably large.
Ablation of Nectin4 Binding Compromises CD46 Usage by a Hybrid Vesicular Stomatitis Virus/Measles Virus

ABSTRACT Measles virus (MV) immunosuppression is due to infection of SLAM-positive immune cells, whereas respiratory shedding and virus transmission are due to infection of nectin4-positive airway epithelial cells. The vaccine lineage MV strain Edmonston (MV-Edm) acquired an additional tropism for CD46 which is the basis of its oncolytic specificity. VSVFH is a vesicular stomatitis virus (VSV) encoding the MV-Edm F and H entry proteins in place of G. The virus spreads faster than MV-Edm and is highly fusogenic and a potent oncolytic. To determine whether ablating nectin4 tropism from VSVFH might prevent shedding, increasing its safety profile as an oncolytic, or might have any effect on CD46 binding, we generated VSVFH viruses with H mutations that disrupt attachment to SLAM and/or nectin4. Disruption of nectin4 binding reduced release of VSVFH from the basolateral side of differentiated airway epithelia composed of Calu-3 cells. However, because nectin4 and CD46 have substantially overlapping receptor binding surfaces on H, disruption of nectin4 binding compromised CD46 binding and greatly diminished the oncolytic potency of these viruses on human cancer cells. Thus, our results support continued preclinical development of VSVFH without ablation of nectin4 binding.
Hantavirus GnT Elements Mediate TRAF3 Binding and Inhibit RIG-I/TBK1-Directed Beta Interferon Transcription by Blocking IRF3 Phosphorylation

ABSTRACT Hantaviruses successfully replicate in primary human endothelial cells by restricting the early induction of beta interferon (IFN-β) and interferon-stimulated genes (ISGs). Gn proteins from NY-1V, ANDV, and TULV, but not PHV, harbor elements in their 142-residue cytoplasmic tails (GnTs) that inhibit RIG-I/MAVS/TBK1-TRAF3-directed IFN-β induction. Here, we define GnT interactions and residues required to inhibit TRAF3-TBK1-directed IFN-β induction and IRF3 phosphorylation. We observed that GnTs bind TRAF3 via residues within the TRAF-N domain (residues 392 to 415) and that binding is independent of the MAVS-interactive TRAF-C domain (residues 415 to 568). We determined that GnT binding to TRAF3 is mediated by C-terminal degrons within NY-1V or ANDV GnTs and that mutations that add degrons to TULV or PHV GnTs confer TRAF3 binding. Further analysis of GnT domains revealed that TRAF3 binding is a discrete GnT function, independent of IFN regulation, and that residues 15 to 42 from the NY-1V GnT C terminus are required for inhibiting TBK1-directed IFN-β transcription. Mutagenesis of the NY-1V GnT revealed that altering tyrosine 627 (Y627A/S/F) abolished GnT regulation of RIG-I/TBK1-directed IRF3 phosphorylation and transcriptional responses of ISRE, κB, and IFN-β promoters. Moreover, GnTs from NY-1V, ANDV, and TULV, but not PHV, inhibited RIG-I-directed IRF3 phosphorylation. Collectively, these findings suggest a novel role for GnTs in regulating RIG-I/TBK1 pathway-directed IRF3 phosphorylation and IFN-β induction and define virulence determinants within GnTs that may permit the attenuation of pathogenic hantaviruses. IMPORTANCE These findings provide a mechanism for selected hantavirus GnT interactions to regulate RIG-I/TBK1 signaling responses required for IFN-β induction by inhibiting TBK1 phosphorylation of IRF3. These studies culminate in showing that a single GnT residue, Y627, is required for the NY-1V GnT to inhibit RIG-I/TBK1-directed IRF3 phosphorylation and IFN-β induction. These findings define a potential virulence determinant within the NY-1V GnT that may permit hantavirus attenuation.