bluuebunny/crossref_metadata_2025_split huggingface dataset:
‘The character rests heavily within me’: drama students as standardized patients in mental health nursing education
Authors: Jacobs A. C. , van Jaarsveldt D. E. 
Published: April 2016

Accessible summaryWhat is known on the subject?

Standardized patient (SP) simulation is an internationally recognized learning strategy that has proven effective in enhancing nursing students’ competencies necessary for mental health practice.

What does this paper add to existing knowledge?

A deeper exploration of the process from the perspective of SPs and more particularly drama students, revealed the complexity they need to navigate and the personal vulnerability they are exposed to when creating an authentic learning opportunity for nursing students.

What are the implications for practice?

Their vulnerability justifies deeper consideration of support, as well as research on the ethical implications of SP simulation.

Nursing students need to be well grounded in therapeutic communication before engaging with mental health users. This should include opportunities to question personal frames of reference that could hinder therapeutic engagement with diverse others.

In future, the drama students can be involved in scenario development to enhance the authenticity of simulations.

AbstractIntroductionThe effectiveness of Standardized patient (SP) simulation in enhancing students’ mental health nursing competencies is well published. Nevertheless, the believable and accurate portrayal of a patient with a mental health issue during SP simulation is complex. Though vital to the creation of safe authentic learning experiences, the perspectives of SPs and particularly of drama students involved in SP simulation are unknown.AimThe aim of this paper is therefore to explore and describe the experiences of 11 drama students engaged in mental health simulations for nursing students.MethodA qualitative approach was taken and data were gathered using various techniques.FindingsThe content analysis revealed that these SPs negotiated three roles during this interdisciplinary learning experience, namely of a facilitator of learning, a drama student and the person within.DiscussionThe study provided valuable insight into the world of an SP, including the complexities they navigate and the vulnerability they experience.Implications for PracticeNurse educators are alerted to SP's need for support and the necessity of establishing good interpersonal skills before nursing students enter the practice setting. Involvement of SPs in scenario development could enhance the authenticity of future simulations. The ethical implications of SP simulation requires further exploration.
Reproducing Disability and Degeneration in the Victorian Fin de Siècle
Authors: Andree Courtney J. 
Published: April 2016

AbstractUnderstandings of disability were in flux in the Victorian fin de siècle as eugenic thought and degeneration theory gained in popularity. Increasingly imagined as a marker of national and familial decline in the scientific and popular literature of the day, people with disabilities were refigured as domestic threats in the late‐19th century, and increasingly immersed in a culture of shame and secret keeping. While fin de siècle works from Conrad, Haggard, and Wells banished disability to the ends of empire and projected it into the distant future, New Woman novelists like Emma Frances Brooke and Sarah Grand sought to “contain” and ultimately eradicate disability from the British home by rationalizing women's role in marriage and reproduction. Brooke'sA Superfluous Woman(1894) synthesizes late‐19th century outlooks on degeneration and heredity as it locates disability and deviance in the upper class home. By engaging with recent histories of disability and literary studies of degeneration and eugenics, this article identifies the dearth of literary scholarship on disability in the fin de siècle and points to future opportunities for inquiry.
An autopsy case of cortical superficial siderosis with persistent abnormal behavior
Authors: Torii Youta , Iritani Shuji , Fujishiro Hiroshige , Sekiguchi Hirotaka , Habuchi Chikako , Umeda Kentaro , Matsunaga Shinji , Mimuro Maya , Ozaki Norio , Yoshida Mari , Fujita Kiyoshi 
Published: April 2016

In recent years, MRI has revealed cortical superficial siderosis (cSS), which exhibits hemosiderin deposition in only the cortical surface. However, the associations between the histological findings and clinical symptoms of cSS remain unclear. We herein report an autopsy case of a 75‐year‐old Japanese man with cSS with persistent abnormal behavior according to cognitive impairment, hallucination and delusion. At 73 years of age, the patient presented with unusual behavior that indicated auditory hallucination and delusion. One year later, he was admitted to the hospital for malignant lymphoma. On admission, cognitive impairment was detected by a screening test. Soon after hospitalization, he presented with active delirium including visual hallucination and delusion. The patient's excited behavior was improved by the administration of a major tranquilizer. However, the abnormal behavior and cognitive impairment persisted. At 75 years of age, he died of heart failure. A neuropathological investigation revealed hemosiderin depositions in the superficial layer of the cortex in the medial and lateral frontal lobe, the lateral temporal lobe, the parietal lobe, and the medial and lateral occipital lobe. Neuritic plaques and diffuse plaques were extensively observed, which corresponded to Braak stage C and CERAD B, although NFTs were observed that corresponded to Braak stage II. Cortical amyloid angiopathy was not observed in any regions. Ischemic change of brain was also mild. Our report suggests that localized deposition of hemosiderin in the cortex might affect the manifestation of cognitive impairments and hallucination. Further clinicopathological studies are needed to clarify the clinical manifestations of patients with cSS.
Asthma, hay fever, and food allergy are associated with caregiver‐reported speech disorders in US children
Authors: Strom Mark A. , Silverberg Jonathan I. 
Published: April 2016

AbstractBackgroundChildren with asthma, hay fever, and food allergy may have several factors that increase their risk of speech disorder, including allergic inflammation, ADD/ADHD, and sleep disturbance. However, few studies have examined a relationship between asthma, allergic disease, and speech disorder. We sought to determine whether asthma, hay fever, and food allergy are associated with speech disorder in children and whether disease severity, sleep disturbance, or ADD/ADHD modified such associations.MethodsWe analyzed cross‐sectional data on 337,285 children aged 2–17 years from 19 US population‐based studies, including the 1997–2013 National Health Interview Survey and the 2003/4 and 2007/8 National Survey of Children's Health.ResultsIn multivariate models, controlling for age, demographic factors, healthcare utilization, and history of eczema, lifetime history of asthma (odds ratio [95% confidence interval]: 1.18 [1.04–1.34], p = 0.01), and one‐year history of hay fever (1.44 [1.28–1.62], p < 0.0001) and food allergy (1.35 [1.13–1.62], p = 0.001) were associated with increased odds of speech disorder. Children with current (1.37 [1.15–1.59] p = 0.0003) but not past (p = 0.06) asthma had increased risk of speech disorder. In one study that assessed caregiver‐reported asthma severity, mild (1.58 [1.20–2.08], p = 0.001) and moderate (2.99 [1.54–3.41], p < 0.0001) asthma were associated with increased odds of speech disorder; however, severe asthma was associated with the highest odds of speech disorder (5.70 [2.36–13.78], p = 0.0001).ConclusionChildhood asthma, hay fever, and food allergy are associated with increased risk of speech disorder. Future prospective studies are needed to characterize the associations.
Incidence and risk factors for postoperative vomiting following atrial septal defect repair in children
Authors: Lee Joshua , Faraoni David , Lee Sandra , Brown Morgan , Odegard Kirsten , Randolph Adrienne , DiNardo James A. , Yuki Koichi 
Published: April 2016

SummaryBackgroundThe incidence and risk factors for postoperative vomiting (POV) after pediatric cardiac surgery has not been studied.AimsThis study sought to assess the incidence and risk factors for POV in children undergoing surgical repair of an atrial septal defect (ASD).MethodsWe retrospectively collected perioperative data from 160 patients who underwent surgical repair of an ASD and met early extubation criteria. Demographic and clinical data that could potentially influence the incidence of POV were collected. Univariate analysis was performed using Student t‐test or Wilcoxon rank test to identify factors associated with POV. Continuous variables were dichotomized based on the cutoff values derived from the receiver operating characteristic (ROC) curve analysis and the Youden‐J index. We used multivariate logistic regression analysis using backward selection to determine the independent predictors using a univariate cutoff of P < 0.10 for inclusion and P > 0.05 for removal to determine factors independently associated with POV. The accuracy of our multivariate model was assessed by the area under the ROC curve (AUC).ResultsOverall the incidence of POV was 37.5% in all the children who underwent surgical ASD repair. POV did not significantly differ between patients who received and did not receive antiemetics intraoperatively. Age of ≥4 years and cardiopulmonary bypass (CPB) time ≥51 min were identified as independent risk predictors for POV and the AUC of logistic regression model was 0.650 (95% confidence interval; 0.565–0.735).ConclusionsThe incidence of POV in children undergoing surgical ASD repair was 37.5%. Age ≥4 years and CPB time ≥51 min were identified as independent predictors.
Volatile compounds emitted by diverse phytopathogenic microorganisms promote plant growth and flowering through cytokinin action
Authors: Sánchez‐López Ángela María , Baslam Marouane , De Diego Nuria , Muñoz Francisco José , Bahaji Abdellatif , Almagro Goizeder , Ricarte‐Bermejo Adriana , García‐Gómez Pablo , Li Jun , Humplík Jan F. , Novák Ondřej , Spíchal Lukáš , Doležal Karel , Baroja‐Fernández Edurne , Pozueta‐Romero Javier 
Published: April 2016

AbstractIt is known that volatile emissions from some beneficial rhizosphere microorganisms promote plant growth. Here we show that volatile compounds (VCs) emitted by phylogenetically diverse rhizosphere and non‐rhizhosphere bacteria and fungi (including plant pathogens and microbes that do not normally interact mutualistically with plants) promote growth and flowering of various plant species, including crops. In Arabidopsis plants exposed to VCs emitted by the phytopathogen Alternaria alternata, changes included enhancement of photosynthesis and accumulation of high levels of cytokinins (CKs) and sugars. Evidence obtained using transgenic Arabidopsis plants with altered CK status show that CKs play essential roles in this phenomenon, because growth and flowering responses to the VCs were reduced in mutants with CK‐deficiency (35S:AtCKX1) or low receptor sensitivity (ahk2/3). Further, we demonstrate that the plant responses to fungal VCs are light‐dependent. Transcriptomic analyses of Arabidopsis leaves exposed to A. alternata VCs revealed changes in the expression of light‐ and CK‐responsive genes involved in photosynthesis, growth and flowering. Notably, many genes differentially expressed in plants treated with fungal VCs were also differentially expressed in plants exposed to VCs emitted by the plant growth promoting rhizobacterium Bacillus subtilis GB03, suggesting that plants react to microbial VCs through highly conserved regulatory mechanisms.
A review of antiviral drugs and other compounds with activity against feline herpesvirus type 1
Authors: Thomasy Sara M. , Maggs David J. 
Published: April 2016

AbstractFeline herpesvirus type 1 (FHV‐1) is a common and important cause of ocular surface disease, dermatitis, respiratory disease, and potentially intraocular disease in cats. Many antiviral drugs developed for the treatment of humans infected with herpesviruses have been used to treat cats infected withFHV‐1. Translational use of drugs in this manner ideally requires methodical investigation of theirin vitroefficacy againstFHV‐1 followed by pharmacokinetic and safety trials in normal cats. Subsequently, placebo‐controlled efficacy studies in experimentally inoculated animals should be performed followed, finally, by carefully designed and monitored clinical trials in client‐owned animals. This review is intended to provide a concise overview of the available literature regarding the efficacy of antiviral drugs and other compounds with proven or putative activity againstFHV‐1, as well as a discussion of their safety in cats.
Frequency and Distribution of Tuberculosis Resistance-Associated Mutations between Mumbai, Moldova, and Eastern Cape
Authors: Georghiou S. B. , Seifert M. , Catanzaro D. , Garfein R. S. , Valafar F. , Crudu V. , Rodrigues C. , Victor T. C. , Catanzaro A. , Rodwell T. C. 
Published: April 2016

ABSTRACTMolecular diagnostic assays, with their ability to rapidly detect resistance-associated mutations in bacterial genes, are promising technologies to control the spread of drug-resistant tuberculosis (DR-TB). Sequencing assays provide detailed information for specific gene regions and can help diagnostic assay developers prioritize mutations for inclusion in their assays. We performed pyrosequencing of sevenMycobacterium tuberculosisgene regions (katG,inhA,ahpC,rpoB,gyrA,rrs, andeis) for 1,128 clinical specimens from India, Moldova, and South Africa. We determined the frequencies of each mutation among drug-resistant and -susceptible specimens based on phenotypic drug susceptibility testing results and examined mutation distributions by country. The most common mutation among isoniazid-resistant (INHr) specimens was thekatG315ACC mutation (87%). However, in the Eastern Cape, INHrspecimens had a lower frequency ofkatGmutations (44%) and higher frequencies ofinhA(47%) andahpC(10%) promoter mutations. The most common mutation among rifampin-resistant (RIFr) specimens was therpoB531TTG mutation (80%). The mutation was common in RIFrspecimens in Mumbai (83%) and Moldova (84%) but not the Eastern Cape (17%), where the 516GTC mutation appeared more frequently (57%). The most common mutation among fluoroquinolone-resistant specimens was thegyrA94GGC mutation (44%). Therrs1401G mutation was found in 84%, 84%, and 50% of amikacin-resistant, capreomycin-resistant, and kanamycin (KAN)-resistant (KANr) specimens, respectively. Theeispromoter mutation −12T was found in 26% of KANrand 4% of KAN-susceptible (KANs) specimens. Inclusion of theahpCandeispromoter gene regions was critical for optimal test sensitivity for the detection of INH resistance in the Eastern Cape and KAN resistance in Moldova. (This study has been registered atClinicalTrials.govunder registration number NCT02170441.)
Daptomycin in Combination with Ceftolozane-Tazobactam or Cefazolin against Daptomycin-Susceptible and -Nonsusceptible Staphylococcus aureus in an
In Vitro
, Hollow-Fiber Model
Authors: Smith Jordan R. , Arya Anu , Yim Juwon , Barber Katie E. , Hallesy Jessica , Singh Nivedita B. , Rybak Michael J. 
Published: April 2016

ABSTRACT

Ceftolozane-tazobactam (TOL-TAZ) is a novel cephalosporin/beta-lactamase inhibitor with activity against several Gram-negative pathogens. Daptomycin (DAP) has demonstrated synergistic activity with beta-lactams against methicillin-resistant
Staphylococcus aureus
(MRSA) isolates with reduced lipopeptide and glycopeptide susceptibilities. Our objective was to determine if DAP and TOL-TAZ possess synergy in hollow-fiber pharmacokinetic/pharmacodynamic (PK/PD) models. One isogenic pair of daptomycin-susceptible and daptomycin-nonsusceptible MRSA strains was evaluated. DAP, TOL-TAZ, and cefazolin (CFZ) MIC determinations were performed. DAP MIC determinations were also performed in the presence of subinhibitory concentrations of TOL-TAZ and CFZ. Ninety-six-hour
in vitro
models were run, simulating DAP at 10 mg/kg of body weight/day; TOL-TAZ at 1,500 mg every 8 h; TOL at 1,000 mg every 8 h; and DAP combined with TOL-TAZ (DAP+TOL-TAZ), DAP+TOL, DAP+TAZ, and DAP+CFZ at 2,000 mg every 8 h. DAP MICs were 0.5 and 4 μg/ml for strains R8845 and R8846, respectively. In the presence of CFZ, R8845 and R8846 DAP MICs were reduced 8-fold and 16-fold, respectively. TOL and TAZ had no effect on DAP MICs. PK/PD models demonstrated bactericidal activity with DAP+CFZ against both strains. The combination of DAP+TOL-TAZ was bactericidal against R8845 but was not bactericidal against daptomycin-nonsusceptible strain R8846. DAP+TOL and DAP+TAZ were not bactericidal. No other regimens were bactericidal. DAP+TOL-TAZ did not demonstrate synergistic activity against daptomycin-nonsusceptible
S. aureus
but prevented daptomycin-nonsusceptible MRSA emergence. Because DAP+TOL or TAZ alone did not prevent daptomycin-nonsusceptible MRSA emergence, the combination TOL-TAZ may be necessary for synergy with DAP. DAP+CFZ demonstrated enhancement against both strains. The combination of DAP+CFZ warrants further clinical study.
Effect of Fidaxomicin versus Vancomycin on Susceptibility to Intestinal Colonization with Vancomycin-Resistant Enterococci and Klebsiella pneumoniae in Mice
Authors: Deshpande Abhishek , Hurless Kelly , Cadnum Jennifer L. , Chesnel Laurent , Gao Lihong , Chan Luisa , Kundrapu Sirisha , Polinkovsky Alexander , Donskey Curtis J. 
Published: April 2016

ABSTRACT

The use of oral vancomycin or metronidazole for treatment of
Clostridium difficile
infection (CDI) may promote colonization by health care-associated pathogens due to disruption of the intestinal microbiota. Because the macrocyclic antibiotic fidaxomicin causes less alteration of the intestinal microbiota than vancomycin, we hypothesized that it would not lead to a loss of colonization resistance to vancomycin-resistant enterococci (VRE) and extended-spectrum-β-lactamase-producing
Klebsiella pneumoniae
(ESBL-Kp). Mice (8 per group) received orogastric saline, vancomycin, or fidaxomicin daily for 5 days at doses resulting in stool concentrations in mice similar to those measured in humans. The mice were challenged with 10
5
CFU of orogastric VRE or ESBL-Kp on day 2 of treatment and concentrations of the pathogens in stool were monitored. The impact of drug exposure on the microbiome was measured by cultures, real-time PCR for selected anaerobic bacteria, and deep sequencing. In comparison to saline controls, oral vancomycin promoted establishment of high-density colonization by VRE and ESBL-Kp in stool (8 to 10 log
10
CFU/g;
P
< 0.001), whereas fidaxomicin did not (<4 log
10
CFU;
P
> 0.5). Vancomycin treatment resulted in significant reductions in enterococci,
Bacteroides
spp., and
Clostridium leptum
, whereas the population of aerobic and facultative Gram-negative bacilli increased; deep-sequencing analysis demonstrated suppression of
Firmicutes
and expansion of
Proteobacteria
during vancomycin treatment. Fidaxomicin did not cause significant alteration of the microbiota. In summary, in contrast to vancomycin, fidaxomicin treatment caused minimal disruption of the intestinal microbiota and did not render the microbiota susceptible to VRE and ESBL-Kp colonization.
The Periodontal Pathogen Porphyromonas gingivalis Preferentially Interacts with Oral Epithelial Cells in S Phase of the Cell Cycle
Authors: Al-Taweel Firas B. , Douglas C. W. Ian , Whawell Simon A. 
Published: April 2016

ABSTRACT

Porphyromonas gingivalis
, a key periodontal pathogen, is capable of invading a variety of cells, including oral keratinocytes, by exploiting host cell receptors, including alpha-5 beta-1 (α5β1) integrin. Previous studies have shown that
P. gingivalis
accelerates the cell cycle and prevents apoptosis of host cells, but it is not known whether the cell cycle phases influence bacterium-cell interactions. The cell cycle distribution of oral keratinocytes was characterized by flow cytometry and BrdU (5-bromo-2-deoxyuridine) staining following synchronization of cultures by serum starvation. The effect of cell cycle phases on
P. gingivalis
invasion was measured by using antibiotic protection assays and flow cytometry, and these results were correlated with gene and surface expression levels of α5 integrin and urokinase plasminogen activator receptor (uPAR). There was a positive correlation (
R
= 0.98) between the number of cells in S phase and
P. gingivalis
invasion, the organism was more highly associated with cells in S phase than with cells in G
2
and G
1
phases, and S-phase cells contained 10 times more bacteria than did cells that were not in S phase. Our findings also show that α5 integrin, but not uPAR, was positively correlated with cells in S phase, which is consistent with previous reports indicating that
P. gingivalis
invasion of cells is mediated by α5 integrin. This study shows for the first time that
P. gingivalis
preferentially associates with and invades cells in the S phase of the cell cycle. The mechanism of targeting stable dividing cells may have implications for the treatment of periodontal diseases and may partly explain the persistence of this organism at subgingival sites.
Enhanced Clearance of Pseudomonas aeruginosa by Peroxisome Proliferator-Activated Receptor Gamma
Authors: Bedi Brahmchetna , Yuan Zhihong , Joo Myungsoo , Zughaier Susu M. , Goldberg Joanna B. , Arbiser Jack L. , Hart C. Michael , Sadikot Ruxana T. 
Published: April 2016

ABSTRACT

The pathogenic profile of
Pseudomonas aeruginosa
is related to its ability to secrete a variety of virulence factors. Quorum sensing (QS) is a mechanism wherein small diffusible molecules, specifically acyl-homoserine lactones, are produced by
P. aeruginosa
to promote virulence. We show here that macrophage clearance of
P. aeruginosa
(PAO1) is enhanced by activation of the nuclear hormone receptor peroxisome proliferator-activated receptor gamma (PPARγ). Macrophages treated with a PPARγ agonist (pioglitazone) showed enhanced phagocytosis and bacterial killing of PAO1. It is known that PAO1 QS molecules are inactivated by PON-2. QS molecules are also known to inhibit activation of PPARγ by competitively binding PPARγ receptors. In accord with this observation, we found that infection of macrophages with PAO1 inhibited expression of PPARγ and PON-2. Mechanistically, we show that PPARγ induces macrophage paraoxonase 2 (PON-2), an enzyme that degrades QS molecules produced by
P. aeruginosa
. Gene silencing studies confirmed that enhanced clearance of PAO1 in macrophages by PPARγ is PON-2 dependent. Further, we show that PPARγ agonists also enhance clearance of
P. aeruginosa
from lungs of mice infected with PAO1. Together, these data demonstrate that
P. aeruginosa
impairs the ability of host cells to mount an immune response by inhibiting PPARγ through secretion of QS molecules. These studies define a novel mechanism by which PPARγ contributes to the host immunoprotective effects during bacterial infection and suggest a role for PPARγ immunotherapy for
P. aeruginosa
infections.