Speaking up for patient safety by hospital-based health care professionals: a literature review

BACKGROUND: Speaking up is important for patient safety, but often, health care professionals hesitate to voice concerns. Understanding the influencing factors can help to improve speaking-up behaviour and team communication. This review focused on health care professionals’ speaking-up behaviour for patient safety and aimed at (1) assessing the effectiveness of speaking up, (2) evaluating the effectiveness of speaking-up training, (3) identifying the factors influencing speaking-up behaviour, and (4) developing a model for speaking-up behaviour. METHODS: Five databases (PubMed, MEDLINE, CINAHL, Web of Science, and the Cochrane Library) were searched for English articles describing health care professionals’ speaking-up behaviour as well as those evaluating the relationship between speaking up and patient safety. Influencing factors were identified and then integrated into a model of voicing behaviour. RESULTS: In total, 26 studies were identified in 27 articles. Some indicated that hesitancy to speak up can be an important contributing factor in communication errors and that training can improve speaking-up behaviour. Many influencing factors were found: (1) the motivation to speak up, such as the perceived risk for patients, and the ambiguity or clarity of the clinical situation; (2) contextual factors, such as hospital administrative support, interdisciplinary policy-making, team work and relationship between other team members, and attitude of leaders/superiors; (3) individual factors, such as job satisfaction, responsibility toward patients, responsibility as professionals, confidence based on experience, communication skills, and educational background; (4) the perceived efficacy of speaking up, such as lack of impact and personal control; (5) the perceived safety of speaking up, such as fear for the responses of others and conflict and concerns over appearing incompetent; and (6) tactics and targets, such as collecting facts, showing positive intent, and selecting the person who has spoken up. CONCLUSIONS: Hesitancy to speak up can be an important contributing factor to communication errors. Our model helps us to understand how health care professionals think about voicing their concerns. Further research is required to investigate the relative importance of different factors

Upregulation of Transglutaminase andε(γ-Glutamyl)-Lysine in the Fisher-Lewis Rat Model of Chronic Allograft Nephropathy

Background. Tissue transglutaminase (TG2), a cross-linking enzyme, modulates deposition of extracellular matrix protein in renal fibrosis. This study aimed to examine TG2 and its cross-link product ε(γ-glutamyl)-lysine in the Fisher-Lewis rat renal transplantation (RTx) model of chronic allograft nephropathy (CAN). Materials and Methods. Left renal grafts from male Fisher and Lewis were transplanted into Lewis rats, generating allografts and isografts, respectively. Blood pressure, renal function, and proteinuria were monitored for up to 52 weeks. At termination, CAN was assessed in the renal tissue by light and electron microscopy, TG2 and ε(γ-glutamyl)-lysine by immunofluorescence, and the urinary ε(γ-glutamyl)-lysine by high performance liquid chromatography. Results. Compared to the isograft, the allografts were hypertensive, proteinuric, and uraemic and developed CAN. Extracellular TG2 (glomerulus: 64.55 + 17.61 versus 2.11 + 0.17, P<0.001; interstitium: 13.72 + 1.62 versus 3.19 + 0.44, P<0.001), ε(γ-glutamyl)-lysine (glomerulus: 21.74 + 2.71 versus 1.98 + 0.37, P<0.01; interstitium: 37.96 + 17.06 versus 0.42 + 0.11, P<0.05), TG2 enzyme activity (1.09 + 0.13 versus 0.41 + 0.03 nmol/h/mg protein, P<0.05), TG2 mRNA (20-fold rise), and urinary ε(γ-glutamyl)-lysine (534.2 + 198.4 nmol/24 h versus 57.2 + 4.1 nmol/24 h,P<0.05) levels were significantly elevated in the allografts and showed a positive linear correlation with tubulointerstitial fibrosis. Conclusion. CAN was associated with upregulation of renal TG2 pathway, which has a potential for pharmacological intervention. The elevated urinary ε(γ-glutamyl)-lysine, measured for the first time in RTx, is a potential biomarker of CA

High-global warming potential F-gas emissions in California: comparison of ambient-based versus inventory-based emission estimates, and implications of refined estimates.

To provide information for greenhouse gas reduction policies, the California Air Resources Board (CARB) inventories annual emissions of high-global-warming potential (GWP) fluorinated gases, the fastest growing sector of greenhouse gas (GHG) emissions globally. Baseline 2008 F-gas emissions estimates for selected chlorofluorocarbons (CFC-12), hydrochlorofluorocarbons (HCFC-22), and hydrofluorocarbons (HFC-134a) made with an inventory-based methodology were compared to emissions estimates made by ambient-based measurements. Significant discrepancies were found, with the inventory-based emissions methodology resulting in a systematic 42% under-estimation of CFC-12 emissions from older refrigeration equipment and older vehicles, and a systematic 114% overestimation of emissions for HFC-134a, a refrigerant substitute for phased-out CFCs. Initial, inventory-based estimates for all F-gas emissions had assumed that equipment is no longer in service once it reaches its average lifetime of use. Revised emission estimates using improved models for equipment age at end-of-life, inventories, and leak rates specific to California resulted in F-gas emissions estimates in closer agreement to ambient-based measurements. The discrepancies between inventory-based estimates and ambient-based measurements were reduced from -42% to -6% for CFC-12, and from +114% to +9% for HFC-134a

The Grizzly, September 1, 2005

Class of 2009 Arrives on Campus • Residence Life Office Hires Three New RDs • Construction Projects Underway • CIE Continues to Attract Attention • Kaleidoscope: Perfect Combination of Style and Function • Left Side of the Hallway, Slow Down • For Sexual Health, Ursinus Students Need Not Look Far • If We Knew Then, What We Know Now: Tips for Freshmen from Experienced Classmates • Opinions: A Day at Citizen\u27s Bank Park; Three Decent Reasons for Approving John Roberts (A Democrat\u27s Opinion); Marching with the Penguins; How to Build a Stronger Facebook Profile • Bears Look to Bounce Back in 2005 • Field Hockey Looks to Defend Title on New Fieldhttps://digitalcommons.ursinus.edu/grizzlynews/1586/thumbnail.jp

Deletions of CDKN2A and MTAP Detected by Copy-Number Variation Array Are Associated with Loss of p16 and MTAP Protein in Pleural Mesothelioma

CDKN2A deletion is a common alteration in pleural mesothelioma (PM) and frequently associated with co-deletion of MTAP. Since the standard detection method for CDKN2A deletion and FISH analysis is relatively expensive, we here investigated the suitability of inexpensive p16 and MTAP IHC by comparing concordance between IHC and OncoScan CNV arrays on samples from 52 PM patients. Concordance was determined using Cohen's kappa statistics. Loss of CDKN2A was associated with co-deletion of MTAP in 71% of cases. CDKN2A-MTAP copy-number normal cases were also IHC positive in 93% of cases for p16 and 100% for MTAP, while homozygous deletion of CDKN2A-MTAP was always associated with negative IHC for both proteins. In cases with heterozygous CDKN2A-MTAP loss, IHC expression of p16 and MTAP was negative in 100% and 71%, respectively. MTAP and p16 IHC showed high sensitivity (MTAP 86.5%, p16 100%) and specificity (MTAP 100%, p16 93.3%) for the detection of any gene loss. Loss of MTAP expression occurred exclusively in conjunction with loss of p16 labeling. Both p16 and MTAP IHC showed high concordance with Oncoscan CNV arrays (kappa = 0.952, p < 0.0001, and kappa = 0.787, p < 0.0001 respectively). We recommend combined MTAP and p16 immunohistochemistry to confirm the diagnosis of PM

Identification of Burkholderia pseudomallei Near-Neighbor Species in the Northern Territory of Australia

Identification and characterization of near-neighbor species are critical to the development of robust molecular diagnostic tools for biothreat agents. One such agent, Burkholderia pseudomallei, a soil bacterium and the causative agent of melioidosis, is lacking in this area because of its genomic diversity and widespread geographic distribution. The Burkholderia genus contains over 60 species and occupies a large range of environments including soil, plants, rhizospheres, water, animals and humans. The identification of novel species in new locations necessitates the need to identify the true global distribution of Burkholderia species, especially the members that are closely related to B. pseudomallei. In our current study, we used the Burkholderia-specific recA sequencing assay to analyze environmental samples from the Darwin region in the Northern Territory of Australia where melioidosis is endemic. Burkholderia recA PCR negative samples were further characterized using 16s rRNA sequencing for species identification. Phylogenetic analysis demonstrated that over 70% of the bacterial isolates were identified as B. ubonensis indicating that this species is common in the soil where B. pseudomallei is endemic. Bayesian phylogenetic analysis reveals many novel branches within the B. cepacia complex, one novel B. oklahomensis-like species, and one novel branch containing one isolate that is distinct from all other samples on the phylogenetic tree. During the analysis with recA sequencing, we discovered 2 single nucleotide polymorphisms in the reverse priming region of B. oklahomensis. A degenerate primer was developed and is proposed for future use. We conclude that the recA sequencing technique is an effective tool to classify Burkholderia and identify soil organisms in a melioidosis endemic area

The Grizzly, April 13, 2006

Relay a Success • New Healthcare Scholarship Available • Lurking Beneath the Skin: Scabies Infection • Day of Museums • Shopping with Eco-labels • Airband a Hit • Opinions: Drawing the Line: Moral Predicament of Abortion, Part II • Importance of CoSA: A Message • Bears Battle Back • Real Deal on Steroidshttps://digitalcommons.ursinus.edu/grizzlynews/1712/thumbnail.jp

The Grizzly, February 16, 2006

Hoodoo Man Arthur Flowers Delivers Captivating Speech at Ursinus • USGA Holds First Meeting of Semester • Francophone Film Festival: Almost Peaceful • Georgetown Professor to Lecture at Ursinus • Getting to Know Your Glands • Spiritual Experiences in Paris • Meet the New Director of Facilities Services and Keep Current with Bomberger Renovations • Recycling Myths Revealed • Retraction on Parking Article • Broken Social Scene a Must Have for Indie Fans • Lone Senior Walks Off a Winnerhttps://digitalcommons.ursinus.edu/grizzlynews/1706/thumbnail.jp

Case report:Thirty-year progression of an EMPF1 encephalopathy due to defective mitochondrial and peroxisomal fission caused by a novel de novo heterozygous DNM1L variant

Mutations in DNM1L (DRP1), which encode a key player of mitochondrial and peroxisomal fission, have been reported in patients with the variable phenotypic spectrum, ranging from non-syndromic optic atrophy to lethal infantile encephalopathy. Here, we report a case of an adult female patient presenting with a complex neurological phenotype that associates axonal sensory neuropathy, spasticity, optic atrophy, dysarthria, dysphasia, dystonia, and ataxia, worsening with aging. Whole-exome sequencing revealed a heterozygous de novo variant in the GTPase domain of DNM1L [NM_001278464.1: c.176C>A p.(Thr59Asn)] making her the oldest patient suffering from encephalopathy due to defective mitochondrial and peroxisomal fission-1. In silico analysis suggested a protein destabilization effect of the variant Thr59Asn. Unexpectedly, Western blotting disclosed profound decrease of DNM1L expression, probably related to the degradation of DNM1L complexes. A detailed description of mitochondrial and peroxisomal anomalies in transmission electron and 3D fluorescence microscopy studies confirmed the exceptional phenotype of this patient