Wissenskonversion und Behandlungsfehler im Krankenhaus

Rund jeder tausendste Krankenhauspatient stirbt aufgrund vermeidbarer unerwünschter Ereignisse. Empirische Studien zeigen Zusammenhänge zwischen der Sicherheitskultur in Krankenhäusern und der Fehlerhäufigkeit. Die bisherige Forschung weist allerdings Theoriedefizite auf. Unter Heranziehung des Konzeptes der Wissenskonversion nach Nonaka und Takeuchi (1995) wird versucht, einen theoretischen Bezugsrahmen für das Lernen aus Fehlern zu erarbeiten. Auf empirischer Basis wird eine Skala entwickelt, die unterschiedliche Profile der Wissenskonversion im Umgang mit Fehlern misst. Anhand einer 420 Probanden umfassenden Stichprobe aus 11 Abteilungen von sieben Krankenhäusern gelingt der Nachweis, dass eine lernende Sicherheitskultur die Fehlerhäufigkeit zu reduzieren imstande ist. Zudem zeigt sich, dass dem Prozess der Internalisierung der höchste Stellenwert zukommt.Approximately one in every thousand hospital patients dies because of preventable adverse events. Empirical findings show that safety culture is essential for improving the quality of health care. However, the research so far has theoretical deficits. Using Nonaka and Takeuchi's (1995) concept of knowledge conversion, our paper develops a theoretical and empirical framework to show how people can learn from mistakes. On the basis of results of 420 probands from 11 departments in seven hospitals it was possible to prove that a learning safety culture does indeed reduce the frequency of errors. In addition, it reveals that the process of internalisation contributes most to this reduction

Attitude is everything? The impact of workload, safety climate, and safety tools on medical errors: A study of intensive care units

Background: Hospitals face an increasing pressure towards efficiency and cost reduction while ensuring patient safety. This warrants a closer examination of the trade-off between production and protection posited in the literature for a high-risk hospital setting (intensive care). Purposes: Based on extant literature and concepts on both safety management and organizational/safety culture, this study investigates to which extent production pressure (i.e., increased staff workload and capacity utilization) and safety culture (consisting of safety climate among staff and safety tools implemented by management) influence the occurrence of medical errors and if/how safety climate and safety tools interact. Methodology / Approach: A prospective, observational, 48-hour cross-sectional study was conducted in 57 intensive care units. The dependent variable is the incidence of errors affecting those 378 patients treated throughout the entire observation period. Capacity utilization and workload were measured by indicators such as unit occupancy, nurse-/physician-to-patient ratios, levels of care, or NEMS scores. The safety tools considered include Critical Incidence Reporting Systems, audits, training, mission statements, SOPs/checklists and the use of barcodes. Safety climate was assessed using a psychometrically validated four-dimensional questionnaire. Linear regression was employed to identify the effects of the predictor variables on error rate, as well as interaction effects between safety tools and safety climate. Findings: Higher workload has a detrimental effect on safety while safety climate - unlike the examined safety tools - has a virtually equal opposite effect. Correlations between safety tools and safety climate as well as their interaction effects on error rate are mostly nonsignificant. Practice Implications: Increased workload and capacity utilization increase the occurrence of medical error; an effect that can be offset by a positive safety climate but not by formally implemented safety procedures and policies

Strongly nonequilibrium flux flow in the presence of perforating submicron holes

We report on the effects of perforating submicron holes on the vortex dynamics of amorphous Nb0.7Ge0.3 microbridges in the strongly nonequilibrium mixed state, when vortex properties change substantially. In contrast to the weak nonequilibrium - when the presence of holes may result in either an increase (close to Tc) or a decrease (well below Tc) of the dissipation, in the strong nonequilibrium an enhanced dissipation is observed irrespectively of the bath temperature. Close to Tc this enhancement is similar to that in the weak nonequilibrium, but corresponds to vortices shrunk due to the Larkin-Ovchinnikov mechanism. At low temperatures the enhancement is a consequence of a weakening of the flux pinning by the holes in a regime where electron heating dominates the superconducting properties.Comment: 6 pages, 5 figure

Attitude is everything? The impact of workload, safety climate, and safety tools on medical errors: A study of intensive care units

Background: Hospitals face an increasing pressure towards efficiency and cost reduction while ensuring patient safety. This warrants a closer examination of the trade-off between production and protection posited in the literature for a high-risk hospital setting (intensive care). Purposes: Based on extant literature and concepts on both safety management and organizational/safety culture, this study investigates to which extent production pressure (i.e., increased staff workload and capacity utilization) and safety culture (consisting of safety climate among staff and safety tools implemented by management) influence the occurrence of medical errors and if/how safety climate and safety tools interact. Methodology / Approach: A prospective, observational, 48-hour cross-sectional study was conducted in 57 intensive care units. The dependent variable is the incidence of errors affecting those 378 patients treated throughout the entire observation period. Capacity utilization and workload were measured by indicators such as unit occupancy, nurse-/physician-to-patient ratios, levels of care, or NEMS scores. The safety tools considered include Critical Incidence Reporting Systems, audits, training, mission statements, SOPs/checklists and the use of barcodes. Safety climate was assessed using a psychometrically validated four-dimensional questionnaire. Linear regression was employed to identify the effects of the predictor variables on error rate, as well as interaction effects between safety tools and safety climate. Findings: Higher workload has a detrimental effect on safety while safety climate - unlike the examined safety tools - has a virtually equal opposite effect. Correlations between safety tools and safety climate as well as their interaction effects on error rate are mostly nonsignificant. Practice Implications: Increased workload and capacity utilization increase the occurrence of medical error; an effect that can be offset by a positive safety climate but not by formally implemented safety procedures and policies

Tetraspanin CD9 affects HPV16 infection by modulating ADAM17 activity and the ERK signalling pathway

Human papillomaviruses (HPV) are causative agents of various tumours such as cervical cancer. HPV binding to the cell surface of keratinocytes leads to virus endocytosis at tetraspanin enriched microdomains. Complex interactions of the capsid proteins with host proteins as well as ADAM17-dependent ERK1/2 signal transduction enable the entry platform assembly of the oncogenic HPV type 16. Here, we studied the importance of tetraspanin CD9, also known as TSPAN29, in HPV16 infection of different epithelial cells. We found that both overexpression and loss of the tetraspanin decreased infection rates in cells with low endogenous CD9 levels, while reduction of CD9 expression in keratinocytes that exhibit high-CD9 protein amounts, led to an increase of infection. Therefore, we concluded that low-CD9 supports infection. Moreover, we found that changes in CD9 amounts affect the shedding of the ADAM17 substrate transforming growth factor alpha (TGFα) and the downstream phosphorylation of ERK. These effects correlate with those on infection rates suggesting that a specific CD9 optimum promotes ADAM17 activity, ERK signalling and virus infection. Together, our findings implicate that CD9 regulates HPV16 infection through the modulation of ADAM17 sheddase activity

HPV16 induces formation of virus-p62-PML hybrid bodies to enable infection

Human papillomaviruses (HPVs) inflict a significant burden on the human population. The clinical manifestations caused by high-risk HPV types are cancers at anogenital sites, including cervical cancer, as well as head and neck cancers. Host cell defense mechanisms such as autophagy are initiated upon HPV entry. At the same time, the virus modulates cellular antiviral processes and structures such as promyelocytic leukemia nuclear bodies (PML NBs) to enable infection. Here, we uncover the autophagy adaptor p62, also known as p62/sequestosome-1, as a novel proviral factor in infections by the high-risk HPV type 16 (HPV16). Proteomics, imaging and interaction studies of HPV16 pseudovirus-treated HeLa cells display that p62 is recruited to virus-filled endosomes, interacts with incoming capsids, and accompanies the virus to PML NBs, the sites of viral transcription and replication. Cellular depletion of p62 significantly decreased the delivery of HPV16 viral DNA to PML NBs and HPV16 infection rate. Moreover, the absence of p62 leads to an increase in the targeting of viral components to autophagic structures and enhanced degradation of the viral capsid protein L2. The proviral role of p62 and formation of virus-p62-PML hybrid bodies have also been observed in human primary keratinocytes, the HPV target cells. Together, these findings suggest the previously unrecognized virus-induced formation of p62-PML hybrid bodies as a viral mechanism to subvert the cellular antiviral defense, thus enabling viral gene expression. Keywords: human papillomavirus; HPV16; L2; p62; sequestosome-1; autophagy; antiviral defense; promyelocytic leukemia nuclear bodies (PML NB); hybrid bodie

Mindfulness and skills-based eHealth intervention to reduce distress in cancer-affected patients in the Reduct trial: Intervention protocol of the make it training optimized.

Introduction Cancer-affected patients experience high distress due to various burdens. One way to expand psycho-oncological support is through digital interventions. This protocol describes the development and structure of a web-based psycho-oncological intervention, the Make It Training optimized. This intervention is currently evaluated in the Reduct trial, a multicenter randomized controlled trial. Methods The Make It Training optimized was developed in six steps: A patient need and demand assessment, development and acceptability analysis of a prototype, the formation of a patient advisory council, the revision of the training, implementation into a web app, and the development of a motivation and evaluation plan. Results Through a process of establishing cancer-affected patients' needs, prototype testing, and patient involvement, the Make It Training optimized was developed by a multidisciplinary team and implemented in a web app. It consists of 16 interactive self-guided modules which can be completed within 16 weeks. Discussion Intervention protocols can increase transparency and increase the likelihood of developing effective web-based interventions. This protocol describes the process and results of developing a patient-oriented intervention. Future research should focus on the further personalization of web-based psycho-oncological interventions and the potential benefits of combining multiple psychotherapeutic approaches

A cancer stem cell-like phenotype is associated with miR-10b expression in aggressive squamous cell carcinomas

Background Cutaneous squamous cell carcinomas (cSCC) are the primary cause of premature deaths in patients suffering from the rare skin-fragility disorder recessive dystrophic epidermolysis bullosa (RDEB), which is in marked contrast to the rarely metastasizing nature of these carcinomas in the general population. This remarkable difference is attributed to the frequent development of chronic wounds caused by impaired skin integrity. However, the specific molecular and cellular changes to malignancy, and whether there are common players in different types of aggressive cSCCs, remain relatively undefined. Methods MiRNA expression profiling was performed across various cell types isolated from skin and cSCCs. Microarray results were confirmed by qPCR and by an optimized in situ hybridization protocol. Functional impact of overexpression or knock-out of a dysregulated miRNA was assessed in migration and 3D-spheroid assays. Sample-matched transcriptome data was generated to support the identification of disease relevant miRNA targets. Results Several miRNAs were identified as dysregulated in cSCCs compared to control skin. These included the metastasis-linked miR-10b, which was significantly upregulated in primary cell cultures and in archival biopsies. At the functional level, overexpression of miR-10b conferred the stem cell-characteristic of 3D-spheroid formation capacity to keratinocytes. Analysis of miR-10b downstream effects identified a novel putative target of miR-10b, the actin- and tubulin cytoskeleton-associated protein DIAPH2. Conclusion The discovery that miR-10b mediates an aspect of cancer stemness – that of enhanced tumor cell adhesion, known to facilitate metastatic colonization – provides an important avenue for future development of novel therapies targeting this metastasis-linked miRNA