A Systematic Review and Integration of Concept Analyses of Self-Care and Related Concepts

Purpose This systematic review identified, synthesized, and integrated concept analyses on self‐care and related concepts. Design The guidelines for systematic literature reviews of the Joanna Briggs Institute were followed. Methods The Cumulative Index to Nursing and Allied Health Literature (CINAHL), PubMed, PsycINFO, and EMBASE databases were searched for concept analyses published in the past 20 years. Findings A total of 26 concept analyses were identified that had been published on self‐care, self‐care agency, self‐monitoring, self‐management, self‐management support, symptom management, and self‐efficacy. Differences and commonalities in the examined literature were identified, and a model was delineated, explaining the relations among the various concepts from the nursing perspective. Conclusions The healthcare literature has broadly described self‐care and related concepts; however, consensus on the definitions remains beyond our reach and should not be expected, due to the different perspectives and paradigms from which the concepts are interpreted. From a nursing perspective, self‐care can be considered a broad concept encompassing the other concepts, which describe more specific individual levels of activities and processes. Clinical Relevance Nurses are actively involved in disease management and self‐management support as well as in promoting self‐care in healthy and sick people. Referring to a model on self‐care and related concepts could avoid misinterpretations in nursing practice, research, and policy

Analysis of Parametric Oscillatory Instability in Power Recycled LIGO Interferometer

We present the analysis of a nonlinear effect of parametric oscillatory instability in power recycled LIGO interferometer with the Fabry-Perot (FP) cavities in the arms. The basis for this effect is the excitation of the additional (Stokes) optical mode and the mirror elastic mode, when the optical energy stored in the main FP cavity main mode exceeds the certain threshold and the frequencies are related so that sum of frequencies of Stokes and elastic modes are approximately equal to frequencyof main mode. The presence of anti-Stokes modes (with frequency approximately equal to sum of frequencies of main and elastic modes) can depress parametric instability. However, it is very likely that the anti-Stokes modes will not compensate the parametric instability completely.Comment: 9 pages, 2 figures. submitted to Physics Letters

Delineation of fault zones using imaging radar

The assessment of earthquake hazards and mineral and oil potential of a given region requires a detailed knowledge of geological structure, including the configuration of faults. Delineation of faults is traditionally based on three types of data: (1) seismicity data, which shows the location and magnitude of earthquake activity; (2) field mapping, which in remote areas is typically incomplete and of insufficient accuracy; and (3) remote sensing, including LANDSAT images and high altitude photography. Recently, high resolution radar images of tectonically active regions have been obtained by SEASAT and Shuttle Imaging Radar (SIR-A and SIR-B) systems. These radar images are sensitive to terrain slope variations and emphasize the topographic signatures of fault zones. Techniques were developed for using the radar data in conjunction with the traditional types of data to delineate major faults in well-known test sites, and to extend interpretation techniques to remote areas

Serafino Zappacosta: An Enlightened Mentor and Educator

With this article, the authors aim to honor the memory of Serafino Zappacosta, who had been their mentor during the early years of their career in science. The authors discuss how the combination of Serafino Zappacosta's extraordinary commitment to teaching and passion for science created a fostering educational environment that led to the creation of the “Ruggero Ceppellini Advanced School of Immunology.” The review also illustrates how the research on the MHC and the inspirational scientific context in the Zappacosta's laboratory influenced the authors' early scientific interests, and subsequent professional work as immunologists

Transitions between care settings after enrolment in a palliative care service in Italy: a retrospective analysis

This study was a retrospective analysis of prospectively collected data that aimed to map patients' care transitions following admission to a specialist palliative care service in Italy called Antea Centre. Patients' data was extracted from the Antea local database from 2007 to 2011. External transitions were defined as a change in the setting of care, with the patient no longer being cared for by Antea staff. Internal transitions were defined as a change in the setting of care, with the care still being provided by Antea staff. A total of 1123 patients out of 5313 admitted to the palliative service (21%) experienced transitions. Patients who experienced no transitions after their admission to the palliative care service were more likely to have a Karnofsky Performance Scale Index <30, to have been referred by a hospital physician, to have a shorter survival time, and to have home as their place of death (P<0.001). Although the patients with no transitions had worse clinical conditions, organisations should pay attention to reducing the possible negative effects of transitions, such as discontinuity of care and poor coordination

Genome-wide modeling of transcription kinetics reveals patterns of RNA production delays

Genes with similar transcriptional activation kinetics can display very different temporal mRNA profiles because of differences in transcription time, degradation rate, and RNA-processing kinetics. Recent studies have shown that a splicing-associated RNA production delay can be significant. To investigate this issue more generally, it is useful to develop methods applicable to genome-wide datasets. We introduce a joint model of transcriptional activation and mRNA accumulation that can be used for inference of transcription rate, RNA production delay, and degradation rate given data from high-throughput sequencing time course experiments. We combine a mechanistic differential equation model with a nonparametric statistical modeling approach allowing us to capture a broad range of activation kinetics, and we use Bayesian parameter estimation to quantify the uncertainty in estimates of the kinetic parameters. We apply the model to data from estrogen receptor alpha activation in the MCF-7 breast cancer cell line. We use RNA polymerase II ChIP-Seq time course data to characterize transcriptional activation and mRNA-Seq time course data to quantify mature transcripts. We find that 11% of genes with a good signal in the data display a delay of more than 20 min between completing transcription and mature mRNA production. The genes displaying these long delays are significantly more likely to be short. We also find a statistical association between high delay and late intron retention in pre-mRNA data, indicating significant splicing-associated production delays in many genes.Peer reviewe

PD-1-induced T cell exhaustion is controlled by a Drp1-dependent mechanism

Programmed cell death-1 (PD-1) signaling downregulates the T-cell response, promoting an exhausted state in tumor-infiltrating T cells, through mostly unveiled molecular mechanisms. Dynamin-related protein-1 (Drp1)-dependent mitochondrial fission plays a crucial role in sustaining T-cell motility, proliferation, survival, and glycolytic engagement. Interestingly, such processes are exactly those inhibited by PD-1 in tumor-infiltrating T cells. Here, we show that PD-1pos CD8+ T cells infiltrating an MC38 (murine adenocarcinoma)-derived murine tumor mass have a downregulated Drp1 activity and more elongated mitochondria compared with PD-1neg counterparts. Also, PD-1pos lymphocytic elements infiltrating a human colon cancer rarely express active Drp1. Mechanistically, PD-1 signaling directly prevents mitochondrial fragmentation following T-cell stimulation by downregulating Drp1 phosphorylation on Ser616, via regulation of the ERK1/2 and mTOR pathways. In addition, downregulation of Drp1 activity in tumor-infiltrating PD-1pos CD8+ T cells seems to be a mechanism exploited by PD-1 signaling to reduce motility and proliferation of these cells. Overall, our data indicate that the modulation of Drp1 activity in tumor-infiltrating T cells may become a valuable target to ameliorate the anticancer immune response in future immunotherapy approaches

CD8+ T cells specific for cryptic apoptosis-associated epitopes exacerbate experimental autoimmune encephalomyelitis

The autoimmune immunopathology occurring in multiple sclerosis (MS) is sustained by myelin-specific and -nonspecific CD8(+) T cells. We have previously shown that, in MS, activated T cells undergoing apoptosis induce a CD8(+) T cell response directed against antigens that are unveiled during the apoptotic process, namely caspase-cleaved structural proteins such as non-muscle myosin and vimentin. Here, we have explored in vivo the development and the function of the immune responses to cryptic apoptosis-associated epitopes (AEs) in a well-established mouse model of MS, experimental autoimmune encephalomyelitis (EAE), through a combination of immunization approaches, multiparametric flow cytometry, and functional assays. First, we confirmed that this model recapitulated the main findings observed in MS patients, namely that apoptotic T cells and effector/memory AE-specific CD8(+) T cells accumulate in the central nervous system of mice with EAE, positively correlating with disease severity. Interestingly, we found that AE-specific CD8(+) T cells were present also in the lymphoid organs of unprimed mice, proliferated under peptide stimulation in vitro, but failed to respond to peptide immunization in vivo, suggesting a physiological control of this response. However, when mice were immunized with AEs along with EAE induction, AE-specific CD8(+) T cells with an effector/memory phenotype accumulated in the central nervous system, and the disease severity was exacerbated. In conclusion, we demonstrate that AE-specific autoimmunity may contribute to immunopathology in neuroinflammation