Abstract Background: This paper describes quality improvement strategies implemented following the identification of a significantly high prevalence rate and severity of pressure injuries in a regional health care facility in a large health district in Queensland, Australia. Aim: The aim of this paper is to inform health professionals of processes employed to reduce the incidence and financial burden of pressure injuries following the detection of rates that were significantly above the State average. Method: An audit of pressure injury prevalence data was conducted on a single day throughout a regional hospital. Prevalence data was compared to State averages and hospital strategies used to prevent injuries were examined. Findings: Audit reports for this acute setting revealed that despite best practice guidelines, prevalence was a major concern. Lack of accountability, poor documentation, limited education and knowledge of risk assessment and prevention were central to the need to implement quality improvement processes. Conclusion: This paper outlines the results associated with implementing quality measures to reduce the prevalence of pressure injuries. Following an audit of pressure injury prevalence data, strategies were implemented to reduce noteworthy rates. Employing specific techniques can result in significantly decreasing hospital acquired pressure injuries in health care settings throughout the world.
Mitochondrial abnormalities may lead to metabolic complications in HIV-infected children who have been receiving long-term antiretroviral treatment. We conducted a matched, case-control study comparing 21 HIV-infected children with insulin resistance (cases) to 21 HIV-infected children without insulin resistance (controls) to assess differences in mitochondrial DNA (mtDNA) copies/cell and oxidative phosphorylation NADH dehydrogenase (C1) and cytochrome c oxidase (C4) enzyme activities in peripheral blood mononuclear cells. MtDNA copies/cell tended to be lower in cases, and fasting serum glucose levels were inversely and significantly correlated with C1 enzyme activity, more so in cases. Larger pediatric studies should evaluate mitochondrial etiologies of insulin resistance and determine the role of antiretroviral therapies or HIV infection on mitochondrial dysfunction.
Long-chain polyunsaturated fatty acids (LC-PUFA) and their metabolites are critical players in cell biology and embryonic development. Here we show that long-chain acyl-CoA synthetase 4a (Acsl4a), an LC-PUFA activating enzyme, is essential for proper patterning of the zebrafish dorsoventral axis. Loss of Acsl4a results in dorsalized embryos due to attenuated bone morphogenetic protein (Bmp) signaling. We demonstrate that Acsl4a modulates the activity of Smad transcription factors, the downstream mediators of Bmp signaling. Acsl4a promotes the inhibition of p38 mitogen-activated protein kinase and the Akt-mediated inhibition of glycogen synthase kinase 3, critical inhibitors of Smad activity. Consequently, introduction of a constitutively active Akt can rescue the dorsalized phenotype of Acsl4a-deficient embryos. Our results reveal a critical role for Acsl4a in modulating Bmp-Smad activity and provide a potential avenue for LC-PUFAs to influence a variety of developmental processes.
Quaternary plant ecology in much of the world has historically relied on morphological identification of macro- and microfossils from sediments of small freshwater lakes. Here, we report new protocols that reliably yield DNA sequence data from Holocene plant macrofossils and bulk lake sediment used to infer ecological change. This will allow changes in census populations, estimated from fossils and associated sediment, to be directly associated with population genetic changes.
MRI is a sensitive method for detecting subtle anatomic abnormalities in the neonatal brain. To optimize the usefulness for neonatal and pediatric care, systematic research, based on quantitative image analysis and functional correlation, is required. Normalization-based image analysis is one of the most effective methods for image quantification and statistical comparison. However, the application of this methodology to neonatal brain MRI scans is rare. Some of the difficulties are the rapid changes in T1 and T2 contrasts and the lack of contrast between brain structures, which prohibits accurate cross-subject image registration. Diffusion tensor imaging (DTI), which provides rich and quantitative anatomical contrast in neonate brains, is an ideal technology for normalization-based neonatal brain analysis. In this paper, we report the development of neonatal brain atlases with detailed anatomic information derived from DTI and co-registered anatomical MRI. Combined with a diffeomorphic transformation, we were able to normalize neonatal brain images to the atlas space and three-dimensionally parcellate images into 122 regions. The accuracy of the normalization was comparable to the reliability of human raters. This method was then applied to babies of 37-53 post-conceptional weeks to characterize developmental changes of the white matter, which indicated a posterior-to-anterior and a central-to-peripheral direction of maturation. We expect that future applications of this atlas will include investigations of the effect of prenatal events and the effects of preterm birth or low birth weights, as well as clinical applications, such as determining imaging biomarkers for various neurological disorders.
Magnetic resonance phase images can yield superior gray and white matter contrast compared to conventional magnitude images. However, the underlying contrast mechanisms are not yet fully understood. Previous studies have been limited to high field acquisitions in adult volunteers and patients. In this study, phase imaging in the neonatal brain is demonstrated for the first time. Compared to adults, phase differences between gray and white matter are significantly reduced but not inverted in neonates with little myelination and iron deposits in their brains. The remaining phase difference between the neonatal and adult brains may be due to a different macromolecule concentration in the unmyelinated brain of the neonates and thus a different frequency due to water macromolecule exchange. Additionally, the susceptibility contrast from brain myelination can be separately studied in neonates during brain development. Therefore, magnetic resonance phase imaging is suggested as a novel tool to study neonatal brain development and pathologies in neonates.
Although a recent study of white spruce using chloroplast DNA uncovered the presence of a glacial refuge in Alaska, chloroplast failed to provide information on the number or specific localities of refugia. Recent studies have demonstrated the utility of nuclear microsatellites to refine insights into postglacial histories. The greater relative rate of mutation may allow finer scale resolution of historic dynamics, including the number, location, and sizes of refugia. Genetic data were acquired from screening 6 microsatellite loci on approximately 14 trees from each of 22 populations located across the central and western boreal forests of Canada and Alaska. Our studies combining microsatellites with Bayesian analyses of population structure in white spruce support the phylogeographic patterns uncovered using chloroplast, separating Alaskan from non-Alaskan regions. Results also support the idea that north-central Alaska served as a glacial refugium during the last glacial maximum. Additionally, the relationship between the degree of genetic differentiation and geographic distance indicated that gene flow played a more important role in structuring non-Alaskan populations, whereas drift played a more important role in structuring Alaskan populations (R(ST)s for non-Alaskan populations 0.029 ± 0.007 and 0.083 ± 0.012 for Alaskan populations). Microsatellites also substantiate the bidirectional patterns of gene flow previously uncovered using chloroplast DNA but indicate much greater movement and mixing. Results from our Bayesian analyses also suggest the existence of additional cryptic refugia. However, the locations have been obscured by high gene flow (R(ST) averaging 0.057 ± 0.004).
This case depicts an unusual presentation of septo-optic dysplasia. A four-year-old female presented with monocular nystagmus and temporal optic disc pallor in her left eye. Despite a normal sized optic nerve head, magnetic resonance imaging (MRI) showed a hypoplastic intraorbital and intracranial left optic nerve in the absence of a septum pellucidum. She was subsequently diagnosed with septo-optic dysplasia with sectoral optic nerve head hypoplasia.
With the expansion of online nursing courses and programs, many nurse educators are faced with the challenge of designing online courses. This article provides an example of how traditional face-to-face nursing content was transformed into an online problem-based learning experience. A framework and specific course examples are provided to help with the redesign process. The article concludes with the instructor and instructional designer sharing lessons learned from this experience and recommendations for future course designers.
The membranes of healthy lymphocytes normally resist hydrolysis by secretory phospholipase A(2). However, they become susceptible during the process of apoptosis. Previous experiments have demonstrated the importance of certain physical changes to the membrane during cell death such as a reduction in membrane lipid order and exposure of phosphatidylserine on the membrane surface. Nevertheless, those investigations also showed that at least one additional factor was required for rapid hydrolysis by the human group IIa phospholipase isozyme. This study was designed to test the possibility that oxidation of membrane lipids is the additional factor. Flow cytometry and confocal microscopy with a fluorescent probe of oxidative potential suggested that oxidation of the plasma membrane occurs during apoptosis stimulated by thapsigargin. When oxidative potential was high, the activity of human group IIa secretory phospholipase A(2) was enhanced 30- to 100-fold compared to that observed with conditions sufficient for maximal hydrolysis by other secretory phospholipase A(2) isoforms. Direct oxidation of cell membranes with either of two oxidizing agents also stimulated hydrolysis by secretory phospholipase A(2). Both oxidizers caused externalization of phosphatidylserine, but a change in lipid order did not always occur. These results demonstrated that membrane oxidation strongly stimulates human group IIa secretory phospholipase A(2) activity toward apoptotic cells. Interestingly, the change in membrane order, previously thought to be imperative for high rates of hydrolysis, was not required when membrane lipids were oxidized. Whether phosphatidylserine exposure is still necessary with oxidation remains unresolved since the two events could not be deconvoluted.
Normal human lymphocytes resisted the hydrolytic action of secretory phospholipase A(2) but became susceptible to the enzyme following treatment with a calcium ionophore, ionomycin. To test the hypothesis that this susceptibility requires exposure of the anionic lipid phosphatidylserine on the external face of the cell membrane, experiments were repeated with a human Burkitts lymphoma cell line (Raji cells). In contrast to normal lymphocytes or S49 mouse lymphoma cells, most of the Raji cells (83%) did not translocate phosphatidylserine to the cell surface upon treatment with ionomycin. Those few that did display exposed phosphatidylserine were hydrolyzed immediately upon addition of phospholipase A(2). Interestingly, the remaining cells were also completely susceptible to the enzyme but were hydrolyzed at a slower rate and after a latency of about 100s. In contradistinction to the defect in phosphatidylserine translocation, Raji cells did display other physical membrane changes upon ionomycin treatment that may be relevant to hydrolysis by phospholipase A(2). These changes were detected by merocyanine 540 and trimethylammonium diphenylhexatriene fluorescence and were common among normal lymphocytes, S49 cells, and Raji cells. The levels of these latter effects corresponded well with the relative rates of hydrolysis among the three cell lines. These results suggested that while phosphatidylserine enhances the rate of cell membrane hydrolysis by secretory phospholipase A(2), it is not an absolute requirement. Other physical properties such as membrane order contribute to the level of membrane susceptibility to the enzyme independent of phosphatidylserine.
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