Parent's perceptions of paediatric care in two radiology departments within Johannesburg, South Africa.

BACKGROUND: A referral to the Radiology department may be a very frightening, and at times a stressful experience for a child and their parents. The radiographer plays an important role as a healthcare professional to simultaneously produce high-quality diagnostic X-ray images and facilitate a high standard of care in a limited timeframe. METHODS: The purpose of this qualitative, phenomenological study was thus to explore and describe parents' perceptions of paediatric care in two Radiology departments within Gauteng. A total of 12 semi-structured individual interviews were conducted with parents, until data saturation was achieved. RESULTS: Braun and Clarke's six-step thematic analysis was used which unveiled three themes: 1) Recognition of overall positive, high standard of care received by paediatrics who underwent an X-ray examination 2) Limitations prohibiting a caring environment 3) The need for parent-centered paediatric care through the implementation of Family Centered Care (FCC). CONCLUSION: Overall, there was positive feedback from the parents' perspectives and general satisfaction with the quality of care received by the child whilst in the Radiology department. Although there were some negative categories particularly referring to an unknown environment, parents overall appreciated the qualities of caring and effective communication that the radiographers displayed during their visit. IMPLICATIONS FOR PRACTICE: The lack of literature regarding parents' perceptions of paediatric care within the context of radiography led to the current study. Recommendations for future best practice would be incorporating the concept of FCC within the curriculum of the radiography degree to improve overall patient and parent satisfaction.

International audit of simulation use in pre-registration medical radiation science training.

INTRODUCTION: Simulation-based education (SBE) can replicate the challenging aspects of real-world clinical environments, while providing a safe and less intimidating setting. Literature supports its use within medical radiation science (MRS) training for safe practice of psychomotor skills, development of problem solving, team working, interpersonal and decision-making skills and embedding awareness of patient safety. This project aimed to quantify usage of SBE resources and activities internationally and to evaluate how this changed during COVID-19 restrictions. METHODS: An anonymous online survey tool gathered data relating to programme demographics, simulation resources, simulation activities and future plans. A link to the survey was distributed to programme leads via social media, professional bodies and national networks. RESULTS: A total of 72 responses were received from a range of countries and representing a range of programme structures. Most respondents reported up to 100 h of SBE per student per year with low fidelity resources and image viewing software featuring most prominently. There was low reported engagement of service users within simulation activities. Respondents also indicated that COVID-19 had been a trigger for rapid uptake of simulation resources. CONCLUSION: SBE forms an important aspect of MRS training internationally with low-fidelity resources being widely deployed. Where available, high fidelity virtual reality and specialised profession-specific resources were used heavily. There was a low level of reported engagement with service users or expert patients in simulation activities. Future research will identify whether the rapid uptake of SBE during COVID-19 continues and clarify the role of service users in SBE provision. IMPLICATIONS FOR PRACTICE: Increased collaboration between MRS education providers may help to improve parity of SBE provision and identify additional opportunities to engage service users within SBE.

Correlation between intima-to-media ratio, apolipoprotein B-100, myeloperoxidase, and hypochlorite-oxidized proteins in human atherosclerosis.

The oxidative modification of low-density lipoprotein (LDL) is thought to contribute to atherogenesis, and there is evidence that oxidants derived from myeloperoxidase (MPO) contribute to such oxidative damage. Using human iliac arteries we investigated the relationship between lesion stage indicated by the intima-to-media (I/M) ratio and the presence of apolipoprotein B-100 (apoB, a marker for LDL), MPO, and hypochlorite (HOCl)-oxidized proteins identified by immunohistochemistry in the intima, media, and adventitia. More staining for apoB, MPO, and HOCl-oxidized proteins was observed in diseased than healthy vessels. Diseased segments also stained more for the three parameters than healthy segments in the same diseased vessel, highlighting the variability that can occur within a single cross-section of a vessel. However, significant positive correlation between I/M ratio and positive staining for apoB, MPO, and HOCl-oxidized proteins in different segments of individual arteries were apparent in segments with an I/M ratio of > 1.8. Also, the overall extent of intimal staining for apoB, MPO, and HOCl-oxidized proteins increased with increasing I/M ratio. In addition, the extent of apoB staining was greater and appeared at comparatively lower I/M ratios than that of MPO and HOCl-oxidized proteins. Our results support a contribution to atherogenesis of all three parameters assessed, although MPO and HOCl-oxidized proteins appear to participate in the disease process at a later stage than apoB.

Secondary radicals derived from chloramines of apolipoprotein B-100 contribute to HOCl-induced lipid peroxidation of low-density lipoproteins.

Oxidation of low-density lipoproteins (LDL) is thought to contribute to atherogenesis. Although there is increasing evidence for a role of myeloperoxidase-derived oxidants such as hypochlorite (HOCl), the mechanism by which HOCl modifies LDL remains controversial. Some studies report the protein component to be the major site of attack, whereas others describe extensive lipid peroxidation. The present study addresses this controversy. The results obtained are consistent with the hypothesis that radical-induced oxidation of LDL's lipids by HOCl is a secondary reaction, with most HOCl consumed via rapid, non-radical reaction with apolipoprotein B-100. Subsequent incubation of HOCl-treated LDL gives rise to lipid peroxidation and antioxidant consumption in a time-dependent manner. Similarly, with myeloperoxidase/H2O2/Cl- (the source of HOCl in vivo), protein oxidation is rapid and followed by an extended period of lipid peroxidation during which further protein oxidation does not occur. The secondary lipid peroxidation process involves EPR-detectable radicals, is attenuated by a radical trap or treatment of HOCl-oxidized LDL with methionine, and occurs less rapidly when the lipoprotein was depleted of alpha-tocopherol. The initial reaction of low concentrations of HOCl (400-fold or 800-fold molar excess) with LDL therefore seems to occur primarily by two-electron reactions with side-chain sites on apolipoprotein B-100. Some of the initial reaction products, identified as lysine-residue-derived chloramines, subsequently undergo homolytic (one-electron) reactions to give radicals that initiate antioxidant consumption and lipid oxidation via tocopherol-mediated peroxidation. The identification of these chloramines, and the radicals derived from them, as initiating agents in LDL lipid peroxidation offers potential new targets for antioxidative therapy in atherogenesis.

Alpha-tocopherol does not inhibit hypochlorite-induced oxidation of apolipoprotein B-100 of low-density lipoprotein.

The amount of alpha-tocopherol (alpha-TOH) can dramatically alter the extent of radical-induced oxidation of low density lipoprotein (LDL) lipids, a process generally thought to be important in atherogenesis. However, LDL with atherogenic features can also be formed in vitro by exposure to the strong non-radical oxidant hypochlorite (HOCl), which preferentially oxidises LDL apolipoprotein B-100. Here we show that varying LDL content of alpha-TOH by vitamin supplementation or depletion has no effect on the extent of HOCI-induced oxidation of apolipoprotein B-100 as measured by the loss of lysine and tryptophan residues, and the alteration in relative electrophoretic mobility of the lipoprotein particle.

Presence of hypochlorite-modified proteins in human atherosclerotic lesions.

Oxidation of LDL may contribute to atherogenesis, though the nature of the in vivo oxidant(s) remains obscure. Myeloperoxidase, the enzyme responsible for hypochlorous acid/hypochlorite (HOCl) production in vivo, is present in active form in human atherosclerotic lesions, and HOCl aggregates and transforms LDL into a high-uptake form for macrophages in vitro. Here we demonstrate HOCl-modified proteins in human lesions using an mAb raised against HOCl-modified LDL that recognizes HOCl-oxidized proteins but does not cross-react with Cu2+-, malondialdehyde-, or 4-hydroxynonenal-modified LDL. This antibody detected significantly more material in advanced atherosclerotic lesions than normal arteries, even though azide and methionine were included during sample work-up to inhibit myeloperoxidase and to scavenge HOCl. The epitope(s) recognized was predominantly cell associated and present in monocyte/macrophages, smooth muscle, and endothelial cells. The intima and cholesterol clefts stained more heavily than the center of the thickened vessels; adventitial staining was apparent in some cases. Immunostaining was also detected in a very early lesion from an accident victim, beside healthy areas that were unreactive. LDL oxidized by HOCl in vitro, but not native LDL, effectively competed with the epitopes in lesions for antibody binding. Density centrifugation of plaque homogenates and Western blot analysis showed that, in the apo B-containing lipoprotein fraction, the mAb recognized protein(s) of molecular mass greater than apo B, similar to those produced during oxidation of LDL with HOCl in vitro. Three major proteins were recognized by the anti-HOCl-modified protein antibody but not by an anti-apo B antibody in the apo B-free fraction. Together, these results demonstrate HOCl-oxidized proteins in human atherosclerotic lesions, implicating this oxidant in LDL modification in vivo.

Oxidation of low-density lipoprotein by hypochlorite causes aggregation that is mediated by modification of lysine residues rather than lipid oxidation.

Peroxidation of low-density lipoprotein (LDL) lipid is generally thought to represent the initial step in a series of modification reactions that ultimately transform the protein moiety of the lipoprotein into a form recognized by receptors different from those that bind native LDL. Uptake of LDL via these alternative receptors can lead to the formation of lipid-laden cells, which are typical for the early stages of atherogenesis. We have studied the oxidative modification of LDL by hypochlorite (-OCl), a powerful oxidant produced from H2O2 and chloride via the action of myeloperoxidase which is released from activated neutrophils and monocytes. Exposure of LDL to reagent or enzymically generated -OCl at 4 or 37 degrees C resulted in immediate and preferential oxidation of amino acid residues of apolipoprotein B-100, the single protein associated with LDL. Lysine residues quantitatively represented the major target and, like tryptophan, were oxidized to approximately the same extent with reagent or enzymically generated -OCl. In contrast, LDL lipid oxidation was less favoured than protein oxidation, as judged by the amounts of lipid hydroperoxides, chlorohydrins, cholesterol or fatty acid oxidation products formed. Treatment with -OCl caused aggregation of LDL, as shown by an increased turbidity of the oxidized LDL solution and elution from a size-exclusion h.p.l.c. column of high-molecular-mass LDL complexes. Chemical modification of lysine residues before oxidation with -OCl prevented aggregation, while it enhanced the extent of lipid peroxidation. Treatment of LDL with -OCl also caused the formation of carbonyl groups and release of ammonia; both these modifications were inhibited by lysine-residue modification before oxidation. These results demonstrate that aggregation reactions are dependent on initial lysine oxidation by -OCl, followed by deamination and carbonyl formation, but do not involve lipid (per)oxidation. We propose that the observed -OCl-mediated aggregation of LDL is caused, at least in part, by cross-linking of apoproteins by Schiff-base formation independently of lipid peroxidation.

Oxidation of low-density lipoprotein with hypochlorite causes transformation of the lipoprotein into a high-uptake form for macrophages.

Oxidation of low-density lipoprotein (LDL) lipid is thought to represent the initial step in a series of oxidative modification reactions that ultimately transform this lipoprotein into an atherogenic high-uptake form that can cause lipid accumulation in cells. We have studied the effects of hypochlorite, a powerful oxidant released by activated monocytes and neutrophils, on isolated LDL. Exposure of LDL to reagent hypochlorite (NaOCl) at 4 degrees C resulted in immediate and preferential oxidation of amino acid residues of apoprotein B-100, the single protein associated with LDL. Neither lipoprotein lipid nor LDL-associated antioxidants, except ubiquinol-10, represented major targets for this oxidant. Even when high concentrations of NaOCl were used, only low levels of lipid hydroperoxides could be detected with the highly sensitive h.p.l.c. post-column chemiluminescence detection method. Lysine residues of apoprotein B-100 quantitatively represented the major target, scavenging some 68% of the NaOCl added, with tryptophan and cysteine together accounting for an additional 10% of the oxidant. Concomitant with the loss of LDL's amino groups, chloramines were formed and the anionic surface charge of the lipoprotein particle increased, indicated by a 3-4-fold increase in electrophoretic mobility above that of native LDL on agarose gels. While both these changes could be initially reversed by physiological reductants such as ascorbic acid and methionine, incubation of the NaOCl-modified LDL at 37 degrees C resulted in increasing resistance of the modified lysine residues against reductive reversal. Exposure of mouse peritoneal macrophages to NaOCl-oxidized LDL resulted in increased intracellular concentrations of cholesterol and cholesteryl esters. These findings suggest that lipid-soluble antioxidants associated with LDL do not efficiently protect the lipoprotein against oxidative damage mediated by hypochlorite, and that extensive lipid oxidation is not a necessary requirement for oxidative LDL modification that leads to a high-uptake form of the lipoprotein.