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To describe the implementation of a trauma-informed model of care in the Post COVID Respiratory Clinic of a large tertiary referral centre in NSW.
Discussion paper.
Evidence gathered from a literature search (2008–2022) was used to develop a framework for management of patients presenting to this Post COVID Respiratory Clinic. This paper outlines the personal reflections of the clinic staff as they developed and implemented this framework. Ethical approval was obtained to report the data collected from patient reviews.
The literature highlights the high prevalence of trauma in patients following COVID-19 infection, as well as the larger population both during and after the pandemic. This experience of trauma was observed in patients seen within the clinic, indicating a need for specialized care. In response, a trauma-informed model of care was implemented.
Reconceptualizing COVID-19 as a ‘collective trauma’ can help healthcare workers understand the needs of post-COVID patients and enable them to respond empathetically. A trauma-informed model is complementary to this cohort as it specifically addresses vulnerable populations, many of whom have been further marginalized by the pandemic.
Frontline healthcare workers, particularly nurses, are well positioned to implement trauma-informed care due to their high-level of patient contact. Adequate allocation of resources and investment in staff is essential to ensure such care can be provided.
The COVID-19 pandemic has led to adverse physical and mental health outcomes for many. Trauma-informed care is a way to promote reengagement with the healthcare system in this group. Post COVID patients globally may benefit from this approach, as it aims to build trust and independence.
Feedback was sought from a patient representative to ensure this paper adequately reflected the experience of the post-COVID patient.
by Ashley G. Holtz, Troy L. Lowe, Yusuke Aoki, Yutaro Kubota, Robert M. Hoffman, Steven G. Clarke
The methionine addiction of cancer cells is known as the Hoffman effect. While non-cancer cells in culture can utilize homocysteine in place of methionine for cellular growth, most cancer cells require exogenous methionine for proliferation. It has been suggested that a biochemical basis of this effect is the increased utilization of methionine for S-adenosylmethionine, the major methyl donor for a variety of cellular methyltransferases. Recent studies have pointed to the role of S-adenosylmethionine-dependent protein arginine methyltransferases (PRMTs) in cell proliferation and cancer. To further understand the biochemical basis of the methionine addiction of cancer cells, we compared protein arginine methylation in two previously described isogenic cell lines, a methionine-addicted 143B human osteosarcoma cell line and its less methionine-dependent revertant. Previous work showed that the revertant cells were significantly less malignant than the parental cells. In the present study, we utilized antibodies to detect the asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA) products of PRMTs in polypeptides from cellular extracts and purified histone preparations of these cell lines fractionated by SDS-PAGE. Importantly, we observed little to no differences in the banding patterns of ADMA- and SDMA-containing species between the osteosarcoma parental and revertant cell lines. Furthermore, enzymatic activity assays using S-adenosyl-ʟ-[methyl-3H] methionine, recombinantly purified PRMT enzymes, cell lysates, and specific PRMT inhibitors revealed no major differences in radiolabeled polypeptides on SDS-PAGE gels. Taken together, these results suggest that changes in protein arginine methylation may not be major contributors to the Hoffman effect and that other consequences of methionine addiction may be more important in the metastasis and malignancy of osteosarcoma and potentially other cancers.
FreshRSS 