14 research outputs found

    Developing and Evaluating a Stigma Scale for People with COPD

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    Chronic obstructive pulmonary disease (COPD) is a prevalent respiratory disease and the third leading cause of death worldwide. Tobacco smoking is not only a major contributor to the prevalence of and high mortality in COPD, but a history of smoking predisposes people with COPD to being stigmatized. Stigma, like in anxiety and depression, can adversely affect psychological functioning and essential functions for disease management. Guided by “the conceptual model representing the effects of stigma processes on health,” this three-paper dissertation includes a) a systematic review of stigma in people with COPD compared to lung cancer-related stigma, b) a qualitative study to evaluate and refine a 52-item preliminary COPD stigma scale using cognitive interviewing, and c) a quantitative study to examine the validity and reliability of the refined COPD stigma scale. In a systematic review, people with COPD or lung cancer are similar in their perceptions of stigma: “they did it to themselves.” Studies have shown that lung cancer-related stigma is associated with patient outcomes including increased psychological distress, poor quality of life, low help-seeking, poor medication adherence, and low social support. A small number of qualitative studies have described the phenomenon of stigma in people with COPD, and less is known about COPD-related stigma in part because there are no existing measures of COPD-related stigma. In a qualitative study, nineteen people with COPD participated in semi-structured cognitive interviews to assess comprehension of the 52-item preliminary COPD stigma scale. Most questionnaire items were understood and interpreted as intended. Of 52 total items, one item was dropped because it was identified as so offensive that many subjects were reluctant to answer. Eleven items were revised to improve the flow of responses to the questionnaire. Regarding response options, subjects selected the mid-point (i.e., neutral) response for various reasons. The most frequent reason for choosing the mid-point response was “both equal parts of agree and disagree,” followed by “not applicable.” This qualitative study provided the foundation required for further revision and evaluation of the stigma questionnaire using psychometric methods. In the quantitative study, we identified the underlying structure and assessed the psychometric properties of the revised version of the COPD-related Stigma Scale. People with COPD (n = 148) participated in the mailed questionnaire, including the 51-item COPD-related Stigma Scale. The exploratory factor analysis indicated that the four-factor model with 28 items provided a good fit to the data with high internal consistency (α = 0.96). The COPD-related Stigma Scale estimated by 28 items was significantly correlated with other measures—chronic illness-related stigma, psychological distress, and physical function—establishing the construct validity of the scale. This finding provided the foundation required for the further evaluation of confirming the underlying structure of the COPD-related Stigma Scale. In conclusion, the findings in the studies above support that COPD-related stigma may adversely affect psychological and physical health. Researchers may consider further investigating the potential harmful effects of stigma on COPD management as well as developing strategies to reduce the negative influence of COPD-related stigma in this population.PHDNursingUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttps://deepblue.lib.umich.edu/bitstream/2027.42/153482/1/sywoo_1.pd

    Testing the influence of cultural determinants on help-seeking theory.

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    Effects of perioperative exercise interventions on lung cancer patients: An overview of systematic reviews

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    Aims and ObjectivesTo identify, appraise and summarise systematic reviews of exercise interventions for surgical lung cancer patients.BackgroundLow exercise capacity, reduced pulmonary function, impaired health‐related quality of life and postoperative pulmonary complications are common in surgical lung cancer patients. Numerous systematic reviews address these health problems and examine the effects of exercise intervention. However, differences in the quality and scope of the systematic reviews and discordant findings from the reviews make it difficult for decisions‐makers to interpret the evidence and establish best practices in the clinical settings.DesignOverview of systematic reviews.MethodsThis overview was conducted following the PRISMA guideline. A literature search of PubMed, CINAHL, EMBASE, Cochrane Library, SPORTDiscus and PEDro was conducted (October 2019). Peer‐reviewed systematic reviews of randomised controlled trials focusing on the effects of exercise interventions for lung cancer patients who underwent surgery were included. The methodological quality of included reviews was assessed using AMSTAR 2. The results of reviews with meta‐analysis were synthesised and presented by each health outcome.ResultsSeven systematic reviews published between 2013 and 2019 were included. High/moderate‐quality evidence showed that postoperative exercise interventions could increase the exercise capacity and muscle strength, and low/very‐low‐quality evidence showed that postoperative exercise interventions may increase the physical component of health‐related quality of life and decease dyspnoea. Low‐quality evidence showed that preoperative exercise interventions may increase exercise capacity and pulmonary function, decrease the risk of postoperative pulmonary complications and reduce the length of hospital stay.ConclusionsPostoperative and preoperative exercises have the potential to improve health outcomes in surgical lung cancer patients. Further research is needed to evaluate the effects of different types of exercise and varying amounts of exercise.Relevance to clinical practiceThis study provides evidence to support the implementation of exercise interventions for surgical lung cancer patients.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/163626/2/jocn15511_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/163626/1/jocn15511.pd

    sj-docx-1-jtt-10.1177_1357633X231167613 - Supplemental material for Artificial intelligence assisted telehealth for nursing: A scoping review

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    Supplemental material, sj-docx-1-jtt-10.1177_1357633X231167613 for Artificial intelligence assisted telehealth for nursing: A scoping review by Jeeyae Choi, Seoyoon Woo and Anastasiya Ferrell in Journal of Telemedicine and Telecare</p

    Effect of Baicalin on Wound Healing in a Mouse Model of Pressure Ulcers

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    One of the most frequent comorbidities that develop in chronically ill or immobilized patients is pressure ulcers, also known as bed sores. Despite ischemia-reperfusion (I/R)-induced skin lesion having been identified as a primary cause of pressure ulcers, wound management efforts have so far failed to significantly improve outcomes. Baicalin, or 5,6,7-trihydroxyflavone, is a type of flavonoid which has been shown to possess a variety of biological characteristics, including antioxidative and anti-inflammatory effects and protection of I/R injury. In vitro wound scratch assay was first used to assess the function of baicalin in wound healing. We established a mouse model of advanced stage pressure ulcers with repeated cycles of I/R pressure load. In this model, topically applied baicalin (100 mg/mL) induced a significant increase in the wound healing process measured by wound area. Histological examination of the pressure ulcer mouse model showed faster granulation tissue formation and re-epithelization in the baicalin-treated group. Next, baicalin downregulated pro-inflammatory cytokines (IL-6 and IL-1ÎČ), while upregulating the anti-inflammatory IL-10. Additionally, baicalin induced an increase in several growth factors (VEGF, FGF-2, PDGF-ÎČ, and CTGF), promoting the wound healing process. Our results suggest that baicalin could serve as a promising agent for the treatment of pressures ulcers

    A study on longitudinal relationship between ultrafine dust and the prevalence of depression

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    Abstract Background Recently, the fine dust problem caused by rapid industrialization and science and technological development has emerged as a severe social issue worldwide. This also increases the interest in its effect on human life. In particular, there is a growing concern about the harm of fine dust in Korea. Methods This study is based on the PM 2.5 data from 2017 to 2021 provided by Air Korea to estimate changes in ultrafine dust. In addition, the data from the Community Health Survey provided by the Korea Centers for Disease Control and Prevention (KCDC) from 2017 to 2021 were used to examine the effect between the change in ultra-fine dust and the prevalence of depression. A total of 229 local governments were included in the analysis. The Latent Growth Modeling was carried out to estimate the change in ultra-fine dust and the prevalence of depressions and verify the relationship between ultra-fine dust and the prevalence of depression. Results The analysis result revealed that the ultra-fine dust concentration continued to decrease from 2017 to 2021. However, the depression prevalence increased from an average of 2.60% in 2017 to an average of 3.12% in 2021, suggesting the need for adequate and sufficient welfare policies for depression treatment. As a result of estimating the initial value and change rate of ultra-fine dust and depression prevalence, the higher the initial value of ultra-fine dust, the greater the decrease in ultra-fine dust. In terms of depression, the lower the initial value of the prevalence of depression, the larger the increase in depression prevalence. Conclusions This study is significant in that it revealed the strong association of the longitudinal relationship between ultra-fine dust and depression, one of the biggest issues in Korea, by utilizing large-scale longitudinal data

    Pellino1 promotes chronic inflammatory skin disease via keratinocyte hyperproliferation and induction of the T helper 17 response

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    Psoriasis: Regulatory protein linked to chronic inflammation An immune-regulating protein that mediates chronic inflammation in the skin offers a new therapeutic target for the autoimmune disorder psoriasis. A research team from South Korea led by Chang-Woo Lee from Sungkyunkwan University School of Medicine in Suwon and Heounjeong Go from the University of Ulsan College of Medicine in Seoul have discovered that Pellino1, a protein known to modulate immune responses to pathogens, is also found in abundance in the skin lesions of people with psoriasis. Using mouse models, the researchers showed how Pellino1 induces the proliferation of certain skin cells and triggers an inflammatory state through the activation of small proteins and immune cells normally involved in defense against infection. Targeting strategy that inactivate Pellino1 could help blunt the inflammatory signaling in the skin that drives the development of psoriatic lesions

    Oxalomalate reduces expression and secretion of vascular endothelial growth factor in the retinal pigment epithelium and inhibits angiogenesis: Implications for age-related macular degeneration

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    AbstractClinical and experimental observations indicate a critical role for vascular endothelial growth factor (VEGF), secreted by the retinal pigment epithelium (RPE), in pathological angiogenesis and the development of choroidal neovascularization (CNV) in age-related macular degeneration (AMD). RPE-mediated VEGF expression, leading to angiogenesis, is a major signaling mechanism underlying ocular neovascular disease. Inhibiting this signaling pathway with a therapeutic molecule is a promising anti-angiogenic strategy to treat this disease with potentially fewer side effects. Oxalomalate (OMA) is a competitive inhibitor of NADP+-dependent isocitrate dehydrogenase (IDH), which plays an important role in cellular signaling pathways regulated by reactive oxygen species (ROS). Here, we have investigated the inhibitory effect of OMA on the expression of VEGF, and the associated underlying mechanism of action, using in vitro and in vivo RPE cell models of AMD. We found that OMA reduced the expression and secretion of VEGF in RPE cells, and consequently inhibited CNV formation. This function of OMA was linked to its capacity to activate the pVHL-mediated HIF-1α degradation in these cells, partly via a ROS-dependent ATM signaling axis, through inhibition of IDH enzymes. These findings reveal a novel role for OMA in inhibiting RPE-derived VEGF expression and angiogenesis, and suggest unique therapeutic strategies for treating pathological angiogenesis and AMD development
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