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        Primary Purulent Pericarditis with Cardiac Tamponade due to Oropharyngeal Polymicrobial Infection: A Case Report and Literature Review

        Mukul Bhatarai,Gregory Yost,Christopher W Good,Charles F White,Hitekshya Nepal 대한흉부외과학회 2014 Journal of Chest Surgery (J Chest Surg) Vol.47 No.2

        Cardiac tamponade due to purulent pericarditis with a characteristic greenish fluid is rare in this antibiotic era. It is highly fatal despite early diagnosis and advanced treatment. Gram-positive cocci are the leading cause of purulent pericarditis, which usually results from a direct or hematogenous spread of organisms to the pericardium from the primary foci of infection. We describe an index case of rapidly developing pericardial tamponade caused by oropharyngeal polymicrobial infection in the absence of a primary source of infection in a 62-year-old man, who was successfully managed with emergency large-volume pericardiocentesis followed by pericardiectomy.

      • Systematic Review on Cancer Care Teams in Adolescents and Young Adult Patients with Cancer: How Multidisciplinary Teams Influence the Quality of Care

        Hyewon Shin,Angela Kabbe,Olivia Palermo,Molly Yost 한국간호과학회 2021 한국간호과학회 학술대회 Vol.2021 No.10

        Aim(s): The use of multidisciplinary teamwork has been found to result in effective care for patients with cancer in general but there is a lack of research surrounding teamwork in adolescent and young adult patients with cancer. This integrative review examines the teamwork among health care providers determining the plan of care for this population. Method(s): The preferred reporting items for systematic reviews and meta-analysis guidelines informed this review of studies that were conducted from 2000 to 2020. Eligible studies involved health care providers caring for a young patient diagnosed with cancer between 15-39 years of age, encompassed at least one phase of the cancer care continuum (cancer diagnosis to survivorship), and included multidisciplinary teamwork among health care providers. Result(s): Ten articles met inclusion criteria. Four themes were identified: 1) unique features of multidisciplinary teams in adolescent and young adult cancer care; 2) components of the multidisciplinary team effort; 3) how multidisciplinary teams were implemented, and ; 4) the impact of the multidisciplinary teams. These populations have psychosocial and informational needs related to their developmental stages. Multidisciplinary team efforts varied and included education and care delivery foci. Medicine, nursing, and social work were the commonly included disciplines on multidisciplinary teams. Communication and team member cooperation were deemed important to multidisciplinary team processes. Conclusion(s): Multidisciplinary team efforts demonstrated positive impacts on adolescent and young adult cancer care and improved outcomes. Emerging evidence indicates multidisciplinary teams have positive impacts on the experience and outcomes of this population. Further research focused on evaluating existing multidisciplinary team efforts for adolescent and young adult patients with cancer are needed. The development of comprehensive cancer care programs utilizing multidisciplinary teams should be considered.

      • Structure-activity relationship of capsaicin analogs and transient receptor potential vanilloid 1-mediated human lung epithelial cell toxicity.

        Thomas, Karen C,Ethirajan, Manivannan,Shahrokh, Kiumars,Sun, Hao,Lee, Jeewoo,Cheatham, Thomas E,Yost, Garold S,Reilly, Christopher A Williams Wilkins 2011 The Journal of pharmacology and experimental thera Vol.337 No.2

        <P>Activation of intracellular transient receptor potential vanilloid-1 (TRPV1) in human lung cells causes endoplasmic reticulum (ER) stress, increased expression of proapoptotic GADD153 (growth arrest- and DNA damage-inducible transcript 3), and cytotoxicity. However, in cells with low TRPV1 expression, cell death is not inhibited by TRPV1 antagonists, despite preventing GADD153 induction. In this study, chemical variants of the capsaicin analog nonivamide were synthesized and used to probe the relationship between TRPV1 receptor binding, ER calcium release, GADD153 expression, and cell death in TRPV1-overexpressing BEAS-2B, normal BEAS-2B, and primary normal human bronchial epithelial lung cells. Modification of the 3-methoxy-4-hydroxybenzylamide vanilloid ring pharmacophore of nonivamide reduced the potency of the analogs and rendered several analogs mildly inhibitory. Correlation analysis of analog-induced calcium flux, GADD153 induction, and cytotoxicity revealed a direct relationship for all three endpoints in all three lung cell types for nonivamide and N-(3,4-dihydroxybenzyl)nonanamide. However, the N-(3,4-dihydroxybenzyl)nonanamide analog also produced cytotoxicity through redox cycling/reactive oxygen species formation, shown by inhibition of cell death by N-acetylcysteine. Molecular modeling of binding interactions between the analogs and TRPV1 agreed with data for reduced potency of the analogs, and only nonivamide was predicted to form a 'productive' ligand-receptor complex. This study provides vital information on the molecular interactions of capsaicinoids with TRPV1 and substantiates TRPV1-mediated ER stress as a conserved mechanism of lung cell death by prototypical TRPV1 agonists.</P>

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        Transient receptor potential vanilloid-1 (TRPV1) is a mediator of lung toxicity for coal fly ash particulate material.

        Deering-Rice, Cassandra E,Johansen, Mark E,Roberts, Jessica K,Thomas, Karen C,Romero, Erin G,Lee, Jeewoo,Yost, Garold S,Veranth, John M,Reilly, Christopher A American Society for Pharmacology and Experimental 2012 Molecular pharmacology Vol.81 No.3

        <P>Environmental particulate matter (PM) pollutants adversely affect human health, but the molecular basis is poorly understood. The ion channel transient receptor potential vanilloid-1 (TRPV1) has been implicated as a sensor for environmental PM and a mediator of adverse events in the respiratory tract. The objectives of this study were to determine whether TRPV1 can distinguish chemically and physically unique PM that represents important sources of air pollution; to elucidate the molecular basis of TRPV1 activation by PM; and to ascertain the contributions of TRPV1 to human lung cell and mouse lung tissue responses exposed to an insoluble PM agonist, coal fly ash (CFA1). The major findings of this study are that TRPV1 is activated by some, but not all of the prototype PM materials evaluated, with rank-ordered responses of CFA1 > diesel exhaust PM > crystalline silica; TRP melastatin-8 is also robustly activated by CFA1, whereas other TRP channels expressed by airway sensory neurons and lung epithelial cells that may also be activated by CFA1, including TRPs ankyrin 1 (A1), canonical 4α (C4α), M2, V2, V3, and V4, were either slightly (TRPA1) or not activated by CFA1; activation of TRPV1 by CFA1 occurs via cell surface interactions between the solid components of CFA1 and specific amino acid residues of TRPV1 that are localized in the putative pore-loop region; and activation of TRPV1 by CFA1 is not exclusive in mouse lungs but represents a pathway by which CFA1 affects the expression of selected genes in lung epithelial cells and airway tissue.</P>

      • Contributions of TRPV1, endovanilloids, and endoplasmic reticulum stress in lung cell death in vitro and lung injury.

        Thomas, Karen C,Roberts, Jessica K,Deering-Rice, Cassandra E,Romero, Erin G,Dull, Randal O,Lee, Jeewoo,Yost, Garold S,Reilly, Christopher A American Physiological Society 2012 American journal of physiology. Lung cellular and Vol.302 No.1

        <P>Endogenous agonists of transient receptor potential vanilloid-1 (TRPV1) (endovanilloids) are implicated as mediators of lung injury during inflammation. This study tested the hypothesis that endovanilloids produced following lipopolysaccharide (LPS) treatment activate TRPV1 and cause endoplasmic reticulum stress/GADD153 expression in lung cells, representing a mechanistic component of lung injury. The TRPV1 agonist nonivamide induced GADD153 expression and caused cytotoxicity in immortalized and primary human bronchial, bronchiolar/alveolar, and microvascular endothelial cells, proportional to TRPV1 mRNA expression. In CF-1 mice, Trpv1 mRNA was most abundant in the alveoli, and intratracheal nonivamide treatment promoted Gadd153 expression in the alveolar region. Treatment of CF-1 mice with LPS increased Gadd153 in the lung, lactate dehydrogenase (LDH) in bronchoalveolar lavage (BAL) fluid, and lung wet-to-dry weight ratio. Cotreating mice with LPS and the TRPV1 antagonist LJO-328 reduced Gadd153 induction and LDH in BAL but did not inhibit increases in lung wet-to-dry ratio. In Trpv1(-/-) mice treated with LPS, Gadd153 induction and LDH in BAL were reduced relative to wild-type mice, and the wet-to-dry weight ratios of lungs from both wild-type and Trpv1(-/-) mice decreased. Organic extracts of blood collected from LPS-treated mice were more cytotoxic to TRPV1-overexpressing cells compared with BEAS-2B cells and extracts from control mice, however, most pure endovanilloids did not produce cytotoxicity in a characteristic TRPV1-dependent manner. Collectively, these data indicate a role for TRPV1, and endogenous TRPV1 agonists, in ER stress and cytotoxicity in lung cells but demonstrate that ER stress and cytotoxicity are not essential for pulmonary edema.</P>

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