3,341 research outputs found

    Roles of Inflammatory Biomarkers in Exhaled Breath Condensates in Respiratory Clinical Fields

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    Background Exhaled condensates contain inflammatory biomarkers; however, their roles in the clinical field have been under-investigated. Methods We prospectively enrolled subjects admitted to pulmonology clinics. We collected exhaled breath condensates (EBC) and analysed the levels of six and 12 biomarkers using conventional and multiplex enzyme-linked immunosorbent assay, respectively. Results Among the 123 subjects, healthy controls constituted the largest group (81 participants; 65.9%), followed by the preserved ratio impaired spirometry group (21 patients; 17.1%) and the chronic obstructive pulmonary disease (COPD) group (21 patients; 17.1%). In COPD patients, platelet derived growth factor-AA exhibited strong positive correlations with COPD assessment test (ρ=0.5926, p=0.0423) and COPD-specific version of St. George’s Respiratory Questionnaire (SGRQ-C) score (total, ρ=0.6725, p=0.0166; activity, ρ=0.7176, p=0.0086; and impacts, ρ=0.6151, p=0.0333). Granzyme B showed strong positive correlations with SGRQ-C score (symptoms, ρ=0.6078, p=0.0360; and impacts, ρ=0.6007, p=0.0389). Interleukin 6 exhibited a strong positive correlation with SGRQ-C score (activity, ρ=0.4671, p=0.0378). The absolute serum eosinophil and basophil counts showed positive correlations with pro-collagen I alpha 1 (ρ=0.6735, p=0.0164 and ρ=0.6295, p=0.0283, respectively). In healthy subjects, forced expiratory volume in 1 second (FEV1)/forced vital capacity demonstrated significant correlation with CC chemokine ligand 3 (CCL3)/macrophage inflammatory protein 1 alpha (ρ=0.3897 and p=0.0068). FEV1 exhibited significant correlation with CCL11/eotaxin (ρ=0.4445 and p=0.0017). Conclusion Inflammatory biomarkers in EBC might be useful to predict quality of life concerning respiratory symptoms and serologic markers. Further studies are needed

    Multimodality treatment for esophageal squamous cell carcinoma

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    This thesis aims to optimize multimodality treatments for locally advanced esophageal squamous cell carcinoma (ESCC), specifically in East-Asia, recognizing that ESCC may differ in biology and response to treatment in different parts of the world. Part I of the thesis introduces the subtype ESCC and its characteristics from different geographical perspectives followed by an exposition of the differences between ESCC in eastern and western worlds. Part II optimizes trimodal therapy of ESCC in Taiwan, as a representative region of East-Asia. Finally, in Part III, the accuracy of liquid biopsies in identifying patients who may not need surgery after trimodal therapy is assessed.

    Impact of indoor environment on children's pulmonary health.

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    IntroductionA child's living environment has a significant impact on their respiratory health, with exposure to poor indoor air quality (IAQ) contributing to potentially lifelong respiratory morbidity. These effects occur throughout childhood, from the antenatal period through to adolescence. Children are particularly susceptible to the effects of environmental insults, and children living in socioeconomic deprivation globally are more likely to breathe air both indoors and outdoors, which poses an acute and long-term risk to their health. Adult respiratory health is, at least in part, determined by exposures and respiratory system development in childhood, starting in utero.Areas coveredThis narrative review will discuss, from a global perspective, what contributes to poor IAQ in the child's home and school environment and the impact that indoor air pollution exposure has on respiratory health throughout the different stages of childhood.Expert opinionAll children have the right to a living and educational environment without the threat of pollution affecting their health. Action is needed at multiple levels to address this pressing issue to improve lifelong respiratory health. Such action should incorporate a child's rights-based approach, empowering children, and their families, to have access to clean air to breathe in their living environment

    Effects of municipal smoke-free ordinances on secondhand smoke exposure in the Republic of Korea

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    ObjectiveTo reduce premature deaths due to secondhand smoke (SHS) exposure among non-smokers, the Republic of Korea (ROK) adopted changes to the National Health Promotion Act, which allowed local governments to enact municipal ordinances to strengthen their authority to designate smoke-free areas and levy penalty fines. In this study, we examined national trends in SHS exposure after the introduction of these municipal ordinances at the city level in 2010.MethodsWe used interrupted time series analysis to assess whether the trends of SHS exposure in the workplace and at home, and the primary cigarette smoking rate changed following the policy adjustment in the national legislation in ROK. Population-standardized data for selected variables were retrieved from a nationally representative survey dataset and used to study the policy action’s effectiveness.ResultsFollowing the change in the legislation, SHS exposure in the workplace reversed course from an increasing (18% per year) trend prior to the introduction of these smoke-free ordinances to a decreasing (−10% per year) trend after adoption and enforcement of these laws (β2 = 0.18, p-value = 0.07; β3 = −0.10, p-value = 0.02). SHS exposure at home (β2 = 0.10, p-value = 0.09; β3 = −0.03, p-value = 0.14) and the primary cigarette smoking rate (β2 = 0.03, p-value = 0.10; β3 = 0.008, p-value = 0.15) showed no significant changes in the sampled period. Although analyses stratified by sex showed that the allowance of municipal ordinances resulted in reduced SHS exposure in the workplace for both males and females, they did not affect the primary cigarette smoking rate as much, especially among females.ConclusionStrengthening the role of local governments by giving them the authority to enact and enforce penalties on SHS exposure violation helped ROK to reduce SHS exposure in the workplace. However, smoking behaviors and related activities seemed to shift to less restrictive areas such as on the streets and in apartment hallways, negating some of the effects due to these ordinances. Future studies should investigate how smoke-free policies beyond public places can further reduce the SHS exposure in ROK

    Winonan

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    This issue of the Winonan was published on February 8, 2023.https://openriver.winona.edu/thewinonan2020s/1024/thumbnail.jp

    Interaction between Cigarette Smoke and Human Papillomavirus 16 E6/E7 Oncoproteins to Induce SOD2 Expression and DNA Damage in Head and Neck Cancer

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    Even though epidemiological studies suggest that tobacco smoking and high-risk human papillomavirus (HR-HPV) infection are mutually exclusive risk factors for developing head and neck cancer (HNC), a portion of subjects who develop this heterogeneous group of cancers are both HPV-positive and smokers. Both carcinogenic factors are associated with increased oxidative stress (OS) and DNA damage. It has been suggested that superoxide dismutase 2 (SOD2) can be independently regulated by cigarette smoke and HPV, increasing adaptation to OS and tumor progression. In this study, we analyzed SOD2 levels and DNA damage in oral cells ectopically expressing HPV16 E6/E7 oncoproteins and exposed to cigarette smoke condensate (CSC). Additionally, we analyzed SOD2 transcripts in The Cancer Genome Atlas (TCGA) Head and Neck Cancer Database. We found that oral cells expressing HPV16 E6/E7 oncoproteins exposed to CSC synergistically increased SOD2 levels and DNA damage. Additionally, the SOD2 regulation by E6, occurs in an Akt1 and ATM-independent manner. This study suggests that HPV and cigarette smoke interaction in HNC promotes SOD2 alterations, leading to increased DNA damage and, in turn, contributing to development of a different clinical entity

    The Bidirectional Gut-Lung Axis in COPD

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    Epidemiological studies indicate that chronic obstructive pulmonary disease (COPD) is associated with the incidence of changes in intestinal health. Cigarette smoking, as one of the major causes of COPD, can have an impact on the gastrointestinal system and promotes intestinal diseases. This points to the existence of gut-lung interactions, however, an overview of the underlying mechanisms of the bidirectional connection between the lungs and the gut in COPD is lacking. The interaction between the lungs and the gut can occur through circulating inflammatory cells and mediators. Moreover, gut microbiota dysbiosis, observed in both COPD and intestinal disorders, can lead to a disturbed mucosal environment, including the intestinal barrier and immune system, and hence, may negatively affect both the gut and the lungs. Furthermore, systemic hypoxia and oxidative stress that occurs in COPD may also be involved in intestinal dysfunction and play a role in the gut-lung axis. This review summarizes data from clinical research, animal models and in vitro studies that may explain the possible mechanisms of gut-lung interactions associated with COPD. Interesting observations on the possibility of promising future add-on therapies for intestinal dysfunction in COPD patients will be highlighted

    Mechanisms of Cigarette Smoke-Induced Mitochondrial Dysfunction in Striated Muscle and Aorta

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    Cigarette Smoke is a significant cause of morbidity and mortality in the United States, accounting for over 480,000 annual deaths. Of these deaths, the most common cause of mortality in chronic smokers is cardiometabolic diseases. Likewise, a significant portion of smokers experience some form of cardiac, vascular, or metabolic dysfunction throughout their lifetime. More specifically, smoking is shown to induce mitochondrial dysfunction in these tissues, causing an increase in oxidative damage and poor overall health. However, despite the advances in the health outcomes related to cigarette smoke exposure, the mechanisms underlying mitochondrial dysfunction in striated muscle and the vasculature remain largely unexplained. Particularly, no investigations have been conducted to (1) characterize the acute inhibitory effects of cigarette smoke to the mitochondria in these tissues, (2) assess the changes in mitochondrial substrate oxidation with exposure to cigarette smoke, or (3) identify the mechanisms by which cigarette smoke induces deleterious effects on the mitochondrial electron transport chain. Therefore, the purpose of this dissertation is to use high-resolution respirometry to characterize the toxicity of cigarette smoke in the mitochondria of the aorta, heart, and two types of skeletal muscle, determine the capacity for cigarette smoke to induce a shift in mitochondrial carbohydrate- or fatty acid-stimulated mitochondrial respiration, and further investigate the mechanisms by which cigarette smoke impairs the mitochondrial electron transport chain. Herein, we first demonstrate that cigarette smoke-induced inhibition of mitochondrial respiration is tissue-specific and depends on the intrinsic qualities of the mitochondria in each tissue (e.g. morphology) as well as the tissue-specific mitochondrial content. Second, we show that mitochondrial pyruvate oxidation, not fatty acid oxidation, is a primary mechanism for cigarette smoke-induced mitochondrial dysfunction. Third, we further support the hypothesis that mitochondrial complex I is a primary site of smoke-induced mitochondrial dysfunction. However, we also identify the ADP/ATP transporter, ANT, as another site of smoke-induced mitochondrial impairment. Lastly, we discuss the clinical implications of each of these findings as well as future research directions

    Individual and Social Influences on Cigarette Smoking During Pregnancy

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    Population-level trends on sociodemographic risk factors for cigarette smoking during pregnancy (SDP) and outcomes for offspring exposed to maternal SDP are well established. However, the more complex task of understanding individual risk-prediction, including differences by maternal race/ethnicity, and its clinical application, remains incomplete. Characterizing the relative influence of environmental and individual characteristics as risk or protective factors for continued SDP is a necessary next step for informing individual- and public health-level interventions to produce successful smoking cessation prior to pregnancy, substantially reducing smoking-related mortality in child-bearing people. In this dissertation, I wanted to explore how multiple levels of influence, from individual, to family, to neighborhood, interact to confer risk or protection for SDP. First, I used a population-level birth cohort from state birth records of first births including geocoded maternal address at time of childbirth to compare individual and neighborhood level sociodemographics as risk and protective influences for SDP. I found important social influences on cigarette smoking during first pregnancy—marital status, reproductive partner acknowledgement of paternity, and census tract-level SDP rate. Moreover, there were differences in risk factors by maternal race/ethnicity, in particular, among Black/African Americans, where SDP was higher in tracts with a greater proportion of white non-Hispanic residents. To examine how clinical factors, namely nicotine dependence, modulate risk for SDP, I used research data from a well-characterized like-sex female twin pair sample, connected to birth records for children born to the twin participants. I found that lifetime heaviness of nicotine dependence contributed as much risk to SDP as maternal sociodemographics at time of childbirth; however, the contribution of nicotine dependence to SDP risk was diminished at high levels of sociodemographic risk. These findings were limited to white non-Hispanic participants, as there was insufficient sample size from Black/African American participants. Finally, I wanted to use findings from administrative data to inform research design and address the needs of historically excluded populations, considering protective as well as risk factors. I wanted to identify protective factors for SDP among women who identify as American Indian or Alaska Native, as most existing research either excludes Native women, or only identifies higher rates of smoking, including SDP, without considering risk and protective factors. I conducted a pilot data collection from ten women recruited from birth records to examine the roles of positive racial identity, engagement with traditional tobacco use, and social influence by reproductive partner and cohabitants during pregnancy that might be associated with SDP. While I did not achieve a sufficient sample size for statistical analysis, I identified ways future work could explore these questions, including by working with a specific Tribe or Nation to address their questions about pregnancy and perinatal health and/or partnering with Tribal Epidemiology Centers to improve recruitment opportunities
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