Browsing by Subject "Lungs"

Now showing 1 - 10 of 11
  • Thumbnail Image
    Item
    During the COVID-19 Pandemic, Lung Specialists of the World Implore You: Inhale Only Clean Air
    (American Thoracic Society, 2020-08-14) Santhosh, Lekshmi; Oh, Anita; Alismail, Abdullah; Breiburg, Anna; Kaminski, Naftali; Carlos, Graham; Jamil, Shazia; Department of Medicine, IU School of Medicine
    Recent social media and lay news report that nicotine may help protect from COVID-19. However, lung specialists of the American Thoracic Society and California Thoracic Society recommend that you inhale only clean air. Research shows that exposure to smoke, vapors, and air pollution all contribute to worse outcomes in COVID-19 infection. This fact sheet summarizes some of the common public questions addressed to lung healthcare professionals.
  • Thumbnail Image
    Item
  • Thumbnail Image
    Item
    The Effects of SRT1720 Treatment on Endothelial Cells Derived from the Lung and Bone Marrow of Young and Aged, Male and Female Mice
    (MDPI, 2021-10-14) Dadwal, Ushashi Chand; Bhatti, Fazal Ur Rehman; Awosanya, Olatundun Dupe; Staut, Caio de Andrade; Nagaraj, Rohit U.; Perugini, Anthony Joseph, III.; Tewari, Nikhil Prasad; Valuch, Conner Riley; Sun, Seungyup; Mendenhall, Stephen Kyle; Zhou, Donghui; Mostardo, Sarah Lyn; Blosser, Rachel Jean; Li, Jiliang; Kacena, Melissa Ann; Orthopaedic Surgery, School of Medicine
    Angiogenesis is critical for successful fracture healing. Age-related alterations in endothelial cells (ECs) may cause impaired bone healing. Therefore, examining therapeutic treatments to improve angiogenesis in aging may enhance bone healing. Sirtuin 1 (SIRT1) is highly expressed in ECs and its activation is known to counteract aging. Here, we examined the effects of SRT1720 treatment (SIRT1 activator) on the growth and function of bone marrow and lung ECs (BMECs and LECs, respectively), derived from young (3-4 month) and old (20-24 month) mice. While aging did not alter EC proliferation, treatment with SRT1720 significantly increased proliferation of all LECs. However, SRT1720 only increased proliferation of old female BMECs. Vessel-like tube assays showed similar vessel-like structures between young and old LECs and BMECs from both male and female mice. SRT1720 significantly improved vessel-like structures in all LECs. No age, sex, or treatment differences were found in migration related parameters of LECs. In males, old BMECs had greater migration rates than young BMECs, whereas in females, old BMECs had lower migration rates than young BMECs. Collectively, our data suggest that treatment with SRT1720 appears to enhance the angiogenic potential of LECs irrespective of age or sex. However, its role in BMECs is sex- and age-dependent.
  • Thumbnail Image
    Item
    Fatty acid synthesis in the perfused rat lung
    (1978) Buechler, Kenneth Francis
  • Thumbnail Image
    Item
    Innovative Use of High-Fidelity Lung Simulators to Test a Ventilator Splitter Device
    (Wolters Kluwer, 2020-06-02) Boyer, Tanna J.; Mitchell, Sally A.; Cartwright, Johnny F.; Ahmed, Rami A.; Anesthesia, School of Medicine
    The coronavirus disease 2019 (COVID-19) pandemic has rapidly exposed health care system inadequacies. Hospital ventilator shortages in Italy compelled US physicians to consider cre-ative solutions, such as using Y-pieces or T-pieces, to preclude the need to make decisions of life or death based on medical equipment availability. We add to current knowledge and testing capacity for ventilator splitters by reporting the ability to examine the functionality of ventilator splitters by using 2 high-fidelity lung simulators. Data obtained by the high-fidelity lung simula-tors included: tidal volume, respiratory rate, minute ventilation, peak inspiratory pressure, peak plateau pressure, and positive end-expiratory pressure.
  • Thumbnail Image
    Item
    Oxygen radical-induced microvascular injury in the lung
    (1987) Barnard, Joseph Wade
  • Thumbnail Image
    Item
  • Thumbnail Image
    Item
    The role of ceramides in cigarette smoke-induced alveolar cell death
    (2012-11) Kamocki, Krzysztof; Petrache, Irina; Gunst, Susan J.; Quilliam, Laurence; Atkinson, Simon
    The complex pathogenesis of emphysema involves disappearance of alveolar structures, in part attributed to alveolar cell apoptosis. The mechanism by which cigarette smoke (CS) induces alveolar cell apoptosis is not known. We hypothesized that ceramides are induced by CS via specific enzymatic pathways that can be manipulated to reduce lung cell apoptosis. CS increased ceramides in the whole lung and in cultured primary structural lung cells. Exposure to CS activated within minutes the acid sphingomyelinase, and within weeks the de novo- ceramide synthesis pathways. Pharmacological inhibition of acid sphingomyelinase significantly attenuated CS-induced apoptosis. To understand the mechanisms by which ceramides induce apoptosis, we investigated the cell types affected and the involvement of RTP801, a CS-induced pro-apoptotic and pro-inflammatory protein. Direct lung augmentation of ceramide caused apoptosis of both endothelial and epithelial type II cells. Ceramide upregulated RTP801 and the transgenic loss of RTP801 inhibited only epithelial, but not endothelial cell apoptosis induced by ceramide. In conclusion, CS induces acid sphingomyelinase-mediated ceramide upregulation and apoptosis in a cell-specific manner, which in epithelial cells involves induction of stress response proteins that may further amplify lung injury. Molecular targeting of amplification pathways may provide therapeutic opportunities to halt emphysema progression.
  • Thumbnail Image
    Item
  • Thumbnail Image
    Item
    Sensitivity of Mouse Lung Nuclear Receptors to Electronic Cigarette Aerosols and Influence of Sex Differences: A Pilot Study
    (MDPI, 2024-06-20) Sharma, Shikha; Rousselle, Dustin; Parker, Erik; Damilola Ekpruke, Carolyn; Alford, Rachel; Babayev, Maksat; Commodore, Sarah; Silveyra, Patricia; Medicine, School of Medicine
    The emerging concern about chemicals in electronic cigarettes, even those without nicotine, demands the development of advanced criteria for their exposure and risk assessment. This study aims to highlight the sensitivity of lung nuclear receptors (NRs) to electronic cigarette e-liquids, independent of nicotine presence, and the influence of the sex variable on these effects. Adult male and female C57BL/6J mice were exposed to electronic cigarettes with 0%, 3%, and 6% nicotine daily (70 mL, 3.3 s, 1 puff per min/30 min) for 14 days, using the inExpose full body chamber (SCIREQ). Following exposure, lung tissues were harvested, and RNA extracted. The expression of 84 NRs was determined using the RT2 profiler mRNA array (Qiagen). Results exhibit a high sensitivity to e-liquid exposure irrespective of the presence of nicotine, with differential expression of NRs, including one (females) and twenty-four (males) in 0% nicotine groups compared to non-exposed control mice. However, nicotine-dependent results were also significant with seven NRs (females), fifty-three NRs (males) in 3% and twenty-three NRs (female) twenty-nine NRs (male) in 6% nicotine groups, compared to 0% nicotine mice. Sex-specific changes were significant, but sex-related differences were not observed. The study provides a strong rationale for further investigation.