Section of Respiratory Medicine, Department of Experimental and Clinical Medicine, University of Florence, Florence, 50134, Italy.
Published: June 2014
AI Article Synopsis
Article Abstract
The purpose of this study was to assess lung function in runners with marathon-induced lung edema. Thirty-six (24 males) healthy subjects, 34 (SD 9) years old, body mass index 23.7 (2.6) kg/m(2) had posterior/anterior (PA) radiographs taken 1 day before and 21 (6) minutes post marathon finish. Pulmonary function was performed 1-3 weeks before and 73 (27) minutes post finish. The PA radiographs were viewed together, as a set, and evaluated by two experienced readers separately who were blinded as to time the images were obtained. Radiographs were scored for edema based on four different radiological characteristics such that the summed scores for any runner could range from 0 (no edema) to a maximum of 8 (severe interstitial edema). Overall, the mean edema score increased significantly from 0.2 to 1.0 units (P < 0.01), and from 0.0 to 2.9 units post exercise in the six subjects that were edema positive (P = 0.03). Despite a 2% decrease in forced vital capacity (FVC, P = 0.024) and a 12% decrease in alveolar-membrane diffusing capacity for carbon monoxide (DmCO, P = 0.01), there was no relation between the change in the edema score and the change in DmCO or FVC. In conclusion, (1) mild pulmonary edema occurs in at least 17% of subjects and that changes in pulmonary function cannot predict the occurrence or severity of edema, (2) lung edema is of minimal physiological significance as marathon performance is unaffected, exercise-induced arterial hypoxemia is unlikely, and postexercise pulmonary function changes are mild.
Department of Respiratory and Critical Care Medicine, West China Hospital, Sichuan University, No. 37, Guoxue Lane, Wuhou District, Chengdu, 610000, Sichuan, China.
Background: Alveolar macrophages (AMs) is critical to exacerbate acute lung injury (ALI) induced by lipopolysaccharide (LPS) via inhibiting inflammation, which could by shifted by mesenchymal stem cell-derived exosomes (MSC-exos). But the underlying rationale is not fully clarified. Our study aimed to analyze the significance of itaconic acid (ITA) in mediating the protective effects of MSC-exos on LPS-induced ALI.
A positive-sense single-stranded RNA virus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), caused the coronavirus disease 2019 (COVID-19) pandemic that devastated the world. While this is a respiratory virus, one feature of the SARS-CoV-2 infection was recognized to cause pathogenesis of other organs. Because the membrane fusion protein of SARS-CoV-2, the spike protein, binds to its major host cell receptor angiotensin-converting enzyme 2 (ACE2) that regulates a critical mediator of cardiovascular diseases, angiotensin II, COVID-19 is largely associated with vascular pathologies.
Perioperative and critical care management following penetrating thoracic trauma represents a complex challenge. Those who survive the early trauma approach and reach the hospital alive often remain in critical condition, with cardiocirculatory complications and major pulmonary injuries. Additional difficulty arises from the presence of a weapon , particularly in a dorsal location, which limits patient positioning, and the safe manipulation of both the weapon and the patient.
Background: Swimming-induced pulmonary edema (SIPE), also called immersion pulmonary edema, is a form of exertional pulmonary edema associated with swimming and/or water immersion without aspiration. Most case reports on SIPE feature young, healthy patients who were scuba-diving, surface swimming, snorkeling, or breath-hold diving before experiencing symptoms of dyspnea, chest pain/tightness, cough, and hemoptysis. The incidence of SIPE is thought to be between 0.
College of Medicine, Graduate School, Kyung Hee University, 02447, Republic of Korea; Division of Cardiology, Department of Internal Medicine, Kyung-Hee University Hospital, Kyung Hee University, 02447, Republic of Korea. Electronic address:
In the current study, we dosed Didecyldimethylammonium chloride (DDAC) in mice by pharyngeal aspiration for 28 days or 90 days (weekly) and tried to elucidate the relationship between lamellar body formation and the lesions. When exposed for 28 days (0, 5, 10, 50, and 100 μg/head), all the mice in the 50 and 100 μg/head groups died since Day 2 after the third dosing (Day 16 after the first dosing). Edema, necrosis of bronchiolar and alveolar epithelium, and fibrinous exudate were observed in the lungs of all the dead mice, and chronic inflammatory lesions were observed in the lung tissues of alive mice.
