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2.
Toxicol Lett ; 334: 4-13, 2020 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-32949624

RESUMO

Radon exposure is the most frequent cause of lung cancer in non-smokers. The high linear energy transfer alpha-particles from radon decay cause the accumulation of multiple genetic changes and lead to cancer development. Epithelial-mesenchymal transition (EMT) plays an important role in oncogenesis. However, the mechanisms underlying chronic radon exposure-induced EMT attributed to carcinogenesis are not understood. This study aimed to explore the EMT and potential molecular mechanisms induced by repeated radon exposure. The EMT model of 16HBE and BEAS-2B cells was established with radon exposure (20000 Bq/m3, 20 min each time every 3 days). We found repeated radon exposure facilitated epithelial cell migration, proliferation, reduced cell adhesion and ability to undergo EMT through a decrease in epithelial markers and an increase in mesenchymal markers. Radon regulated the expression of matrix metalloproteinase 2 (MMP2) and tissue inhibitors of metalloproteinase 2 (TIMP2) to disrupt the balance of MMP2/TIMP2. In vivo, BALB/c mice were exposed to 105 Bq/m3 radon gas for cumulative doses of 60 and 120 Working Level Months (WLM). Radon inhalation caused lung damage and fibrosis in mice, which was aggravated with the increase of exposure dose. EMT-like transformation also occurred in lung tissues of radon-exposure mice. Moreover, radon radiation increased p-PI3K, p-AKT and p-mTOR in cells and mice. Radon reduced the GSK-3ß level and elevated the active ß-catenin in 16HBE cells. The m-TOR and AKT inhibitors attenuated radon exposure-induced EMT by regulation related biomarkers. These data demonstrated that radon exposure induced EMT through the PI3K/AKT/mTOR pathway in epithelial cells and lung tissue.


Assuntos
Poluentes Radioativos do Ar/toxicidade , Células Epiteliais/efeitos dos fármacos , Transição Epitelial-Mesenquimal/efeitos dos fármacos , Lesão Pulmonar/induzido quimicamente , Pulmão , Radônio/toxicidade , Animais , Linhagem Celular , Movimento Celular/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Relação Dose-Resposta à Radiação , Humanos , Exposição por Inalação/efeitos adversos , Pulmão/efeitos dos fármacos , Pulmão/metabolismo , Pulmão/patologia , Lesão Pulmonar/metabolismo , Lesão Pulmonar/patologia , Camundongos , Camundongos Endogâmicos BALB C , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Produtos de Decaimento de Radônio/toxicidade , Transdução de Sinais , Serina-Treonina Quinases TOR/metabolismo
3.
PLoS One ; 15(9): e0238140, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32881943

RESUMO

Vitamin E acetate (VEA) is strongly linked to the outbreak of electronic-cigarette or vaping product use-associated lung injury (EVALI). It has been proposed that VEA decomposition to ketene-a respiratory poison that damages lungs at low ppm levels-may play a role in EVALI. However, there is no information available on the temperature at which VEA decomposes and how this correlates with the vaping process. We have studied the temperature-dependent kinetics of VEA decomposition using quantum chemical and statistical mechanical modelling techniques, developing a chemical kinetic model of the vaping process. This model predicts that, under typical vaping conditions, the use of VEA contaminated e-cigarette products is unlikely to produce ketene at harmful levels. However, at the high temperatures encountered at low e-cigarette product levels, which produce 'dry hits', ketene concentrations are predicted to reach acutely toxic levels in the lungs (as high as 30 ppm). We therefore hypothesize that dry hit vaping of e-cigarette products containing VEA contributes to EVALI.


Assuntos
Etilenos/metabolismo , Cetonas/metabolismo , Lesão Pulmonar/patologia , Vaping/efeitos adversos , Vitamina E/metabolismo , Etilenos/química , Etilenos/toxicidade , Humanos , Cetonas/química , Cetonas/toxicidade , Cinética , Lesão Pulmonar/induzido quimicamente , Temperatura , Vitamina E/química
4.
Life Sci ; 260: 118426, 2020 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-32937159

RESUMO

AIMS: Tobacco smoking is a major health problem associated with lung and liver damage. Lung and liver damage secondary to tobacco smoking is mediated through nicotine-induced oxidative stress. Therefore, we hypothesized that antioxidant treatment with tiron may improve nicotine-induced lung and liver damage. MATERIALS AND METHODS: Rats were divided into six groups, a control, nicotine (10 mg/kg/day, i.p.; for 8 weeks) and tiron (100 or 200 mg/kg/day, i.p.; for 8 weeks) with or without nicotine administration. KEY FINDINGS: Tiron improved survival rate and attenuated lung and liver damage as reflected by decreased total and differential cell counts, lactate dehydrogenase (LDH) activity in bronchoalveolar lavage fluid (BALF) and decreased alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) in serum; also histopathological examination confirmed the protective effect of tiron in lung and liver tissues of nicotine treated rats. Tiron attenuated dyslipidemia, which is associated with nicotine. These ameliorative effects of tiron may be mainly due to its antioxidant effect as proved by a significant decrease in malondialdehyde (MDA) content, reactive oxygen species (ROS) and total nitrite/nitrate (NOx) levels, and increase in reduced glutathione (GSH) level, catalase (CAT) and superoxide dismutase (SOD) activities. This is likely related to suppression of protein levels of NADPH oxidase enzyme (NOX1), inducible nitric oxide synthase (iNOS), nuclear factor kappa B (NF-κB) and tumor necrosis factor alpha (TNF-α); and up-regulation of protein levels of nuclear factor erythroid-2 (Nrf2). SIGNIFICANCE: This makes tiron (synthetic analogue of vitamin E) good candidate for future use to minimize nicotine's hazards among smokers.


Assuntos
Sal Dissódico do Ácido 1,2-Di-Hidroxibenzeno-3,5 Dissulfônico/farmacologia , Antioxidantes/farmacologia , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle , Lesão Pulmonar/prevenção & controle , Nicotina/toxicidade , Animais , Anti-Inflamatórios não Esteroides/farmacologia , Peso Corporal/efeitos dos fármacos , Líquido da Lavagem Broncoalveolar/química , Contagem de Células , Doença Hepática Induzida por Substâncias e Drogas/etiologia , Doença Hepática Induzida por Substâncias e Drogas/mortalidade , Doença Hepática Induzida por Substâncias e Drogas/patologia , Enzimas/sangue , L-Lactato Desidrogenase/metabolismo , Lipídeos/sangue , Lesão Pulmonar/induzido quimicamente , Lesão Pulmonar/mortalidade , Lesão Pulmonar/patologia , Masculino , NADPH Oxidase 1/sangue , NADPH Oxidase 1/metabolismo , NF-kappa B/sangue , NF-kappa B/metabolismo , Óxido Nítrico Sintase Tipo II/metabolismo , Substâncias Protetoras/farmacologia , Ratos Sprague-Dawley
5.
J Am Heart Assoc ; 9(18): e017368, 2020 09 15.
Artigo em Inglês | MEDLINE | ID: mdl-32896206

RESUMO

E-cigarette or vaping product use-associated lung injury was recognized in the United States in the summer of 2019 and is typified by acute respiratory distress, shortness of breath, chest pain, cough, and fever, associated with vaping. It can mimic many of the manifestations of coronavirus disease 2019 (COVID-19). Some investigators have suggested that E-cigarette or vaping product use-associated lung injury was due to tetrahydrocannabinol or vitamin E acetate oil mixed with the electronic cigarette liquid. In experimental rodent studies initially designed to study the effect of electronic cigarette use on the cardiovascular system, we observed an E-cigarette or vaping product use-associated lung injury-like condition that occurred acutely after use of a nichrome heating element at high power, without the use of tetrahydrocannabinol, vitamin E, or nicotine. Lung lesions included thickening of the alveolar wall with foci of inflammation, red blood cell congestion, obliteration of alveolar spaces, and pneumonitis in some cases; bronchi showed accumulation of fibrin, inflammatory cells, and mucus plugs. Electronic cigarette users should be cautioned about the potential danger of operating electronic cigarette units at high settings; the possibility that certain heating elements may be deleterious; and that E-cigarette or vaping product use-associated lung injury may not be dependent upon tetrahydrocannabinol, vitamin E, or nicotine.


Assuntos
Dronabinol/toxicidade , Vapor do Cigarro Eletrônico/toxicidade , Sistemas Eletrônicos de Liberação de Nicotina , Lesão Pulmonar/induzido quimicamente , Pulmão/efeitos dos fármacos , Pneumonia/induzido quimicamente , Vaping/efeitos adversos , Vitamina E/toxicidade , Animais , Exposição por Inalação , Pulmão/patologia , Lesão Pulmonar/patologia , Modelos Animais , Óleos , Pneumonia/patologia , Ratos , Medição de Risco
6.
Orv Hetil ; 161(31): 1281-1285, 2020 08.
Artigo em Húngaro | MEDLINE | ID: mdl-32750017

RESUMO

The electronic cigarette and vaping associated lung injury (EVALI) syndrome was first described in the United States (US) and was presumably strongly associated with cannabinoid vaping and exposure to vitamin E acetate, an oily additive used to dilute/cut cannabinoids vape liquids. As the case numbers were relatively low (epidemiologically) and the available data was inconsistent, several assumptions were made to explain the phenomenon. The lack of standardization of sampling, the self-reported, inhomogeneous user habits, the huge number of potential etiologies, and certain trade/legal loopholes (such as online distribution, black market penetration, or the inefficient regulatory control regarding the quantity and/or quality of ingredients/cutting agents) might question the validity of the data and the consequent conclusions. Furthermore, an interesting but by no means negligible question is the fact why no EVALI cases have been registered outside the US when electronic cigarettes and vapes have become increasingly popular worldwide. The present review seeks to answer whether vitamin E acetate is indeed the cause of this complex syndrome, what potentially non-healthcare related factors might have contributed to the rapid increase and decline in EVALI cases, and last but not least the minimum standards of safe vaping (as potential for drug delivery route for cannbinoids). Orv Hetil. 2020; 161(31): 1281-1285.


Assuntos
Canabinoides/efeitos adversos , Sistemas Eletrônicos de Liberação de Nicotina , Lesão Pulmonar/induzido quimicamente , Vaping/efeitos adversos , Canabinoides/administração & dosagem , Humanos , Autorrelato , Estados Unidos , Vitamina E
7.
Nat Commun ; 11(1): 3559, 2020 07 16.
Artigo em Inglês | MEDLINE | ID: mdl-32678092

RESUMO

The cell type specific sequences of transcriptional programs during lung regeneration have remained elusive. Using time-series single cell RNA-seq of the bleomycin lung injury model, we resolved transcriptional dynamics for 28 cell types. Trajectory modeling together with lineage tracing revealed that airway and alveolar stem cells converge on a unique Krt8 + transitional stem cell state during alveolar regeneration. These cells have squamous morphology, feature p53 and NFkB activation and display transcriptional features of cellular senescence. The Krt8+ state appears in several independent models of lung injury and persists in human lung fibrosis, creating a distinct cell-cell communication network with mesenchyme and macrophages during repair. We generated a model of gene regulatory programs leading to Krt8+ transitional cells and their terminal differentiation to alveolar type-1 cells. We propose that in lung fibrosis, perturbed molecular checkpoints on the way to terminal differentiation can cause aberrant persistence of regenerative intermediate stem cell states.


Assuntos
Células Epiteliais Alveolares/metabolismo , Queratina-8/metabolismo , Alvéolos Pulmonares/fisiologia , Fibrose Pulmonar/patologia , Regeneração , Células-Tronco/metabolismo , Células Epiteliais Alveolares/citologia , Animais , Comunicação Celular , Modelos Animais de Doenças , Feminino , Perfilação da Expressão Gênica , Humanos , Queratina-8/genética , Lesão Pulmonar/induzido quimicamente , Lesão Pulmonar/metabolismo , Lesão Pulmonar/patologia , Camundongos , Camundongos Endogâmicos C57BL , Alvéolos Pulmonares/citologia , Fibrose Pulmonar/metabolismo , Análise de Célula Única , Células-Tronco/citologia
8.
Am J Physiol Lung Cell Mol Physiol ; 319(4): L585-L595, 2020 10 01.
Artigo em Inglês | MEDLINE | ID: mdl-32726146

RESUMO

In 2019, the United States experienced the emergence of the vaping-associated lung injury (VALI) epidemic. Vaping is now known to result in the development and progression of severe lung disease in the young and healthy. Lack of regulation on electronic cigarettes in the United States has resulted in over 2,000 patients and 68 deaths. We examine the clinical representation of VALI and the delve into the scientific evidence of how deadly exposure to electronic cigarettes can be. E-cigarette vapor is shown to affect numerous cellular processes, cellular metabolism, and cause DNA damage (which has implications for cancer). E-cigarette use is associated with a higher risk of developing crippling lung conditions such as chronic obstructive pulmonary disease (COPD), which would develop several years from now, increasing the already existent smoking-related burden. The role of vaping and virus susceptibility is yet to be determined; however, vaping can increase the virulence and inflammatory potential of several lung pathogens and is also linked to an increased risk of pneumonia. As it has emerged for cigarette smoking, great caution should also be given to vaping in relation to SARS-CoV-2 infection and the COVID-19 pandemic. Sadly, e-cigarettes are continually promoted and perceived as a safer alternative to cigarette smoking. E-cigarettes and their modifiable nature are harmful, as the lungs are not designed for the chronic inhalation of e-cigarette vapor. It is of interest that e-cigarettes have been shown to be of no help with smoking cessation. A true danger lies in vaping, which, if ignored, will lead to disastrous future costs.


Assuntos
Vapor do Cigarro Eletrônico/toxicidade , Doenças Pulmonares Intersticiais/epidemiologia , Lesão Pulmonar/epidemiologia , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Vaping/efeitos adversos , Adolescente , Betacoronavirus , Infecções por Coronavirus/patologia , Suscetibilidade a Doenças/induzido quimicamente , Sistemas Eletrônicos de Liberação de Nicotina/estatística & dados numéricos , Feminino , Humanos , Doenças Pulmonares Intersticiais/induzido quimicamente , Lesão Pulmonar/induzido quimicamente , Lesão Pulmonar/mortalidade , Masculino , Pessoa de Meia-Idade , Pandemias , Pneumonia/epidemiologia , Pneumonia Viral/patologia , Doença Pulmonar Obstrutiva Crônica/induzido quimicamente , Doença Pulmonar Obstrutiva Crônica/mortalidade , Abandono do Hábito de Fumar/métodos , Estados Unidos/epidemiologia , Vaping/epidemiologia , Vaping/mortalidade
10.
Am J Physiol Lung Cell Mol Physiol ; 318(6): L1198-L1210, 2020 06 01.
Artigo em Inglês | MEDLINE | ID: mdl-32320623

RESUMO

The pulmonary epithelial glycocalyx, an anionic cell surface layer enriched in glycosaminoglycans such as heparan sulfate and chondroitin sulfate, contributes to the alveolar barrier. Direct injury to the pulmonary epithelium induces shedding of heparan sulfate into the air space; the impact of this shedding on recovery after lung injury is unknown. Using mass spectrometry, we found that heparan sulfate was shed into the air space for up to 3 wk after intratracheal bleomycin-induced lung injury and coincided with induction of matrix metalloproteinases (MMPs), including MMP2. Delayed inhibition of metalloproteinases, beginning 7 days after bleomycin using the nonspecific MMP inhibitor doxycycline, attenuated heparan sulfate shedding and improved lung function, suggesting that heparan sulfate shedding may impair lung recovery. While we also observed an increase in air space heparanase activity after bleomycin, pharmacological and transgenic inhibition of heparanase in vivo failed to attenuate heparan sulfate shedding or protect against bleomycin-induced lung injury. However, experimental augmentation of airway heparanase activity significantly worsened post-bleomycin outcomes, confirming the importance of epithelial glycocalyx integrity to lung recovery. We hypothesized that MMP-associated heparan sulfate shedding contributed to delayed lung recovery, in part, by the release of large, highly sulfated fragments that sequestered lung-reparative growth factors such as hepatocyte growth factor. In vitro, heparan sulfate bound hepatocyte growth factor and attenuated growth factor signaling, suggesting that heparan sulfate shed into the air space after injury may directly impair lung repair. Accordingly, administration of exogenous heparan sulfate to mice after bleomycin injury increased the likelihood of death due to severe lung dysfunction. Together, our findings demonstrate that alveolar epithelial heparan sulfate shedding impedes lung recovery after bleomycin.


Assuntos
Heparitina Sulfato/metabolismo , Lesão Pulmonar/induzido quimicamente , Lesão Pulmonar/metabolismo , Alvéolos Pulmonares/metabolismo , Alvéolos Pulmonares/patologia , Animais , Bleomicina , Linhagem Celular , Glucuronidase/metabolismo , Heparitina Sulfato/administração & dosagem , Peptídeos e Proteínas de Sinalização Intercelular/metabolismo , Lesão Pulmonar/fisiopatologia , Metaloproteinases da Matriz/metabolismo , Camundongos Endogâmicos C57BL , Alvéolos Pulmonares/fisiopatologia , Testes de Função Respiratória , Mecânica Respiratória , Fatores de Risco , Transdução de Sinais , Regulação para Cima
11.
Am J Respir Crit Care Med ; 202(6): 795-802, 2020 09 15.
Artigo em Inglês | MEDLINE | ID: mdl-32243764

RESUMO

The NHLBI convened a working group on October 23, 2019, to identify the most relevant and urgent research priorities and prevailing challenges in e-cigarette or vaping product use-associated lung injury (EVALI). Experts across multiple disciplines discussed the complexities of the EVALI outbreak, identified research priorities, and recommended strategies to address most effectively its causal factors and improve diagnosis, treatment, and prevention of this disease. Many research priorities were identified, including the need to create national and international registries of patients with EVALI, to track accurately those affected and assess outcomes. The group concluded that biospecimens from subjects with EVALI are urgently needed to help define EVALI pathogenesis and that vaping has disease risks that are disparate from smoking, with the occurrence of EVALI highlighting the importance of broadening e-cigarette research beyond comparators to smoking-related diseases.


Assuntos
Sistemas Eletrônicos de Liberação de Nicotina , Lesão Pulmonar/induzido quimicamente , Lesão Pulmonar/epidemiologia , Lesão Pulmonar/terapia , Guias de Prática Clínica como Assunto , Terapia Respiratória/normas , Vaping/efeitos adversos , Adulto , Idoso , Idoso de 80 Anos ou mais , Congressos como Assunto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , National Heart, Lung, and Blood Institute (U.S.) , National Institutes of Health (U.S.) , Relatório de Pesquisa , Estados Unidos/epidemiologia
12.
Zhonghua Zhong Liu Za Zhi ; 42(4): 305-311, 2020 Apr 23.
Artigo em Chinês | MEDLINE | ID: covidwho-5530

RESUMO

Objective: To investigate the principles of differential diagnosis of pulmonary infiltrates in cancer patients during the outbreak of novel coronavirus (2019-nCoV) by analyzing one case of lymphoma who presented pulmonary ground-glass opacities (GGO) after courses of chemotherapy. Methods: Baseline demographics and clinicopathological data of eligible patients were retrieved from medical records. Information of clinical manifestations, history of epidemiology, lab tests and chest CT scan images of visiting patients from February 13 to February 28 were collected. Literatures about pulmonary infiltrates in cancer patients were searched from databases including PUBMED, EMBASE and CNKI. Results: Among the 139 cancer patients who underwent chest CT scans before chemotherapy, pulmonary infiltrates were identified in eight patients (5.8%), five of whom were characterized with GGOs in lungs. 2019-nCoV nuclear acid testing was performed in three patients and the results were negative. One case was a 66-year-old man who was diagnosed with non-Hodgkin lymphoma and underwent CHOP chemotherapy regimen. His chest CT scan image displayed multiple GGOs in lungs and the complete blood count showed decreased lymphocytes. This patient denied any contact with confirmed/suspected cases of 2019-nCoV infection, fever or other respiratory symptoms. Considering the negative result of nuclear acid testing, this patient was presumptively diagnosed with viral pneumonia and an experiential anti-infection treatment had been prescribed for him. Conclusions: The 2019 novel coronavirus disease (COVID-19) complicates the clinical scenario of pulmonary infiltrates in cancer patients. The epidemic history, clinical manifestation, CT scan image and lab test should be taken into combined consideration. The 2019-nCoV nuclear acid testing might be applied in more selected patients. Active anti-infection treatment and surveillance of patient condition should be initiated if infectious disease is considered.


Assuntos
Antineoplásicos/uso terapêutico , Infecções por Coronavirus/diagnóstico por imagem , Coronavirus , Lesão Pulmonar/induzido quimicamente , Lesão Pulmonar/diagnóstico por imagem , Pulmão/diagnóstico por imagem , Neoplasias/tratamento farmacológico , Pneumonia Viral/diagnóstico por imagem , Idoso , Antineoplásicos/efeitos adversos , Betacoronavirus , Coronavirus/patogenicidade , Infecções por Coronavirus/epidemiologia , Infecção Hospitalar/prevenção & controle , Diagnóstico Diferencial , Surtos de Doenças/prevenção & controle , Humanos , Masculino , Neoplasias/patologia , Pandemias , Pneumonia Viral/epidemiologia , Tomografia Computadorizada por Raios X
13.
Pediatr Pulmonol ; 55(5): 1224-1236, 2020 05.
Artigo em Inglês | MEDLINE | ID: mdl-32168438

RESUMO

Alongside the epidemic use of electronic cigarettes (e-cigarettes) across the country, evidence of multiple pulmonary complications has emerged, with the most immediately life-threatening being the new clinical condition of e-cigarette/vaping-associated lung injury (EVALI), with investigation actively underway to further define this entity and determine the cause or causes. We present a series of cases of respiratory illnesses associated with e-cigarette use, many of which meet criteria for suspected or confirmed EVALI, managed at a pediatric tertiary care center, demonstrating notable variation in presenting symptoms and severity. Most cases improved with supportive respiratory care and the administration of corticosteroids and antibiotics, although generally no infection was found. The cases also tend to show improvement with discontinuation of the use of e-cigarettes. We discuss challenges in determining the contribution of e-cigarettes to the case pathology and review possible diagnostic and treatment options. In patients suffering from e-cigarette-related respiratory illness including EVALI, the primary treatment goal should be the cessation of e-cigarette use and avoidance of other possible pulmonary toxins, including conventional cigarettes. Prevention of e-cigarette use is critical in the youth population, as these patients are typically nicotine naïve and do not engage in smoking conventional cigarettes before initiation of vaping.


Assuntos
Lesão Pulmonar/induzido quimicamente , Vaping/efeitos adversos , Adolescente , Corticosteroides/uso terapêutico , Adulto , Antibacterianos/uso terapêutico , Sistemas Eletrônicos de Liberação de Nicotina , Feminino , Humanos , Pulmão/diagnóstico por imagem , Lesão Pulmonar/diagnóstico por imagem , Lesão Pulmonar/terapia , Masculino , Tomografia Computadorizada por Raios X , Adulto Jovem
14.
Radiology ; 295(2): 430-438, 2020 05.
Artigo em Inglês | MEDLINE | ID: mdl-32125258

RESUMO

Background Electronic cigarette or vaping product use-associated lung injury (EVALI) is a serious public health concern with substantial morbidity and mortality, particularly in young individuals. Purpose To evaluate chest radiographic and chest CT findings of EVALI in the pediatric population. Materials and Methods This was a retrospective study of children who presented to a tertiary pediatric hospital from December 2018 to December 2019. Patients fulfilled the Centers for Disease Control and Prevention criteria for EVALI and had chest radiographs and CT images available at initial presentation. Two pediatric radiologists independently reviewed imaging for pattern, distribution, and extent of pulmonary abnormalities, as well as for extrapulmonary abnormalities. Clinical information, management, and outcomes were reviewed. Interobserver agreement was measured with Cohen κ coefficient. Results Seven male patients (50%) and seven female patients (50%) (mean age, 16 years; range, 13-18 years) were evaluated. All patients underwent chest radiography and CT within 4 days of presentation (range, 0-4 days). Chest radiographic findings included ground-glass opacity in 14 of 14 (100%) and consolidation in eight of 14 (57%). CT findings included ground-glass opacity in 14 of 14 (100%), consolidation in nine of 14 (64%), and interlobular septal thickening in two of 14 (14%). At CT, subpleural sparing was seen in 11 of 14 (79%) and a reversed halo sign was seen in five of 14 (36%). Chest radiographic and CT abnormalities were predominately bilateral in 14 of 14 (100%) and symmetric in 13 of 14 (93%), with lower lobe predominance in seven of 14 (50%). Extent of abnormality was predominately diffuse at both chest radiography and CT. There was almost perfect interobserver agreement between two reviewers for detecting abnormalities on chest radiographs (κ = 0.99; 95% confidence interval: 0.97, 1.00) and CT (κ = 0.99; 95% confidence interval: 0.98, 1.00). Conclusion In pediatric patients, electronic cigarette or vaping product use-associated lung injury is characterized by bilateral symmetric ground-glass opacities, consolidation, and a lower lobe predominance at CT. © RSNA, 2020.


Assuntos
Sistemas Eletrônicos de Liberação de Nicotina , Lesão Pulmonar/induzido quimicamente , Lesão Pulmonar/diagnóstico por imagem , Radiografia Torácica , Tomografia Computadorizada por Raios X , Vaping/efeitos adversos , Adolescente , Feminino , Humanos , Masculino , Estudos Retrospectivos , Estados Unidos
15.
Zhonghua Zhong Liu Za Zhi ; 42(4): 305-311, 2020 Apr 23.
Artigo em Chinês | MEDLINE | ID: mdl-32133833

RESUMO

Objective: To investigate the principles of differential diagnosis of pulmonary infiltrates in cancer patients during the outbreak of novel coronavirus (2019-nCoV) by analyzing one case of lymphoma who presented pulmonary ground-glass opacities (GGO) after courses of chemotherapy. Methods: Baseline demographics and clinicopathological data of eligible patients were retrieved from medical records. Information of clinical manifestations, history of epidemiology, lab tests and chest CT scan images of visiting patients from February 13 to February 28 were collected. Literatures about pulmonary infiltrates in cancer patients were searched from databases including PUBMED, EMBASE and CNKI. Results: Among the 139 cancer patients who underwent chest CT scans before chemotherapy, pulmonary infiltrates were identified in eight patients (5.8%), five of whom were characterized with GGOs in lungs. 2019-nCoV nuclear acid testing was performed in three patients and the results were negative. One case was a 66-year-old man who was diagnosed with non-Hodgkin lymphoma and underwent CHOP chemotherapy regimen. His chest CT scan image displayed multiple GGOs in lungs and the complete blood count showed decreased lymphocytes. This patient denied any contact with confirmed/suspected cases of 2019-nCoV infection, fever or other respiratory symptoms. Considering the negative result of nuclear acid testing, this patient was presumptively diagnosed with viral pneumonia and an experiential anti-infection treatment had been prescribed for him. Conclusions: The 2019 novel coronavirus disease (COVID-19) complicates the clinical scenario of pulmonary infiltrates in cancer patients. The epidemic history, clinical manifestation, CT scan image and lab test should be taken into combined consideration. The 2019-nCoV nuclear acid testing might be applied in more selected patients. Active anti-infection treatment and surveillance of patient condition should be initiated if infectious disease is considered.


Assuntos
Antineoplásicos/uso terapêutico , Infecções por Coronavirus/diagnóstico por imagem , Coronavirus , Lesão Pulmonar/induzido quimicamente , Lesão Pulmonar/diagnóstico por imagem , Pulmão/diagnóstico por imagem , Neoplasias/tratamento farmacológico , Pneumonia Viral/diagnóstico por imagem , Idoso , Antineoplásicos/efeitos adversos , Betacoronavirus , Coronavirus/patogenicidade , Infecções por Coronavirus/epidemiologia , Infecção Hospitalar/prevenção & controle , Diagnóstico Diferencial , Surtos de Doenças/prevenção & controle , Humanos , Masculino , Neoplasias/patologia , Pandemias , Pneumonia Viral/epidemiologia , Tomografia Computadorizada por Raios X
16.
Ecotoxicol Environ Saf ; 195: 110473, 2020 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-32199220

RESUMO

To investigate the effect of fermented black barley on cooking oil fume (COF)-induced lung injury, male ICR mice were randomized into five groups: normal control (NC), fermented black barley treatment (NF), COF exposure (O), COF + fermented black barley treatment (OF) and COF + Lactobacillus treatment (OL). The exposure of mice to COF was performed for 5 min per day and 4 days per week for a total of 9 weeks, and the mice in the OF, NF and OL groups were administered fermented black barley or Lactobacillus continuously for 9 weeks (1 mL/100 g). Our results showed that the gamma-aminobutyric acid (GABA), total phenolic, and flavonoid contents significantly increased after fermentation (P < 0.01). In addition, fermented black barley significantly increased SOD activity in the lung tissue, decreased the wet pulmonary coefficient, inhibited the reduction of microbial diversity and richness, and upregulated genes involved in cilium assembly and the cilium axoneme. These findings support the notion that fermented black barley can ameliorate COF-induced lung injury in mice.


Assuntos
Poluentes Atmosféricos/toxicidade , Microbioma Gastrointestinal , Hordeum , Lesão Pulmonar/terapia , Animais , Antioxidantes/química , Antioxidantes/metabolismo , Cílios/metabolismo , Culinária , Fermentação , Flavonoides/metabolismo , Hordeum/química , Hordeum/metabolismo , Lactobacillus , Pulmão/enzimologia , Lesão Pulmonar/induzido quimicamente , Lesão Pulmonar/enzimologia , Lesão Pulmonar/microbiologia , Masculino , Camundongos Endogâmicos ICR , Fenóis/metabolismo , Superóxido Dismutase/metabolismo , Ácido gama-Aminobutírico/metabolismo
17.
Proc Natl Acad Sci U S A ; 117(12): 6349-6355, 2020 03 24.
Artigo em Inglês | MEDLINE | ID: mdl-32156732

RESUMO

A combined analytical, theoretical, and experimental study has shown that the vaping of vitamin E acetate has the potential to produce exceptionally toxic ketene gas, which may be a contributing factor to the upsurge in pulmonary injuries associated with using e-cigarette/vaping products. Additionally, the pyrolysis of vitamin E acetate also produces carcinogen alkenes and benzene for which the negative long-term medical effects are well recognized. As temperatures reached in vaping devices can be equivalent to a laboratory pyrolysis apparatus, the potential for unexpected chemistries to take place on individual components within a vape mixture is high. Educational programs to inform of the danger are now required, as public perception has grown that vaping is not harmful.


Assuntos
Etilenos/análise , Cetonas/análise , Lesão Pulmonar , Vaping , Vitamina E/química , Acetatos/análise , Acetatos/química , Sistemas Eletrônicos de Liberação de Nicotina , Etilenos/toxicidade , Cetonas/toxicidade , Lesão Pulmonar/induzido quimicamente , Estrutura Molecular , Fenóis/análise , Fenóis/química , Pirólise , Vaping/efeitos adversos , Vitamina E/análise
18.
Orv Hetil ; 161(11): 413-418, 2020 Mar.
Artigo em Húngaro | MEDLINE | ID: mdl-32148093

RESUMO

Over 1000 respiratory cases have been linked to vaping at the Centers for Disease Control and Prevention (Atlanta, GA, USA). So far at least 800 cases were confirmed as vaping-associated lung injuries (VALI) with 18 patients succumbing to the illness. To our present knowledge, vape fluids may contain certain compounds with toxic properties. It is not yet understood though what component or components are responsible for the cluster of cases. However, federal and state investigators are focusing on vape cartridges that likely contained cannabinoids as most patients vaped legal or illegal cannabinoids. Until recently, USA and UK public health authorities have welcomed vaping as a safer alternative to smoking. In countries where cannabis has been legalised, vaporizers became an increasingly popular form of administration, however, no human studies have been performed with vaporized cannabinoid oils, hence the safety of such device is unknown. A 2018 review concluded that although vaping might not necessarily be safe, it is still preferable for both patients and their environment to smoking cannabis. Since 2015, Hungarian, Australian and European scientific bodies have called for ban on the unregulated e-cigarettes, but encouraged future research to understand all aspects of vaping cannabinoids. Should vaping itself prove harmless, it might open new avenues for research and potential administration of medical cannabis, however, the contrary may cause landslide in the tobacco industry. Orv Hetil. 2020; 161(11): 413-418.


Assuntos
Canabinoides/efeitos adversos , Sistemas Eletrônicos de Liberação de Nicotina , Lesão Pulmonar/induzido quimicamente , Vaping/efeitos adversos , Austrália , Canabinoides/administração & dosagem , Humanos , Fumar Maconha
19.
Nat Commun ; 11(1): 1064, 2020 02 28.
Artigo em Inglês | MEDLINE | ID: mdl-32111836

RESUMO

Idiopathic pulmonary fibrosis (IPF) is a fatal and incurable form of interstitial lung disease in which persistent injury results in scar tissue formation. As fibrosis thickens, the lung tissue loses the ability to facilitate gas exchange and provide cells with needed oxygen. Currently, IPF has few treatment options and no effective therapies, aside from lung transplant. Here we present a series of studies utilizing lung spheroid cell-secretome (LSC-Sec) and exosomes (LSC-Exo) by inhalation to treat different models of lung injury and fibrosis. Analysis reveals that LSC-Sec and LSC-Exo treatments could attenuate and resolve bleomycin- and silica-induced fibrosis by reestablishing normal alveolar structure and decreasing both collagen accumulation and myofibroblast proliferation. Additionally, LSC-Sec and LSC-Exo exhibit superior therapeutic benefits than their counterparts derived from mesenchymal stem cells in some measures. We showed that an inhalation treatment of secretome and exosome exhibited therapeutic potential for lung regeneration in two experimental models of pulmonary fibrosis.


Assuntos
Exossomos/transplante , Fibrose Pulmonar Idiopática/terapia , Lesão Pulmonar/terapia , Pulmão/citologia , Esferoides Celulares/metabolismo , Administração por Inalação , Células Epiteliais Alveolares/efeitos dos fármacos , Células Epiteliais Alveolares/metabolismo , Células Epiteliais Alveolares/patologia , Animais , Apoptose/efeitos dos fármacos , Bleomicina/toxicidade , Proliferação de Células , Modelos Animais de Doenças , Exossomos/metabolismo , Humanos , Fibrose Pulmonar Idiopática/induzido quimicamente , Fibrose Pulmonar Idiopática/metabolismo , Fibrose Pulmonar Idiopática/patologia , Pulmão/metabolismo , Lesão Pulmonar/induzido quimicamente , Lesão Pulmonar/metabolismo , Lesão Pulmonar/patologia , Células-Tronco Mesenquimais/metabolismo , Camundongos , Miofibroblastos/citologia , Proteômica , Dióxido de Silício/toxicidade
20.
Int J Mol Sci ; 21(3)2020 Jan 30.
Artigo em Inglês | MEDLINE | ID: mdl-32019239

RESUMO

Acute pancreatitis is an inflammatory disorder of the pancreas. Its presentation ranges from self-limiting disease to acute necrotizing pancreatitis (ANP) with multiorgan failure and a high mortality. Polyethylene glycols (PEGs) are non-immunogenic, non-toxic, and water-soluble chemicals composed of repeating units of ethylene glycol. The present article explores the effect of PEG35 administration on reducing the severity of ANP and associated lung injury. ANP was induced by injection of 5% sodium taurocholate into the biliopancreatic duct. PEG35 was administered intravenously either prophylactically or therapeutically. Three hours after ANP induction, pancreas and lung tissue samples and blood were collected and ANP severity was assessed. To evaluate the inflammatory response, gene expression of pro-inflammatory cytokines and chemokine and the changes in the presence of myeloperoxidase and adhesion molecule levels were determined in both the pancreas and the lung. To evaluate cell death, lactate dehydrogenase (LDH) activity and apoptotic cleaved caspase-3 localization were determined in plasma and in both the pancreatic and lung tissue respectively. ANP-associated local and systemic inflammatory processes were reduced when PEG35 was administered prophylactically. PEG35 pre-treatment also protected against acute pancreatitis-associated cell death. Notably, the therapeutic administration of PEG35 significantly decreased associated lung injury, even when the pancreatic lesion was equivalent to that in the untreated ANP-induced group. Our results support a protective role of PEG35 against the ANP-associated inflammatory process and identify PEG35 as a promising tool for the treatment of the potentially lethal complications of the disease.


Assuntos
Inflamação/prevenção & controle , Lesão Pulmonar/tratamento farmacológico , Pancreatite Necrosante Aguda/tratamento farmacológico , Polietilenoglicóis/farmacologia , Ácido Taurocólico/toxicidade , Animais , Colagogos e Coleréticos/toxicidade , Inflamação/etiologia , Inflamação/patologia , Interleucina-6/metabolismo , Lesão Pulmonar/induzido quimicamente , Lesão Pulmonar/patologia , Masculino , Pancreatite Necrosante Aguda/induzido quimicamente , Pancreatite Necrosante Aguda/patologia , Ratos , Ratos Wistar , Fator de Necrose Tumoral alfa/metabolismo
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