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1.
PLoS One ; 15(8): e0236988, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32764771

RESUMO

Exposure to secondhand cigarette smoke is associated with the development of diverse diseases. Resistance training has been considered one of the most useful tools for patients with pulmonary disease, improving their quality of life. This study aimed to evaluate the effect of resistance training (RT) on the prevention of thickening of the right ventricle wall of rats exposed to secondhand cigarette smoke. Thirty-two Wistar rats were divided into four groups: Control (C), Smoker (S), Exercised (E) and Exercised Smoker (ES). The smoker groups were exposed to the smoke of four cigarettes for 30 min, twice daily, five days a week, for 16 weeks. The exercised groups climbed on a vertical ladder with progressive load, once a day, five days a week, for 16 weeks. The heart, trachea, lung, liver and gastrocnemius muscle were removed for histopathological analysis. Pulmonary emphysema (S and ES vs C and E, P < 0.0001) and pulmonary artery thickness enlargement (S vs C and E, P = 0.003, ES vs C, P = 0.003) were detected in the smoking groups. There was an increase in the right ventricle thickness in the S group compared with all other groups (P < 0.0001). An increase in resident macrophages in the liver was detected in both smoking groups compared with the C group (P = 0.002). Additionally, a relevant reduction of the diameter of the muscle fibers was detected only in ES compared with the C, S and E groups (P = 0.0002), impairing, at least in part, the muscle mass in exercised smoking rats. Therefore, it was concluded that resistance training prevented the increase of thickness of the right ventricle in rats exposed to secondhand cigarette smoke, but it may be not so beneficial for the skeletal muscle of smoking rats.


Assuntos
Fumar Cigarros/efeitos adversos , Hipertrofia Ventricular Direita/prevenção & controle , Condicionamento Físico Animal/métodos , Poluição por Fumaça de Tabaco/efeitos adversos , Animais , Fumar Cigarros/patologia , Fumar Cigarros/fisiopatologia , Modelos Animais de Doenças , Humanos , Hipertrofia Ventricular Direita/patologia , Hipertrofia Ventricular Direita/fisiopatologia , Masculino , Músculo Esquelético/patologia , Artéria Pulmonar/fisiologia , Enfisema Pulmonar/etiologia , Enfisema Pulmonar/patologia , Enfisema Pulmonar/fisiopatologia , Ratos , Ratos Wistar , Treinamento de Resistência
2.
PLoS One ; 15(8): e0238107, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32834016

RESUMO

BACKGROUND: In CT-guided transthoracic lung biopsy (CTLB), pneumothorax can occur as a late complication (delayed pneumothorax). The incidence, risk factors, and clinical significance of delayed pneumothorax are not well known. OBJECTIVES: To compare the risk factors for immediate and delayed pneumothorax after CTLB and to know their clinical significance. METHODS: Images and medical records of 536 consecutive patients who underwent CTLB were reviewed. All biopsies were performed as inpatient procedures. Follow-up chest radiographs were obtained at least twice at 4 h after procedure and before discharge. Risk factors for immediate and delayed pneumothorax were assessed based on patient-, lesion-, and procedure-related variables. Rates of chest tube insertion were also compared. RESULTS: Pneumothorax developed in 161 patients (30.0%) including 135 (25.2%) immediate and 26 (4.9%) delayed cases. Lesion size was an independent risk factor for both immediate and delayed pneumothorax (OR = 0.813; CI = 0.717-0.922 and OR = 0.610; CI = 0.441-0.844, respectively). While emphysema, lower lobe location, and long intrapulmonary biopsy track were risk factors (OR = 1.981; CI = 1.172-3.344, OR = 3.505; CI = 2.718-5.650, and OR = 1.330; CI = 1.132-1.563, respectively) for immediate pneumothorax, upper lobe location and increased number of pleural punctures were independent risk factors (OR = 5.756; CI = 1.634-20.274 and OR = 3.738; CI = 1.860-7.511, respectively) for delayed pneumothorax. The rate of chest tube insertion was significantly (p < 0.001) higher in delayed pneumothorax. CONCLUSION: Pneumothorax tends to occur immediately after CTLB in patients with emphysema, lower lobe lesion, and long intrapulmonary biopsy track. Further attention and warnings are needed for those with multiple punctures of small lesions involving upper lobes due to the possibility of delayed development of pneumothorax and higher requirement for chest tube drainage.


Assuntos
Biópsia Guiada por Imagem/efeitos adversos , Pneumotórax/etiologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Biópsia por Agulha/métodos , Tubos Torácicos , Enfisema/patologia , Feminino , Humanos , Incidência , Pulmão/patologia , Masculino , Pessoa de Meia-Idade , Paracentese/efeitos adversos , Enfisema Pulmonar/patologia , Punções/efeitos adversos , Radiografia Intervencionista/efeitos adversos , Estudos Retrospectivos , Fatores de Risco , Tórax , Tomografia Computadorizada por Raios X/efeitos adversos , Tomografia Computadorizada por Raios X/métodos
3.
Sci Rep ; 10(1): 10949, 2020 07 02.
Artigo em Inglês | MEDLINE | ID: mdl-32616814

RESUMO

Marfan syndrome (MFS) is a heritable disorder of connective tissue, caused by mutations in the fibrillin-1 gene. Pulmonary functional abnormalities, such as emphysema and restrictive lung diseases, are frequently observed in patients with MFS. However, the pathogenesis and molecular mechanism of pulmonary involvement in MFS patients are underexplored. Notch signaling is essential for lung development and the airway epithelium regeneration and repair. Therefore, we investigated whether Notch3 signaling plays a role in pulmonary emphysema in MFS. By using a murine model of MFS, fibrillin-1 hypomorphic mgR mice, we found pulmonary emphysematous-appearing alveolar patterns in the lungs of mgR mice. The septation in terminal alveoli of lungs in mgR mice was reduced compared to wild type controls in the early lung development. These changes were associated with increased Notch3 activation. To confirm that the increased Notch3 signaling in mgR mice was responsible for structure alterations in the lungs, mice were treated with N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglucine t-butyl ester (DAPT), a γ-secretase inhibitor, which inhibits Notch signaling. DAPT treatment reduced lung cell apoptosis and attenuated pulmonary alteration in mice with MFS. This study indicates that Notch3 signaling contributes to pulmonary emphysema in mgR mice. Our results may have the potential to lead to novel strategies to prevent and treat pulmonary manifestations in patients with MFS.


Assuntos
Modelos Animais de Doenças , Síndrome de Marfan/complicações , Enfisema Pulmonar/patologia , Receptor Notch3/metabolismo , Animais , Feminino , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Enfisema Pulmonar/etiologia , Enfisema Pulmonar/metabolismo , Receptor Notch3/genética
4.
Am J Respir Crit Care Med ; 202(7): 983-995, 2020 10 01.
Artigo em Inglês | MEDLINE | ID: mdl-32515984

RESUMO

Rationale: Endothelial injury may provoke emphysema, but molecular pathways of disease development require further discernment. Emphysematous lungs exhibit decreased expression of HIF-2α (hypoxia-inducible factor-2α)-regulated genes, and tobacco smoke decreases pulmonary HIF-2α concentrations. These findings suggest that decreased HIF-2α expression is important in the development of emphysema.Objectives: The objective of this study was to evaluate the roles of endothelial-cell (EC) HIF-2α in the pathogenesis of emphysema in mice.Methods: Mouse lungs were examined for emphysema after either the loss or the overexpression of EC Hif-2α. In addition, SU5416, a VEGFR2 inhibitor, was used to induce emphysema. Lungs were evaluated for HGF (hepatocyte growth factor), a protein involved in alveolar development and homeostasis. Lungs from patients with emphysema were measured for endothelial HIF-2α expression.Measurements and Main Results: EC Hif-2α deletion resulted in emphysema in association with fewer ECs and pericytes. After SU5416 exposure, EC Hif-2α-knockout mice developed more severe emphysema, whereas EC Hif-2α-overexpressing mice were protected. EC Hif-2α-knockout mice demonstrated lower levels of HGF. Human emphysema lung samples exhibited reduced EC HIF-2α expression.Conclusions: Here, we demonstrate a unique protective role for pulmonary endothelial HIF-2α and how decreased expression of this endogenous factor causes emphysema; its pivotal protective function is suggested by its ability to overcome VEGF antagonism. HIF-2α may maintain alveolar architecture by promoting vascular survival and associated HGF production. In summary, HIF-2α may be a key endogenous factor that prevents the development of emphysema, and its upregulation has the potential to foster lung health in at-risk patients.


Assuntos
Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética , Células Endoteliais/metabolismo , Subunidade alfa do Fator 1 Induzível por Hipóxia/genética , Pulmão/metabolismo , Enfisema Pulmonar/genética , Inibidores da Angiogênese/toxicidade , Animais , Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo , Desferroxamina/farmacologia , Modelos Animais de Doenças , Células Endoteliais/patologia , Fator de Crescimento de Hepatócito/genética , Fator de Crescimento de Hepatócito/metabolismo , Humanos , Indóis/toxicidade , Quelantes de Ferro/farmacologia , Pulmão/irrigação sanguínea , Pulmão/citologia , Pulmão/efeitos dos fármacos , Camundongos , Camundongos Knockout , Microvasos , Pericitos/metabolismo , Circulação Pulmonar , Doença Pulmonar Obstrutiva Crônica/metabolismo , Enfisema Pulmonar/induzido quimicamente , Enfisema Pulmonar/metabolismo , Enfisema Pulmonar/patologia , Pirróis/toxicidade , Fumaça/efeitos adversos
5.
Am J Physiol Lung Cell Mol Physiol ; 318(6): L1222-L1228, 2020 06 01.
Artigo em Inglês | MEDLINE | ID: mdl-32320267

RESUMO

Parametric response mapping (PRM) is a computed tomography (CT)-based method to phenotype patients with chronic obstructive pulmonary disease (COPD). It is capable of differentiating emphysema-related air trapping with nonemphysematous air trapping (small airway disease), which helps to identify the extent and localization of the disease. Most studies evaluating the gene expression in smokers and COPD patients related this to spirometric measurements, but none have investigated the relationship with CT-based measurements of lung structure. The current study aimed to examine gene expression profiles of brushed bronchial epithelial cells in association with the PRM-defined CT-based measurements of emphysema (PRMEmph) and small airway disease (PRMfSAD). Using the Top Institute Pharma (TIP) study cohort (COPD = 12 and asymptomatic smokers = 32), we identified a gene expression signature of bronchial brushings, which was associated with PRMEmph in the lungs. One hundred thirty-three genes were identified to be associated with PRMEmph. Among the most significantly associated genes, CXCL11 is a potent chemokine involved with CD8+ T cell activation during inflammation in COPD, indicating that it may play an essential role in the development of emphysema. The PRMEmph signature was then replicated in two independent data sets. Pathway analysis showed that the PRMEmph signature is associated with proinflammatory and notch signaling pathways. Together these findings indicate that airway epithelium may play a role in the development of emphysema and/or may act as a biomarker for the presence of emphysema. In contrast, its role in relation to functional small airways disease is less clear.


Assuntos
Brônquios/diagnóstico por imagem , Brônquios/patologia , Perfilação da Expressão Gênica , Processamento de Imagem Assistida por Computador , Enfisema Pulmonar/diagnóstico por imagem , Tomografia Computadorizada por Raios X , Idoso , Brônquios/fisiopatologia , Feminino , Volume Expiratório Forçado , Regulação da Expressão Gênica , Humanos , Masculino , Pessoa de Meia-Idade , Doença Pulmonar Obstrutiva Crônica/diagnóstico por imagem , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Enfisema Pulmonar/patologia , Enfisema Pulmonar/fisiopatologia
6.
Am J Respir Cell Mol Biol ; 63(3): 293-305, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32338993

RESUMO

Chronic exposure to cigarette smoke (CS) causes chronic inflammation, oxidative stress, and apoptosis of epithelial cells, which results in destruction of the lung matrix. However, the mechanism by which the lung fails to repair the CS-induced damage, thereby succumbing to emphysema, remains unclear. Alveolar type 2 (AT2) cells comprise the stem cells of the alveolar compartments and are responsible for repairing and maintaining lung tissues. In this study, we examined the effect of chronic CS on AT2 stem cells. Adult mice expressing GFP in their AT2 cells were exposed to CS for > 3 months. Histological assessment showed that CS not only induced emphysematous changes but also increased the number of AT2 cells compared with that of air-exposed lungs. Assessment of sorted GFP+/AT2 cells via the stem cell three-dimensional organoid/colony-forming assay revealed that the number and size of the colonies formed by the CS-exposed AT2 stem cells were significantly higher than those of air-exposed control AT2 cells. Although CS-exposed lungs had more apoptotic cells, examination of the surviving AT2 stem cells in two-dimensional in vitro culture revealed that they developed a higher ability to resist apoptosis. Microarray analysis of CS-exposed AT2 stem cells revealed the upregulation of genes related to circadian rhythm and inflammatory pathways. In conclusion, we provide evidence that AT2 stem cells respond to chronic CS exposure by activating their stem cell function, thereby proliferating and differentiating faster and becoming more resistant to apoptosis. Disturbances in expression levels of several circadian rhythm-related genes might be involved in these changes.


Assuntos
Células Epiteliais Alveolares/efeitos dos fármacos , Enfisema Pulmonar/patologia , Fumaça/efeitos adversos , Tabaco/toxicidade , Células Epiteliais Alveolares/metabolismo , Células Epiteliais Alveolares/patologia , Animais , Apoptose/efeitos dos fármacos , Pulmão/patologia , Camundongos Endogâmicos C57BL , Estresse Oxidativo/efeitos dos fármacos , Doença Pulmonar Obstrutiva Crônica/patologia , Fumar
7.
Am J Physiol Lung Cell Mol Physiol ; 318(6): L1172-L1182, 2020 06 01.
Artigo em Inglês | MEDLINE | ID: mdl-32130031

RESUMO

Pulmonary emphysema is a major manifestation of chronic obstructive pulmonary disease and is associated with chronic pulmonary inflammation caused by cigarette smoking, with contributions from immune cells such as neutrophils, macrophages, and lymphocytes. Although matrix metalloproteinases are well known to contribute to emphysema progression, the role of a disintegrin and metalloproteinase (ADAM) family proteins, other major metalloproteinases, in disease pathogenesis is largely unknown. ADAM17 is a major sheddase that cleaves various cell surface proteins, including CD62L, an adhesion molecule that plays a critical role in promoting the migration of immune cells to the site of inflammation. In the present study, we aimed to investigate the potential role of ADAM17 and CD62L in the development of elastase-induced emphysema. Control and Adam17flox/flox/Mx1-Cre (Adam17ΔMx1) mice (8-10 wk old) were intratracheally injected with 5 units of porcine pancreas elastase and monitored for 35 days after injection. Lung alveolar destruction was evaluated by analyzing the mean linear intercepts of lung tissue specimens and by histopathological examination. Mean linear intercepts data indicated that the degree of elastase-induced emphysema was significantly more severe in Adam17ΔMx1 mice. Furthermore, flow cytometry showed that CD62L+ neutrophil, CD62L+ macrophage, and CD62L+ B lymphocyte numbers were significantly increased in Adam17ΔMx1 mice. Moreover, the pharmacological depletion of CD62L+ cells with a CD62L-neutralizing antibody ameliorated the extent of emphysema in Adam17ΔMx1 mice. Collectively, these results suggest that ADAM17 possibly suppresses the progression of emphysema by proteolytically processing CD62L in immune cells and that ADAM17 and CD62L could be novel therapeutic targets for treating pulmonary emphysema.


Assuntos
Proteína ADAM17/metabolismo , Selectina L/metabolismo , Leucócitos/metabolismo , Enfisema Pulmonar/induzido quimicamente , Enfisema Pulmonar/imunologia , Animais , Antioxidantes/metabolismo , Apoptose , Líquido da Lavagem Broncoalveolar , Contagem de Células , Quimiocinas/metabolismo , Células Epiteliais/metabolismo , Regulação da Expressão Gênica , Pulmão/patologia , Macrófagos/patologia , Metaloproteinase 12 da Matriz/metabolismo , Camundongos Endogâmicos C57BL , Testes de Neutralização , Oxidantes/metabolismo , Elastase Pancreática , Enfisema Pulmonar/genética , Enfisema Pulmonar/patologia
8.
Artif Cells Nanomed Biotechnol ; 48(1): 656-663, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-32070140

RESUMO

Smoking is an important factor in the pathogenesis of chronic obstructive pulmonary disease (COPD), which is commonly characterised by cellular senescence and inflammation. Recently, miR-200b has emerged as an important target to cure lung disease; however, the function of miR-200b in reducing cellular senescence and inflammatory responses has not been reported. In this study, we found that miR-200b was downregulated in the lungs of COPD model mice, and its expression is correlated with cellular senescence and inflammatory responses. We hypothesised that miR-200b may be a potential novel therapy for treating COPD. We performed senescence-Associated-ß-galactosidase (SA-ß-GAL) staining, western blot, qRT-PCR and ELISA; our data suggested that miR-200b is an anti-aging factor in the lungs that is involved in inflammatory responses. We also confirmed that ZEB2 (Zinc finger E-box binding homeobox 2) is a target gene of miR-200b using luciferase reporter assay. In addition, we verified the function of ZEB2 in cellular senescence and inflammatory responses through transfection experiments. Moreover, we found that the protective effects of miR-200b are inhibited when cells overexpress the ZEB2 protein. In conclusion, our results suggest that miR-200b may attenuate cellular senescence and inflammatory responses by targeting ZEB2 in pulmonary emphysema.


Assuntos
Senescência Celular/genética , Inflamação/genética , MicroRNAs/genética , Enfisema Pulmonar/patologia , Homeobox 2 de Ligação a E-box com Dedos de Zinco/genética , Animais , Linhagem Celular , Modelos Animais de Doenças , Expressão Gênica , Regulação da Expressão Gênica , Pulmão/metabolismo , Pulmão/patologia , Camundongos , Enfisema Pulmonar/genética , Homeobox 2 de Ligação a E-box com Dedos de Zinco/metabolismo
9.
Surg Pathol Clin ; 13(1): 141-163, 2020 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-32005429

RESUMO

Cystic diseases of the lung encompass a fairly broad variety of different diseases with causes including genetic abnormalities, smoking-related problems, developmental disorders, malignant neoplasms, and inflammatory processes. In addition, there are several diagnoses that closely resemble cystic lung disease, including cavitary diseases, cystic bronchiectasis, emphysema, and cystic changes in fibrosing interstitial lung disease. This article provides a review of cystic lung disease and its gross and histologic mimics.


Assuntos
Pneumopatias/patologia , Síndrome de Birt-Hogg-Dubé/diagnóstico , Síndrome de Birt-Hogg-Dubé/patologia , Bronquiectasia/diagnóstico , Bronquiectasia/patologia , Diagnóstico Diferencial , Histiocitose de Células de Langerhans/diagnóstico , Histiocitose de Células de Langerhans/patologia , Humanos , Pneumonias Intersticiais Idiopáticas/diagnóstico , Pneumonias Intersticiais Idiopáticas/patologia , Pulmão/patologia , Pneumopatias/diagnóstico , Neoplasias Pulmonares/secundário , Linfangioleiomiomatose/diagnóstico , Linfangioleiomiomatose/patologia , Infecções por Papillomavirus/diagnóstico , Infecções por Papillomavirus/patologia , Enfisema Pulmonar/diagnóstico , Enfisema Pulmonar/patologia , Infecções Respiratórias/diagnóstico , Infecções Respiratórias/patologia
10.
Am J Respir Cell Mol Biol ; 63(1): 67-78, 2020 07.
Artigo em Inglês | MEDLINE | ID: mdl-32101459

RESUMO

Epithelial dysfunction in the small airways may cause the development of emphysema in chronic obstructive pulmonary disease. C/EBPα (CCAAT/enhancer binding protein-α), a transcription factor, is required for lung maturation during development, and is also important for lung homeostasis after birth, including the maintenance of serine protease/antiprotease balance in the bronchiolar epithelium. This study aimed to show the roles of C/EBPα in the distal airway during chronic cigarette smoke exposure in mice and in the small airways in smokers. In a model of chronic smoke exposure using epithelial cell-specific C/EBPα-knockout mice, significant pathological phenotypes, such as higher protease activity, impaired ciliated cell regeneration, epithelial cell barrier dysfunction via reduced zonula occludens-1 (Zo-1), and decreased alveolar attachments, were found in C/EBPα-knockout mice compared with control mice. We found that Spink5 (serine protease inhibitor kazal-type 5) gene (encoding lymphoepithelial Kazal-type-related inhibitor [LEKTI], an anti-serine protease) expression in the small airways is a key regulator of protease activity in this model. Finally, we showed that daily antiprotease treatment counteracted the phenotypes of C/EBPα-knockout mice. In human studies, CEBPA (CCAAT/enhancer binding protein-α) gene expression in the lung was downregulated in patients with emphysema, and six smokers with centrilobular emphysema (CLE) showed a significant reduction in LEKTI in the small airways compared with 22 smokers without CLE. LEKTI downregulation in the small airways was associated with disease development during murine small airway injury and CLE in humans, suggesting that LEKTI might be a key factor linking small airway injury to the development of emphysema.


Assuntos
Pulmão/metabolismo , Pulmão/patologia , Doença Pulmonar Obstrutiva Crônica/metabolismo , Doença Pulmonar Obstrutiva Crônica/patologia , Enfisema Pulmonar/metabolismo , Enfisema Pulmonar/patologia , Serina Proteases/metabolismo , Animais , Bronquíolos/metabolismo , Bronquíolos/patologia , Proteínas Estimuladoras de Ligação a CCAAT/metabolismo , Humanos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Camundongos Transgênicos , Inibidor de Serinopeptidase do Tipo Kazal 5/metabolismo , Fumar/metabolismo
11.
Zhonghua Er Ke Za Zhi ; 58(1): 19-24, 2020 Jan 02.
Artigo em Chinês | MEDLINE | ID: mdl-31905471

RESUMO

Objective: To summarize the diagnosis, clinical manifestations, treatment and prognosis of congenital cystic lung lesions. Methods: A retrospective study described the clinical course of 96 patients (46 female and 50 male) diagnosed with congenital cystic lung lesions treated at the Tianjin Children's Hospital from January 2010 to March 2019. The clinical findings, imaging examinations, pathological findings, treatment and follow-up were analyzed. Results: Totally 96 patients (aged from 4 days to 13 years) with congenital cystic lung lesions were included in this study. Eighty-six patients (90%) were diagnosed when they had cough and fever symptoms. Forty (42%) patients exhibited congenital cystic adenomatoid malformation, 30 underwent surgical excision, two were at emergency operations and one dead. There were 12 (13%) patients with pulmonary sequestration and four were surgical treated. Twelve (13%) patients with bronchogenic cyst were included and 4 were surgically treated. There were 3 (3%) patients with congenital lobar emphysema and one was surgically treated. Another patient with pneumothorax was operated in other hospital 2 months after discharge. Twenty-nine (30%) patients with unclassified congenital cystic lung lesions could not be definitively diagnosed by CT. Some of them were difficult to be distinguished from necrotizing pneumonia. Finally, 2 patients were diagnosed as necrotizing pneumonia after 6, 10 months follow-up. After operation 37 out of 39 patients recovered well. Conclusions: The diagnosis of congenital pulmonary cystic disease depend on imaging and pathological examination. Most patients are diagnosed when they have respiratory tract infection. The main clinical manifestations are cough and fever. The prognosis of operative management is good.


Assuntos
Cisto Broncogênico/diagnóstico , Cisto Broncogênico/cirurgia , Malformação Adenomatoide Cística Congênita do Pulmão/diagnóstico , Enfisema Pulmonar/patologia , Adolescente , Cisto Broncogênico/congênito , Sequestro Broncopulmonar/diagnóstico , Sequestro Broncopulmonar/cirurgia , Criança , Pré-Escolar , Malformação Adenomatoide Cística Congênita do Pulmão/cirurgia , Feminino , Humanos , Lactente , Masculino , Pneumonectomia , Enfisema Pulmonar/cirurgia , Estudos Retrospectivos , Resultado do Tratamento
12.
J Pak Med Assoc ; 70(1): 197-199, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31954057

RESUMO

Congenital Lobar Hyperinflation is an overinflation of one or more than one lobes of the lung and is caused by an abnormal development of broncho-pulmonary segment. We report a case of a 2-month-old female who presentedin outpatient department with complaints of fever, cough and difficulty in breathing. This case was seen in January, 2018. Congenital Lobar Hyperinflation was diagnosed on chest x-rays and Computed Tomography (CT ) scan. Immediate surgical excision (lobectomy) of the affected lobe was conducted.


Assuntos
Enfisema Pulmonar , Erros de Diagnóstico , Feminino , Cardiopatias Congênitas , Humanos , Lactente , Pulmão/diagnóstico por imagem , Pulmão/patologia , Pulmão/cirurgia , Enfisema Pulmonar/diagnóstico , Enfisema Pulmonar/patologia , Enfisema Pulmonar/cirurgia
13.
Bull Exp Biol Med ; 168(3): 334-340, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31940128

RESUMO

The changes in endothelial progenitor cells and progenitor cells of angiogenesis, pericytes and smooth muscle cells, were studied in female C57BL/6 mice with a combination of metabolic impairments induced by injections of sodium glutamate and lung emphysema modeled by the administration of cigarette smoke extract. It was observed that sodium glutamate significantly enhances pathological changes in the lungs (inflammation and lung emphysema) induced by the administration of cigarette smoke extract. Recruiting of endothelial progenitor cells (CD45-CD31+CD34+ and CD31+CD34+CD146-) and progenitor cells of angiogenesis (CD45-CD117+CD309+) was registered in the injured lungs. Angiogenesis impairment induced by combined exposure is related to altered migration of pericytes (CD31-CD34-CD146+) and smooth muscle cells (CD31-CD34+CD146+) in emphysema-like enlarged lung tissue.


Assuntos
Miócitos de Músculo Liso/citologia , Miócitos de Músculo Liso/metabolismo , Pericitos/citologia , Pericitos/metabolismo , Enfisema Pulmonar/metabolismo , Enfisema Pulmonar/patologia , Animais , Antígenos CD34/metabolismo , Antígeno CD146/metabolismo , Fumar Cigarros/efeitos adversos , Células Progenitoras Endoteliais/citologia , Células Progenitoras Endoteliais/efeitos dos fármacos , Células Progenitoras Endoteliais/metabolismo , Feminino , Antígenos Comuns de Leucócito/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , Miócitos de Músculo Liso/efeitos dos fármacos , Molécula-1 de Adesão Celular Endotelial a Plaquetas/metabolismo , Proteínas Proto-Oncogênicas c-kit/metabolismo
16.
J Pathol ; 250(5): 624-635, 2020 04.
Artigo em Inglês | MEDLINE | ID: mdl-31691283

RESUMO

Chronic obstructive pulmonary disease (COPD) is a devastating lung disease with a high personal and societal burden. Exposure to toxic particles and gases, including cigarette smoke, is the main risk factor for COPD. Together with smoking cessation, current treatment strategies of COPD aim to improve symptoms and prevent exacerbations, but there is no disease-modifying treatment. The biggest drawback of today's COPD treatment regimen is the 'one size fits all' pharmacological intervention, mainly based on disease severity and symptoms and not the individual's disease pathology. To halt the worrying increase in the burden of COPD, disease management needs to be advanced with a focus on personalized treatment. The main pathological feature of COPD includes a chronic and abnormal inflammatory response within the lungs, which results in airway and alveolar changes in the lung as reflected by (small) airways disease and emphysema. Here we discuss recent developments related to the abnormal inflammatory response, ECM and age-related changes, structural changes in the small airways and the role of sex-related differences, which are all relevant to explain the individual differences in the disease pathology of COPD and improve disease endotyping. Furthermore, we will discuss the most recent developments of new treatment strategies using biologicals to target specific pathological features or disease endotypes of COPD. © 2020 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.


Assuntos
Pulmão/patologia , Medicina de Precisão , Doença Pulmonar Obstrutiva Crônica/patologia , Enfisema Pulmonar/patologia , Humanos , Pneumopatias/etiologia , Pneumopatias/patologia , Enfisema Pulmonar/etiologia , Tabaco/efeitos adversos
17.
Forensic Sci Int ; 305: 110029, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31726327

RESUMO

The question whether an injury was sustained during life or not is one of the most important subjects in forensic medicine. Therefore, vital reactions have been a main research topic in forensic medicine for a long period and many renowned forensic pathologists have devoted important papers to this field. The research area ranges from macroscopically visible organ reactions, over tissue alterations (enzyme histochemistry, later on immunohistochemistry with a wide range of enzymes and other analytes, molecular pathology) to biochemical responses to injury. Especially in the field of immunohistochemistry and molecular pathology much progress has been achieved in the last years (e.g. heat-shock-proteins or positive aquaporine3-staining in mechanical skin trauma). Furthermore, 20 years after its implementation postmortem imaging also contributes to the detection and visualization of vital signs. The aim of the present review is to provide an update on forensically relevant vital signs/vital reactions. Systemic vital reactions especially of the circulatory and respiratory system as well as local vital reactions will be addressed. Vital reactions of different organ systems will be discussed in detail regarding pathogenesis and possible postmortem evolution. Current research on immunohistochemically detectable vital reactions (heat-shock-protein expression, aquaporine3-staining in mechanical trauma of the skin) will be addressed as well as biochemical vital reactions (agonochemical stress reaction, myoglobine in electrocution death, hypoxanthine as marker of hypoxia).


Assuntos
Medicina Legal/métodos , Ferimentos e Lesões/patologia , Catecolaminas/sangue , Tosse , Deglutição , Embolia/patologia , Exsanguinação/patologia , Hemorragia/patologia , Humanos , Imuno-Histoquímica , Insulina/sangue , Absorção Intestinal , Isquemia/patologia , Pneumotórax/patologia , Proteínas/metabolismo , Enfisema Pulmonar/patologia , Ventilação Pulmonar , Púrpura/patologia , Aspiração Respiratória/patologia , Salivação
18.
Chin Med J (Engl) ; 132(20): 2465-2475, 2019 Oct 20.
Artigo em Inglês | MEDLINE | ID: mdl-31567388

RESUMO

OBJECTIVE: Chronic obstructive pulmonary disease (COPD) is a common chronic respiratory disease of human beings characterized by not fully reversible airflow limitation. Emphysema is the main pathological feature of COPD which causes high mortality worldwide every year and consumes a large amount of medical expenses. This paper was to review the establishment and evaluation methods of animal models of emphysema or COPD, and put forward some new ideas on animal selection, method of modeling, and model evaluation. DATA SOURCES: The author retrieved information from the PubMed database up to July 2019, using various combinations of search terms, including emphysema, model, and animal. STUDY SELECTION: Original articles, reviews, and other articles were searched and reviewed for animal models of emphysema. RESULTS: This review summarized animal models of emphysema from the perspectives of animal selection, emphysema mechanism, modeling method and model evaluation, and found that passive smoking is the classic method for developing animal model of emphysema, mice are more suitable for experimental study on emphysema. Compared with pulmonary function indicators, airway inflammation indicators and oxidative stress indicators, pathomorphological indicators of lung tissue are the most important parameters for evaluating the establishment of the animal model of emphysema. CONCLUSIONS: Mice model induced by passive smoking is the classic animal model of emphysema. Pathomorphological indicators are the most important parameters for evaluating the establishment of the animal model of emphysema.


Assuntos
Modelos Animais de Doenças , Enfisema Pulmonar/etiologia , Animais , Humanos , Inflamação/complicações , Elastase Pancreática/fisiologia , Doença Pulmonar Obstrutiva Crônica/complicações , Enfisema Pulmonar/genética , Enfisema Pulmonar/patologia , Tabaco/efeitos adversos , Poluição por Fumaça de Tabaco/efeitos adversos , Estimulação do Nervo Vago
19.
Front Immunol ; 10: 2169, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31608051

RESUMO

Ozone exposure causes irritation, airway hyperreactivity (AHR), inflammation of the airways, and destruction of alveoli (emphysema), the gas exchange area of the lung in human and mice. This review focuses on the acute disruption of the respiratory epithelial barrier in mice. A single high dose ozone exposure (1 ppm for 1 h) causes first a break of the bronchiolar epithelium within 2 h with leak of serum proteins in the broncho-alveolar space, disruption of epithelial tight junctions and cell death, which is followed at 6 h by ROS activation, AHR, myeloid cell recruitment, and remodeling. High ROS levels activate a novel PGAM5 phosphatase dependent cell-death pathway, called oxeiptosis. Bronchiolar cell wall damage and inflammation upon a single ozone exposure are reversible. However, chronic ozone exposure leads to progressive and irreversible loss of alveolar epithelial cells and alveoli with reduced gas exchange space known as emphysema. It is further associated with chronic inflammation and fibrosis of the lung, resembling other environmental pollutants and cigarette smoke in pathogenesis of asthma, and chronic obstructive pulmonary disease (COPD). Here, we review recent data on the mechanisms of ozone induced injury on the different cell types and pathways with a focus on the role of the IL-1 family cytokines and the related IL-33. The relation of chronic ozone exposure induced lung disease with asthma and COPD and the fact that ozone exacerbates asthma and COPD is emphasized.


Assuntos
Barreira Alveolocapilar/imunologia , Ozônio/toxicidade , Mucosa Respiratória/imunologia , Doença Aguda , Animais , Asma/induzido quimicamente , Asma/imunologia , Asma/patologia , Barreira Alveolocapilar/patologia , Fumar Cigarros/efeitos adversos , Fumar Cigarros/imunologia , Humanos , Camundongos , Fosfoproteínas Fosfatases/imunologia , Pneumonia/induzido quimicamente , Pneumonia/imunologia , Pneumonia/patologia , Doença Pulmonar Obstrutiva Crônica/induzido quimicamente , Doença Pulmonar Obstrutiva Crônica/imunologia , Doença Pulmonar Obstrutiva Crônica/patologia , Enfisema Pulmonar/induzido quimicamente , Enfisema Pulmonar/imunologia , Enfisema Pulmonar/patologia , Espécies Reativas de Oxigênio/imunologia , Mucosa Respiratória/patologia , Junções Íntimas/imunologia , Junções Íntimas/patologia
20.
J Vis Exp ; (151)2019 09 26.
Artigo em Inglês | MEDLINE | ID: mdl-31609316

RESUMO

Emphysema is a significant feature of chronic obstructive pulmonary disease (COPD). Studies involving an emphysematous mouse model require optimal lung fixation to produce reliable histological specimens of the lung. Due to the nature of the lung's structural composition, which consists largely of air and tissue, there is a risk that it collapses or deflates during the fixation process. Various lung fixation methods exist, each of which has its own advantages and disadvantages. The lung fixation method presented here utilizes constant pressure to enable optimal tissue evaluation for studies using an emphysematous mouse lung model. The main advantage is that it can fix many lungs with the same condition at one time. Lung specimens are obtained from chronic cigarette smoke-exposed mice. Lung fixation is performed using specialized equipment that enables the production of constant pressure. This constant pressure maintains the lung in a reasonably inflated state. Thus, this method generates a histological specimen of the lung that is suitable to evaluate cigarette smoke-induced mild emphysema.


Assuntos
Pulmão/patologia , Enfisema Pulmonar/diagnóstico , Fixação de Tecidos , Animais , Modelos Animais de Doenças , Masculino , Camundongos Endogâmicos C57BL , Camundongos Knockout , Enfisema Pulmonar/patologia , Vácuo
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