RESUMO
Purpose: To develop a novel method for calculating small airway resistance using computational fluid dynamics (CFD) based on CT data and evaluate its value to identify COPD. Patients and Methods: 24 subjects who underwent chest CT scans and pulmonary function tests between August 2020 and December 2020 were enrolled retrospectively. Subjects were divided into three groups: normal (10), high-risk (6), and COPD (8). The airway from the trachea down to the sixth generation of bronchioles was reconstructed by a 3D slicer. The small airway resistance (RSA) and RSA as a percentage of total airway resistance (RSA%) were calculated by CFD combined with airway resistance and FEV1 measured by pulmonary function test. A correlation analysis was conducted between RSA and pulmonary function parameters, including FEV1/FVC, FEV1% predicted, MEF50% predicted, MEF75% predicted and MMEF75/25% predicted. Results: The RSA and RSA% were significantly different among the three groups (p<0.05) and related to FEV1/FVC (r = -0.70, p < 0.001; r = -0.67, p < 0.001), FEV1% predicted (r = -0.60, p = 0.002; r = -0.57, p = 0.004), MEF50% predicted (r = -0.64, p = 0.001; r = -0.64, p = 0.001), MEF75% predicted (r = -0.71, p < 0.001; r = -0.60, p = 0.002) and MMEF 75/25% predicted (r = -0.64, p = 0.001; r = -0.64, p = 0.001). Conclusion: Airway CFD is a valuable method for estimating the small airway resistance, where the derived RSA will aid in the early diagnosis of COPD.
Assuntos
Resistência das Vias Respiratórias , Hidrodinâmica , Pulmão , Valor Preditivo dos Testes , Doença Pulmonar Obstrutiva Crônica , Tomografia Computadorizada por Raios X , Humanos , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Doença Pulmonar Obstrutiva Crônica/diagnóstico por imagem , Masculino , Estudos Retrospectivos , Feminino , Pessoa de Meia-Idade , Idoso , Volume Expiratório Forçado , Pulmão/fisiopatologia , Pulmão/diagnóstico por imagem , Capacidade Vital , Simulação por Computador , Interpretação de Imagem Radiográfica Assistida por Computador , Testes de Função Respiratória/métodosRESUMO
Cardiovascular diseases (CVDs) are the leading cause of death and disability worldwide. It is essential to develop novel interventions to prevent/delay CVDs by targeting their fundamental cellular and molecular processes. Melatonin is a small indole molecule acting both as a hormone of the pineal gland and as a local regulator molecule in various tissues. It has multiple features that may contribute to its cardiovascular protection. Moreover, melatonin enters all cells and subcellular compartments and crosses morphophysiological barriers. Additionally, this indoleamine also serves as a safe exogenous therapeutic agent. Increasing evidence has demonstrated the beneficial effects of melatonin in preventing and improving cardiovascular risk factors. Exogenous administration of melatonin, as a result of its antioxidant and anti-inflammatory properties, has been reported to decrease blood pressure, protect against atherosclerosis, attenuate molecular and cellular damage resulting from cardiac ischemia/reperfusion, and improve the prognosis of myocardial infarction and heart failure. This review aims to summarize the beneficial effects of melatonin against these conditions, the possible protective mechanisms of melatonin, and its potential clinical applicability in CVDs.
Assuntos
Doenças Cardiovasculares , Melatonina , Infarto do Miocárdio , Humanos , Melatonina/farmacologia , Melatonina/fisiologia , Melatonina/uso terapêutico , Doenças Cardiovasculares/tratamento farmacológico , Antioxidantes , Isquemia/tratamento farmacológico , Infarto do Miocárdio/tratamento farmacológicoRESUMO
Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation of the joints and joint destruction. Monocyte chemoattractant protein 1 (MCP1) is highly expressed in the joints of patients suffering from RA. The present study aimed to evaluate the effects of MCP1 on the phenotype of fibroblastlike synoviocytes (FLSs) and their differentiation potential towards vascular endothelial cells. The expression of MCP1 in collageninduced arthritis (CIA) rats was investigated by PCR, ELISA and immunohistology. Cell proliferation induced by MCP1 was measured using a Cell Counting Kit8 (CCK8) and 5Bromo2deoxyuridine ELISA assay. In addition, the effects of MCP1 on the migration of FLSs was examined using a Transwell assay. Activation of PI3K and P38 were investigated by western blotting following MCP1 treatment. The vascular endothelial cell markers, tumor necrosis factor alpha (TNFα) and interleukin1 beta (ILß), were also examined by western blotting. LY294002 [PI3K inhibitor, (LY)] and SB203580 [P38 inhibitor, (SB)] were used to examine the proliferative and prodifferentiation effect of PI3K and P38. The present findings showed that the expression level of MCP1 in the synovium of CIA rats was significantly higher compared with controls. The present in vitro study suggested that MCP1 increased the FLSs cell numbers with a maximal effect at 200 ng/ml, and induced the maximal phosphorylation of PI3K at 15 min and P38 at 30 min. In addition, MCP1 stimulation significantly increased the migration of FLSs. Furthermore, MCP1induced the expression of vascular endothelial growth factor and CD31 in FLSs. Suppression of PI3K and P38 was found to reduce MCP1 induced FLSs proliferation and migration, and decreased the expression levels of angiogenesis markers increased following MCP1 treatment. MCP1 was also found to increase the expression levels of both TNFα and ILß. Therefore, MCP1 could promote the proliferation and migration of FLSs, and was found to increase the expression levels of various angiogenesis markers via PI3K/P38, suggesting a role for this pathway in synovium hyperplasia in RA.