Prevalência de tabagismo e morbimortalidade por câncer de pulmão nos estados brasileiros / Smoking prevalence and lung cancer morbimortality in Brazilian states / Prevalencia del tabaquismo y morbimortalidad por cáncer de pulmón en los estados brasileños

Introdução: O câncer de pulmão é uma doença grave, sendo a segunda maior causa de morte em todo o mundo, entretanto, em alguns países desenvolvidos, tornou-se já a primeira causa de morte. Cerca de 90% dos casos de neoplasia pulmonares são causados pela inalação da fumaça do cigarro. Objetivo: Correlacionar a prevalência de tabagismo e morbimortalidade por câncer de pulmão nos estados brasileiros, além de demonstrar a associação destes com sexo e faixa etária. Métodos: Estudo de caráter ecológico acerca da prevalência de tabagismo e morbimortalidade por câncer de pulmão nos estados brasileiros, nos períodos de 2013 e 2019, dividida por sexo e faixa etária. Foram utilizados bancos de coleta de dados como o Tabnet e Pesquisa Nacional de Saúde. Resultados: As maiores taxas de mortalidade e internações hospitalares foram do público masculino, em 2013, com taxa de 2,7 e 10, respectivamente, e em 2019 com 3,3 e 11,9, respectivamente. Ademais, a maior prevalência de tabagismo foi encontrada nos homens; entretanto seu índice tem caído, enquanto a quantidade de mulheres tabagistas tem aumentado. A Região Sul demonstrou maiores números de mortalidade em ambos os períodos estudados, com taxas de 4,9 e 5,8 por 100 mil habitantes, e morbidade hospitalar com 19,9 e 23,5 por 100 mil habitantes. Já a Região Norte se configurou com as menores prevalências: em 2013 apresentou taxa de óbito por câncer de pulmão de 1,0 e morbidade hospitalar de 3,5/100 mil habitantes, em 2019 apresentou taxa de mortalidade de 4,6 e internações de 1,6/100 mil habitantes. Os coeficientes de correlação de morbidade hospitalar e prevalência de tabagismo foram R2=0,0628, r=0,251 e p=0,042, enquanto os de mortalidade e prevalência de tabagismo foram R2=0,0337, r=0,183 e p=0,140. Conclusões: Na presente pesquisa, pode-se inferir que houve associação positiva na comparação entre taxa de morbidade hospitalar e prevalência de tabagismo; em contrapartida, não foi possível observar associação positiva na correlação da taxa de mortalidade por câncer de pulmão e prevalência de tabagismo.

Introduction: Lung cancer is a serious disease, being the second leading cause of death worldwide. Moreover, in some developed countries, it has already become the leading cause of death. About 90% of lung cancer cases are caused by cigarette smoking. Objective: To correlate the prevalence of smoking and lung cancer morbidity and mortality in Brazilian states, and to demonstrate their association with sex and age group as well. Methods: An ecological study on the prevalence of smoking and lung cancer morbidity and mortality in Brazilian states between 2013 and 2019, divided by sex and age group. The data collection databases Tabnet and National Health Survey were used. Results: The highest rates of mortality and hospital admissions were among men, in 2013 with a rate of 2.7 and 10, respectively, and in 2019 with 3.3 and 11.9, respectively. In addition, the highest prevalence of smoking was found in men, but this rate has fallen, while the number of women smokers has increased. The South region showed higher mortality rates in both periods studied, with rates of 4.9 and 5.8 per 100,000 inhabitants, and hospital morbidity with 19.9 and 23.5 per 100,000 inhabitants. The North region had the lowest prevalence, where in 2013, it had a death rate from lung cancer of 1.0 and hospital morbidity of 3.5/100 thousand inhabitants, and where in 2019, it had a mortality rate of 4.6 and hospitalizations of 1.6/100 thousand inhabitants. The correlation coefficients for hospital morbidity and smoking prevalence were R2=0.0628, r=0.251 and p=0.042, while for mortality and smoking prevalence, these were R2=0.0337, r=0.183 and p=0.140. Conclusions: In the present study, it can be inferred that there was a positive association between hospital morbidity rate and prevalence of smoking, while it was not possible to observe a correlation between lung cancer mortality rate and prevalence of smoking.

Introducción: El cáncer de pulmón es una enfermedad grave, siendo la segunda causa de muerte en todo el mundo, sin embargo, en algunos países desarrollados, ya se ha convertido en la primera causa de muerte. Alrededor del 90% de los casos de neoplasias pulmonares están causados por la inhalación del humo del cigarrillo. Objetivo: Correlacionar la prevalencia de tabaquismo y la morbimortalidad por cáncer de pulmón en los estados brasileños, además de demostrar la asociación de estos con el género y el grupo de edad. Métodos: estudio ecológico sobre la prevalencia de tabaquismo y morbimortalidad por cáncer de pulmón en los estados brasileños, dentro de los períodos 2013 y 2019, divididos por sexo y grupo de edad. Se utilizaron bancos de recogida de datos como Tabnet y la Encuesta Nacional de Salud. Resultados: las mayores tasas de mortalidad e ingresos hospitalarios se dieron en el público masculino, en 2013 con una tasa de 2,7 y 10, respectivamente, y en 2019 con 3,3 y 11,9, respectivamente. Además, la mayor prevalencia del tabaquismo se encontró en los hombres, sin embargo, su tasa ha disminuido, mientras que la cantidad de mujeres fumadoras ha aumentado. La región Sur presentó cifras más altas de mortalidad en ambos periodos estudiados, con tasas de 4,9 y 5,8 por 100.000 habitantes, y de morbilidad hospitalaria con 19,9 y 23,5 por 100.000 habitantes. Mientras que la región Norte se configuró con las prevalencias más bajas, en 2013 presentó una tasa de mortalidad por cáncer de pulmón de 1,0 y una morbilidad hospitalaria de 3,5/100.000 habitantes, en 2019 presentó una tasa de mortalidad de 4,6 y hospitalizaciones de 1,6/100.000 habitantes. Los coeficientes de correlación para la morbilidad hospitalaria y la prevalencia del tabaquismo fueron R2=0,0628, r=0,251 y p=0,042, mientras que para la mortalidad y la prevalencia del tabaquismo fueron R2=0,0337, r=0,183 y p=0,140. Conclusiones: En la presente investigación se puede inferir que existe una asociación positiva en la comparación entre la tasa de morbilidad hospitalaria y la prevalencia de tabagismo, en contrapartida, no fue posible observar una asociación positiva en la correlación de la tasa de mortalidad por cáncer de pulmón y la prevalencia de tabagismo.

Controles de salud durante la pandemia e impacto clínico del COVID-19 en niños con enfermedad neuromuscular / Health checkups during the pandemic and clinical impact of COVID-19 in children with neuromuscular disease

Introducción. Los niños con enfermedad neuromuscular (ENM) requieren cuidados crónicos de salud (CCS) y podrían presentar COVID-19 grave. Objetivos. Describir CCS para niños con ENM durante la pandemia y evolución del COVID-19 en este grupo. Población y métodos. Cohorte prospectiva unicéntrica. Se incluyeron pacientes de 2-18 años, con ≥ 1 año de seguimiento previo a la pandemia. Se recolectaron variables demográficas, relativas a los CCS y al COVID-19 mediante historias clínicas y encuestas telefónicas. Resultados. Se incluyeron 226 pacientes; el 71 % varones, mediana de edad 11,3 años. Presentaban distrofias musculares (55,7 %) y atrofia muscular espinal (23 %). Comparando el primer año de pandemia con el previo, el 30 % no realizó controles médicos y el 25 % no realizó kinesioterapia. Otros disminuyeron la frecuencia. Hubo 52 casos de COVID-19. Fueron sintomáticos el 82 %: el 88,4 % leves/moderados y el 11,6 % graves. No hubo fallecidos. Conclusiones. La pandemia impactó negativamente en los CCS y los casos de COVID-19 fueron mayormente leves.

Introduction. Children with neuromuscular disease (NMD) require chronic health care (CHC) and may develop severe COVID-19. Objectives. To describe CHC for children with NMD during the pandemic and the course of COVID-19 in this group. Population and methods. Prospective, single-center cohort. Patients aged 2 to 18 years with ≥ 1 year of follow-up prior to the pandemic were included. Demographic variables in relation to CHC and COVID-19 were collected from medical records and via telephone surveys. Results. A total of 226 patients with a median age of 11.3 years were included; 71% were males. They had muscular dystrophy (55.7%) and spinal muscular atrophy (23%). When comparing the first year of the pandemic with the previous year, 30% did not have a health checkup and 25% did not receive kinesiotherapy. Others did, but with a lower frequency. A total of 52 COVID-19 cases were reported; 82% were symptomatic: 88.4% were mild/moderate and 11.6%, severe. No patient died. Conclusions. The pandemic had a negative impact on CHC, and COVID-19 cases were mostly mild.

Disfunciones del metabolismo del surfactante pulmonar: caso clínico pediátrico / Pulmonary surfactant metabolism dysfunction: A pediatric clinical case report

Las enfermedades pulmonares intersticiales son patologías poco frecuentes en pediatría. Dentro de ellas, se incluyen las disfunciones del metabolismo del surfactante pulmonar, molécula anfipática cuya función es disminuir la tensión superficial y evitar el colapso alveolar. Se presenta el caso de un lactante de 6 meses, en seguimiento por bajo peso, que presentó dificultad respiratoria aguda y cianosis; la radiografía de tórax evidenció infiltrado intersticial, neumomediastino y neumotórax bilateral. Al interrogatorio, surgió antecedente materno de internación al año de vida, con requerimiento de oxigenoterapia prolongada y diagnóstico desconocido; presenta signos de hipoxia crónica. El paciente cursó internación con requerimiento de oxigenoterapia. Se realizaron estudios complementarios en búsqueda de etiología, sin resultados positivos. La tomografía de tórax evidenció opacidades en vidrio esmerilado, engrosamiento del intersticio septal y áreas de atrapamiento aéreo; con resultado de biopsia pulmonar y estudio genético se llegó al diagnóstico de disfunción del metabolismo del surfactante pulmonar.

Interstitial lung diseases are rare in pediatrics. They include dysfunctions in the metabolism of pulmonary surfactant, an amphipathic molecule that reduces surface tension and prevents alveolar collapse. Here we describe the case of a 6-month-old infant controlled for low weight, who presented with acute respiratory distress and cyanosis; his chest X-ray showed interstitial infiltrate, pneumomediastinum, and bilateral pneumothorax. During history-taking, it was noted that his mother had a history of hospitalization at 1 year old with unknown diagnosis, requiring prolonged oxygen therapy; she now shows signs of chronic hypoxia. The patient was hospitalized and required oxygen therapy. Ancillary tests were done to look for the etiology of the condition, with no positive results. A chest computed tomography showed groundglass opacities, thickening of the septal interstitium, and areas of air trapping; based on the results of a lung biopsy and a genetic study, pulmonary surfactant metabolism dysfunction was diagnosed.

Hipertensão Arterial Pulmonar com Características de Envolvimento Venoso: Um Trabalho Investigativo / Pulmonary Arterial Hypertension with Features of Venous Involvement: A Detective's Task

Resumo A doença veno-oclusiva pulmonar (DVOP) e a hemangiomatose capilar pulmonar são tipos raros de substratos histopatológicos dentro do espectro da hipertensão arterial pulmonar (HAP) com prognóstico muito ruim. Caracterizam-se por um processo fibroproliferativo generalizado das veias e/ou capilares de pequeno calibre com preservação das veias maiores, resultando em um fenótipo de hipertensão pulmonar pré-capilar. A apresentação clínica é inespecífica e semelhante a outras etiologias de HAP. O diagnóstico definitivo é obtido por meio de análise histológica, embora a biópsia pulmonar não seja aconselhada devido ao maior risco de complicações. No entanto, alguns achados adicionais podem permitir um diagnóstico clínico presuntivo de DVOP, especialmente história de tabagismo, uso de drogas quimioterápicas, exposição a solventes orgânicos (particularmente tricloroetileno), baixa capacidade de difusão do monóxido de carbono (DLCO), dessaturação ao esforço e evidências de doença venosa sem doença cardíaca esquerda no exame de imagem, manifestada por uma tríade clássica de opacidades em vidro fosco, linhas septais, e linfadenopatias. O transplante pulmonar é o único tratamento eficaz e os pacientes devem ser encaminhados no momento do diagnóstico, devido à rápida progressão da doença e ao prognóstico ruim. Apresentamos o caso de um homem de 58 anos com HAP com características de envolvimento venoso/capilar em que a suspeita clínica, o pronto diagnóstico e o encaminhamento precoce para transplante pulmonar foram determinantes para um bom desfecho.

Abstract Pulmonary veno-occlusive disease (PVOD) and pulmonary capillary hemangiomatosis are rare types of histopathological substrates within the spectrum of pulmonary arterial hypertension (PAH) with a very poor prognosis. They are characterized by a widespread fibroproliferative process of the small caliber veins and/or capillaries with sparing of the larger veins, resulting in a pre-capillary pulmonary hypertension phenotype. Clinical presentation is unspecific and similar to other PAH etiologies. Definitive diagnosis is obtained through histological analysis, although lung biopsy is not advised due to a higher risk of complications. However, some additional findings may allow a presumptive clinical diagnosis of PVOD, particularly a history of smoking, chemotherapy drug use, exposure to organic solvents (particularly trichloroethylene), low diffusing capacity for carbon monoxide (DLCO), exercise induced desaturation, and evidence of venous congestion without left heart disease on imaging, manifested by a classical triad of ground glass opacities, septal lines, and lymphadenopathies. Lung transplant is the only effective treatment, and patients should be referred at the time of diagnosis due to the rapid progression of the disease and associated poor prognosis. We present a case of a 58-year-old man with PAH with features of venous/capillary involvement in which clinical suspicion, prompt diagnosis, and early referral for lung transplantation were determinant factors for the successful outcome.

Edema pulmonar por reexpansión. Reporte de Caso / Pulmonary edema due to re-expansion. Case Report

Introducción. El edema pulmonar por reexpansión es una complicación poco frecuente, secundaria a una rápida reexpansión pulmonar posterior al drenaje por toracentesis o toracostomía cerrada. Al día de hoy, se ha descrito una incidencia menor al 1 % tras toracostomía cerrada, con mayor prevalencia en la segunda y tercera década de la vida. Su mecanismo fisiopatológico exacto es desconocido; se ha planteado un proceso multifactorial de daño intersticial pulmonar asociado con un desequilibrio de las fuerzas hidrostáticas. Caso clínico. Presentamos el caso de un paciente que desarrolló edema pulmonar por reexpansión posterior a toracostomía cerrada. Se hizo una revisión de la literatura sobre esta complicación. Resultados. Aunque la clínica sugiere el diagnóstico, la secuencia de imágenes desempeña un papel fundamental. En la mayoría de los casos suele ser autolimitado, por lo que su manejo es principalmente de soporte; sin embargo, se han reportado tasas de mortalidad que alcanzan hasta el 20 %, por tanto, es importante conocer los factores de riesgo y las medidas preventivas. Conclusión. El edema pulmonar de reexpansión posterior a toracostomía es una complicación rara en los casos con neumotórax, aunque es una complicación que se puede presentar en la práctica diaria, por lo cual debe tenerse en mente para poder hacer el diagnóstico y un manejo adecuado.

Introduction. Re-expansion pulmonary edema is a rare complication secondary to rapid pulmonary re-expansion after drainage by thoracentesis and/or closed thoracostomy. As of today, an incidence of less than 1% has been described after closed thoracostomy, with a higher prevalence in the second and third decades of life. Its exact pathophysiological mechanism is unknown; a multifactorial process of lung interstitial damage associated with an imbalance of hydrostatic forces has been proposed. Clinical case. We present the case of a patient who developed pulmonary edema due to re-expansion after closed thoracostomy, conducting a review of the literature on this complication. Results. Although the clinic suggests the diagnosis, the sequence of images plays a fundamental role. In most cases, it tends to be a self-limited disease, so its management is mainly supportive. However, mortality rates of up to 20% have been recorded. Therefore, it is important to identify patients with major risk factors and initiate preventive measures in these patients. Conclusions. Re-expansion pulmonary edema after thoracostomy is a rare complication in cases with pneumothorax; however, it is a complication that can occur in daily practice. Therefore, it must be kept in mind to be able to make the diagnosis and an adequate management.

Upregulation of PGC-1α expression by pioglitazone mediates prevention of sepsis-induced acute lung injury

Abstract The imbalance between pro-inflammatory M1 and anti-inflammatory M2 macrophages plays a critical role in the pathogenesis of sepsis-induced acute lung injury (ALI). Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) may modulate macrophage polarization toward the M2 phenotype by altering mitochondrial activity. This study aimed to investigate the role of the PGC-1α agonist pioglitazone (PGZ) in modulating sepsis-induced ALI. A mouse model of sepsis-induced ALI was established using cecal ligation and puncture (CLP). An in vitro model was created by stimulating MH-S cells with lipopolysaccharide (LPS). qRT-PCR was used to measure mRNA levels of M1 markers iNOS and MHC-II and M2 markers Arg1 and CD206 to evaluate macrophage polarization. Western blotting detected expression of peroxisome proliferator-activated receptor gamma (PPARγ) PGC-1α, and mitochondrial biogenesis proteins NRF1, NRF2, and mtTFA. To assess mitochondrial content and function, reactive oxygen species levels were detected by dihydroethidium staining, and mitochondrial DNA copy number was measured by qRT-PCR. In the CLP-induced ALI mouse model, lung tissues exhibited reduced PGC-1α expression. PGZ treatment rescued PGC-1α expression and alleviated lung injury, as evidenced by decreased lung wet-to-dry weight ratio, pro-inflammatory cytokine secretion (tumor necrosis factor-α, interleukin-1β, interleukin-6), and enhanced M2 macrophage polarization. Mechanistic investigations revealed that PGZ activated the PPARγ/PGC-1α/mitochondrial protection pathway to prevent sepsis-induced ALI by inhibiting M1 macrophage polarization. These results may provide new insights and evidence for developing PGZ as a potential ALI therapy.

Bibliometric and visual analysis of SCI indexed papers on e-cigarette or vaping product use associated lung injury from 2013 to 2022 / 环境与职业医学

Background In recent years, the rising number of e-cigarette users among adolescents and the surging cases of lung injury related to e-cigarette use have attracted the attention of researchers in various fields. Objective To identify the research hotspots and trends of e-cigarette or vaping product use associated lung injury (EVALI) worldwide from 2013 to 2022 by bibliometric and visual analysis. Methods Web of Science Core Collection was selected to obtain literature related to EVALI from 2013 to 2022 across the world, statistics were calculated by country/region, institution, author, journal, cited literature, keyword, etc. CiteSpace 6.2.R1 was used for visual analysis to draw diagrams of publication trend, author cooperation network, co-citation clustering time distribution, and keyword cluster. Results A total of 888 EVALI-related papers published between 2013 and 2022 were retrieved. The number of publications was gradually increased, with a significant increase in 2020 and a decrease from 2021, but the number of citations was increased year by year. The most active country was the United States (631 articles). European and American countries cooperated closely and the centrality was prominent. Among the publishing institutions, the University of California system topped the list with 103 articles. Rahman I (27 articles) published the most articles and had a high degree of centrality; Goniewicz M L was the most cited author; and the network analysis diagram showed relatively weak collaboration between authors. The American Journal of Respiratory and Critical Care Medicine was the journal with the highest number of publications (94 articles). The top 5 cited articles were all cited more than 300 times. The leading high-frequency keywords of EVALI-related studies were nicotine (149 times), exposure (118 times), and oxidative stress (80 times). The cluster of key nodes in the co-citation network and the clustering time distribution diagram indicated youth e-cigarette addiction received widespread attention from society. From the top 25 keywords with the strongest bursts, the focus of research on the pathogenesis of EVALI gradually shifted from the oxidative stress damage associated with e-cigarette vapor to the oxidative effect of flavoring chemicals in the process of lung injury. The current research interests in this field were mainly the mechanisms of various chemicals in e-cigarettes and the heating elements that led to damage to the lungs. Conclusion EVALI is receiving continuous attention from researchers in government, medical institutions, and other organizations. A variety of e-cigarette ingredients such as flavoring chemicals may lead to varying degrees of cytotoxicity, inflammation, and lung damage. However, the pathophysiology of EVALI remains unclear. In the future, more Chinese scholars should be encouraged to participate in this field.

Construction and Verification of A Nomogram Model for Predicting Invasive Risk of Ground Glass Nodules / 肿瘤防治研究

Objective To investigate the importance of a nomogram model based on biomarkers and CT signs in the prediction of the invasive risk of ground glass nodules. Methods A total of 322 patients with ground glass nodule, including 240 and 82 patients in the model and verification groups, respectively, were retrospectively analyzed. Independent risk factors for the invasive risk of ground glass nodules were screened out after using single and multiple Logistic analysis. R software was used to construct the nomogram model, and clinical decision curve analysis (DCA), receiver operating curve (ROC), and calibration curve were used for internal and external verification of the model. Results In this study, the independent risk factors for the invasive risk of ground glass nodules included systemic immune-inflammation index (SII), CYFRA21-1, edge, vascular cluster sign, and nodular consolidation tumor ratio (CTR). The area under the ROC curve of the constructed nomogram model had a value of 0.946, and that of the external validation group reached 0.932, which suggests the good capability of the model in predicting the invasive risk of ground glass nodules. The model was internally verified through drawing of calibration curves of Bootstrap 1000 automatic sampling. The results showed that the consistency index between the model and actual curves reached 0.955, with a small absolute error and good fit. The DCA curve revealed a good clinical practicability. In addition, nodule margin, vascular cluster sign, and CTR were correlated with the grade of pathological subtype of invasive adenocarcinoma. Conclusion A nomogram model based on biomarkers and CT signs has good value and clinical practicability in the prediction of the invasive risk of ground glass nodules.

Research Progress in Mitochondrial Treatment and Mechanism in Occurrence of Lung Cancer / 肿瘤防治研究

Lung cancer is characterized by high incidence and mortality rates and invasiveness, and its occurrence and development are influenced by various factors. Mitochondria, as ubiquitous organelles in the human body, regulate cellular processes, such as metabolism, signal transduction, oxidative stress, and genomic instability, thereby affecting the initiation and progression of lung cancer. This article summarizes the recent research progress on mitochondrial-targeted drugs, mitochondrial transfer, and mitochondrial gene therapy for lung cancer treatment. This work also discusses the principles and prospects of mitochondrial therapy to provide new insights for lung cancer treatment.

Oxidative Stress-related Signaling Pathways in Lung Cancer and Chinese Medicine Intervention： A Review / 中国实验方剂学杂志

Lung cancer has the highest incidence and mortality rate among all cancers in China， with its complex and variable nature， long treatment duration， and often poor prognosis. Currently， the treatment of lung cancer mainly employs classical therapies such as surgery， radiotherapy， and chemotherapy， but some patients may experience a series of adverse reactions， which affect their quality of life， survival period， and treatment outcomes. As reported， oxidative stress is one of the important pathogenic factors of lung cancer， affecting its occurrence and development. Oxidative stress is a state of imbalance between oxidative products and antioxidant defense mechanisms in the body. The intervention of oxidative stress in the occurrence and development of lung cancer is related to multiple signaling pathways， including the Kelch-like ECH-associated protein 1 （Keap1）-nuclear factor erythroid 2-related factor 2 （Nrf2） signaling pathway， phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR） signaling pathway， mitogen-activated protein kinase （MAPK） signaling pathway， and nuclear factor-κB （NF-κB） signaling pathway. Currently， researchers in China and abroad have conducted extensive studies on the occurrence and development of lung cancer and the pathophysiological mechanisms of drug intervention. The results have shown that oxidative stress plays an important role in the occurrence and development of lung cancer. Chinese medicine monomers and compounds can regulate oxidative stress levels and intervene in related signaling pathways， thereby inhibiting or delaying the occurrence and development of lung cancer. Based on this， this article mainly summarized the relevant signaling pathways regulating oxidative stress intervention in lung cancer in recent years， and also reviewed the latest research on Chinese medicine monomers and compounds in regulating oxidative stress to treat lung cancer， aiming to provide new ideas for research on drug treatment of lung cancer and clinical drug development， as well as to provide references and guidance for further in-depth mechanistic studies in the future.

Effectss of persistent obesity on lung function in school age children / 中国学校卫生

Objective@#To analyze the impact of persistent obesity on their lung function, so as to offer insights for implementing intervention measures to increase lung function in obese school age children.@*Methods@#A total of 335 children from the Sheyang Mini Birth Cohort established in 2009 in Yancheng City, Jiangsu Province, who participated in the follow up at the ages of 7 years (2016) and 10 years (2019), were selected as the study participants. Physical measurements including height, weight, and lung function were recorded. According to the World Health Organization standard, that is, gender and age specific to correct the body mass index to calculate the body mass index Z score, was used to evaluate the obesity status of children at the age of 7 and 10. Children were divided into four groups, including sustained non obesity group, restored obesity group, newly classified obesity group, and persistent obesity group. Meanwhile, the lung function prediction equations recommended by the Global Lung Function Initiative were used to standardize the lung function indexes of children. Pulmonary function differences among these groups were examined, and the relationship between childhood obesity and pulmonary function was longitudinally analyzed using generalized estimating equations.@*Results@#The prevalence of obesity were 9.0% and 16.1% at the age of 7 and 10 years, respectively. The proportion of both newly classified and persistent obesity group were 8.1%, respectively. The forced expiratory volume in one second (FEV 1) and forced vital capacity (FVC) were (1 269.90±202.70) and (1 415.70±230.00) mL, respectively, at the age of 7 years. FEV 1 and FVC at the age of 10 years were (1 440.80±403.20) and (1 555.60±517.60) mL, respectively. Cross sectional analysis at age 7 showed that forced expiratory flow at 75% vital capacity (FEF 75 ) ( β=-0.52, 95%CI =-0.96--0.07) and maximal mid expiratary flow (MMEF) ( β=-0.45, 95%CI =-0.89--0.00) were significantly lower in obese children compared to their non obese peers ( P < 0.05). Longitudinal analysis indicated that obese children had lower levels of lung pulmonary function, with a statistically significant difference in FEV 1 ( β=-0.44, 95%CI=-0.85--0.02, P <0.05). There was no significant difference among the various obesity groups ( P >0.05), while gender stratified results revealed significant reductions in FEV 1/FVC in newly classified obese girls at age 10 years ( β=-1.76, 95%CI =-3.13--0.38) and in MMEF in persistently obese girls at age 10 years ( β=-1.44, 95%CI = -2.79- -0.09) ( P <0.05).@*Conclusion@#Obesity may contribute to reduced lung function levels in school aged children, with newly classified and persistent obesity having more pronounced effects on lung function in girls.

Application of multi-disciplinary team mode in prevention and control of multidrug resistant organism infection in lung transplant recipients / 器官移植

<b>Objective</b> To evaluate the effectiveness of multi-disciplinary team (MDT) mode in the prevention and control of multidrug resistant organism (MDRO) infection in lung transplant recipients. <b>Methods</b> Lung transplant recipients admitted to the hospital from 2019 to 2022 were enrolled. MDT expert group was established in January, 2020. A series of prevention and control measures were conducted. The implementation rate of MDRO prevention and control measures and the detection rate of MDRO on the environmental surface from 2020 to 2022, and the detection rate of MDRO in lung transplant recipients from 2019 to 2022 were analyzed. <b>Results</b> The overall implementation rate of MDRO prevention and control measures for medical staff was increased from 64.9% in 2020 to 91.6% in 2022, showing an increasing trend year by year (<i>P</i><0.05). The detection rate of MDRO on the environmental surface was decreased from 28% in 2020 to 9% in 2022, showing a downward trend year by year (<i>P</i><0.05). The detection rate of MDRO in lung transplant recipients was decreased from 66.7% in 2019 to 44.3% in 2022, showing a decreasing trend year by year (<i>P</i><0.001). <b>Conclusions</b> MDT mode management may enhance the implementation of MDRO prevention and control measures for medical staff, effectively reduce the infection rate of MDRO in lung transplant recipients and the detection rate of MDRO on the environmental surface, which is worthy of widespread application.

Clinical analysis of lung transplantation for lung chronic graft-versus-host disease after hematopoietic stem cell transplantation / 器官移植

<b>Objective</b> To evaluate clinical efficacy of lung transplantation for lung chronic graft-versus-host disease (cGVHD) after hematopoietic stem cell transplantation (HSCT). <b>Methods</b> Clinical data of 12 patients undergoing lung transplantation for lung cGVHD were retrospectively analyzed. Preoperative clinical manifestations and involved organs of patients were analyzed. The lung function before and after lung transplantation was compared, and the survival of patients after lung transplantation was analyzed. <b>Results</b> Eleven patients underwent HSCT due to primary hematological malignancies, including 9 cases of leukemia, 1 case of myelodysplastic syndrome, 1 case of lymphoma. And 1 case underwent HSCT for systemic lupus erythematosus. Among 12 cGVHD patients, skin involvement was found in 8 cases, oral cavity involvement in 5 cases, gastrointestinal tract involvement in 4 cases and liver involvement in 3 cases. All 12 patients developed severe respiratory failure caused by cGVHD before lung transplantation, including 9 cases of typeⅡ respiratory failure and 3 cases of type Ⅰ respiratory failure. Two patients underwent right lung transplantation, 2 cases of left lung transplantation and 8 cases of bilateral lung transplantation. The interval from HSCT to lung transplantation was 75 (19-187) months. Upon the date of submission, postoperative follow-up time was 18 (7-74) months. Ten patients survived, 1 died from severe hepatitis at postoperative 22 months, and 1 died from gastrointestinal bleeding at postoperative 6 months. No recurrence of primary diseases was reported in surviving patients. <b>Conclusions</b> Lung transplantation is an efficacious treatment for lung cGVHD after HSCT, which may prolong the survival time and improve the quality of life of the recipients.

Latest research progress in airway stenosis after lung transplantation / 器官移植

With the optimization of surgical technologies and postoperative management regimens, the number of lung transplantation has been significantly increased, which has become an important treatment for patients with end-stage lung disease. However, due to the impact of comprehensive factors, such as bronchial ischemia and immunosuppression, the incidence of airway stenosis after lung transplantation is relatively high, which severely affects postoperative survival and quality of life of lung transplant recipients. In recent years, with the improvement of perioperative management, organ preservation and surgical technologies, the incidence of airway stenosis after lung transplantation has been declined, but it remains at a high level. Early diagnosis and timely intervention play a significant role in enhancing clinical prognosis of patients with airway stenosis. In this article, the general conditions, diagnosis, treatment and prevention of airway stenosis after lung transplantation were reviewed, aiming to provide reference for comprehensive management of airway stenosis after lung transplantation and improving clinical prognosis of lung transplant recipients.

Effect and mechanism of cucurbitacin B preventing sepsis-induced acute lung injury in mice / 中国药房

OBJECTIVE To investigate the preventive effect of cucurbitacin B （CB） on sepsis-induced acute lung injury （ALI） and its mechanism. METHODS The mice were divided into control group， model group， dexamethasone group （positive control， 2 mg/kg）， CB low-dose and high-dose groups （25， 50 mg/kg）. Each group was given relevant medicine intraperitoneally， once a day， for 3 consecutive days. Twenty-four hours after the last administration， those groups were given lipopolysaccharide （10 mg/kg） intraperitoneally to establish sepsis-induced ALI model （finally， 8 mice per group were included in the experiment）， except for control group. Twenty-four hours after medication， blood routine indicators （total white blood cell count， neutrophils count， lymphocytes count）， lung function indicators （total lung resistance， pulmonary outflow resistance， lung dynamic compliance， peak expiratory flow rate， and maximum ventilation volume）， dry wet ratio of lung tissue were measured in each group. The lung tissue level of myeloperoxidase （MPO）， and the serum levels of tumor necrosis factor-α （TNF-α）， interleukin 1β （IL-1β）， IL-6， superoxide dismutase （SOD） and malondialdehyde （MDA） were all detected. The pathological changes of lung tissue were observed； immunohistochemistry was used to detect the positive expression of phosphorylation signal transducer and activator of transcription 3 （p-STAT3） in the lung tissue. Western blot assay was used to detect the expressions of proteins related to IL-6/JAK2/ STAT3 signaling pathway in the lung tissue. RESULTS Compared with control group， total pulmonary resistance， pulmonary flow resistance， dry wet ratio of lung tissue， the total white blood cell count， neutrophils count， lymphocytes count of whole blood， the lung tissue level of MPO and serum levels of MDA， IL-6， IL-1β and TNF-α， the p-STAT3 protein optical density value， the protein expressions of IL-6 and IL-6 receptor， and the phosphorylation levels of JAK2 and STAT3 protein were increased significantly in the model group （P＜0.01）， while lung dynamic compliance， peak expiratory flow rate， maximum ventilation volume and serum level of SOD were decreased significantly （P＜0.05 or P＜0.01）. Pulmonary tissue showed alveolar collapse and infiltration of inflammatory cells. Compared with the model group， the above indexes of mice were reversed significantly in dexamethasone group and CB groups （P＜0.05 or P＜0.01）， the pathological damage of lung tissue was reduced. CONCLUSIONS CB can prevent sepsis-induced ALI by inhibiting the activity of Δ 基金项目遵义市科技计划项目（No.202252） IL-6/JAK2/STAT3 signaling pathway and relieving ＊第一作者主治医师。研究方向：重症医学。E-mail：fjuanxui@ 163.com inflammatory reactions. # 通信作者 主任医师。研究方向：儿童呼吸系统疾病诊断与治

Improvement of Lung Function in Rats with Idiopathic Pulmonary Fibrosis by Shengxiantang via Regulating Cell Senescence Mediated by Wnt3a/β-catenin Signaling Pathway / 中国实验方剂学杂志

ObjectiveTo observe the effect of Shengxiantang （SXT） on cell senescence mediated by wingless/integrated （Wnt）3a/β-catenin pathway in rats with idiopathic pulmonary fibrosis （IPF） and reveal the possible mechanism in improving lung function of IPF rats. MethodA total of 32 SPF level SD rats were randomly divided into sham group， model group， pirfenidone group， and SXT group. The IPF rat model was established by intratracheal instillation of bleomycin （0.005 g·kg-1）. The following day after surgery， rats in the SXT group were given the aqueous solution of SXT granules （0.78 g·kg-1）， and the pirfenidone group was given pirfenidone suspension （0.05 g·kg-1）. The other groups were given deionized water （10 mL·kg-1） for 28 consecutive days. Lung tissue was collected after the lung function was measured. The pathological changes of the lung tissue were observed by hematoxylin-eosin （HE） and Masson staining， and then the Szapiel score and Ashcroft score were performed. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect telomere length. Western blot was applied to detect the expressions of epithelial-mesenchymal transformation （EMT） markers ［α-smooth muscle actin （α-SMA） and E-cadherin］， telomere reverse transcriptase （TRET）， aging-related proteins （p53 and p21）， senescence-associated secretory phenotype ［interleukin-6 （IL-6） and matrix metalloproteinase-1 （MMP-1）］， and key proteins of Wnt signaling pathway ［Wnt3a， glycogen synthase kinase-3β （GSK-3β）， β-catenin， Cyclin D1， and c-Myc］. ResultCompared with those in the Sham group， peak expiratory flow （PEF） and minute ventilation volume （MV） in the model group were significantly decreased （P<0.01）， and the frequency of respiratory （f） was significantly increased （P<0.01）. The Szapiel score， Ashcroft score， and protein expression of α-SMA， p53， p21， IL-6， MMP-1， Wnt3a， GSK3β， β-catenin， Cyclin D1， and c-Myc were increased （P<0.01）. The expressions of E-cadherin and TERT， as well as telomere length were significantly decreased （P<0.01）. Compared with those in the model group， PEF and MV in the SXT group were significantly increased （P<0.01）， while f was significantly decreased （P<0.01）. The Szapiel score， Ashcroft score， and protein expression of α-SMA， p53， p21， IL-6， MMP-1， Wnt3a， GSK3β， β-catenin， Cyclin D1， and c-Myc were significantly decreased （P<0.05， P<0.01）. Nevertheless， the expression of E-cadherin and TERT， as well as telomere length were significantly increased （P<0.01）. ConclusionSXT presents a significant protective effect on lung function in IPF rats， and the prescription may act on the Wnt3a/β-catenin signaling pathway to regulate cell senescence induced by TERT to inhibit EMT.

Mechanism of Wenfei Huaxian Decoction-containing Serum in Delaying Inflammatory Senescence of Lung Mesenchymal Stem Cells Based on NAMPT/SIRT1 / 中国实验方剂学杂志

ObjectiveThe lung mesenchymal stem cells （LMSCs） induced by D-galactose （D-gal） were intervened by Wenfei Huaxian decoction-containing serum to explore the mechanism of Wenfei Huaxian decoction in delaying the senescence of LMSCs through the nicotinamide phosphoribosyltransferase/silent information regulator 1 （NAMPT/SIRT1） signaling pathway. MethodWenfei Huaxian decoction-containing serum was prepared. LMSCs were isolated by gradient density centrifugation， and they were cultured and identified in vitro. The senescence model in vitro was established by stimulating cells via D-gal for 24 h. LMSCs cells were modeled after being treated with different volume fractions （5%， 10%， 20%， 40%， and 80%） of Wenfei Huaxian decoction-containing serum for 24 h， and the cell proliferation level was detected by methyl thiazolyl tetrazolium （MTT） method. The cells were randomly divided into blank serum group， model group， and high， medium， and low dose groups of Wenfei Huaxian decoction-containing serum. Senescence-associated β-galactosidase （SA-β-gal） staining was used to detect the senescence of LMSCs in each group. The content of NAD + was detected by colorimetry. The levels of senescence-associated factors （p16 and p53）， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） in cell culture supernatant were detected by enzyme-linked immunosorbent assay （ELISA）. Western blot was used to detect the relative expression of senescence-associated proteins and NAMPT/SIRT1 signaling pathway-related proteins. ResultCompared with the blank serum group， the proliferation of LMSCs was significantly inhibited after D-gal stimulation for 24 h （P<0.01）. Compared with the model group， the proliferation of LMSCs could be promoted after intervention with the corresponding Wenfei Huaxian decoction-containing serum （P<0.05， P<0.01）. Compared with the blank serum group， the SA-β-gal staining of LMSCs in the model group after D-gal stimulation was enhanced， and the content of NAD+ was increased （P<0.01）. The expression levels of senescence factors p16 and p53， as well as SASP pro-inflammatory factors IL-6 and TNF-α in the cell culture supernatant， were significantly increased （P<0.01）. The expression of senescence-associated proteins p16， p21， and p53 increased （P<0.01）， and the protein expression of NAMPT， SIRT1， peroxisome proliferator-activated receptor γ coactivator 1α （PGC-1α）， and forkhead box family transcription factor O1 （FoxO1） decreased （P<0.01）. Compared with the model group， the SA-β-gal staining of LMSCs in each group of Wenfei Huaxian decoction-containing serum was significantly reduced， and the content of NAD+ was decreased （P<0.01）. The senescence factors （p16 and p53） and inflammatory factors （IL-6 and TNF-α） in the cell culture supernatant were significantly decreased （P<0.01）. The expression of senescence-associated proteins （P16， P21， and P53） decreased （P<0.05， P<0.01）. The protein expressions of NAMPT， SIRT1， PGC-1α， and FoxO1 were significantly up-regulated （P<0.05， P<0.01）. ConclusionWenfei Huaxian decoction can alleviate senescence and inflammatory response damage of D-gal-induced LMSCs， and its mechanism may be related to the regulation of the NAMPT/SIRT1 signaling pathway.

HMGB1 gene knockout alleviates acute lung injury of sepsis mice via inhibiting TLR4/NF-κB pathway / 安徽医科大学学报

Objective To study the effect of high mobility group box B1(HMGB1)gene knockout on alleviating a-cute lung injury and inhibiting toll-like receptor 4(TLR4)/nuclear factor-KB(NF-κB)pathway of sepsis mice.Methods Wild-type(WT)mice were divided into WT-Sham group and WT-model group,and HMGB1 knockout(KO)mice were divided into KO-sham group and KO-model group.Sepsis ALI model was established by cecal ligation and perforation in WT-model group and KO-model group.Sham operation was performed in WT-Sham group and KO-Sham group.24 h after modeling,the partial pressure of arterial oxygen(PaO2)was detected,oxy-genation index(OI)was calculated,pathological changes of lung tissue were detected and lung injury score was calculated,the concentrations of tumor necrosis factor-α(TNF-α),interleukin-1 β(IL-1 β),interleukin-6(IL-6),reactive oxygen species(ROS),malondialdehyde(MDA),superoxide dismutase(SOD),in serum and lung tissues and the expression of HMGB1,TLR4 and nuclear NF-κB in lung tissues were detected.Results The PaO2,OI and the concentration of SOD in serum and lung tissue of WT-model group were lower than those of WT-Sham group,the lung injury scores,the concentrations of TNF-α,IL-1 β,IL-6,ROS and MDA in serum and lung tissue,and the expression levels of HMGB1,TLR4 and nuclear NF-κB in lung tissue were higher than those in WT-Sham group(P＜0.05).HMGB1 was not expressed in lung tissue of KO-model group,and the concentrations of PaO2,OI and the concentration of SOD in serum and lung tissue of KO-model group were higher than those of WT-model group,the lung injury scores,the concentrations of TNF-α,IL-1β,IL-6,ROS and MDA in serum and lung tissue,and the expression levels of TLR4 and nuclear NF-κB in lung tissue were lower than those of the WT-model group(P＜0.05).Conclusion HMGB1 gene knockout alleviates acute lung injury of sepsis mice,the re-lated molecular mechanism may be the inhibition of TLR4/NF-κB pathway mediated inflammation and oxidative stress.

Targeting CDT1 inhibit tumor growth and its mechanism in lung adenocarcinoma / 安徽医科大学学报

Objective To explore the clinical significance and mechanisms of chromatin licensing and DNA repli-cation factor 1(CDT1)in lung adenocarcinoma).Methods The gene expression samples of lung adenocarcinoma tissue and normal lung tissue were downloaded from the TCGA database,and perform differential analysis,GO a-nalysis,independent prognosis analysis,and correlation analysis with immunotherapy using R language.CDT1 ex-pression in lung adenocarcinoma and normal tissues was detected by PCR in clinical samples.The changes of cell proliferation and cycle in si-CDT1 knockdown group and si-NC control group were detected by flow cytometry.The invasive ability of each group was detected by Transwell.The expressions of CDT1,TPX2 and p53 in each group were detected by Western blot.Results The TCGA data analysis revealed CDT1 as a differentially expressed gene.GO analysis indicated that CDT1 was closely associated with the cell cycle.The high expression of CDT1 in lung adenocarcinoma tissues was validated in clinical samples.CDT1 could serve as an independent factor for predicting the prognosis of lung adenocarcinoma and had predictive value for immunotherapy in lung adenocarcinoma.Knock-down of CDT1 resulted in a significant decrease in cell proliferation ability compared to the control group,and cells were noticeably arrested in the G1 phase.Transwell assay results demonstrated a significant reduction in invasive capacity in the CDT1 knockdown group.Knockdown of CDT1 led to a significant decrease in TPX2 expression and a significant increase in p53 expression,while overexpression of CDT1 yielded the opposite effect.Conclusion Re-sults demonstrate the elevated expression of CDT1 in lung adenocarcinoma,its association with prognostic signifi-cance,and its impact on lung adenocarcinoma's occurrence and development by influencing TPX2 and p53.

Exploring the mechanism of traditional Chinese medicine indirubin derivative E804 inhibiting the proliferation and migration of lung cancer A549 cells based on the Nrf2-HO-1/GPX4 pathway / 安徽医科大学学报

Objective To investigate the effects of indirubatin derivative E804 on proliferation and migration of non-small cell lung cancer(NSCLC)A549 cells,and to elucidate the possible mechanism of Nrf2-HO-1/GPX4 pathway.Methods Lung cancer A549 cells were used as the cell model.The proliferation and migration of differ-ent specific inhibitors(Nec-1,CQ,Z-VAD,DFO,Fer-1 and Lip-1)in 0,10 μmol/L E804 and 10 μmol/L E804+groups were observed by MTT and cell scratch assay.The contents of reactive oxygen species(ROS)were de-tected by DCFH-DA fluorescence probe method,the contents of Fe2+were detected by colorimetric method,the contents of reduced glutathione(GSH)were detected by spectrophotometry,and the contents of malondialdehyde(MDA)were detected by micromethod.The expression levels of SLC7A11,Transferrin,GPX4,SLC40A1,Nrf2 and HO-1 were detected by Western blot in cells of 0,2.5,5 and 10 μmol/L E804 groups.Results Compared with the control group(0 μmol/L E804),2.5,5 and 10 μmol/L E804 significantly increased intracellular ROS,Fe2+and MDA levels,and decreased intracellular GSH content(P＜0.01).Meanwhile,the expression levels of SLC7A11,GPX4,SLC40A1,Nrf2 and HO-1 significantly decreased(P＜0.01),and the expression level of Transferrin increased(P＜0.05).Compared with the 10 μmol/L E804 group alone,the apoptosis inhibitor(Z-VAD)group and the ferroptosis inhibitor(DFO,Fer-1 and Lip-1)group could significantly reverse the inhibition of proliferation and migration of A549 cells by 10 μmol/L E804(P＜0.01).Conclution E804 can induce ferrop-tosis and inhibit the proliferation and migration of A549 cells,which may be related to the inhibition of Nrf2-HO-1/GPX4 pathway.