Interventional treatment of giant tracheal lymphoma under rigid bronchoscopy: A case report and literature review.

INTRODUCTION: Lymphoma can appear in all parts of the body and present with different symptoms. However, bronchial lymphoma is rare and can be misdiagnosed as airway malignancy or lung disease.Patient: An older adult woman with tracheal lymphoma experienced severe breathing difficulties, and chest computed tomography indicated severe narrowing of the airway. She did not respond to repeated antibiotic treatment, and she was eventually diagnosed with lymphoma based on pathology after surgical removal of the tumor. DIAGNOSIS: The patient received a diagnosis of thoracic tracheal stenosis due to intratracheal inflammatory granulomatous lesions or a tumor. INTERVENTIONS: Treatment involved the use of a high-frequency electrotome, freezing, and argon plasma coagulation. OUTCOMES: The patient reported improvements in dyspnea, cough, and other symptoms after the operation. The pathological results confirmed follicular lymphoma. Reexamination by fiberbronchoscopy indicated that the degree of stenosis in the middle and upper tracheal segments was significantly reduced following interventional therapy. CONCLUSION: Endoscopic interventional therapy can be an effective treatment for tracheal lymphoma.

Prognostic and clinicopathological significance of long noncoding RNA MALAT-1 expression in patients with non-small cell lung cancer: A meta-analysis.

BACKGROUND: Although expression of long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT-1) in tumor tissues has been assessed in several malignancies. However, the association between lncRNA MALAT-1 expression and prognosis or clinicopathological feature remains controversial. Therefore, we conducted a meta-analysis to verify whether lncRNA MALAT-1 expression was associated with prognosis or clinicopathological features in patients with non-small cell lung cancer (NSCLC). METHODS: We searched Embase, PubMed, Web of Science, Cochrane library, The Chinese National Knowledge Infrastructure, and Wanfang databases from inception to March, 1, 2020. The language restrictions were Chinese and English. The published literature on lncRNA MALAT-l expression and prognosis or clinicopathological characteristics of NSCLC patients was statistically analyzed. Combined hazard ratios (HRs), odds ratios (OR), and 95% confidence intervals (95% CIs) were used to evaluate the effects of lncRNA MALAT-l on the prognosis and clinicopathological features of NSCLC. RESULTS: Fifteen studies with 1477 NSCLC patients were enrolled. The results showed that the elevated expression of lncRNA MALAT-l in tumor tissues was associated with shorter overall survival (OS) (HR: 2.20, 95% CI: 1.53-3.16; P = 0.000). Additionally, high lncRNA MALAT-l expression was also significantly associated with gender (OR: 0.69, 95% CI: 0.51-0.93; P = 0.014), tumor size (OR: 1.87, 95% CI:1.13-3.09; P = 0.016), lymph node metastasis (LNM) (OR: 2.87, 95% CI:1.05-7.83, P = 0.04), tumor differentiation (OR: 1.60, 95% CI:1.17-2.20; P = 0.003), and tumor-node-metastasis (TNM) stage (OR: 0.42, 95% CI: 0.25-0.70; P = 0.001). There was no significant relationship between lncRNA MALAT-l expression and other clinicopathological features including age (OR: 1.03, 95% CI: 0.79-1.34; P = 0.830), number of tumors (OR: 1.02, 95% CI: 0.63-1.64; P = 0.943), vascular invasion (OR: 1.23, 95% CI: 0.50-3.05; P = 0.652), and recurrence (OR: 1.98, 95% CI: 0.67-5.85; P = 0.214). CONCLUSION: The overexpression of lncRNA MALAT-l in NSCLC tissues was correlated with OS, gender, tumor size, LNM, tumor differentiation, and TNM stage. Thus, lncRNA MALAT-l may serve as a prognostic factor for NSCLC.

Cigarette smoke exposure promotes differentiation of CD4+ T cells toward Th17 cells by CD40-CD40L costimulatory pathway in mice.

Purpose: This study aimed to investigate the impact of cigarette smoke exposure upon CD40-CD40L ligation between bone marrow-derived dendritic cells (BMDCs)and CD4+T cells, and to examine the effects of cigarette smoke exposure upon differentiation of CD4+T cells toward Th17 cells through blockade of CD40-CD40L pathway in mice. Methods: The study was processed in vivo and in vitro. In vivo, Th17 cells, CD40, interleukin (IL)-17A, and IL-27 in the lung tissues were quantified and compared between mice with and without cigarette smoke exposure. In vitro, Th17 cells, IL-17A, and IL-27 yielded by multiple cell cultivations in which BMDCs from mice with or without cigarette smoke exposure were fostered with CD4+ T cells from healthy mice spleens in the presence of antagonistic CD40 antibody and/or cigarette smoke extract (CSE) were quantified and compared. The flow cytometry was used to detect expressions of Th17 cells and CD40, and the liquid chip was used to detect levels of IL-17A and IL-27. Results: Both in vivo exposed to cigarette smoke and in vitro to CSE, CD40 expressions noticeably escalated on the surfaces of BMDCs. The presence of Th17 cells, IL-17A, and IL-27 in the lung tissues prominently increased in mice exposed to cigarette smoke. The in vitro culture of CD4+ T cells and BMDCs significantly enhanced the differentiation of CD4+ T cells toward Th17 cells and secretions of IL-17A and IL-27 in the case that BMDCs were produced from mice exposed to cigarette smoke or the culture occurred in the presence of CSE. Usage of antagonistic CD40 antibody evidently reduced the number of Th17 cells, IL-17A, and IL-27 that increased due to cigarette smoke exposure. Conclusion: The CD40-CD40L ligation is associated with the quantities of Th17 cells and relevant cytokines in the context of cigarette smoke exposure. Reducing the number of Th17 cells via the usage of antagonistic CD40 antibody can be an inspiration for pursuing a novel therapeutic target for immune inflammation in COPD.

Indoor environmental factors associated with pulmonary function among adults in an acid rain-plagued city in Southwest China.

OBJECTIVE: To assess the association of indoor environmental risk factors with respiratory function among adults in an acid rain-plagued city in China where coal use is frequent. METHODS: The subjects were randomly selected in the winter season. Information on selected home environmental factors was collected through administered questionnaires. Additionally, pulmonary function tests, including Forced Vital Capacity (FVC), Forced Expiratory Volume in 1 s (FEV1), FEV1/FVC and Peak Expiratory Flow Rate (PEFR) were also performed in participants. RESULTS: This study showed that, among a variety of risk factors, coal fuel use, cooking oil fumes and active and passive smoking exposure together with asthma in childhood were important factors for deterioration of pulmonary function among adults in the winter season (p < 0.05). Additionally, subjects whose kitchen was located in the living room or bedroom, who opened their windows only occasionally or never, who noted the presence of cooking oil fumes and pests, whose bedroom was shared by 3 or more residents and who kept pets tended to exhibit lower values of FVC, FEV1 and PEFR values compared with non-exposed counterparts (p < 0.05). CONCLUSIONS: This study demonstrated impaired pulmonary function among adults who were exposed to indoor risk factors, such as coal fires and cigarette smoking compared to non-users in the winter season and emphasizes the need for public health efforts to decrease exposure to indoor air pollution.

[Depressive effect of cigarette smoke extracts on dendritic cells inducing differentiation of CD4+T cells into CD4+CD25+Foxp3+ Tregs].

OBJECTIVE: To explore the impact of both cigarette smoke extracts (CSE) and CD40-CD40L pathway blocking on mouse myeloid dendritic cells (DCs) inducing CD4(+)T cells differentiation into CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs). METHODS :A combination of recombinant mouse granulocyte-macrophage colony stimulating factor (rmGM-CSF, 40 ng/mL) and recombinant mouse IL-4 (rmIL-4, 10 ng/mL) was applied in vitro to induce the differentiation of BALB/c mouse myeloid monocytes into DCs. DCs were detected for the expression of CD40 molecules through flow cytometry. CD4(+)T cells were sorted out from BALB/c mouse spleen cells with magnetic activated cell sorting technique. Myeloid DCs were co-cultivated with CD4(+)T cells separated from the control-group for 24 hours in the presence of CSE or antagonistic CD40 antibody. CD4(+)CD25(+)Foxp3(+)Tregs were quantified with flow cytometry, and concentrations of IL-10 and IL-6 in cell supernatants were detected with liquid phase chip technology. RESULTS: The co-cultivation of DCs and CD4(+)T cells promoted CD4(+)CD25(+)Foxp3(+)Tregs differentiation. However, after stimulated by CSE, the number of CD4(+)CD25(+)Foxp3(+)Tregs differentiated by co-cultivation of DCs and CD4(+)T cells was reduced, accompanied by the decrease of IL-10 concentration and the increased of IL-6 concentration. In contrast, with the intervention of antagonistic CD40 antibody, the number of CD4(+)CD25(+)Foxp3(+)Tregs increased, IL-10 concentration rose and IL-6 dropped. CONCLUSION: CSE can substantially reduce CD4(+)CD25(+)Foxp3(+)Tregs, but blocking CD40-CD40L pathway in vitro by antagonistic CD40 antibody can promote the process of CD4(+)T cells differentiating into CD4(+)CD25(+)Foxp3(+)Tregs.