Prognostic value of tumor­associated CD177+ neutrophils in lung adenocarcinoma.

The aim of the present study was to detect CD177+ neutrophils in tumor tissues and analyze their association with the clinical characteristics and prognosis of patients with lung adenocarcinoma (LUAD). Immunohistochemistry was used to detect CD177+ neutrophils in tumors and adjacent tissues of 16 patients with LUAD who underwent curative surgical resection. A total of 120 patients with LUAD were recruited, and their clinical data were collected; survival follow-up was performed. CD177+ neutrophils in tumor tissues were detected via immunohistochemistry, and the association between CD177+ neutrophils and clinical characteristics was analyzed. The density of CD177+ neutrophils in tumor tissues and adjacent tissues of patients with LUAD was analyzed using t-test, and the association between CD177+ neutrophils and clinical characteristics was analyzed through the Chi-square test. Survival was calculated using the Kaplan-Meier survival rate curve. Finally, the association between these indicators and the survival of LUAD patients was evaluated using Cox regression analysis. CD177+ neutrophil infiltration was significantly higher in LUAD tumor tissues, and the high density of CD177+ neutrophils was associated with the clinical characteristics of TNM stage, tumor differentiation and poor progression-free and overall survival in LUAD. In conclusion, tumor-associated CD177+ neutrophils associated with malignant progression and poor prognosis may be independent and unfavorable prognostic biomarkers for LUAD.

Modified silicone hourglass stents for the treatment of benign subglottic stenosis: a case series.

Background: Benign subglottic stenosis has been a challenging illness to treat and manage in clinical because of its special anatomical location, and easy recurrence of the condition, which can cause life-threatening asphyxia. For patients who are not suitable for surgery or in urgent need of preoperative transitional treatment, respiratory endoscopy-guided stent placement becomes an alternative treatment option. Case Description: Clinical data were collected from four patients who received treatment at the Jining First People's Hospital due to benign subglottic stenosis, which was achieved after tracheal intubation/tracheotomy. All patients were male, admitted with shortness of breath, with an average of 45±8.95 years. Among them, three patients refused the surgery, and one patient was unable to tolerate the surgery. Despite repeated intervention under bronchoscopy, airway stability was still not maintained. By inserting modified hourglass silicone stents, the patient's symptoms were improved and the clinical efficacy was satisfactory. Regular follow-up showed good stent position and no granulomatous growth at the ends of the stents. Conclusions: This is an initial report of improved hourglass stents used for the treatment of benign subglottic airway stenosis. In these cases, the modified hourglass stents had good efficacy and fewer complications and were also accepted by patients.

A long non-coding RNA LINC01288 facilitates non-small cell lung cancer progression through stabilizing IL-6 mRNA.

The non-small cell lung cancer (NSCLC) denotes a malignant type of cancers. Long non-coding RNAs (lncRNAs) can actively participate in cancer development. However, the exact role of lncRNAs in NSCLC remains largely elusive. In current work, we report a novel intergenic lncRNA LINC01288 involved in NSCLC. We found that LINC01288 is frequently upregulated in NSCLC samples and cell lines. LINC01288 significantly promotes viability, migration, xenograft tumor growth and metastasis in vitro and in vivo. LINC01288 physically interacts with the IL-6 mRNA and increase the stability of IL-6 transcripts. Subsequently, the autocrine induction of IL-6 and enhanced STAT3 activation may facilitate NSCLC progression. Collectively, our data have demonstrated that LINC01288 serves as a crucial mediator of IL-6/STAT3 pathway and created novel interplay between lncRNAs and tumor development.

[IL-33 promotes airway remodeling in a mouse model of asthma via ERK1/2 signaling pathway].

OBJECTIVE: To explore the role of IL-33 in asthmatic airway remodeling. METHODS: Male BALB/c mice were randomly divided into 3 groups: a control group, an ovalbumin (OVA) group, and an anti-IL-33 antibody combined with OVA group. The airway remodeling features in mice were observed by HE staining. In addition, the expressions of IL-33, alpha smooth muscle actin (α-SMA), and type 1 collagen (Col1) in the airway of mice were detected by immunohistochemistry and Western blotting. Finally, Western blotting was used to determine the activation of extracellular signal-regulated kinase 1/2 (ERK1/2) and mitogen- and stress-activated protein kinase 1 (MSK1) in the lungs of mice. In vitro, human lung fibroblasts (HLF-1) were pretreated with the ERK1/2 inhibitor U0126 or the MSK1 inhibitor H89 respectively, and then treated with the human recombinant IL-33 (rIL-33). Then real-time quantitative PCR and Western blotting were used to test the expressions of α-SMA and Col1. Immunofluorescence cytochemistry and Western blotting were also used to observe the phosphorylation of ERK1/2 and MSK1 in HLF-1 cells. RESULTS: The pre-treatment with the ERK1/2 inhibitor U0126 or anti-IL-33 antibody significantly abolished the OVA-induced airway remodeling, increased expressions of IL-33, α-SMA, Col1, and phosphorylation of ERK1/2 and MSK1 in the airway of mice. In vitro, the increased expressions of α-SMA and Col1 and the phosphorylation of ERK1/2 and MSK1 induced by rIL-33 in HLF-1 cells were markedly inhibited by the pre-treatment with U0126 or H89. CONCLUSION: IL-33 promotes airway remodeling in asthmatic mice via the ERK1/2-MSK1 signaling pathway.