ABSTRACT
BACKGROUND: Many patients have inadequate long-term analgesia, respiratory distress, and hypoxemia due to a long-standing substantial smoking history or the presence of primary pulmonary diseases; analgesic treatment is not valid in these patients. Even if the imaging findings of rib fractures are relatively mild, rib fractures may cause severe position limitation, respiratory distress, and hypoxemia. AIM: To investigate the curative effect of surgical treatment for patients with severe non-flail chest rib fractures. METHODS: A total of 78 patients from our hospital with severe noncontinuous thoracic rib fractures from September 2016 to September 2018 were enrolled in our study. Thirty-nine patients underwent surgical treatment, and 39 underwent conservative treatment. The surgical treatment group received surgery performed with titanium plates, and the screws were inserted with open reduction and internal fixation. The conservative treatment group received analgesia and symptomatic treatment. The pain scores at 72 h, 1 wk, 2 wk, 4 wk, 6 wk, 3 mo, and 6 mo were compared, and the SF-36 quality of life scores were compared atthe 3rd and 6th months. RESULTS: Pain relief in the surgical group was significantly better than that in the conservative group at each time point (72 h, 1 wk, 2 wk, 4 wk, 6 wk, 3 mo, and 6 mo after surgery, P < 0.001). ( The SF-36 scores were significantly higher in the surgical group than in the conservative group at 1 mo and 6 mo (P < 0.05). CONCLUSION: Patients with severe non-flail chest rib fractures have a better quality of life following surgical treatment than following conservative treatment, and surgical treatment is also useful for relieving pain. We should pay more attention to the physiological functions and clinical manifestations of patients with severe rib fractures. In patients with non-flail chest rib fractures, surgical treatment is feasible and effective.
ABSTRACT
MicroRNAs (miRNAs) have been demonstrated to participate in a variety of human cancers by functioning as post-transcriptional regulators of oncogenes or antioncogenes including non-small cell lung cancer (NSCLC). The aim of the current study was to identify the role of miR-422a in NSCLC via sulfatase 2 (SULF2) to further elucidate the mechanism of NSCLC. Initially, the expression of miR-422a and SULF2 was determined in NSCLC tissues and cells. The role of miR-422a in NSCLC was identified in relation with a miR-422a mimic or inhibitor, siRNA against SULF2 and TGF-ß1. The regulatory effects of miR-422a were examined following detection of the related epithelial mesenchymal transition (EMT)-related genes, and the apoptosis-related genes and evaluation of their cellular biological functions. The expression pattern of miR-422a, SULF2, and the TGF-ß/SMAD pathway-related genes was detected to elucidate the mechanism by which miR-422a influences the progression of NSCLC. Finally, xenograft tumors in nude mice were observed for tumorigenicity evaluation purposes. Our results showed that miR-422a was poorly expressed while SULF2 was highly expressed in NSCLC. Dual luciferase reporter gene assay further verified that miR-422a targeted SULF2. Altogether, this study demonstrated that miR-422a downregulated SULF2 to inhibit the TGF-ß/SMAD pathway. NSCLC cell proliferation, migration, invasion, colony formation, EMT and tumorigenesis were all inhibited while apoptosis was promoted upon restoration of miR-422a or silencing of SULF2. However, the activation of the TGF-ß/SMAD pathway was determined to reverse the tumor-suppressive effects of si-SULF2. miR-422a restoration, which ultimately inhibited the progression of NSCLC by suppressing the TGF-ß/SMAD pathway via SULF2.
