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Retrograde utilisation of the Outback™ re-entry catheter throughout sophisticated infrainguinal arterial recanalizations.
In recent years, the diagnosis and treatment of gastrointestinal stromal tumors (GISTs) of the small intestine have been a hot topic due to their rarity and non-specific clinical manifestations. With the development of gene and imaging technology, surgery, and molecular targeted drugs, the diagnosis and treatment of GISTs have achieved great success. For a long time, radical resection was prioritized to treat GISTs of the small intestine. At present, preoperative tumor staging is a novel treatment for unresectable malignant tumors. In addition, karyokinesis exponent is the sole independent predictor of progression-free survival of GISTs. The DNA, miRNA, and protein of exosomes have also been found to be biomarkers with prognostic implications. The research on the treatment of GISTs has become a focus in the era of precision medicine, ushering in the use of standardized, normalized, and individualized treatment.Objective This study set out to explore the regulatory mechanism of miR-130a-5p in cisplatin (DDP)-resistant gastric cancer (GC) cells. Materials and methods Forty cases of GC and paracancerous tissues were collected, and the miR-130a-5p and CCL22 levels were detected by qRT-PCR. DDP-resistant cell lines of GC cells were established. Cell viability, invasion, and apoptosis were measured by CCK-8, Transwell, and flow cytometry, respectively. Trilaciclib The relationship between miR-130a-5p and CCL22 was verified by dual-luciferase reporter enzyme, and the protein levels of caspase-3, bax, bcl-2, and CCL22 were determined by Western blot. Results miR-130a-5p was low expressed in GC tissues and cells, while CCL22 showed marked negative correlation, and the area under the curve (AUC) for diagnosing GC was not less than 0.850. Up-regulating miR-130a-5p or knocking down CCL22 expression can inhibit the proliferation and invasion of GC cells and promote their apoptosis, reverse the resistance of NCI-N87/DDP to DDP, and also enhance the chemosensitivity of GC cells. Dual-luciferase reporter enzyme identified that there was a targeted relationship between miR-130a-5p and CCL22. At the same time, miR-130a-5p and CCL22 were up-regulated or down-regulated, and the malignant proliferation, invasion, apoptosis, and DDP chemotherapy resistance of the cells had no difference compared with miR-NC with transfection-unrelated sequences. Conclusion Up-regulating miR-130a-5p can enhance the sensitivity of DDP-resistant GC cells to chemotherapy and regulate their biological function by targeted inhibition of CCL22.Introduction 2019 novel coronavirus disease (COVID-19) outbreaks have been occurring in China and other countries in the world. To prevent further spread of the disease, restrictions of population flow from the government and measures to reduce virus transmission from hospitals may lead to the delay of diagnosis and treatment in patients with nasopharyngeal carcinoma (NPC). Methods All NPC patients with radiotherapy indications were included from 20 weekdays before (group A) and after (group B) January 31, 2020, when the institute began to take measures against COVID-19. The waiting intervals of each step and variation from the diagnosis and treatment path of NPC between two groups were compared. Results Significant differences were found between the group A and group B in the median waiting days for pathological biopsy (5 vs 15, P=0.012), radiotherapy immobilization and simulation (3.5 vs 16.5, P less then 0.001), validation of position and plan (20 vs 61, P less then 0.001) and initiation of radiotherapy (28 vs 36, P=0.005). During the waiting period of radiotherapy, 32.4% of the NPC patients received an additional one cycle of chemotherapy to the original treatment strategy. Conclusion The prevalence of COVID-19 caused delay in the diagnosis and treatment of NPC patients to a certain extent. Additional chemotherapy could be considered to counteract the effect of treatment delay. More specific measures should be taken to balance the risk of delayed diagnosis and treatment of NPC and infection of COVID-19.Purpose To assess the use of video-assisted thoracoscopic surgery to treat lung metastases from refractory choriocarcinoma. Patients and methods We reviewed patients diagnosed with refractory choriocarcinoma who underwent lung resection by video-assisted thoracoscopic surgery combined with chemotherapy between October 2013 and August 2019 at the Peking Union Medical College Hospital. The surgical records, pathologic findings and survival rates were analyzed. Results The study included 73 patients who underwent 78 thoracoscopic surgeries. Most patients underwent lobectomy (48.7%), and 17 patients (21.8%) underwent resection of more than one lobe. The median operation time and bleeding volume were 95 minutes and 50 mL, respectively. The median duration of chest tube use and hospital stay were 3 days and 4 days, respectively. Postoperative complications were documented in 6 patients (7.7%). The thoracic lymph nodes were harvested in 51 patients (65.4%), but none of these patients had positive nodes. A total of 69.2% of the patients had positive pathologic findings. The mean follow-up time was 30 months. During follow-up, 11 patients experienced disease relapse, and 2 of them died because of brain metastasis. The overall disease-free rate was 83.6%, and the survival rate was 97.0% after excluding those lost to follow-up. Patients with decreased postoperative β-hCG showed a higher disease-free rate during follow up (P less then 0.05). Conclusion The minimally invasive video-assisted thoracoscopic approach is a valuable and safe treatment for refractory choriocarcinoma patients with lung metastases. Lymphadenectomy is not suggested for these patients. Patients with decreased postoperative β-hCG levels may achieve a much better prognostic result.Introduction LEF1-AS1 is a characterized oncogenic lncRNA in oral cancer. Analysis of TCGA dataset revealed the upregulation of LEF1-AS1 in non-small-cell lung cancer (NSCLC). This study was therefore carried out to investigate the involvement of LEF1-AS1 in NSCLC. Methods A total of 62 NSCLC patients were included to collect paired cancer and non-tumor tissues. RT-qPCR was performed to measure levels of LEF1-AS1 and miR-221 expression. Transient transfections were performed to explore the interactions between LEF1-AS1, miR-221 and PTEN. Cell proliferation and apoptosis were analyzed by cell proliferation assay and cell apoptosis assay, respectively. Results We found that LEF1-AS1 was upregulated in NSCLC patients. In addition, expression of LEF1-AS1 was negatively correlated with the expression of PTEN but positively correlated with the expression of miR-221 in NSCLC tissue samples. In NSCLC cells, overexpression of LEF1-AS1 led to downregulated expression of PTEN but upregulated expression of miR-221, which can directly target PTEN.
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