Patching with lens cleaning paper under an endoscope can accelerate the closure of large traumatic eardrum perforations.
Abstract. Recombinant hirudin (rH) is a highly potent and specific inhibitor of thrombin, and has been shown to inhibit the growth and metastasis of several types of cancers in experimental tumor models. The objective of this study was to evaluate the antitumor effects and explore the underlying mechanisms of rH in Hep-2 human laryngeal carcinoma (LC) cells. Hep-2 cells were treated with various concentrations of rH for 24 h. The cell viability was evaluated by a water-soluble tetrazolium salt (WST) assay. The adhesion ability of the cells was evaluated by cell adhesion to fibronectin. Cell migration and invasion were measured with the Boyden chamber assay. Cell apoptosis was detected by Hoechst 33324 fluorescence staining. A chicken chorioallantoic membrane (CAM) assay was used to assess the effects of rH on angiogenesis in vivo. Western blotting was used to detect the expression levels of vascular endothelial growth factor receptor (VEGF-R), focal adhesion kinase (FAK), Bcl-2-associated agonist of cell death (Bad) and B-cell CLL/lymphoma 2 (Bcl-2) proteins. rH significantly inhibited the cell viability and induced apoptosis in LC Hep-2 cells in a dose-dependent manner, as compared with phosphate-buffered saline (PBS) as control. These results were accompanied by a decrease in the anti-apoptotic protein Bcl-2 and an increase in the pro-apoptotic protein Bad. Moreover, rH dose-dependently inhibited the adhesion, migration and invasion of the Hep-2 cells, compared to the vehicle PBS. In addition, rH robustly suppressed angiogenesis in the CAM assay. Importantly, the expression of adhesion and angiogenesis-associated proteins FAK and VEGF-R was significantly downregulated by rH in a dose-dependent manner. The present findings demonstrate that rH exerts antitumor effects in Hep-2 human laryngeal cancer cells via multiple mechanisms and suggests that targeting thrombin by rH is a potential strategy for the treatment of LC. IntroductionLaryngeal carcinoma (LC) is a common head and neck malignancy and accounts for ~2.4% of newly diagnosed malignancies worldwide every year (1,2). Surgery, chemotherapy and radiation therapy are the current treatment modules for laryngeal cancer (3-5). Although early-stage laryngeal cancer can be effectively treated with surgery or radiotherapy, the 5-year survival rate of patients with advanced LC is still below 60% even after systematic surgery and post-surgical adjuvant radiotherapy or chemotherapy (6). In addition, surgery may result in complete or partial loss of swallowing and vocal functions. Many patients have to maintain a tracheal cannula on a long-term basis due to laryngeal stenosis after surgery, which markedly impairs their quality of life (6,7). Therefore, there is urgent need to develop novel approaches and strategies for the treatment of these advanced LC patients.The development and progression of cancer are closely associated with thrombosis (8). Thrombin, the key terminal enzyme of coagulation, enhances angiogenesis, stimulates the adhesion of tumor cells to platelet ...
The incidence of autosomal dominant polycystic kidney disease (ADPKD) is about 1 in 1,000, and its mortality rate is high. So far, beyond dialysis and kidney transplants, there is no better way to slow or completely cure the disease. However, both of which bring huge economic burdens to patients and society. Autosomal dominant polycystic kidney disease is characterized by numerous fluid-filled cysts on the surface of the kidneys. This can lead to tubular dilation and kidney failure. Proteinuria, kidney stones, hematuria, and cyst bleeding are common symptoms of ADPKD. Recent studies have found that the occurrence of adpkd is associated with pkd1 and pkd2 gene mutations, in which clinical data show that mutations in Pkd1 cause 60%-78% of Adpkd, while mutations in Pkd2 cause 15%-26%. Some environmental factors, such as kidney stones, can lead to adpkd, but the exact mechanism remains unclear. In this article, which introduce about autosomal dominant from the historical background of PKD, recent research results, the genetic mechanism of ADPKD, the impact of stones on ADPKD, and the basic damage of ADPKD to the kidney. Information about polycystic kidney disease.
To investigate the predictive value of contrast-enhanced ultrasound (CEUS) combined with serum miR-124 level in acute cerebral infarction (ACI) and their association with the contrast enhancement of carotid atherosclerotic plaque. Methods: Totally 60 patients diagnosed with ACI and 60 controls were included in the study. All the subjects had carotid atherosclerotic plaques, and all of them were examined by CEUS and were tested for serum miR-124 levels. Results: Time to peak (TTP) and mean transit time (MTT) in the ACI group were significantly shorter than those in the control group (P < 0.05), but the peak intensity ratio (PIR), the area under the curve (AUC), and relative expression levels of serum miR-124 were notably greater in the ACI group (P < 0.05). There were statistically significant differences in TTP, MTT, PIR, AUC, and serum miR-124 expression in patients with different cerebral infarct areas in the ACI group (P < 0.05). Besides, the sensitivity and specificity of serum miR-124 levels for the prediction of ACI were 71.67% and 90.00%, respectively, with a cut-off value of 1.52, and the sensitivity was 86.67% and specificity was 93.33% of CEUS combined with serum miR-124 in the prediction of ACI. The ACI group showed a higher proportion of grades 2 and 3 (P < 0.001). Pearson correlation analysis showed that the intraplaque contrast enhancement was negatively related to TTP and MTT but had a positive correlation with PIR, AUC, and serum miR-124 levels. Conclusion: Grades 2 and 3 intraplaque contrast enhancement and serum miR-124 level of 1.52 had high sensitivity and specificity to predict ACI. Moreover, the CEUS parameters combined with serum miR-124 level could improve the performance in predicting ACI and had auxiliary value in evaluating the stability of carotid atherosclerotic plaques.
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