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It is very likely that the pandemic will lead to an increase in influenza and pneumococcal vaccine coverage in this at-risk population.Although the margin reflex distance (MRD) is widely used to assess blepharoptosis, it has some drawbacks (e.g. inaccuracy in severe ptosis). A new parameter is desired. We digitally analyzed pre- and post-operative photographs of 95 patients with blepharoptosis. We set a rectangle with the vertical sides at the lateral and medial canthus and the horizontal sides at the highest and lowest points of the eyelids. We calculated the percentage of the vertical side (height) to the horizontal side (width) and defined this value as the vertical percentage of the palpebral fissure. The MRD and the vertical percentage values were strongly correlated (correlation coefficient 0.766). In the 77 bilateral cases, both sides showed significant improvement in vertical percentage (from 28.9 to 37.3%, right) and (28.7 to 36.1%, left). In the 18 unilateral cases, the affected side showed significant improvement in vertical percentage (from 29.6 to 38.7%), while the unaffected side showed no change. In the eight patients who underwent re-operation, the revised side's vertical percentage was not improved after the first operation (from 28.0 to 31.3%), and the revision significantly changed the vertical percentage to 39.0%. In the re-operated patients, the difference between the right and left sides decreased significantly from 6.7 to 1.9% post-revision. The aspect ratio of each palpebral fissure (the percentage of height to width) reflected the progression of blepharoptosis and the post-operative changes. The aspect ratio thus has the potential to be a new parameter for blepharoptosis.Hepatocellular carcinoma (HCC) is generally known as one of the most common cancers in the world. icFSP1 cell line Nowadays, interventional therapies such as transcatheter arterial chemoembolization (TACE) have emerged as an efficient therapy for HCC patients. Accumulating evidence has unveiled that long non-coding RNAs (lncRNAs) are crucial regulators in HCC progression. Nonetheless, the biological function of lncRNA zinc finger and SCAN domain containing 16 antisense RNA 1 (ZSCAN16-AS1) in HCC has not been systematically clarified. RT-qPCR was used to test ZSCAN16-AS1 expression in HCC cells. The biological functions of RP11-757 G1.5 on HCC cell proliferation, migration, invasion and apoptosis were investigated by colony formation, EdU, CCK-8 and transwell assays, as well as flow cytometry analysis. RNA immunoprecipitation (RIP), RNA pull-down and luciferase reporter assays were utilized to explore the specific mechanism of ZSCAN16-AS1. ZSCAN16-AS1 was significantly up-regulated in HCC cells. ZSCAN16-AS1 silence inhibited HCC cell proliferation, migration and invasion, while it accelerated HCC cell apoptosis. ZSCAN16-AS1 worked as a competing endogenous RNA (ceRNA) to regulate sperm associated antigen 9 (SPAG9) expression through sponging miR-181 c-5p. Moreover, SPAG9 could activate the c-Jun-N-terminal kinase (JNK) pathway. Taken together, our study elucidated that ZSCAN16-AS1 expedited HCC progression via modulating the miR-181 c-5p/SPAG9 axis to activate the JNK pathway, which might be a highly potential HCC therapy and treatment target.Thrombopoietin (TPO) and its receptor, MPL, are the primary regulators of platelet production and critical for hematopoietic stem cell (HSC) maintenance. Since TPO was first cloned in 1994, the physiological and pathological roles of TPO and MPL have been well characterized, culminating in the first MPL agonists being approved for the treatment of chronic immune thrombocytopenia in 2008. Dysregulation of the TPO-MPL signaling axis contributes to the pathogenesis of hematological disorders decreased expression or function results in severe thrombocytopenia progressing to bone marrow failure, while hyperactivation of MPL signaling, either by mutations in the receptor or associated Janus kinase 2 (JAK2), results in pathological myeloproliferation. Despite its importance, it was only recently that the long-running debate over the mechanism by which TPO binding activates MPL has been resolved. This review will cover key aspects of TPO and MPL structure and function and their importance in receptor activation, discuss how these are altered in hematological disorders and consider how a greater understanding could lead to the development of better-targeted and more efficacious therapies.RNA pumilio RNA binding family member 1 (circPUM1) has been reported to play important roles in the tumorigenesis of several cancers. However, the underlying molecular role of circPUM1 in non-small cell lung cancer (NSCLC) progression remains unknown. The qRT-PCR and western blot were used to evaluate the expression of RNAs and proteins. In vitro cell proliferation assays, flow cytometric and glucose metabolism analyses were performed to test the effects of circPUM1 and its target on NSCLC cell growth and glycolysis. The interaction between microRNA (miR)-590-5p and circPUM1 or methyltransferase like 3 (METTL3) was analyzed by using dual-luciferase reporter, pull-down or RNA immunoprecipitation (RIP) assays. Murine xenograft model was established to conduct in vivo experiments. CircPUM1 was highly expressed in NSCLC tissues and cell lines. CircPUM1 knockdown suppressed cell proliferation, cell cycle and glycolysis in vitro. Moreover, circPUM1 directly bound to miR-590-5p, and miR-590-5p inhibitor reversed the inhibitory effects of circPUM1 knockdown on NSCLC carcinogenesis. Additionally, miR-590-5p suppressed NSCLC progression by directly targeting and regulating METTL3. Importantly, circPUM1 could regulate METTL3 in NSCLC cells through miR-590-5p. In addition, it was also proved circPUM1 silencing impeded tumor growth and glycolysis in the murine xenograft model by regulating miR-590-5p/METTL3 axis. CircPUM1 promoted NSCLC tumor growth and glycolysis through sequestering miR-590-5p and up-regulating METTL3, providing an improved understanding of NSCLC tumorigenesis and a potential therapeutic target for NSCLC therapy.Atrial fibrillation (AF) is the common arrhythmias. Myocardial fibrosis (MF) is closely related to atrial remodeling and leads to AF. MF is the main cause of cardiovascular diseases and a pathological basis of AF. Thus, the underlying mechanism in MF and AF development should be fully elucidated for AF therapeutic innovation. Autophagy is a highly conserved lysosomal degradation pathway, and the relationship between autophagy and MF has been previously shown. Moreover, research reported that quercetin (Que) could ameliorate MF. The current study aimed to explore the mechanism of Que in MF. The results in this study showed that in clinical AF patients and in aged rats, miR-223-3p was high-expressed, while FOXO3 and autophagy pathway related proteins, such as ATG7, p62/SQSTM1 and the ratio of LC3B-II/LC3B-I were significantly inhibited. In vivo and in vitro studies, we found that Que can effectively inhibit the expression of miR-223-3p in AF model cells and rats myocardial tissues, and meanwhile enhance the expression of FOXO3 and activate the autophagy pathway, and significantly inhibit myocardial fibrosis, and improve myocardial remodeling in atrial fibrillation.