Early neurological deterioration (END) is associated with increased risk of functional disability and mortality. However, data are limited regarding the long-term risk of poor functional outcomes. Thus we explored the association between END and long-term outcomes in patients with acute ischemic stroke.A total of 1064 patients were enrolled with acute ischemic stroke who were consecutively admitted to the 3 stroke units of Huai-He Hospital, Kaifeng, China. END was defined as an increment change of at least one point in motor power or total National Institute of Health Stroke Scale (NIHSS) score deterioration ≥2 points within the first week after admission. We retrospectively assessed the risk factors of END and prospectively explored the relationship between END and the long-term outcomes by multivariable regression models after adjusting the potential confounding factors. Outcomes were evaluated at 18 months based on modified Rankin scale (MRS) scores.Approximately 32% of first-ever ischemic stroke patients experienced END during the acute phase. END was associated with diabetes (odds ratio [OR], 2.218; 95% confidence interval [CI] 1.619–3.037), NIHSS score at admission (OR, 1.052; 95% CI 1.023–1.082), C-reactive protein (CRP) levels (OR, 1.224; 95% CI 1.066–1.406]), and homocysteine (HCY) levels (OR, 1.203; 95% CI 1.061–1.365) after adjusting related factors, such as hypertension, diabetes, NIHSS at admission, and some blood laboratory values, including direct bilirubin, total cholesterol, low-density lipoprotein, glucose, CRP, HCY, and D-dimer levels. During the follow-up period, 52 (4.9%) patients died, 160 (15.0%) recrudesced, and 317 (29.8%) suffered poor outcomes. Multivariate logistic regression analyses revealed that poor outcome was associated with END (OR, 3.366; 95% CI 2.495–4.542), age (OR, 1.028; 95% CI 1.015–1.041), body mass index (OR, 1.096; 95% CI 1.051–1.144), coronary heart disease (OR, 1.637; 95% CI 1.108–2.416), and CRP (OR, 2.474; 95% CI 1.840–3.326).The risk factors of END are multifaceted. Diabetes, NIHSS score at admission, CRP, and HCY are independent predictors of END. In addition, the results of this study indicate that END is an important predictor of poor functional outcome.

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The hypoxia‐reoxygenation (H/R) model helps analyze myocardial infarction triggered by acute myocardial ischemia, which induces cardiomyocyte proliferation and apoptosis. The Gene Expression Omnibus database was used to obtain the GSE74205 and GSE3866 microarray data, including microRNA (miRNA) and messenger RNA profiles, to catalog potential key miRNAs and genes. The role of rno‐mir‐496 expression in cardiomyocyte proliferation within 10 days of birth was established. The microRNA Target Prediction Database (miRDB) database—via Gene Ontology annotation—predicted hook microtubule tethering protein 3 (Hook3), a key target gene of rno‐mir‐496, was closely related to cell proliferation. Upregulation of miR‐496 related to a significant reduction in apoptosis of H9c2 and human cardiomyocytes treatment with H/R. Moreover, transfection of H9c2 cells with miR‐496 mimics, which were pretreated with H/R for 12 hours, increased Ki67 levels, proliferating cell nuclear antigen and Bcl‐2 proteins; and decreased cleaved caspase‐3 and Bax protein levels, as determined by reverse transcription‐polymerase chain reaction and Western blot assays. A dual‐luciferase reporter system confirmed that miR‐496 targets the Hook3 suppressor. Hook3 overexpression stimulated apoptosis in H/R‐treated cells, thus reducing cell proliferation. Upregulated miR‐496 activated phosphatidylinositol‐3‐kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling, while Hook3 exhibited the inverse trend in H/R‐treated H9c2 cells. In summary, with Hook3 functionality's aid, miR‐496 upregulation defends cells from H/R‐induced apoptosis and stimulates cell proliferation. miR‐496 targets Hook3 to trigger the PI3K/Akt/mTOR signaling pathway for antiapoptotic and proliferative effects.

Background Circular RNAs (circRNAs) have been demonstrated to exert crucial mediators in tumor initiation and development. Nevertheless, the roles of circKIF4A in breast cancer (BC) are still not very clear. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to determine the expression of circKIF4A, miR-152, zinc finger E-box binding homeobox 1 (ZEB1) mRNA and caspase-3. Western blot assay was utilized to examine the protein level of ZEB1. Transwell assay and flow-cytometric analysis were adopted for the evaluation of cell migration, invasion and apoptosis, respectively. The associations among circKIF4A, miR-152 and ZEB1 were predicted by online websites and verified by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Results CircKIF4A and ZEB1 were conspicuously upregulated and miR-152 was markedly reduced in BC tissues and cells. Deficiency of circKIF4A repressed migration, invasion and induced apoptosis of BC cells. Moreover, circKIF4A was confirmed to be a sponge of miR-152 and miR-152 could bind to ZEB1. MiR-152 inhibition or ZEB1 overexpression abolished the impacts of circKIF4A knockdown on cell migration, invasion and apoptosis in BC. Conclusion Silencing of circKIF4A hampered cell metastasis and promoted apoptosis by regulating ZEB1 via sponging miR-152 in BC.

Previous studies have demonstrated that various microRNAs (miRNAs or miRs) are abnormally expressed in osteosarcoma (OS) and serve roles in its malignant development. An in-depth understanding of the specific roles of dysregulated miRNAs in OS may be important for cancer research and the identification of novel therapeutic targets. In the current study, reverse transcription-quantitative PCR was performed to determine miR-652 expression in OS tissues and cell lines. Cell Counting Kit-8 and Transwell invasion assays were used for assessing the effect of miR-652 on the proliferation and invasion of OS cells. Herein, miR-652 expression was assessed in OS and the effects and molecular mechanisms of miR-652 in OS cells were examined. The results revealed that miR-652 expression was significantly upregulated in OS tissues and cell lines compared with adjacent normal tissues and a normal human osteoblast cell line. Furthermore, miR-652 downregulation inhibited the proliferation and invasion of OS cells. miR-652 was also demonstrated to directly interact with the 3'-untranslated region of kruppel-like factor 9 (KLF9) and miR-652 negatively regulated KLF9 expression in OS cells. miR-652 and KLF9 mRNA levels were also revealed to be inversely correlated in OS tissues. Treatment with KLF9 small interfering RNA abolished the suppression of OS proliferation and invasion induced by miR-652 downregulation. miR-652 may serve an oncogenic role in OS cells by targeting KLF9 directly. The results also indicated that miR-652 may be an effective novel therapeutic target for the treatment of patients with OS.