This study aimed to explore the relationship of D-dimer level with the risk stratification of ischemic stroke, and determine whether high D-dimer levels could be used as a risk factor of ischemic stroke in patients with nonvalvular atrial fibrillation (NVAF).This single-center, retrospective study recruited NVAF patients who did not undergo anticoagulant therapy. These patients were divided into 2 groups: ischemic stroke group and no-stroke group. The medical records of each patient were reviewed, demographic and clinical analyses were performed, and the laboratory results were summarized.A total of 323 eligible in-patients with NVAF, who did not receive anticoagulant therapy, were recruited (206 male and 117 female patients, median age was 75.18 ± 10.46 years old). Among these patients, 78 patients suffered from acute ischemic stroke. D-dimer level increased with age, and was positively correlated with the risk stratification of stroke, CHADS2 score (rs = 0.441, P < .001), and CHA2DS2-VASC score (rs = 0.412, P < .001), even after adjustment for age and gender (rs = 0.422, P < .001). The difference in baseline D-dimer level between these 2 groups was not statistically significant (0.70 vs 0.66 mg/L, P = .330), but this significantly increased when patients suffered from stroke (1.34 vs 0.70 mg/L, P < .001). The D-dimer level after stroke (≥6 months) was also higher than the baseline (1.16 vs 0.68 mg/L, P = .514) in 6 months, and this level nearly returned to baseline level after one year (0.69 vs 0.68 mg/L, P = .158). However, logistic regression revealed that only the D-dimer level at stroke onset and OMI were independent risk factors for ischemic stroke (P < .001), while the increase from baseline D-dimer levels was not an independent risk factor (P = .125).D-dimer level is positively correlated with the risk stratification of ischemic stroke, but has no predictive value on the occurrence of ischemic stroke in patients with NVAF.
Insulin receptor substrate 1 (IRS1) is a potential oncogene that has been implicated in several malignant tumors. However, the regulatory mechanism of IRS1 remains to be investigated. The aim of our current study is to unveil the mechanism by which IRS1 exerts functions in tumorigenesis of colorectal cancer (CRC). The expression level of IRS1 was found to be higher in CRC cells in comparison with the normal cell. To determine the role of IRS1 in regulating CRC cellular processes, loss‐of‐function assays were designed and carried out in two CRC cell lines. Both in vitro and in vivo functional assays indicated that silencing of IRS1 suppressed CRC cell survival. Based on bioinformatics prediction and mechanism experiments, IRS1 was identified as a downstream target of miR‐30a‐5p. Furthermore, RNA‐binding protein lin‐28 homolog B (LIN28B) was determined to be a stabilizer of IRS1 messenger RNA. More importantly, LIN28B also acted as a target of miR‐30a‐5p.Through rescue assays, we proved that LIN28B‐stablized IRS1 mediated miR‐30a‐5p‐mediated CRC cell growth. In conclusion, this study revealed that LIN28B and LIN28B‐stablized IRS1 promoted CRC cell growth by cooperating with miR‐30a‐5p.
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