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Supplemental Digital Content is available in the text, Thrombotic thrombocytopenic purpura (TTP) is a life-threatening disease, and its mortality rate is 10% to 20%. However, there are currently only a few markers to predict the prognosis in patients with TTP. We aimed to identify several clinical indices and laboratory parameters for predicting the prognosis of TTP at admission. A single-centre observational cohort study that included patients with TTP from the First Affiliated Hospital of Zhengzhou University in China was conducted from January 1, 2012 to November 30, 2018. The primary outcome was prognosis, including in-hospital mortality, major thromboembolic events, or failure to achieve remission at discharge. We used the random forest method to identify the best set of predictors. Eighty-seven patients with TTP were identified, of whom 12 died during the treatment. The total number of patients within-hospital mortality, major thromboembolic events, and failure to achieve remission at discharge was 58. The machine learning method showed that the D-dimer level was the strongest predictor of the primary outcome. Receiver operating characteristic (ROC) analysis demonstrated that the sensitivity and specificity of the D-dimer level alone for identifying high-risk patients were 78% and 81%, respectively, with an optimum diagnostic cut-off value of 770 ng/mL. The area under the ROC curve (AUC) was 0.80, and the 95% confidence interval (CI) was 0.70 to 0.90. This study found that the D-dimer level exhibited a good predictive ability for prognosis in patients with TTP. These findings may aid in the development of new and intensive treatment strategies to achieve remission among high-risk patients. However, external validation is necessary to confirm the generalizability of our approach across populations and treatment practices.

Aims Our study aims to investigate the effect of microRNA-21 (miR-21) on the proliferation, senescence, and apoptosis of glioma cells by targeting SPRY1 via the PTEN/PI3K/AKT signaling pathway. Methods Glioma tissues and brain tissues were collected for this study after surgical decompression for traumatic brain injury. RT-qPCR was employed to measure mRNA levels of miR-21, SPRY1, PTEN, PI3K, and AKT, and Western blotting was conducted to determine protein levels of SPRY1, PTEN, PI3K, AKT, p-AKT, Caspase-3, Caspase-9, P53, GSK3, and p-GSK3. Human glioma U87 cells were assigned into the blank, negative control (NC), miR-21 mimics, miR-21 inhibitors, siRNA-SPRY1, and miR-21 inhibitors + siRNA-SPRY1 groups, with human HEB cells serving as the normal group. Cell proliferation, cell cycle, and apoptosis were determined by MTT and flow cytometry, respectively. Results Compared with control group, an increased expression of miR-21, PI3K, AKT, p-AKT, P53, and p-GSK3, and a decreased expression of SPRY1, PTEN, Caspase-3, and Caspase-9 were observed in the glioma group, and no significant differences were found in the expression of GSK3. SPRY1 was verified to be the target gene of miR-21. Compared with the blank and NC groups, levels of PI3K, AKT, p-AKT, P53, and p-GSK3 increased while levels of SPRY1, PTEN, Caspase-3, and Caspase-9 decreased in the miR-21 mimics and siRNA-SPRY1 groups; the miR-21 inhibitors group reversed the tendency; furthermore, the miR-21 inhibitors group showed decreased cell proliferation but promoted apoptosis, which were opposite to the results of the miR-21 mimics and siRNA-SPRY1 groups. Conclusion MicroRNA-21 might promote cell proliferation and inhibit cell senescence and apoptosis of human glioma cells by targeting SPRY1 via the PTEN/PI3K/AKT signaling pathway.

Isoliquiritigenin (ISL), a member of the flavonoids, has been demonstrated to possess antitumor activity in various cancer cell lines in vitro and in vivo. In this study, we investigated the antitumor effects of ISL on U87 glioma cells in vitro. As determined by MTT assay, ISL inhibited the proliferation of U87 cells in a time-dependent and dose-dependent manner. The results of fluorescence-activated cell sorting (FACS) analysis suggested that ISL induced the apoptosis of the U87 cells and blocked cell cycle progression at the S and G2/M phases. Moreover, it was identified that ISL induced the apoptosis of the U87 cells in a caspase-dependent manner. Although treatment with the pan-caspase inhibitor Z-VAD-FMK efficiently blocked the ISL-induced caspase activation, it did not eliminate the ISL-induced cell death. Further examination using western blot analysis revealed that ISL upregulated p21/WAF1 and p27. These results indicate that cell cycle arrest and the caspase-mediated apoptosis pathway may participate in the antiproliferative activity of ISL in U87 cells by regulating the expression of specific molecules.

AIM This study aims to investigate the influence of different surgical timing on outcome of patients with aneurysmal subarachnoid hemorrhage and to explore the surgical techniques for ruptured intracranial aneurysms. MATERIAL AND METHODS The clinical data were from 327 cases. 304 cases of the surgical group were further assigned to early surgery (89 cases), intermediate surgery(164 cases) and delayed surgery(51 cases) according to the surgical timing. The other 23 cases were the nonsurgical group. The ultimate outcome of all cases was graded according to the Glasgow Outcome Scale. After the cases of the no-surgical group were re-assigned to different surgical subgroups according to the rebleeding time, the ultimate outcome was graded once more. RESULTS There was no significant difference among the 3 groups' pre-operative clinical data. After re-assigning the cases of no-surgical group to the different surgical subgroups, there was no significant difference among the 3 groups' preooperative clinical data, while the ultimate outcome grades of early surgery (3.6 ± 1.8) and intermediate surgery (3.5 ± 2.2) were superior to that of delayed surgery (2.9 ± 2.8). CONCLUSION This retrospective study has demonstrated that early surgery can not only prevent re-rupture of aneurysm to decrease mortality rate but also improve the ultimate outcome.

Background Malignant gliomas represent the most common primary brain tumors. The prognosis of patients with malignant gliomas is poor in spite of current intensive therapy and novel therapeutic modalities are needed. Here we report that norcantharidin is effective in growth inhibition of glioma cell lines in vitro. Methods Glioma cell lines (U87 and C6) were treated with norcantharidin. The effects of norcantharidin on the proliferation and apoptosis of glioma cells were measured by 3-[4,5-dimethylthiazol-2-thiazolyl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and flow cytometry. Western blotting was employed to determine the signaling pathway changes. Results The results showed that norcantharidin effectively inhibited cell growth and induced apoptosis in glioma cells, which was concurrent with inhibition of the expression of phospho-MEK and phospho-ERK. Furthermore, the expression anti-apoptotic proteins Bcl-2 and Mcl-1 significantly reduced, but no changes in Bcl-xL and Bax. Conclusions Our findings demonstrate that norcantharidin is effective for growth inhibition of glioma cell lines and suggest that norcantharidin may be a new therapeutic option for patients with glioma.