Adoption of Magnetic Resonance Image Features under Segmentation Algorithm in Effect Evaluation of Ginkgo Diterpenoid Lactone Glucamine Injection in Treatment of Cerebral Infarction.

Magnetic resonance imaging (MRI) image segmentation based on a segmentation algorithm was performed to assess neurological function in patients with acute cerebral infarction, to investigate the efficacy evaluation of Ginkgo diterpene lactones meglumine injection (GDLI) in the treatment of cerebral infarction and the efficiency of MRI image segmentation algorithm. First, the results of the fast semisupervised segmentation algorithm (algorithm group) and traditional processing (control group) were compared and analyzed. The recall rate, accuracy, recognition accuracy, and segmentation time of the two groups were compared. The control group was given conventional treatment, while the algorithm group was given GDLI based on conventional treatment. Finally, the difference in serum vascular endothelial growth factor (VEGF), hypoxia-inducible factor-la (HIF-la), angiotensin (Ang)-1, Ang-2, and interleukin (IL)-6 protein concentration was analyzed after treatment. The algorithm evaluation results showed that the accuracy and recall rate of MRI images recognized by the algorithm group fluctuate at 90%. In the control group, the accuracy and recall rate of MRI image results fluctuated at 80%, and the data were statistically different (p < 0.05). The clinical index test results showed that the serum VEGF content of the test group was higher than that of the control group, and the data was statistically different (p < 0.05). In addition, the cerebral blood flow (CBF) and cerebral blood volume (CBV) of the lesion side of the algorithm group were greatly higher than those of the control group on the 30th day, and the differences were significant (p < 0.05). There was little difference between the method presented in this study and the manual delineation by a physician. Compared with traditional manual segmentation, this method greatly reduced the time required for the segmentation of lesions. The diagnostic specificity, sensitivity, and accuracy of the images segmented by the fast semisupervised algorithm were higher than those of the conventional method, and the diagnostic accuracy of acute cerebral infarction was high. In addition, it was sensitive and accurate to detect acute cerebral infarction, which provided a reliable reference for early diagnosis and condition judgment of patients.

USP52 inhibits cell proliferation by stabilizing PTEN protein in non-small cell lung cancer.

Non-small cell lung cancer (NSCLC) is the most common subtype of lung cancer. Ubiquitination is closely related to the development of lung cancer. However, the biological importance of newly discovered ubiquitin-specific peptidase (USP) 52 (USP52) in NSCLC remained unclear. Here, our findings identify USP52 as a novel tumor suppressor of NSCLC, the low expression of USP52 predicts a poor prognosis for NSCLC patients. The present study demonstrates that USP52 inhibits cancer cell proliferation through down-regulation of cyclin D1 (CCND1) as well as AKT/mTOR signaling pathway inhibition. Meanwhile, USP25 also suppresses NSCLC progression via enhancing phosphatase and tensin homolog (PTEN) stability in cancer cells, which further indicates the significance/importance of USP52 in NSCLC suppression.

miR-128-3p serves as an oncogenic microRNA in osteosarcoma cells by downregulating ZC3H12D.

Osteosarcoma is the second leading cause of cancer-associated mortality worldwide in children and adolescents. ZC3H12D has been shown to negatively regulate Toll-like receptor signaling and serves as a possible tumor suppressor gene. MicroRNAs (miRNAs/miRs) are known to play an important role in the proliferation of human osteosarcoma cells. However, whether miRNAs can affect tumor development by regulating the expression of ZC3H12D has not yet been investigated. The aim of the present study was to investigate the role of miR128-3p in regulating ZC3H12D expression, as well as its function in tumor cell proliferation, apoptosis, and metastasis. Reverse transcription-quantitative PCR, western blotting and dual luciferase reporter assays were performed to analyze the regulation of ZC3H12D expression by miR-128-3p. MTT, colony formation and flow cytometry assays were also used to analyze the effect of miR-128-3p on cell proliferation and apoptosis. A wound healing assay was performed to investigate the cell migration ability. The results demonstrated that miR-128-3p directly targeted ZC3H12D and downregulated its expression, thereby promoting cell proliferation and migration. miR-128-3p overexpression also improved resistance to cisplatin in MG-63 and 143B cell lines, supporting the hypothesis that miR-128-3p may function as an oncogene in osteosarcoma cells. The potential clinical significance of miR-128-3p as a biomarker and therapeutic target provides rationale for further investigation into the miR-128-3p-mediated molecular pathway and how it is associated with osteosarcoma development.

Propane-2-sulfonic acid octadec-9-enyl-amide, a novel PPARα/γ dual agonist, reverses neuroinflammation in lipopolysaccharide-induced mice.

Our previous study showed that propane-2-sulfonic acid octadec-9-enyl-amide (N15), a novel peroxisome proliferator-activated receptor α and γ (PPARα/γ) dual agonist, inhibits inflammatory responses in tumor necrosis factor alpha (TNFα)-induced vascular endothelial cells or lipopolysaccharide (LPS)-induced human myeloid leukemia mononuclear cells-1. However, little is known about whether N15 applies to other pathological or neuroinflammatory conditions. In the present study, we detected the effect of N15 on the LPS-induced neuroinflammatory response in mice and further investigated whether the effect of N15 on neuroinflammation and neuronal cells survival was related to PPARα/γ dual pathways. We found that N15 decreased the mRNA expression of the proinflammatory cytokines IL-1ß, IL-6, TNFα, inducible nitric oxide synthase and cyclooxygenase-2; inhibited microglial activation; and ameliorated neuronal apoptosis in the hippocampus and cortex of LPS-induced mice. In addition, PPARα antagonist MK886 or PPARγ antagonist T0070907 partially eliminated the effect of N15. These results demonstrate that N15 exerts an anti-inflammatory effect, at least in part, by enhancing PPARα/γ dual signaling. Our study reveals that N15 may be a promising neuronal protective drug for the treatment of neuroinflammatory diseases.