Deep Learning-Based Magnetic Resonance Imaging in Diagnosis and Treatment of Intracranial Aneurysm.

This study was focused on the positioning of the intracranial aneurysm in the magnetic resonance imaging (MRI) images using the deep learning-based U-Net model, to realize the computer-aided diagnosis of the intracranial aneurysm. First, a network was established based on the three-dimensional (3D) U-Net model, and the collected image data were input into the network to realize the automatic location and segmentation of the aneurysm. The 3D convolutional neural network (CNN) network can extract the aneurysm blood vessels to locate and identify the areas of possible aneurysms. Next, 40 patients highly suspected of intracranial aneurysm were selected as research subjects, and they were subjected to magnetic resonance angiography (MRA) and digital subtraction angiography (DSA) examinations. The results showed that based on the U-Net algorithm model, 40 patients' hemangiomas were completely contained in the labeling bounding box, one patient's hemangioma was at the edge of the labeling bounding box, and 4 patients' hemangiomas were outside the labeling box. The final accuracy coefficient was 88.9%, and it was in good agreement with the doctor's manual labelling results. Under the 3D CNN network test, the sensitivity, specificity, and accuracy of DSA for intracranial aneurysm were 91.46%, 86.01%, and 90.2%, respectively; the sensitivity, specificity, and accuracy of MRA for intracranial aneurysm were 95.87%, 100%, and 97.19%, respectively. In conclusion, the 3D CNN can successfully realize the positioning of intracranial aneurysm in MRA images, providing a certain theoretical basis for subsequent imaging diagnosis of aneurysm.

Oxidized low-density lipoprotein contributes to injury of endothelial cells via the circ_0090231/miR-9-5p/TXNIP axis.

Atherosclerosis (AS) has been reported to induce severe clinical complications. Circular RNA (circRNA) circ_0090231 was found to be aberrantly overexpressed in oxidized low-density lipoprotein (ox-LDL)-induced endothelial cells. This study was designed to explore the role and mechanism of circ_0090231 in ox-LDL-triggered endothelial cell injury in AS. Circ_0090231, microRNA-9-5p (miR-9-5p), and thioredoxin interacting protein (TXNIP) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability, angiogenesis, and apoptosis were detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), tube formation, and flow cytometry assay. Bcl-2, Bax, and TXNIP protein levels were gauged by western blot assay. Malondialdehyde (MDA), lactate dehydrogenase (LDH), and superoxide dismutase (SOD) activity were determined by special kits. Tumor necrosis factor α (TNF-α), interleukin-1ß (IL-1ß), and interleukin 6 (IL-6) levels were analyzed using enzyme-linked immunosorbent assay (ELISA) kits. The binding relationship between miR-9-5p and circ_0090231 or TXNIP was predicted by starBase, and then verified by a dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Circ_0090231 and TXNIP were increased, and miR-9-5p was decreased in ox-LDL-treated HUVECs. Moreover, circ_0090231 knockdown mitigated ox-LDL-induced HUVEC injury by boosting angiogenesis, oxidative stress, and inflammation, and hindering apoptosis. The mechanical analysis revealed that circ_0090231 acted as a sponge of miR-9-5p to regulate TXNIP expression. Circ_0090231 could attenuate ox-LDL-mediated HUVEC damage by the miR-9-5p/TXNIP axis, providing a promising therapeutic strategy for AS treatment.

SIRT6 through PI3K/Akt/mTOR signaling pathway to enhance radiosensitivity of non-Small cell lung cancer and inhibit tumor progression.

To explore the effect and mechanism of SIRT6 on radiosensitivity and tumor progression of non-small cell lung cancer (NSCLC). qRT-PCR was performed to detect the expressions of SIRT6 in tumor tissues, adjacent normal tissues and NSCLC cell lines of patients with advanced NSCLC before and after radiotherapy. After overexpression or interference with SIRT6 expression in NSCLC cells, the cells were routinely cultured or transfected for 48 h followed by 4 Gy radiation for 24 h. Then, check the cell proliferation, migration, apoptosis and cell cycle by MTT, wound healing assay and flow cytometry, while detect the expression of PI3K/Akt/mTOR signaling pathway-related proteins by Western blot. In addition, the effect of SIRT6 expression on NSCLC tumor growth was analyzed by xenograft tumor assay. SIRT6 showed a low expression in NSCLC tumor tissues and cell lines, while SIRT6 was significantly increased in NSCLC tissues after radiation treatment. Overexpression of SIRT6 in A549 and NCI-H23 cells inhibited cell proliferation viability, migration ability and promoted apoptosis. By comparison, after radiation treatment, NSCLC cells with high SIRT6 expression had lower ability of proliferation and migration and higher apoptosis rate. Overexpression of SIRT6 evidently down-regulated the activity of PI3K/Akt/mTOR signaling pathway in NSCLC cells before and after radiation. In addition, H2009 cells exhibited opposite cellular functions after interference with SIRT6 expression. In vivo experiments showed that overexpression of SIRT6 promoted the inhibitory effect of radiation on the growth of NSCLC xenograft tumors in nude mice. SIRT6 can promote the radiosensitivity of NSCLC and inhibit the development of tumor by down-regulating the activity of PI3K/Akt/mTOR signaling pathway.

Lentivirus vector-mediated mitofusin-2 overexpression in rat ovary changes endocrine function and promotes follicular development in vivo.

The aim of the present study was to evaluate the expression and effect of rat mitofusin-2 (rMfn2) in the ovaries and other organs in rats. Rat models were developed by the intraovarian microinjection of an rMfn2-overexpressing lentiviral vector. Lenti-green fluorescent protein (GFP)-rMfn2 was microinjected into rat ovaries at a dosage of 2×106 tuberculin units virosome (n=25) and lenti-GFP was microinjected as a control (n=25). The expression of rMfn2 in the ovaries and other tissues was observed by fluorescence microscopy on days 7, 15, 30, 45 and 60 after the microinjection (n=5/day from each group). The serum levels of estradiol (E2), progesterone (P), follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were determined by radioimmunoassay. Western blotting was used for the quantitative analysis of the expression of rMfn2 and the progesterone receptor (PR), estradiol receptor (ER), luteinizing hormone receptor (LHR) and follicle-stimulating hormone receptor (FSHR). The expression of rMfn2 was detected on day 7 after infection, increased with time and was maintained efficiently until day 60. In addition, rMfn2 was highly expressed in the fallopian tubes, uterus, cardiac muscle, liver and kidney, but expressed at a low level in adipose tissue. The serum levels of E2 and P in the model group were significantly increased compared with those in the control group, whereas the FSH and LH levels showed no significant difference between groups. The expression levels of the ER and PR in the model group were higher than those in the control group; however, no significant difference was observed between groups for the expression levels of LHR and FSHR. These findings suggest that the intraovarian microinjection of lenti-GFP-rMfn2 resulted in a significant time-dependent overexpression of rMfn2 in various organs, and that rMfn2 overexpression in rat ovaries changed the endocrine function and promoted follicular development.