Rosenkildeschmidt1211
We propose an algorithm for registration between brain tumor images and normal brain images based on tissue recovery. U-Net is first used in BraTS2018 dataset to segment the brain tumors, and PConv-Net is then used to simulate the generation of missing normal tissues in the tumor region to replace the tumor region. Finally, the normal brain image is registered to the tissue recovery brain image. We evaluated the effectiveness of this method by comparing the registration results of the repaired image and the tumor image corresponding to the surrounding tissues of the tumor area. The experimental results showed that the proposed method could reduce the effect of pathological variation, achieve a high registration accuracy, and effectively simulate and generate normal tissues to replace the tumor regions, thus improving the registration effect between brain tumor images and normal brain images.
To investigate the effects of miR-300 and PTTG1 on osteosarcoma invasion and metastasis and explore the molecular mechanism of osteosarcoma invasion and metastasis.
Western blot was used to detect the expression of PTTG1 in human osteoblasts hFOB1.19 and osteosarcoma cell MG63 and to detect the transfection efficiency of cells transfected with PTTG1-knockdown plasmid; Transwell invasion assay and CCK8 assay detected the effects of knockdown of PTTG1 and overexpression of miR-300 on the invasion and proliferation of osteosarcoma cell MG63. On-line prediction and screening of microRNAs (miRNAs) with complementary PTTG1 binding was conducted. qRT-PCR was performed to examine the expression of miR-300 in hFOB1.19 and MG63 cells, and Western blotting was used to detect the expression of PTTG1 in MG63 cells after transfection with a miR- 300 plasmid. Double luciferase assay was used to detect the targeted binding of miR-300 and PTTG, Transwell invasion assay and CCK8 assay were used to detect the effects of ovevasion and metastasis of osteosarcoma cell MG63 by targeting PTTG1.
Overexpression of miR-300 can inhibit the invasion and metastasis of osteosarcoma cell MG63 by targeting PTTG1.In order to reduce the energy loss during data transmission and storage in the Internet of Things system and improve the transmission efficiency of fetal heart rate data to allow real-time monitoring of the fetus, we used a convolutional codec network (CC-Net) to compress the data. The network has two modules the encoding and decoding modules. The original data are compressed in the encoding module and reconstructed in the decoding module. The internal parameters are continuously updated using the mean square error of the original and the reconstructed signals to minimize the error to obtain effectively compressed data in the encoding module. In this study, the compression ratio of fetal heart rate signals using this method reached 12.07%, and the error between the reconstructed and original signals was 0.03. The proposed CC-Net can achieve a very low compression ratio for fetal heart rate compression while ensuring a high similarity between the reconstructed and the original signals to retain important information in fetal heart rate signals.
To explore the causal relationship between blood metabolites and the risk of coronary artery disease (CAD) using a two-sample Mendelian randomization (MR) approach.
Based on the data from a large-scale metabolome-based genome-wide association study (mGWAS) and the GWAS of CAD, we investigated the causality between blood metabolites and CAD using an inverse variance weighted (IVW) method and another 4 two-sample MR models. Heterogeneity, horizontal pleiotropy, and sensitivity tests were performed to evaluate the stability and reliability of the results.
Among the 486 blood metabolites, 32 metabolites showed nominally causative association with CAD with the IVW method (
< 0.05), including 11 known metabolites and 21 unknown metabolites. Three known metabolites [N-acetylornithine, bradykinin-des-arg(9), and succinylcarnitine] were statistically significant in at least 3 MR models, but their causal effects on CAD were no longer significant after sensitivity analysis using leave-one-out method and elimination of the confounding instrumental variables.
There is no strong evidence to support a robust causal relationship between the 486 blood metabolites and the risk of CAD.
There is no strong evidence to support a robust causal relationship between the 486 blood metabolites and the risk of CAD.
To assess the effect of salt intake on residual renal function in rats and explore the possible mechanism.
SD rats were 5/6-nephrectomized to induce chronic renal failure followed by peritoneal dialysis for 4 weeks (
=18) or without dialysis treatment (control group;
=18). In both groups, the rats were divided into 3 subgroups and were given lowsalt diet (0.02% NaCl), normal salt diet (0.4% NaCl), and high-salt diet (4% NaCl). After 8 and 12weeks, blood pressure and creatinine and sodium levels in the blood, urine, and peritoneal dialysate of the rats were examined. Glomerular sclerosis, tubulointerstitial fibrosis, and protein expression levels of RAS components (ACE-1, AGT, and AT-1) in renal cortical tissue of the rats were evaluated.
The residual renal function of the rats all decreased especially in rats with high salt intake for 8and 12 weeks. In peritoneal dialysis group, the rats with high-salt diet showed signficiantly increased renal interstitial fibrosis score (
=0.036), glomerular scleroion of the renal RAS system, increases blood pressure, and agrevates renal fibrosis to accelerate the decline of residual renal function, and peritoneal dialysis partially reduces the damage of residual renal function induced by high-salt diets by removing excessive sodium.
To explore the effect of
decoction (HQD) on group 3 innate lymphoid cells (ILC3s) and helper T cells (Th) for treatment of ulcerative colitis (UC).
Male Balb/c mice were randomly divided into control group, DSS group, mesalazine group (ME, 400 mg/kg), and 2.275 g/kg, 4.55 g/kg and 9.1 g/kg HQD groups. All the mice were given free access to normal chow. Except for those in the normal control group, all the mice were given 3% DSS solution for 7 days to establish models of UC. The mice in ME group and 3 HQD groups were given mesalazine or HQD via oral gavage at the specified doses once a day. Flow cytometry was performed to analyze the ILC3s, MHC Ⅱ, Th1 and Treg in the lamina propria lymphocytes in the colon. learn more Milliplex was performed to determine cytokine levels of in the colon tissues.
Compared with those in DSS group, the mice in the 3 HQD groups all showed obviously lessened symptoms of UC with significantl decreased DAI score (
< 0.001) and macroscopic score (
< 0.001). The results of flow cytometry showed that HQD treatment significantly increased the percentage of ILC3s (
< 0.05) and expression of MHCⅡ (
< 0.05), obviously reduced the proportion of Th1 (
< 0.05) but increased Treg cells (
< 0.05) in the colon tissues. Milliplex showed that HQD treatment significantly reduced the expressions of Th-related pro-inflammatory cytokines including IL-2 (
< 0.05), IL-17A (
< 0.05), IL-23 (
< 0.05), TNF-α (
< 0.05), and IFN-γ (
< 0.05).
HQD alleviates DSS- induced UC in mice by increasing ILC3s and MHC Ⅱ expression to suppress the function of Th17 and Th1 cells and promote Treg and Th2 cells.
HQD alleviates DSS- induced UC in mice by increasing ILC3s and MHC Ⅱ expression to suppress the function of Th17 and Th1 cells and promote Treg and Th2 cells.
To investigate the efficacy of anlotinib plus S-1 for treatment of patients with recurrent or metastatic esophageal squamous cell carcinoma with failed first-line chemotherapy.
Twenty-six patients with recurrent or metastatic esophageal squamous cell carcinoma patients who experienced progression after first-line paclitaxel plus platinum chemotherapy in our hospital between July, 2018 and February, 2020 were enrolled in this study. The patients received oral anlotinib along with S-1 treatment (anlotinib at 12 mg once daily and S-1 at 50 mg twice daily for two weeks; 3 weeks per cycle). The objective response rate (ORR), disease control rate (DCR), progression-free survival (PFS) and adverse effects were evaluated for all the patients.
No complete remission (CR) was observed in the 26 patients. Partial remission (PR) was achieved in 6 cases, stable disease (SD) in 12 cases, and progressive disease (PD) occurred in 8 cases, with an ORR of 23.1% and a DCR of 69.2% in these patients. The median PFS was 4.5 months (95%
2.7-6.4 months). Univariate analysis showed that the patients with moderate or high tumor differentiation had significantly longer PFS than those with low tumor differentiation (6.1 months
1.9 months,
< 0.05). Multivariate analysis suggested that pathological differentiation grade (HR=6.778, 95%
1.997-23.012) was an independent factor for a prolonged PFS. The adverse effects in the patients included mainly fatigue, hypertension and hand-foot syndrome, mostly of grade 1 to 2.
Patients with recurrent or metastatic esophageal squamous cell carcinoma can benefit from a second-line anlotinib plus S-1 treatment, which has relatively mild adverse effects with a good safety profile.
Patients with recurrent or metastatic esophageal squamous cell carcinoma can benefit from a second-line anlotinib plus S-1 treatment, which has relatively mild adverse effects with a good safety profile.
To propose a motion compensation reconstruction method based on robust principal component analysis (RPCA) to reduce the influence of streak artifacts on accurate estimation of interphase motion deformation fields.
We propose a RPCA motion compensation reconstruction algorithm to improve the estimation of motion deformation fields based on the traditional MC-FDK algorithm. RPCA was used to decompose the cone-beam computed tomography (CBCT) images into low-rank and sparse components, and the motion deformation fields between different phase images were then estimated using Horn and Schunck optical flow method from the low-rank images to reduce the influence of striping artifacts on the accuracy of estimation of interphase motion deformation fields. The performance of the algorithm was evaluated using simulation data and real data. The simulation phantom data was obtained by back-projection of 4D-CT images acquired from Philips 16-slice spiral CT using MATLAB software programming according to the scanning geometry of Varian Edge accelerator. The real patient data were obtained using the Elekta Synergy system of CBCT scanning system with half-fan mode CB projection data from lung cancer patients.
Compared with images reconstructed using the traditional MC-FDK algorithm, the reconstructed image using the proposed method had clearer tissue boundaries with reduced motion artifact was reduced. The results of phantom data reconstruction showed that compared with the MC- FDK algorithm, the proposed algorithms resulted in improvements of PSNR by 25.4% and SSIM by 7.6%; compared with the FDK algorithm, PSNR was improved by 37.9% and SSIM by 17.6%.
The proposed algorithm can achieve accurate estimation of inter-phase motion deformation fields and improve the quality of the reconstructed CBCT images.
The proposed algorithm can achieve accurate estimation of inter-phase motion deformation fields and improve the quality of the reconstructed CBCT images.
