Learning image context for segmentation of the prostate in CT-guided radiotherapy

Accurate segmentation of prostate is the key to the success of external beam radiotherapy of prostate cancer. However, accurate segmentation of prostate in computer tomography (CT) images remains challenging mainly due to three factors: (1) low image contrast between the prostate and its surrounding tissues, (2) unpredictable prostate motion across different treatment days, and (3) large variations of intensities and shapes of bladder and rectum around the prostate. In this paper, an online-learning and patient-specific classification method based on the location-adaptive image context is presented to deal with all these challenging issues and achieve the precise segmentation of prostate in CT images. Specifically, two sets of location-adaptive classifiers are placed, respectively, along the two coordinate directions of the planning image space of a patient, and further trained with the planning image and also the previous-segmented treatment images of the same patient to jointly perform prostate segmentation for a new treatment image (of the same patient). In particular, each location-adaptive classifier, which itself consists of a set of sequential sub-classifiers, is recursively trained with both the static image appearance features and the iteratively-updated image context features (extracted at different scales and orientations) for better identification of each prostate region. The proposed learning-based prostate segmentation method has been extensively evaluated on 161 images of 11 patients, each with more than 9 daily treatment 3D CT images. Our method achieves the mean Dice value 0.908 and the mean ± SD of average surface distance (ASD) value 1.40 ± 0.57 mm. Its performance is also compared with three prostate segmentation methods, indicating the best segmentation accuracy by the proposed method among all methods under comparison

Excessive miR-152-3p Results in Increased BAFF Expression in SLE B-Cells by Inhibiting the KLF5 Expression

The increased BAFF expression in B-cells of patients with systemic lupus erythematosus (SLE) is associated with B-cell hyperstimulation and T-cell hyperactivity, but the underlying mechanisms are still unclear. This study aimed to uncover the mechanisms that regulate the BAFF expression in SLE B-cells. The results demonstrated that the expression of miR-152-3p was significantly increased in SLE B-cells compared with normal controls. This study confirmed that Kruppel-like factor 5 (KLF5) was a direct target of miR-152-3p, and it could bind to the promoter region of BAFF and inhibit its expression in B-cells. The upregulation of miRNA-152-3p expression decreased the KLF5 expression and increased the BAFF expression in SLE B-cells. Knockdown of miR-152-3p expression inhibited the self-reactivity of SLE B-cells, thereby reducing the autoantibody production. The increased miR-152-3p expression in SLE B-cells led to an increase in BAFF expression by inhibiting KLF5 expression. These factors caused B-cell self-reactivity and autoantibody production, allowing participation in the disease process of SLE

The role of tripartite motif-containing 28 in cancer progression and its therapeutic potentials

Tripartite motif-containing 28 (TRIM28) belongs to tripartite motif (TRIM) family. TRIM28 not only binds and degrades its downstream target, but also acts as a transcription co-factor to inhibit gene expression. More and more studies have shown that TRIM28 plays a vital role in tumor genesis and progression. Here, we reviewed the role of TRIM28 in tumor proliferation, migration, invasion and cell death. Moreover, we also summarized the important role of TRIM28 in tumor stemness sustainability and immune regulation. Because of the importance of TRIM28 in tumors, TIRM28 may be a candidate target for anti-tumor therapy and play an important role in tumor diagnosis and treatment in the future

Long noncoding RNA AFAP1-AS1 acts as a competing endogenous RNA of miR-423-5p to facilitate nasopharyngeal carcinoma metastasis through regulating the Rho/Rac pathway

Background: Actin filament-associated protein 1 antisense RNA 1 (AFAP1-AS1), a long noncoding RNA, is significantly highly expressed and associated with metastasis and poor prognosis in many cancers, including nasopharyngeal carcinoma (NPC). In this study, we aim to identify the role of AFAP1-AS1 acting as an oncogenic lncRNA to promote NPC metastasis. Methods: The role of AFAP1-AS1, miR-423-5p, and FOSL2 in NPC metastasis was investigated in vitro and in vivo. Bioinformatics analysis and luciferase activity assays were used to identify the interaction between AFAP1-AS1, miR-423- 5p, and FOSL2. Additionally, real-time PCR and western blotting were used to assess the function of AFAP1-AS1 acting as an oncogenic lncRNA to promote NPC progression by regulating miR-423-5p and the downstream Rho/Rac pathway. Results: In this study, we determined that AFAP1-AS1 functions as a competing endogenous RNA in NPC to regulate the Rho/Rac pathway through miR-423-5p. These interactions can mediate the expression of RAB11B, LASP1, and FOSL2 and accelerate cell migration and invasion via the Rho/Rac signaling pathway or FOSL2. AFAP1-AS1 and FOSL2 could competitively bind with miR-423-5p to regulate several molecules, including RAB11B and LASP1 of the Rho/Rac signaling pathway. AFAP1-AS1 can also regulate the expression of LASP1, which was transcriptionally regulated by FOSL2, resulting in increased migration and invasion of NPC cells via the Rho/Rac signaling pathway. Conclusions: The observations in this study identify an important role for AFAP1-AS1 as a competing endogenous RNA (ceRNA) in NPC pathogenesis and indicate that it may serve as a potential target for cancer diagnosis and treatment

Quantitative Research on Regional Ecological Compensation from the Perspective of Carbon-Neutral: The Case of Hunan Province, China

The reduction in CO2 emissions is very important, as highlighted by the issue of global climate warming. As a developing country, China has great differences in regional economic development, which makes it necessary to implement the ecological compensation of regional carbon emissions to coordinate the relationship between regional economic development and environmental protection. Using the ecological system in Hunan Province, China as the research object, this study analyzed and calculated the carbon emissions and carbon sequestration across different industries and different regions of Hunan using ArcGIS and theoretical model calculation methods. Quantitative research on region ecological compensation was undertaken by establishing the ecological compensation coefficient and ecological compensation model based on the carbon-neutral principal. The results showed that there were significant differences in carbon sources and carbon sequestration in the different cities. Out of all the cities investigated, Changsha had the highest carbon emissions and Huaihua had the largest carbon sequestration. In terms of per capita, Xiangtan had the highest carbon emissions and Zhangjiajie had the largest carbon sequestration. Through the quantification of carbon compensation in the cities of Hunan, we found that Changsha, Zhuzhou, Xiangtan, Hengyang, Yueyang, and Loudi were in a state of ecological deficit, and should pay an amount of ecological compensation, respectively. Meanwhile, the other eight cities (Shaoyang, Changde, Zhangjiajie, Yiyang, Chenzhou, Yongzhou, Huaihua, and Xiangxi) were in a state of ecological surplus; they could receive some ecological compensation, respectively. Our results will provide a reference for areal carbon trading and ecological compensation mechanisms as significant instruments and measures to realize payment for environmental resource services

Down-regulation of MBD4 contributes to hypomethylation and overexpression of CD70 in CD4+ T cells in systemic lupus erythematosus

Abstract Background Systemic lupus erythematosus (SLE) is an autoimmune disease that is characterized by lymphocytic infiltration and overproduction of autoantibodies, leading to significant morbidity and mortality. However, the pathogenesis of this disorder has not yet been completely elucidated. It has been reported that CD70, a B cell costimulatory molecule encoded by the gene TNFSF7 (tumor necrosis factor ligand superfamily member 7), is overexpressed in CD4+ T cells from patients with SLE due to the demethylation of its promoter. We aimed to investigate the expression patterns of MBD4 (methyl-CpG binding domain protein 4) in CD4+ T cells and its contribution to the pathogenesis of SLE by increasing CD70 expression through epigenetic regulation. Results Our results showed that the expression of MBD4 was significantly decreased in CD4+ T cells from SLE patients. We verified that transfection of MBD4 siRNA into healthy CD4+ T cells upregulated expression of CD70 and decreased the methylation level of the CD70 promoter. Overexpression of MBD4 inhibited CD70 expression and enhanced the DNA methylation level of CD70 in CD4+ T cells of SLE patients. Conclusion Our results indicated that downregulation of MBD4 contributed to overexpression and hypomethylation of the CD70 gene in SLE CD4+ T cells. This modulation of MBD4 may provide a novel therapeutic approach for SLE