Geometric Multi-Model Fitting by Deep Reinforcement Learning

This paper deals with the geometric multi-model fitting from noisy, unstructured point set data (e.g., laser scanned point clouds). We formulate multi-model fitting problem as a sequential decision making process. We then use a deep reinforcement learning algorithm to learn the optimal decisions towards the best fitting result. In this paper, we have compared our method against the state-of-the-art on simulated data. The results demonstrated that our approach significantly reduced the number of fitting iterations

Amygdalin protects apoptosis of retinal ganglionic cells in glaucoma rats by regulating the expressions of anti- and pro-apoptotic proteins

Purpose: To evaluate the protective effect of amygdalin against glaucoma.Methods: Glaucoma was induced in rats via ischemia/reperfusion. The rats were treated with amygdalin (1 mg/kg) intraperitoneally (ip) for 5 weeks. Intra-ocular pressure (IOP), viability of retinal ganglion cell (RGCs) and histopathological changes in the retinal tissue of the glaucoma rats were determined. The expression levels of inflammatory cytokines and expressions of apoptotic factors were assessed in retinal tissues of all groups.Results: Intra-ocular pressure was reduced in amygdalin-treated group, when compared with the glaucoma group (p < 0.05). Moreover, the viability and thickness of RGCs in the amygdalin-treated group were enhanced, relative to untreated glaucoma rats. There was decrease in retinal cytokinelevels in amygdalin-treated group, when compared with untreated glaucoma rats. Amygdalin treatment ameliorated altered expressions of apoptosis proteins in the retinal tissue of ischemia/reperfusioninduced glaucoma rats.Conclusion: Amygdalin has a protective effect against ischemia/reperfusion-induced glaucoma in rats. Thus, it has a potential for use in the clinical management of glaucoma. Keywords: Glaucoma, Amygdalin, Cytokines, Ischemia/reperfusion, Apoptosi

miR-126 promotes angiogenesis and attenuates inflammation after contusion spinal cord injury in rats

AbstractMicroRNAs are a class of small RNAs that regulate the expression of target mRNAs by inhibiting translation or destabilizing target mRNAs. miR-126 is a microRNA that is highly enriched in endothelial cells. miR-126 has been found to promote angiogenesis and inhibit vascular inflammation in endothelial cells by repressing three target genes Sprouty-related EVH1 domain-containing protein 1 (SPRED1), phosphoinositol-3 kinase regulatory subunit 2 (PIK3R2), and vascular cell adhesion molecule 1 (VCAM1). Our previous study showed that the expression of miR-126 was downregulated after spinal cord injury (SCI). Therefore, we wanted to examine whether upregulation of miR-126 could promote angiogenesis, inhibit inflammation, and exert a positive effect on recovery after contusion SCI. In this study, we found that increased levels of miR-126 promoted angiogenesis, and inhibited leukocyte extravasation into the injured spinal cord, which was concurrent with downregulation of mRNA and protein expression of three validated miR-126 target genes, SPRED1, PIK3R2, and VCAM1. Moreover, a dose-dependent effect of miR-126 was observed in rescuing tissue damage and improving the functional deficit after SCI. Thus, the present study indicated that miR-126 played an important role in angiogenesis and inflammation after SCI

Roles of microRNA on cancer cell metabolism

Advanced studies of microRNAs (miRNAs) have revealed their manifold biological functions, including control of cell proliferation, cell cycle and cell death. However, it seems that their roles as key regulators of metabolism have drawn more and more attention in the recent years. Cancer cells display increased metabolic autonomy in comparison to non-transformed cells, taking up nutrients and metabolizing them in pathways that support growth and proliferation. MiRNAs regulate cell metabolic processes through complicated mechanisms, including directly targeting key enzymes or transporters of metabolic processes and regulating transcription factors, oncogenes / tumor suppressors as well as multiple oncogenic signaling pathways. MiRNAs like miR-375, miR-143, miR-14 and miR-29b participate in controlling cancer cell metabolism by regulating the expression of genes whose protein products either directly regulate metabolic machinery or indirectly modulate the expression of metabolic enzymes, serving as master regulators, which will hopefully lead to a new therapeutic strategy for malignant cancer. This review focuses on miRNA regulations of cancer cell metabolism,including glucose uptake, glycolysis, tricarboxylic acid cycle and insulin production, lipid metabolism and amino acid biogenesis, as well as several oncogenic signaling pathways. Furthermore, the challenges of miRNA-based strategies for cancer diagnosis, prognosis and therapeutics have been discussed

MiR-455 targeting SOCS3 improve liver lipid disorders in diabetic mice

MiR-455 has been verified a key regulator of brown adipose tissue and adipose tissue-specific overexpression of miR-455 (ap2-miR-455) mice could combat high-fat-diet-induced obesity. This study is to verify overexpression of miR-455 could ameliorate the lipid accumulation and metabolism in the liver of db/db diabetic mice and explore the potential mechanisms. Diabetic mice (db/db) and control mice (db/m) were randomly divided into four groups. After overexpression of miR-455 in the liver of db/db mice, the triglycerides level in both serum and liver decreased, the lipid deposit in liver was improved, the expression of fatty acid synthase, stearoyl-CoA desaturase 1, sterol regulatory element binding protein 1c (SREBP-1c) and acetyl-CoA carboxylase (ACCα) was also significantly down-regulated. TargetScan indicated that suppressor of cytokine signalling 3 (SOCS3) is predicated to target miR-455 and the protein of SOCS3 in the liver of db/db mice after intervention was significantly decreased. The dual luciferase reporter assay showed that SOCS3 was target gene of miR-455. In vitro, in Palmitate (PA)-stimulated human normal liver (LO2) cells, transfected miR-455 mimic could significantly inhibit the expression of SOCS3, while transfected miR-455 inhibitor could up-regulate the expression of SOCS3. Transfecting LO2 cells with siRNA of SOCS3 could significantly down-regulate the protein expression of SREBP-1c and ACCα. Our study showed that overexpression of miR-455 in the liver could improve lipid metabolism in diabetic mice by down-regulating its target gene SOCS3