Imprinting, methylation, and expression characterization of the maize ETHYLENE-INSENSITIVE 2-like gene

The endosperm plays essential roles in embryogenesis and seed germination and provides abundant resources for human food and industrial products. Identification of genes regulating the development of the endosperm and elucidation of their functions is of great importance for maize genetics and breeding. This study showed that the gene-specific imprinted gene, ETHYLENE-INSENSITIVE 2-like (EIN2-like), is maternally expressed in both endosperm and embryo. The maternally expressed pattern was maintained throughout later seed developmental stages. Bisulfite sequencing using DNA obtained from hybrid endosperm tissues showed that the upstream regions of the alleles of EIN2-like were highly methylated at symmetrical sites (CG and CHG). A differentially methylated region in the upstream part of the maternal allele of EIN2-like was identified and found to be hypomethylated. Expression analysis showed that EIN2-like was highly expressed in the maize endosperm as well as at different stages of cell differentiation (8–12 days after pollination) in the hybrid endosperm. These results suggest that the maternally expressed gene EIN2-like may play crucial roles in the regulation of seed development. Keywords: Maize, Gene imprinting, Methylation, EIN2-lik

Uncertainty Quantification of Neural Reflectance Fields for Underwater Scenes

Neural radiance fields and neural reflectance fields are novel deep learning methods for generating novel views of 3D scenes from 2D images. To extend the neural scene representation techniques to complex underwater environments, beyond neural reflectance fields underwater (BNU) was proposed, which considers the relighting conditions of on-aboard light sources by using neural reflectance fields, and approximates the attenuation and backscatter effects of water with an additional constant. Because the quality of the neural representation of underwater scenes is critical to downstream tasks such as marine surveying and mapping, the model reliability should be considered and evaluated. However, current neural reflectance models lack the ability of quantifying the uncertainty of underwater scenes that are not directly observed during training, which hinders their widespread use in the field of underwater unmanned autonomous navigation. To address this issue, we introduce an ensemble strategy to BNU that quantifies cognitive uncertainty in color space and unobserved regions with the expectation and variance of RGB values and termination probabilities along the ray. We also employ a regularization method to smooth the density of the underwater neural reflectance model. The effectiveness of the present method is demonstrated in numerical experiments

Characteristic MicroRNA Expression Induced by δ-Opioid Receptor Activation in the Rat Liver Under Prolonged Hypoxia

Background/Aims: Hypoxic/ischemic injury to the liver is a frequently encountered clinical problem with limited therapeutic options. Since microRNAs (miRNAs) are involved in hypoxic/ ischemic events, and δ-opioid receptor (DOR) is protective against hypoxic/ischemic injury, we asked if pharmacological activation of DOR can alter hypoxic events by regulating miRNA expression in the liver. As the first step, the present work aimed at testing the effect of DOR activation on hepatic miRNA expression in hypoxia. Methods: Male Sprague Dawley rats were exposed to hypoxia (9.5-10% O2) for 1, 5, or 10 days with or without DOR activation. The target miRNAs were selected according to TaqMan low-density array (TLDA) data and analyzed by quantitative real-time PCR. Results: We found that: 1) 1-day hypoxia caused the upregulation of 9 miRNAs (miR-7a-5p, miR-10a-5p, miR-25-3p, miR-26b-5p, miR-122-5p, miR-128a-3p, miR-135b-5p, miR-145-5p, and miR-181a-5p) and the downregulation of 2 miRNAs (miR-34a-5p and miR-182); 2) 5 and 10-days hypoxia altered the expression of 4 miRNAs (miR-34c-5p, miR-184, miR-107-3p and miR192-5p); 3) DOR activation shifted the expression of 8 miRNAs (miR-122-5p, miR-146a-5p, miR-30e-5p, miR-128a-3p, miR-182, miR-192-5p miR-107-3p and miR-184) in normoxic condition; and 4) DOR activation modified hypoxia-induced changes in 6 miRNAs (miR-142-5p, miR-145-5p, miR-146a-5p, miR-204-5p, miR-34a-5p and miR-192-5p). Conclusion: Hypoxia significantly modifies the miRNA profile in the liver, while DOR activation can modify the hypoxic modification. Therefore, it is potentially possible to alter hypoxic/ischemic pathophysiology in the liver through DOR pharmacotherapy

Neonatal Plasma Exosomes Contribute to Endothelial Cell-Mediated Angiogenesis and Cardiac Repair after Acute Myocardial Infarction

Acute myocardial infarction (AMI) accompanied by cardiac remodeling still lacks effective treatment to date. Accumulated evidences suggest that exosomes from various sources play a cardioprotective and regenerative role in heart repair, but their effects and mechanisms remain intricate. Here, we found that intramyocardial delivery of plasma exosomes from neonatal mice (npEXO) could help to repair the adult heart in structure and function after AMI. In-depth proteome and single-cell transcriptome analyses suggested that npEXO ligands were majorly received by cardiac endothelial cells (ECs), and npEXO-mediated angiogenesis might serve as a pivotal reason to ameliorate the infarcted adult heart. We then innovatively constructed systematical communication networks among exosomal ligands and cardiac ECs and the final 48 ligand–receptor pairs contained 28 npEXO ligands (including the angiogenic factors, Clu and Hspg2), which mainly mediated the pro-angiogenic effect of npEXO by recognizing five cardiac EC receptors (Kdr, Scarb1, Cd36, etc.). Together, the proposed ligand–receptor network in our study might provide inspiration for rebuilding the vascular network and cardiac regeneration post-MI

Reliability Analysis on One-Step Overall Transportation of Composite Bucket Foundation for Offshore Wind Turbine

Composite bucket foundations, which have been successfully transported, installed, and operated at the Qidong, Xiangshui, and Dafeng offshore wind farms in China, are economically advantageous due to the relatively simple transportation and installation process. The innovative one-step transportation and installation technology of foundation-tower-nacelle is the key phase in saving costs. In this paper, a “foundation lift ship” overall transport mode is proposed and introduced for the first time. Prototype data measurement, preliminary numerical simulation, and theoretical calculations were conducted to investigate whether the foundation-ship integrity, tower hoop stability, and various indexes of the nacelle met the requirements under the influences of various environmental factors. The multi-system coupling motion mechanism and analysis method of this new structure and transportation mode were expounded. Through the prototype observation data of the one-step overall transportation, the ship-foundation system reliability of the structure in the case of large wind and wave was confirmed. Furthermore, it was found that in the one-step overall transportation, the importance of factors to nacelle acceleration decreased in the order of wave height, current speed, and wind speed by the time and frequency domain analysis and data statistics

Effect of Annealing on the Microstructure and SERS Performance of Mo-48.2% Ag Films

Mo-48.2% Ag films were fabricated by direct current (DC) magnetron sputtering and annealed in an argon atmosphere. The effects of annealing on the surface morphology, resistivity and surface-enhanced Raman scattering (SERS) performance of Mo-48.2% Ag films were investigated. Results show a mass of polyhedral Ag particles grown on the annealed Mo-48.2% Ag films’ surface, which are different from that of as-deposited Mo-Ag film. Moreover, the thickness and the resistivity of Mo-48.2% Ag films gradually decrease as the annealing temperature increases. Furthermore, finite-difference time-domain (FDTD) simulations proved that the re-deposition Ag layer increases the “hot spots” between adjacent Ag nanoparticles, thereby greatly enhancing the local electromagnetic (EM) field. The Ag layer/annealed Mo-48.2% Ag films can identify crystal violet (CV) with concentration lower than 5 × 10−10 M (1 mol/L = 1 M), which indicated that this novel type of particles/films can be applied as ultrasensitive SERS substrates

Prevention of liver fibrosis by intrasplenic injection of high-density cultured bone marrow cells in a rat chronic liver injury model.

Endothelial progenitor cells (EPCs) from bone marrow have proven to be functional for the prevention of liver fibrosis in chronic liver injury. However, expansion of EPCs in culture is complicated and expansive. Previously, we have established a simple method that could enrich and expand EPCs by simple seeding bone marrow cells in high density dots. The purpose of this study is to evaluate whether cells derived from high-density (HD) culture of rat bone marrow cells could prevent the liver fibrosis in a chronic liver injury rat model, induced by carbon tetrachloride (CCl4). Flow cytometric analysis showed that cells from HD culture were enriched for EPCs, expressing high levels of EPC markers. Intrasplenic injection of HD cultured bone marrow cells in the CCl4-induced liver injury rat showed an enhanced antifibrogenic effect compared with animals treated with cells from regular-density culture. The antifibrogenic effect was demonstrated by biochemical and histological analysis 4 weeks post-transplantation. Furthermore, cells from HD culture likely worked through increasing neovascularization, stimulating liver cell proliferation, and suppressing pro-fibrogenic factor expression. HD culture, which is a simple and cost-effective procedure, could potentially be used to expand bone marrow cells for the treatment of liver fibrosis

MiR-181b-5p downregulates NOVA1 to suppress proliferation, migration and invasion and promote apoptosis in astrocytoma.

MicroRNAs (miRNAs) are small, short noncoding RNAs that modulate the expression of numerous genes by targeting their mRNA. Numerous abnormal miRNA expression patterns are observed in various human malignancies, and certain miRNAs can act as oncogenes or tumor suppressors. Astrocytoma, the most common neuroepithelial cancer, represents the majority of malignant brain tumors in humans. In our previous studies, we found that the downregulation of miR-181b-5p in astrocytomas is associated with a poor prognosis. The aim of the present study was to investigate the functional role of miR-181b-5p and its possible target genes. miR-181b-5p was significantly downregulated in astrocytoma specimens, and the reduced expression of miR-181b-5p was inversely correlated with the clinical stage. The ectopic expression of miR-181b-5p inhibited proliferation, migration and invasion and induced apoptosis in astrocytoma cancer cells in vitro. The NOVA1 (neuro-oncological ventral antigen 1) gene was further identified as a novel direct target of miR-181b-5p. Specifically, miR-181b-5p bound directly to the 3'-untranslated region (UTR) of NOVA1 and suppressed its expression. In clinical specimens, NOVA1 was overexpressed, and its protein levels were inversely correlated with miR-181b-5p expression. Furthermore, the changing level of NOVA1 was significantly associated with a poor survival outcome. Similar to restoring miR-181b-5p expression, downregulating NOVA1 inhibited cell growth, migration and invasion. Overexpression of NOVA1 reversed the inhibitory effects of miR-181b-5p. Our results indicate that miR-181b-5p is a tumor suppressor in astrocytoma that inhibits tumor progression by targeting NOVA1. These findings suggest that miR-181b-5p may serve as a novel therapeutic target for astrocytoma

δ-Opioid Receptor Activation and MicroRNA Expression in the Rat Heart Under Prolonged Hypoxia

Background: Hypoxic/ischemic injury to the heart is a frequently encountered clinical problem with limited therapeutic options. Since microRNAs (miRNAs) are involved in hypoxic/ischemic events, and δ-opioid receptor (DOR) activation is known to protect against hypoxic/ischemic injury, we speculated on the involvement of DOR activation in altering miRNA expression in the heart under hypoxic conditions. The present study aimed to test our hypothesis. Methods: Male Sprague Dawley rats were exposed to hypoxia (9.5-10% O2) for 1, 5, or 10 days with or without DOR activation. The target miRNAs were selected from TaqMan low-density array (TLDA) data and were further analyzed by quantitative real-time PCR. Results: We found that: 1) hypoxia alters the miRNA expression profiles depending on the hypoxic duration; 2) DOR activation shifts miRNA expression profiles in normoxic conditions and upregulates miR-128a-3p, miR-134-5p, miR-135a, miR-193a-3p, miR-196a, miR-324-3p, and miR-338; and 3) DOR activation modifies hypoxia-induced changes in miRNA expression and increases the levels of miR-128a-3p, miR-134-5p, miR-135a, miR-193a-3p, miR-196a, miR-324-3p, miR-141, miR-200b, and miR-324-3p. For example, miR-196c-5p decreased by 50% while miR-135a-5p increased 2.9 fold after 10 days under hypoxic conditions. Moreover, DOR activation further strengthened the hypoxia-induced increase of the levels of miR-7a-5p. When DOR was activated using UFP-512, the level of miR-107-3p significantly increased 1 day after the administration of UFP-512, but gradually decreased back to normal under normoxia. Conclusion: Hypoxia significantly modifies the miRNA profile in the heart, which can be mimicked or modified by DOR activation. Defining the targeted pathways that regulate the diverse cellular and molecular functions of miRNAs may provide new insights into potential therapies for hypoxic/ischemic injury of the heart