Mechanisms of pressure-induced water infiltration process through graphene nanopores

Understanding the mechanism of water infiltration through nanopores is essential for wide applications ranging from membrane separation to gene therapy. In this paper, the molecular dynamics simulation method is used to investigate the pressure-assisted water transport process through graphene nanopores. Various factors including the hydrophobicity of nanopore surface, nanopore dimension, temperature as well as external electric field that affect water in permeation into graphene nanopores are discussed. It is found that classic Laplace-Young equation fails and the relationship between pressure and diameter (D) does not follow the 1/D dependence as the characteristic dimension of a nanopore is sufficiently small (smaller than 1?nm). The critical pressure significantly depends on both the pore length and electric field as D is smaller than 5?nm. Besides, enhancing temperature and electric field intensity are obviously beneficial for water infiltration through those nanopores with a diameter smaller than 5?nm.     

Phloem Unloading Strategies and Mechanisms in Crop Fruits

Journal of Plant Growth Regulation - Carbohydrate produced by photosynthesis is loaded into phloem via collection phloem, translocated via the transport phloem, and unloaded by release phloem into...     

MicroRNA-25 aggravates Aβ1-42-induced hippocampal neuron injury in Alzheimer's disease by downregulating KLF2 via the Nrf2 signaling pathway in a mouse model

Recently, numerous microRNAs (miRNAs) have been considered as key players in the regulation of neuronal processes. The purpose of the present study is to explore the effect of miR-25 on hippocampal neuron injury in Alzheimer's disease (AD) induced by amyloid β (Aβ) peptide fragment 1 to 42 (Aβ1-42) via Kruppel-like factor 2 (KLF2) through the nuclear factor-E2-related factor 2 (Nrf2) signaling pathway. A mouse model of AD was established through Aβ1-42 induction. The underlying regulatory mechanisms of miR-25 were analyzed through treatment of miR-25 mimics, miR-25 inhibitors, or small interfering RNA (siRNA) against KLF2 in hippocampal tissues and cells isolated from AD mice. The targeting relationship between miR-25 and KLF2 was predicted using a target prediction program and verified by luciferase activity determination. MTT assay was used to evaluate the proliferative ability and flow cytometry to detect cell cycle distribution and apoptosis. KLF2 was confirmed as a target gene of miR-25. When the mice were induced by Aβ1-42, proliferation was suppressed while apoptosis was promoted in hippocampal neurons as evidenced by lower levels of KLF2, Nrf2, haem oxygenase, glutathione S transferase α1, glutathione, thioredoxin, and B-cell lymphoma-2 along with higher bax level. However, such alternations could be reversed by treatment of miR-25 inhibitors. These findings indicate that miR-25 may inhibit hippocampal neuron proliferation while promoting apoptosis, thereby aggravating hippocampal neuron injury through downregulation of KLF2 via the Nrf2 signaling pathway.     

GDF-15 promotes mitochondrial function and proliferation in neuronal HT22 cells

The neuronal cell line HT22 is an excellent model for studying Parkinson's disease. Growth differentiation factor 15 (GDF15) plays a critical role in Parkinson's disease, but the molecular mechanism involved are not well understood. We constructed the GDF15 overexpression HT22 cells and detected the effects of overexpression of GDF15 on the viability, oxygen consumption, mitochondrial membrane potential of oligomycin-treated HT22 cells. In addition, we used a high-throughput RNA-sequencing to study the lncRNA and mRNA expression profiling and obtained key lncRNAs, mRNA, gene ontology (GO), and Kyoto encyclopedia of genes and genomes (KEGG) pathway. The expression of selected DElncRNAs was validated by quantitative real-time PCR (qRT-PCR). Our results showed that overexpression of GDF15 significantly reversed the cells viability, oxygen consumption, and mitochondrial membrane potential effect caused by oligomycin in HT22 cells. The 1093 DEmRNAs and 395 DElncRNAs in HT22 cells between GDF15-oligomycin non-intervention group and a normal control-oligomycin un-intervention group were obtained, and 394 DEmRNAs and 271 DElncRNAs in HT22 cells between GDF15-oligomycin intervention group and normal control-oligomycin intervention group were identified. Base on the GO and KEGG enrichment analysis of between GDF15-oligomycin intervention group and normal control-oligomycin intervention group, positive regulation of cell proliferation was most significantly enriched GO terms, and Cav1 was enriched in positive regulation of cell proliferation pathway. PI3K-Akt signaling pathway was one significantly enriched pathway in GDF15-oligomycin intervention group. The qRT-PCR results were consistent with RNA-sequencing, generally. GDF15 might promote mitochondrial function and proliferation of HT22 cells by regulating PI3K/Akt signaling pathway. Our study may be helpful in understanding the potential molecular mechanism of GDF15 in Parkinson's disease.     

基于AnyBodyTM技术的人体运动建模方法

人体运动的建模与仿真是当今运动生物力学研究的一个热点.利用数值模型研究人体的运动规律,是人体运动研究的一个重要手段和有效工具.其关键技术在于应用逆向运动学方法求解人体运动,并获取人体运动中各个肌肉力学上技术参数.文中主要探讨基于AnyBodyTM System软件人体运动仿真的建模方法来研究人体运动力学规律,结合The AnyBodyTM system对人体运动具体应用,说明The AnyBodyTM system技术在人体运动仿真领域的优势.