Canonical nilpotent structure under bounded Ricci curvature and Reifenberg local covering geometry over regular limits

It is known that a closed collapsed Riemannian $n$-manifold $(M,g)$ of bounded Ricci curvature and Reifenberg local covering geometry admits a nilpotent structure in the sense of Cheeger-Fukaya-Gromov with respect to a smoothed metric $g(t)$. We prove that a canonical nilpotent structure over a regular limit space that describes the collapsing of original metric $g$ can be defined and uniquely determined up to a conjugation, and prove that the nilpotent structures arising from nearby metrics $g_\epsilon$ with respect to $g_\epsilon$'s sectional curvature bound are equivalent to the canonical one.Comment: 26 page

Study of the relationship between AGEs and oxidative stress damage to trophoblast cell mitochondria

Objectives: To study the influence of AGEs on placental trophoblast mitochondria oxidative stress, and to explore the possible pathogenesis which may participate in pre-eclampsia. Material and methods: Human trophoblast cells from early pregnancy were cultured by an enzyme-digestion method. When trophoblast cells reached approximately 70–80% after passages, they were incubated with pre-eclampsia serum for 24 hours. A fluorescent dye assay was applied to measure the mitochondrial membrane potential; ELISA was used to measure the activity of the mitochondrial permeability transition pore. mtDNA was detected by Real-time fluorescence quantitative Reverse Transcription-Polymerase Chain Reaction (RT-PCR). We continued to culture one group of cells with pre-eclampsia maternal serum, and other cells were pulsed with 600 mg/L AGEs. Cells were incubated for 16 hours before assaying the levels of mitochondrial oxidative stress damage. Results: The levels of mitochondria oxidative stress damage in the AGEs group were higher than in the pre-eclampsia group 1 and pre-eclampsia group 2. There was no statistically significant difference in mitochondrial oxidative stress damage between the pre-eclampsia group 1 and group 2. Conclusions: The AGEs are involved in the pathogenesis of pre-eclampsia, possibly through the enhancement of mito­chondrial oxidative stress damage

A conserved but plant-specific CDK-mediated regulation of DNA replication protein A2 in the precise control of stomatal terminal division

The R2R3-MYB transcription factor FOUR LIPS (FLP) controls the stomatal terminal division through transcriptional repression of the cell cycle genes CYCLIN-DEPENDENT KINASE (CDK) B1s (CDKB1s), CDKA; 1, and CYCLIN A2s (CYCA2s). We mutagenized the weak mutant allele flp-1 seeds with ethylmethane sulfonate and screened out a flp-1 suppressor 1 (fsp1) that suppressed the flp-1 stomatal cluster phenotype. FSP1 encodes RPA2a subunit of Replication Protein A (RPA) complexes that play important roles in DNA replication, recombination, and repair. Here, we show that FSP1/RPA2a functions together with CDKB1s and CYCA2s in restricting stomatal precursor proliferation, ensuring the stomatal terminal division and maintaining a normal guard-cell size and DNA content. Furthermore, we provide direct evidence for the existence of an evolutionarily conserved, but plant-specific, CDK-mediated RPA regulatory pathway. Serine-11 and Serine-21 at the N terminus of RPA2a are CDK phosphorylation target residues. The expression of the phosphorylation-mimic variant RPA2a(S11,21/D) partially complemented the defective cell division and DNA damage hypersensitivity in cdkb1;1 1;2 mutants. Thus, our study provides a mechanistic understanding of the CDK-mediated phosphorylation of RPA in the precise control of cell cycle and DNA repair in plants

2.79-μm high peak power LiNbO3 acousto-optic Q-switched Er,Cr:YSGG laser with thermal lensing effect compensation

A new type of lithium niobate (LiNbO3) acousto-optic Q-switched Er,Cr:YSGG laser with high peak power was designed and the thermal lensing effect compensation was studied. The values of thermal focal length in the gain medium were calculated theoretically and measured experimentally. The experimental results validate the designed plane-convex resonator validity, and the output performance of the 2.79 μm Er,Cr:YSGG laser was obviously improved. When the laser operated at free running region, the maximum values of pulse energy was 160 mJ at 60 Hz, compared with the plane-parallel resonator, the pulse energy was increased by 2 times in the plane-convex resonator. When the LiNbO3 Q-switched laser operated at 60 Hz, the maximum values of pulse energy was 8.5 mJ, and the minimum values of pulse duration was 60.8 ns, and the corresponding peak power approximately was 140 kW, respectively. Compared with the plane-parallel resonator, the pulse energy was increased by 1.6 times in the plane-convex resonator, the corresponding peak power was increased by 2.3 times

Magnetoelectric Effect at the Ni/HfO\u3csub\u3e2\u3c/sub\u3e Interface Induced by Ferroelectric Polarization

Driven by the technological importance of the recently discovered ferroelectric HfO2, we explore a magnetoelectric effect at the HfO2-based ferroelectric-ferromagnetic interface. Using density-functionaltheory calculations of the Ni/HfO2/Ni (001) heterostructure as a model system, we predict a stable and sizable ferroelectric polarization in a few-nm-thick HfO2 layer. For the Ni/HfO2 interface with opposite polarization directions (pointing to or away from the interface), we find a sizable difference in the interfacial Ni—O bonding, resulting in dissimilar degrees of depletion of the electron density around the interface. The latter affects the relative population of the exchange-split majority and minority spin bands at the interface and thus the interfacial magnetic moments. The sizable change in the interface magnetization with ferroelectric polarization reversal of HfO2 manifests a significant ferroelectrically induced magnetoelectric effect at the Ni/HfO2 interface. Our results reveal promising prospects of ferroelectric-ferromagnetic composite multiferroics based on HfO2-based ferroelectric materials

Expression of Cripto-1 in the placenta and its role in placenta accreta and placenta previa

Objectives: This study Aims to explore the role of placental Cripto-1 in the incidence of an adherent placenta.  Material and methods: Ten pregnant women with placenta increta, 20 pregnant women with placenta previa and 30 women with normal pregnant were enrolled in this study. Reverse transcription-polymerase chain reaction (RT-PCR) was used to measure the expression of Cripto-1 in the placenta while as the analysis of placental Cripto-1 was performed by Western blotting  Results: The placenta increta group showed higher levels of Cripto-1 in the center of the increta as compared to the non-implantation area. The level of placental Cripto-1 in the placenta increta was higher than that of the placenta accrete. The expression of placental Cripto-1 in the placenta increta and placenta previa groups was higher than that of control.  Conclusions: Placental Cripto-1 is involved in the regulation of placental tissue invasion. Additionally, excessive placental growth or penetration into the myometrium are likely to be involved in the development of placenta increta.

Triperyleno[3,3,3]propellane Triimides: Achieving a New Generation of Quasi-\u3cem\u3eD\u3c/em\u3e\u3csub\u3e3h\u3c/sub\u3e Symmetric Nanostructures in Organic Electronics

Rigid three-dimensional (3D) polycyclic aromatic hydrocarbons (PAHs), in particular 3D nanographenes, have garnered interest due to their potential use in semiconductor applications and as models to study through-bond and through-space electronic interactions. Herein we report the development of a novel 3D-symmetric rylene imide building block, triperyleno[3,3,3]propellane triimides (6), that possesses three perylene monoimide subunits fused on a propellane. This building block shows several promising characteristics, including high solubility, large π-surfaces, electron-accepting capabilities, and a variety of reactive sites. Further, the building block is compatible with different reactions to readily yield quasi-D3h symmetric nanostructures (9, 11, and 13) of varied chemistries. For the 3D nanostructures we observed red-shift absorption maxima and amplification of the absorption coefficients when compared to the individual subunits, indicating intramolecular electronic coupling among the subunits. In addition, the microplates of 9 exhibit comparable mobilities in different directions in the range of 10−3 cm2 V−1 s−1, despite the rather limited intermolecular overlap of the π-conjugated moieties. These findings demonstrate that these quasi-D3h symmetric rylene imides have potential as 3D nanostructures for a range of materials applications, including in organic electronic devices

Cdc42-mediated supracellular cytoskeleton induced cancer cell migration under low shear stress

Tumor microenvironment is composed of biological, chemical and physical factors. Mechanical factors are more and more focused these years. Therefore, mimicking mechanical factors' contribution to cancer cell malignancy will greatly improve the advance in this field. Although the induced malignant behaviors are present under many stimuli such as growth or inflammatory factors, the cell key physical migration mechanisms are still missing. In this study, we identify that low shear stress significantly promotes the formation of needle-shaped membrane protrusions, which is called filopodia and important for the sense and interact of a cell with extracellular matrix in the tumor microenvironment. Under low shear stress, the migration is promoted while it is inhibited in the presence of ROCK inhibitor Y27632, which could abolish the F-actin network. Using cell imaging, we further unravel that key to these protrusions is Cell division cycle 42 (Cdc42) dependent. After Cdc42 activation, the filopodia is more and longer, acting as massagers to pass the information from a cell to the microenvironment for its malignant phenotype. In the Cdc42 inhibition, the filopodia is greatly reduced. Moreover, small GTPases Cdc42 rather than Rac1 and Rho directly controls the filopodia formation. Our work highlights that low shear stress and Cdc42 activation are sufficient to promote filopodia formation, it not only points out the novel structure for cancer progression but also provides the experimental physical basis for the efficient drug anti-cancer strategies