The Physiological Occlusion of the Central Canal May Be a Prerequisite for Syringomyelia Formation

Objective Syringomyelia is a common central nervous system disease characterized by the dilation of the central canal (CC). Regarding the pathogenesis of syringomyelia, cerebrospinal fluid (CSF) circulation obstruction in the subarachnoid space (SAS) of the spinal cord has been widely accepted. However, clinical and animal studies on obstructing the CSF in SAS failed to form syringomyelia, challenging the theory of SAS obstruction. The precise pathogenesis remains unknown. Methods We utilized an extradural compression rat model to investigate the pathogenesis underlying syringomyelia. Magnetic resonance imaging enabled detection of syringomyelia formation. To assess CSF flow within the SAS, Evans blue was infused into the cisterna magna. Histological analysis allowed morphological examination of the CC. Furthermore, CSF flow through the CC was traced using Ovalbumin Alexa-Flour 647 conjugate (OAF-647). Scanning electron microscopy (SEM) enabled visualization of ependymal cilia. Results The findings showed that the dura mater below the compression segment exhibited lighter coloration relative to the region above the compression, indicative of partial obstruction within the SAS. However, the degree of SAS occlusion did not significantly differ between syringomyelia (SM-Y group) and those without (SM-N group). Intriguingly, hematoxylin and eosin staining and CSF tracing revealed occlusion of the CC accompanied by reduced CSF flow in the SM-Y group compared to SM-N and control groups. SEM images uncovered impairment of ependymal cilia inside the syringomyelia. Conclusion CC occlusion may represent a physiological prerequisite for syringomyelia formation, while SAS obstruction serves to initiate disease onset. The impairment of ependymal cilia appears to facilitate progression of syringomyelia

A Common SMAD7 Variant Is Associated with Risk of Colorectal Cancer: Evidence from a Case-Control Study and a Meta-Analysis

<div><h3>Background</h3><p>A common genetic variant, rs4939827, located in <em>SMAD7</em>, was identified by two recent genome-wide association (GWA) studies to be strongly associated with the risk of colorectal cancer (CRC). However, the following replication studies yielded conflicting results.</p> <h3>Method and Findings</h3><p>We conducted a case-control study of 641 cases and 1037 controls in a Chinese population and then performed a meta-analysis, integrating our and published data of 34313 cases and 33251 controls, to clarify the relationship between rs4939827 and CRC risk. In our case-control study, the dominant model was significant associated with increased CRC risk [Odds Ratio (OR) = 1.46; 95% confidence interval (95% CI), 1.19–1.80]. The following meta-analysis further confirmed this significant association for all genetic models but with significant between-study heterogeneity (all <em>P</em> for heterogeneity <0.1). By stratified analysis, we revealed that ethnicity, sample size, and tumor sites might constitute the source of heterogeneity. The cumulative analysis suggested that evident tendency to significant association was seen with adding study samples over time; whilst, sensitive analysis showed results before and after removal of each study were similar, indicating the highly stability of the current results.</p> <h3>Conclusion</h3><p>Results from our case-control study and the meta-analysis collectively confirmed the significant association of the variant rs4939827 with increased risk of colorectal cancer. Nevertheless, fine-mapping of the susceptibility loci defined by rs4939287 should be imposed to reveal causal variant.</p> </div

Effects of Ultrasonic Shot Peening on the Corrosion Resistance and Antibacterial Properties of Al_0.3Cu_0.5CoCrFeNi High-Entropy Alloys

Cu-bearing high-entropy alloys (HEAs) have been proposed for use as structural materials in the marine environment due to their superior mechanical and antimicrobial properties. However, the Al, Cu-enriched precipitations in HEAs damage their corrosion resistance. In this study, we used ultrasonic shot peening (USSP) technology to solve this problem. USSP caused severe plastic deformation of the Al0.3Cu0.5CoCrFeNi HEA surface and dispersed the long-strip Al, Cu-enriched phases into scattered dots, which reduced the galvanic corrosion of the HEA and enhanced passive film formation. The Al, Cu-enriched scattered precipitations also increased the number of Cu2+ ion dissolution sites, leading to the improvement of the alloy’s antibacterial properties

Rapid Identification of Corn Sugar Syrup Adulteration in Wolfberry Honey Based on Fluorescence Spectroscopy Coupled with Chemometrics

Honey adulteration has become a prominent issue in the honey market. Herein, we used the fluorescence spectroscopy combined with chemometrics to explore a simple, fast, and non-destructive method to detect wolfberry honey adulteration. The main parameters such as the maximum fluorescence intensity, peak positions, and fluorescence lifetime were analyzed and depicted with a principal component analysis (PCA). We demonstrated that the peak position of the wolfberry honey was relatively fixed at 342 nm compared with those of the multifloral honey. The fluorescence intensity decreased and the peak position redshifted with an increase in the syrup concentration (10–100%). The three-dimensional (3D) spectra and fluorescence lifetime fitting plots could obviously distinguish the honey from syrups. It was difficult to distinguish the wolfberry honey from another monofloral honey, acacia honey, using fluorescence spectra, but it could easily be distinguished when the fluorescence data were combined with a PCA. In all, fluorescence spectroscopy coupled with a PCA could easily distinguish wolfberry honey adulteration with syrups or other monofloral honeys. The method was simple, fast, and non-destructive, with a significant potential for the detection of honey adulteration

OSU53 Rescues Human OB-6 Osteoblastic Cells from Dexamethasone through Activating AMPK Signaling.

Excessive dexamethasone (Dex) application causes osteoblast cell death, which could lead to osteoporosis or osteonecrosis. AMP-activated protein kinase (AMPK) activation is shown to protect osteoblasts/osteoblastic cells from Dex. In this report, we tested the potential effect of OSU53, a novel AMPK activator, in Dex-treated osteoblastic cells. We show that OSU53 activated AMPK signaling in human OB-6 osteoblastic cells. Further, Dex-induced osteoblastic OB-6 cell death and apoptosis were largely attenuated with pre-treatment with OSU53. OSU53 was more efficient than other known AMPK activators (A-769662 and Compound 13) in protecting OB-6 cells against Dex. AMPK activation is required for OSU53-induced actions in OB-6 cells. AMPKα shRNA knockdown or dominant-negative mutation (dn-AMPKα T172A) almost completely blocked OSU53-induced AMPK activation and OB-6 cell protection against Dex. Further studies showed that OSU53 increased NADPH (nicotinamide adenine dinucleotide phosphate) activity and alleviated Dex-induced oxidative stress in OB-6 cells. Such effects by OSU53 were again almost abolished with AMPKα shRNA or dn-AMPKα in OB-6 cells. Together, these results demonstrate that OSU53 protects osteoblastic cells from Dex possibly via activating AMPK-dependent signaling

Efficient Suppression of Chain Transfer and Branching via Cs-Type Shielding in a Neutral Ni(II) Catalyst

An effective shielding of both apical positions of a neutral Ni(II) active site is achieved by dibenzosuberyl groups, both attached via the same donors' N -aryl group in a C s -type arrangement. The key aniline building block is accessible in a single step from commercially available dibenzosuberol. This shielding approach suppresses chain transfer and branch formation to such an extent that ultrahigh molecular weight polyethylenes (5 × 10 6 g mol -1 ) are accessible, with a strictly linear microstructure (< 0.1 branches/1000C). Key features of this highly active (4.3 × 10 5 turnovers h -1 ) catalyst are an exceptionally facile preparation, thermal robustness (up to 90 o C polymerization temperature), ability for living polymerization and compatibility with THF as a polar reaction medium.publishe

Fibroblast growth factor 5 overexpression ameliorated lipopolysaccharide-induced apoptosis of hepatocytes through regulation of the phosphoinositide-3-kinase/protein kinase B pathway

Abstract. Background:. Sepsis is a systemic inflammatory syndrome induced by several infectious agents. Multiple organs are affected by sepsis, including the liver, which plays an important role in metabolism and immune homeostasis. Fibroblast growth factors (FGFs) participate in several biological processes, although the role of FGF5 in sepsis is unclear. Methods:. In this study, lipopolysaccharide (LPS) was administrated to mice to establish a sepsis-induced liver injury. A similar in vitro study was conducted using L-02 hepatocytes. Western blot and immunohistochemistry staining were performed to evaluate the FGF5 expression level in liver tissues and cells. Inflammatory cell infiltrations, cleaved-caspase-3 expressions, reactive oxygen species and levels of inflammatory cytokines were detected by immunofluorescence, dihydroethidium staining, and reverse transcription quantitative polymerase chain reaction analysis, respectively. Flow cytometry was used to detect the apoptosis level of cells. In addition, ribonucleic acid (RNA)-sequencing was applied to explore the possible mechanism by which FGF5 exerted effects. Results:. LPS administration caused FGF5 down-regulation in the mouse liver as well as in L-02 hepatocytes. Additionally, with FGF5 overexpression, liver injury and the level of hepatocyte apoptosis were ameliorated. Further, RNA sequencing performed in hepatocytes revealed the phosphoinositide-3-kinase/protein kinase B (PI3K/AKT) pathway as a possible pathway regulated by FGF5. This was supported using an inhibitor of the PI3K/AKT pathway, which abrogated the protective effect of FGF5 in LPS-induced hepatocyte injury. Conclusion:. The anti-apoptotic effect of FGF5 on hepatocytes suffering from LPS has been demonstrated and was dependent on the activation of the PI3K/AKT signaling pathway

Tip-enhanced electric field : a new mechanism promoting mass transfer in oxygen evolution reactions

The slow kinetics of oxygen evolution reaction (OER) causes high power consumption for electrochemical water splitting. Various strategies have been attempted to accelerate the OER rate, but there are few studies on regulating the transport of reactants especially under large current densities when the mass transfer factor dominates the evolution reactions. Herein, Nix Fe1- x alloy nanocones arrays (with ≈2 nm surface NiO/NiFe(OH)2 layer) are adopted to boost the transport of reactants. Finite element analysis suggests that the high-curvature tips can enhance the local electric field, which induces an order of magnitude higher concentration of hydroxide ions (OH- ) at the active sites and promotes intrinsic OER activity by 67% at 1.5 V. Experimental results show that a fabricated NiFe nanocone array electrode, with optimized alloy composition, has a small overpotential of 190 mV at 10 mA cm-2 and 255 mV at 500 mA cm-2 . When calibrated by electrochemical surface area, the nanocones electrode outperforms the state-of-the-art OER electrocatalysts. The positive effect of the tip-enhanced local electric field in promoting mass transfer is also confirmed by comparing samples with different tip curvature radii. It is suggested that this local field enhanced OER kinetics is a generic effect to other OER catalysts.Accepted versio

OSU53 activates AMPK to alleviate Dex-mediated oxidative stress in osteoblastic cells.

<p>Stable OB-6 cells expressing dominant-negative AMPKα (“dn-AMPKα”, T172A, “Line-1”), AMPKα shRNA (“-a”), or the scramble control shRNA (“scr shRNA”) were treated with Dex (1 μM) or plus OSU53 (10 μM, 1 hour pretreatment), ROS intensity (DCFH-DA fluorescent OD, 6 hours, A) was tested; Relative NADPH activity in above cells was also shown (4 hours, B). Experiments in this figure were repeated three times, and similar results were obtained. *<i>p</i><0.05 vs. “scr shRNA” cells.</p