Effect of inflammatory factor‐induced cyclo‐oxygenase expression on the development of reperfusion‐related no‐reflow phenomenon in acute myocardial infarction

No reflow after reperfusion therapy for myocardial infarction is a strong predictor of clinical outcome. Increased levels of inflammatory factors, including C‐reactive protein (CRP), in patients with acute myocardial infarction (AMI) undergoing primary percutaneous coronary intervention (PCI) may affect myocardial perfusion. However, why the no‐reflow phenomenon increases in inflammation stress after PCI is not clear. The aim of the present study was to determine the effects and molecular mechanisms underlying the effects of CRP on the expression of cyclo‐oxygenase (COX) on the development of the no‐reflow phenomenon. There was a significant increase in plasma levels of CRP and interleukin (IL)‐6 in no‐reflow patients, suggesting that inflammatory factors play an important role in the development of the no‐reflow phenomenon. The mechanisms involved were further evaluated after reperfusion in a rat model mimicking the no‐reflow phenomenon. Compared with normal reflow rats, there were significant increases in both COX‐1 and COX‐2 in cardiac tissue from no‐reflow rats. The COX inhibitor indomethacin (5 mg/kg, i.p.) significantly reduced the no‐reflow area. In another series of experiments, human coronary artery endothelial cells (HCAEC) were treated with CRP at clinically relevant concentrations (5–25 μg/mL). C‐Reactive protein significantly increased COX‐1 and COX‐2 levels in a time‐ and concentration‐dependent manner. In addition, extracellular signal‐regulated kinase (ERK) and Jun N‐terminal kinase (JNK) were activated in CRP (5, 10, 25 μg/mL)‐treated HCAEC cultures. Furthermore, the ERK inhibitor pd98059 (30 μmol/L) and the JNK inhibitor sp600125 (10 μmol/L) blocked CRP‐induced COX‐1 and COX‐2 expression for 12 h. Together, the findings of the present study suggest that CRP can promote the development of the no‐reflow phenomenon by increasing COX‐1 and COX‐2 expression, which is regulated, in part, via ERK and JNK activity.     

Curcumin alleviates lung injury in diabetic rats by inhibiting nuclear factor‐κB pathway

Curcumin is a polyphenolic compound that is extracted from Curcuma longa. It has broad anti‐inflammation and anti‐tumor activities. Curcumin was previously reported to exert beneficial effects on diabetes. However, the effect of curcumin on diabetes‐induced lung injury is not yet clear. In this study, the effects of curcumin on lung injury induced by diabetes was explored using quantitative real time polymerase chain reaction (PCR), enzyme‐linked immunosorbent assay (ELISA), immunohistochemistry and electrophoretic mobility shift assay. The results of this study showed that curcumin reduced oxidative stress level, inhibited the synthesis of nitric oxide and prostaglandin E2, and reduced inflammatory responses in the lungs of diabetic rats, thereby alleviating diabetes‐induced lung injury. Further study of the mechanism revealed that curcumin inhibited the activation of nuclear factor (NF)‐κB which is a key player in inflammatory responses. In summary, our study demonstrated that curcumin inhibited the activation of NF‐κB in the lungs of diabetic rats, thus reducing pulmonary inflammatory responses and oxidative stress, and ultimately relieving diabetes‐induced lung injury. This study suggests that curcumin may be a promising agent to alleviate diabetic lung injury and also provides theoretical foundation for the development of diabetes therapy.     

Preparation of MoS2-based polydopamine-modified core–shell nanocomposites with elevated adsorption performances

New molybdenum disulfide (MoS₂)-based core–shell nanocomposite materials were successfully prepared through the self-assembly of mussel-inspired chemistry. Characterization by Fourier transform infrared, thermogravimetric analysis, scanning electron microscope and transmission electron microscopy revealed that the surface of the flaked MoS₂ was homogeneously coated with a thin layer of polydopamine (PDA). Dye adsorption performances of the synthesized MoS₂–PDA nanocomposites were investigated at different pH values and reaction times. Compared with pure MoS₂ nanosheets, the obtained core–shell nanocomposites showed elevated adsorption performances and high stability, indicating their potential applications in wastewater treatment and composite materials.

New core–shell MoS₂–PDA nanocomposites are prepared via mussel-inspired chemistry and a simple interfacial self-assembly process, demonstrating potential applications in wastewater treatment and self-assembled core–shell composite materials.     

Production of Ti–Fe alloys via molten oxide electrolysis at a liquid iron cathode

This work studies the direct electrochemical preparation of Ti–Fe alloys through molten oxide electrolysis (MOE) at a liquid iron cathode. Cyclic voltammetry and potentiostatic electrolysis have been employed to study the cathodic process of titanium ions. The results show that cathodic behavior happens during the negative sweep at a potential range from −0.80 to −1.25 V (vs. QRE-Mo), corresponding to the electro-reduction of titanium ions. Importantly, Ti–Fe and titanium-rich Ti–Fe alloys have been successfully produced by galvanostatic electrolysis at different current densities of 0.15 and 0.30 A cm⁻², respectively. The results show that it is feasible to directly prepare Ti–Fe alloys by the MOE method at a liquid iron cathode.

This work studies the direct electrochemical preparation of Ti–Fe alloys through molten oxide electrolysis (MOE) at a liquid iron cathode.     

Retracted Article: Resveratrol attenuates inflammation and reduces matrix-metalloprotease expression by inducing autophagy via suppressing the Wnt/β-catenin signaling pathway in IL-1β-induced osteoarthritis chondrocytes

Resveratrol (Res), a naturally occurring polyphenolic compound, has been reported to exert many biological effects like anti-inflammatory and anti-oxidant effects. In this study, we investigated the role of Res on IL-1β-induced osteoarthritis (OA) chondrocytes and its possible mechanism. Results demonstrated that Res suppressed IL-1β-induced IL-1, IL-6 and TNF-α production in a dose-dependent manner. Res also decreased MMP-1, MMP-3 and MMP-13 production in IL-1β-induced OA chondrocytes. These results suggested that Res suppressed IL-1β-induced inflammation and matrix-metalloproteases (MMP) expression in OA chondrocytes. In addition, Res was found to reverse the decreased autophagy level through increasing the expression of Beclin1, LC3 II/I ratio and LC3⁺ puncta in IL-1β-induced OA chondrocytes. Inhibition of autophagy by 3-methyladenine (3-MA) abolished the inhibitory effect of Res on inflammation and MMP expression in IL-1β-induced OA chondrocytes. Moreover, the Wnt/β-catenin signaling pathway was activated in IL-1β-induced OA chondrocytes. However, Res was found to suppress this activated Wnt/β-catenin signaling pathway. Activation of the Wnt/β-catenin signaling pathway counteracted the promoted effect on autophagy and inhibitory effect on inflammation and MMP expression of Res in IL-1β-induced OA chondrocytes. Taken together, our data demonstrated that Res attenuated inflammation and reduced MMP expression through inducing autophagy via inhibiting the Wnt/β-catenin signaling pathway in IL-1β-induced OA chondrocytes. Res may be used as a potential therapeutic agent for OA treatment.

Resveratrol (Res), a naturally occurring polyphenolic compound, has been reported to exert many biological effects like anti-inflammatory and anti-oxidant effects.     

探索基于码头完全信息化的空箱码头查验模式

目的大力推进码头信息化建设,分析和探索先进的进境集装箱空箱检疫模式,以完善空箱检疫机制,有效防范疫病疫情和有毒有害物质传播入境。方法借鉴国内外先进口岸的进境集装箱空箱检疫模式和码头信息化建设,分析现有模式的弊端及工作中存在的问题,探讨进境空箱的检疫风险,研究进境空箱检疫新模式及与之配套的口岸码头信息化建设。结果进境集装箱空箱检疫风险较大且复杂,现有的堆场查验模式常出现漏检现象,码头信息化管理落后,无法将检关港高效有序协调起来,大大降低了工作效率和服务质量。结论现有进境集装箱空箱检疫模式存在的问题不容忽视,需积极推进口岸码头的信息化建设,并在此基础上积极稳妥地探索和实践空箱检疫码头查验新模式。     

早产儿喂养不耐受肠道菌群多样性研究

目的：采用变性梯度凝胶电泳聚合酶链反应（ PCR－DGGE）技术从微生物生态学的角度分析比较喂养不耐受（ FI）与健康早产儿肠道细菌群落结构的多样性及相似性。方法以2013年11月至2014年9月在第四军医大学附属唐都医院儿科新生儿病房诊断为FI的早产儿为FI组。选择与FI组胎龄、日龄、出生体重相匹配的非FI早产儿作为对照组。采集出现FI时和同时间段对照组的粪便标本,进行16SrDNAV3区扩增和变性梯度凝胶电泳（DGGE）,从而分析比较两组间肠道菌群多样性指数及相似性。结果细菌多样性检测显示FI组的肠道菌群多样性指数香农－维纳指数（H）、丰度（S）、均衡度指数（E）和辛普森多样性指数（D）均低于对照组（均P＜0．05）;相似性矩阵图及聚类分析结果显示组内菌群相似性较组间高（P＜0．05）;PCA结果同聚类分析一致。结论肠道微生物群落多样性的改变及群落结构紊乱可能是引起早产儿FI的重要因素。     

Resveratrol Inhibits the Invasion of Glioblastoma-Initiating Cells via Down-Regulation of the PI3K/Akt/NF-κB Signaling Pathway

Invasion and metastasis of glioblastoma-initiating cells (GICs) are thought to be responsible for the progression and recurrence of glioblastoma multiforme (GBM). A safe drug that can be applied during the rest period of temozolomide (TMZ) maintenance cycles would greatly improve the prognosis of GBM patients by inhibiting GIC invasion. Resveratrol (RES) is a natural compound that exhibits anti-invasion properties in multiple tumor cell lines. The current study aimed to evaluate whether RES can inhibit GIC invasion in vitro and in vivo. GICs were identified using CD133 and Nestin immunofluorescence staining and tumorigenesis in non-obese diabetic severe combined immunodeficient (NOD/SCID) mice. Invasive behaviors, including the adhesion, invasion and migration of GICs, were determined by tumor invasive assays in vitro and in vivo. The activity of matrix metalloproteinases (MMPs) was measured by the gelatin zymography assay. Western blotting analysis and immunofluorescence staining were used to determine the expression of signaling effectors in GICs. We demonstrated that RES suppressed the adhesion, invasion and migration of GICs in vitro and in vivo. Moreover, we proved that RES inhibited the invasion of GICs via the inhibition of PI3K/Akt/NF-κB signal transduction and the subsequent suppression of MMP-2 expression.