Intravenous Administration of Multiwalled Carbon Nanotubes Affects the Formation of Atherosclerosis in Sprague‐Dawley Rats: Yu‐Ying XU, et al. Zhejiang University School of Medicine, China—
Background
Carbon nanotubes (CNTs) have many potential applications, including as delivery systems for a variety of diagnostic or therapeutic agents. However, it has been suggested that exposure to carbon nano‐materials may be a risk for the development of vascular diseases due to its impact on the vascular endothelium.
Materials and Methods
Male Sprague‐Dawley rats (180−200 g) were used to generate an atherosclerosis (AS) model, and the effect of intravenous administration of multi‐walled carbon nanotubes (MWCNTs) on AS was studied. To further understand the underlying mechanisms, the effects of exposure of human umbilical vascular endothelial cells (HUVECs) to MWCNTs were examined.
Results
Exposure to 200 μg/kg MWCNTs aggravated AS in this model. In addition, exposure to 50, 100 and 200 μg/kg MWCNTs increased the calcification of the aorta in the model. Short‐term exposure also revealed that 200 μg/kg MWCNTs injured the endothelium in the aorta. MWCNTs disrupted the endothelial tight junction and induced endothelial cell death.
Conclusion
The results demonstrated that MWCNTs could induce structural and functional changes in the endothelium, probably through vascular endotheliocyte injury, which eventually affected the development of AS in SD rats.
Objective: Dendritic cells (DCs) activation is important in atherosclerosis and coronary heart disease, but the mechanisms regulating activation of dendritic cells remain largely unclear. The aim of this study was to evaluate the effect of transcription factor Kruppel-like factor 2 (KLF2) in the proinflammatory activation of DCs in acute coronary syndrome. Methods and Results: In this study, the expression of CD80 and KLF2 was detected in DCs in normal health controls, patients with stable angina (SA), and acute coronary syndrome (ACS). Our study found that compared with normal control and SA, KLF2 expression in DCs is reduced in patients with ACS. Moreover, the surface expression of CD80 was increased in ACS. In vitro experiment, we found that ox-LDL could increase CD80 expression and decrease KLF2 expression. Furthermore, down-regulated KLF2 could in turn increase CD80 expression via NF-κB pathway. Conclusions: These observations identify KLF2 as a novel negative regulator of DC function and it may play an essential role in DC activation in ACS.
With widespread use of the Internet, there is an increase 20 28.3.1.2 in concern over users' privacy. In particular, an adversary may identify the receiver involved in a communication session by observing the packet traffic. We propose a new routing mechanism, which we call packet cloaking, to protect 127.8.3.2 the privacy of a receiver The main idea ofpacket cloaking 27832 2035Internet is to transmit multiple copies of a sent packet to a selected group of k receivers, so that an adversary may only identify Router the true receiver with a probability of k. We present the system design to supportpacket cloaking. We also propose two metrics that measure the receiver privacy, based on evalu-Sender ating the similarity between the sender/receiver traffic pat-127 832 terns. We have performed experimental evaluations to ver-127.8.3.3 Tu ify the effectiveness of our approach.
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