MCP-1, ICAM-1 and VCAM-1 are present in early aneurysmal dilatation in experimental rats.

Recent studies have suggested that inflammation actively participates in ascending aortic aneurysm formation. The aim of the present study was to evaluate the expression changes of adhesion molecules and MMPs in an experimental model of ascending aortic aneurysm induced by ascending aorta banding in Wistar rats. Twelve rats developed aortic dilation after ascending aorta banding treatment, while nine normal animals underwent surgery without banding were used as controls. Light microscope and scanning electron microscope showed that the wall of the ascending aorta became disorganized as well as infiltration by inflammatory cells in aneurysmal rats. By using immunohistochemical techniques, a significant increase in the immunostaining of MCP-1 was observed in the aneurysmal wall as compared to the normal aortic wall. Under similar experimental conditions, we also found that the immunostaining of ICAM-1 and VCAM-1 was markedly increased in the aneurysmal wall. In addition, gelatin zymographic analysis showed that the expression and activities of MMP-2 and MMP-9 were remarkably enhanced in the ascending aorta of ascending aortic aneurysmal rats as compared to normal rats. These results demonstrate that MCP-1, ICAM-1 and VCAM-1 are involved in the pathogenesis of ascending aortic aneurysm and an increase in the immunostaining and activity of MMP-2 and MMP-9 may promote the progression of ascending aortic aneurysm

p38b Mitogen-Activated Protein Kinase Signaling Mediates Exenatide-Stimulated Microglial b-Endorphin Expression

ABSTRACT Recent discoveries established that activation of glucagon-like peptide-1 receptors (GLP-1Rs) mediates neuroprotection and antinociception through microglial b-endorphin expression. This study aimed to explore the underlying signaling mechanisms of microglial b-endorphin. GLP-1Rs and b-endorphin were coexpressed in primary cultures of microglia. Treatment with the GLP-1R agonist exenatide concentration-dependently stimulated microglial expression of the b-endorphin precursor gene proopiomelanocortin (POMC) and peptides, with EC 50 values of 4.1 and 7.5 nM, respectively. Exenatide also significantly increased intracellular cAMP levels and expression of pprotein kinase A (PKA), p-p38, and p-cAMP response element binding protein (CREB) in cultured primary microglia. Furthermore, exenatide-induced microglial expression of POMC was completely blocked by reagents that specifically inhibit adenylyl cyclase and activation of PKA, p38, and CREB. In addition, knockdown of p38b (but not p38a) using short interfering RNA (siRNA) eliminated exenatide-induced microglial p38 phosphorylation and POMC expression. In contrast, lipopolysaccharide increased microglial activation of p38, and knockdown of p38a (but not p38b) partially suppressed expression of proinflammatory factors (including tumor necrosis factor-a, interleukin-1b, and interleukin-6). Exenatideinduced phosphorylation of p38 and CREB was also totally blocked by the PKA inhibitor and siRNA/p38b, but not by siRNA/p38a. Seven-day intrathecal injections of siRNA/p38b (but not siRNA/p38a) completely blocked exenatide-induced spinal p38 activation, b-endorphin expression, and mechanical antiallodynia in rats with established neuropathy, although siRNA/p38b and siRNA/p38a were not antiallodynic. To our knowledge, our results are the first to show a causal relationship between the PKA-dependent p38b mitogen-activated protein kinase/CREB signal cascade and GLP-1R agonismmediated microglial b-endorphin expression. The differential role of p38a and p38b activation in inflammation and nociception was also highlighted

Integral equation method for the electromagnetic wave propagation in stratified anisotropic dielectric-magnetic materials

We investigate the propagation of electromagnetic waves in stratified anisotropic dielectric-magnetic materials using the integral equation method (IEM). Based on the superposition principle, we use Hertz vector formulations of radiated fields to study the interaction of wave with matter. We derive in a new way the dispersion relation, Snell's law and reflection/transmission coefficients by self-consistent analyses. Moreover, we find two new forms of the generalized extinction theorem. Applying the IEM, we investigate the wave propagation through a slab and disclose the underlying physics which are further verified by numerical simulations. The results lead to a unified framework of the IEM for the propagation of wave incident either from a medium or vacuum in stratified dielectric-magnetic materials.Comment: 14pages, 3figure

Genetic polymorphisms of TLR3 are associated with Nasopharyngeal carcinoma risk in Cantonese population

<p>Abstract</p> <p>Background</p> <p>Nasopharyngeal carcinoma is endemic in Southern China, displays a strong relationship with genetic susceptibility and associates with Epstein-Barr virus infection. Toll-like receptor 3 (TLR3) plays an important role in the antivirus response. Therefore, we examined the association between <it>TLR3 </it>gene polymorphisms and NPC susceptibility.</p> <p>Methods</p> <p>We performed a case-control study of 434 NPC cases and 512 healthy controls matched on age, sex and residence. Both cases and controls are of Cantonese origin from Southern China. Genetic variants in <it>TLR3 </it>were determined by polymerase chain reaction (PCR)-based DNA direct sequencing and four SNPs were genotyped in all samples.</p> <p>Results</p> <p>Our results showed that allele C for SNP 829A/C increased NPC risk significantly ((p = 0.0068, OR = 1.49, 95%CI:1.10–2.00). When adjusted for age, gender and VCA-IgA antibody titers, the NPC risk was reduced significantly among individuals who carried the haplotype "ATCT" compared to those who carried the most common haplotype "ACCT" (p = 0.0054, OR = 0.028; 95% CI (0.002–0.341).</p> <p>Conclusion</p> <p>The <it>TLR3 </it>polymorphisms may be relevant to NPC susceptibility in the Cantonese population, although the reduction in NPC risk is modest and the biological mechanism of the observed association merits further investigation.</p

A peripherally inserted central vein catheter fractured and slid into the right pulmonary artery: A case report

AbstractCatheter fracture is a rare but serious complication of a peripherally inserted central catheter (PICC). An adolescent patient was sent to Tianjin Medical University General Hospital (Tianjin, China) because the PICC was fractured when removed by a nurse. Chest X-ray showed that the PICC fragment slid into the right pulmonary artery. Through emergency surgery, the remainder of the PICC was successfully retrieved by an interventional operation percutaneously via the right femoral vein. PICC fracture is less common and always without significant discomfort if not found timely, and it may lead to serious complications, such as pulmonary embolism, and even death. Thus, nurses, patients and their family members should pay enough attention to the daily maintenance of PICC and have a deep understanding of the reasons associated with PICC fracture as well as how to prevent it. Interventional operation is minimally invasive, which is a good choice for the removal of intravascular foreign bodies, leading to fewer complications and a good prognosis

Tet and TDG Mediate DNA Demethylation Essential for Mesenchymal-to-Epithelial Transition in Somatic Cell Reprogramming

SummaryTet-mediated DNA oxidation is a recently identified mammalian epigenetic modification, and its functional role in cell-fate transitions remains poorly understood. Here, we derive mouse embryonic fibroblasts (MEFs) deleted in all three Tet genes and examine their capacity for reprogramming into induced pluripotent stem cells (iPSCs). We show that Tet-deficient MEFs cannot be reprogrammed because of a block in the mesenchymal-to-epithelial transition (MET) step. Reprogramming of MEFs deficient in TDG is similarly impaired. The block in reprogramming is caused at least in part by defective activation of key miRNAs, which depends on oxidative demethylation promoted by Tet and TDG. Reintroduction of either the affected miRNAs or catalytically active Tet and TDG restores reprogramming in the knockout MEFs. Thus, oxidative demethylation to promote gene activation appears to be functionally required for reprogramming of fibroblasts to pluripotency. These findings provide mechanistic insight into the role of epigenetic barriers in cell-lineage conversion

AI safety of film capacitors.

With a large number of film capacitors being deployed in critical locations in electrical and electronic systems, artificial intelligence (AI) technology is also expected to address the problems encountered in this process. According to our findings, AI applications can cover the entire lifecycle of film capacitors. However, the AI safety hazards in these applications have not received the attention they deserve. To meet this, the authors argue, with specific examples, risks that flawed, erratic, and unethical AI can introduce in the design, operation, and evaluation of film capacitors. Human-AI common impact and more multi-dimensional evaluation for AI are proposed to better cope with unknown, ambiguity, and known risks brought from AI in film capacitors now and in the future