The interaction between graphene and metal was investigated by studying the G band splitting in surface-enhanced Raman scattering (SERS) spectra of single-, bi-, trilayer graphene. Ag deposition on induced large enhancement signal graphene, indicating SERS In particular, split into two distinct peaks spectrum extent 13.0 cm−1 for single-layer, 9.6 bilayer, 9.4 whereas a thick multilayer not split. average factor 24 15 10 These results indicate that there is correlation splitting, strongest...

A new approach for the fabrication of reduced graphene oxide (rGO) multilayers which can be used transparent and conducting thin films was developed. This achieved by using layer-by-layer (LbL) assembly positively negatively charged rGO sheets, could provide highly controllable in terms thickness, transmittance, sheet resistance. In particular, thickness multilayer able to controlled precisely subnanometre scale ∼0.46 nm via simply varying number stacking layers. Therefore, this method...

Surface-enhanced Raman scattering (SERS) of graphene on a SiO(2)(300 nm)/Si substrate was investigated by depositing Au nanoparticles using thermal evaporation. This provided maximum enhancement 120 times for single-layer at 633 nm excitation. SERS spectra and scan images few-layer were acquired. Single-layer provides much larger compared to graphene, while in the G band than that 2D band. Furthermore, D bands identified spectra; these not observed normal spectrum without deposition....

Abstract Malignant gliomas are characterized by aggressive tumor growth with a mean survival of 15 to 18 months and frequently developed resistance temozolomide. Therefore, strategies that sensitize glioma cells temozolomide have high translational impact. We studied focal adhesion kinase (FAK), tyrosine emerging therapeutic target is known be highly expressed activated in glioma. In this report, we tested the FAK autophosphorylation inhibitor, Y15, DBTRG U87 glioblastoma cells. Y15...

Abstract Gliomas generally infiltrate the surrounding normal brain parenchyma, a process associated with increased vascular permeability (VP) and dysregulation of blood–brain barrier (BBB). However, molecular mechanisms underlying glioma-induced VP in remain poorly understood. Using conditional, endothelium-specific deletion focal adhesion kinase (FAK) mouse (FAK CKO), we show that FAK is critical for destabilization tumor endothelium tumor-bearing mice, mutant mice exhibiting relatively...

CNS injury including stroke, infection, and tumor growth lead to astrogliosis, a process that involves upregulation of glial fibrillary acidic protein (GFAP) in astrocytes. However, the kinetics astrogliosis is related these insults (i.e. tumor) largely unknown.Using transgenic mice expressing firefly luciferase under regulation GFAP promoter (GFAP-luc), we developed model system monitor upon rapid, non-invasive manner. A biphasic induction was observed our xenograft which an early phase...

Extensive infiltration of brain tumors by microglia and macrophages is a hallmark tumor progression, yet the overall microenvironment characterized an immunosuppressive phenotype. Here we identify esophageal cancer-related gene 4 (Ecrg4) as novel thrombin-processed monocyte chemoattractant that recruits myeloid cells, promotes their activation, leads to blockade progression. Both xenograft glioma syngeneic models were used measure orthotopic progression survival. Flow cytometry...

Leukocyte ECRG4 amplifies neutrophil recruitment and regulates CD44 expression to mediate inflammation in cutaneous injury.

We identified fresh human leukocytes as an abundant source of the candidate epithelial tumor suppressor gene, Ecrg4, epigenetically regulated which unlike other genes, encodes orphan-secreted, ligand-like protein. In cell lines, Ecrg4 gene expression was low, protein undetectable, and promoter hypermethylation high (45-90%) reversible by methylation inhibitor 5-AzaC. contrast, in fresh, normal PBMCs PMNs 600-800 times higher than cultured low (<3%), levels were readily detectable lysates on...

Abstract: In humans, esophageal cancer-related gene 4 (ECRG4) is encoded by four exons in the c2orf40 locus of chromosome 2. Translation ECRG4 messenger ribonucleic acid produces a 148 amino acid-secreted 17 KDa protein that then processed to 14, ten, eight, six, four, and two peptides, depending on cell which expressed. As hypermethylation at inhibits expression many epithelial cancers, several investigators have speculated candidate tumor suppressor. Indeed, overexpression proliferation...

Traumatic brain injury (TBI)-induced cerebral inflammation involves several mediators including activation of resident microglia, infiltration leukocytes, and release proinflammatory cytokines chemokines at the site injury. Invading mainly neutrophil inflammatory monocytes, contribute to ongoing post-TBI edema neuronal Based on beneficial effect ghrelin hormone treatment following TBI, we hypothesized that may alter infiltrating cell profile.A weight drop model was used create severe TBI....

Abstract Myeloid cells regulate tumor angiogenesis and promote invasion, yet few strategies exist to exploit their presence reverse the overall immunosuppressive microenvironment. Based on bioinformatic mining of sentinel genes encoding biologically active peptides, we have recently identified Ecrg4 (Esophageal Cancer-Related Gene 4), as a novel secreted pro-inflammatory mediator macrophage activation. While higher expression levels correlate with improved survival in cancers esophagus,...

Abstract Tumor-associated microglia generally promote tumor invasion, adopting an immunosuppressive phenotype that is distinct from their pro-inflammatory functions. Based on bioinformatic mining of novel sentinel genes encoding biologically active peptides, we have recently identified Ecrg4, as a secreted mediator macrophage activation. While downregulation Ecrg4 expression occurs in various cells, this study, demonstrate the biological activity cancer functions through paracrine mechanism,...

Supplementary Figure 2 from Conditional Deletion of the Focal Adhesion Kinase FAK Alters Remodeling Blood–Brain Barrier in Glioma

Supplementary Figure 3 from Conditional Deletion of the Focal Adhesion Kinase FAK Alters Remodeling Blood–Brain Barrier in Glioma

Supplementary Figure 1 from Conditional Deletion of the Focal Adhesion Kinase FAK Alters Remodeling Blood–Brain Barrier in Glioma

Supplementary Figure 3 from Conditional Deletion of the Focal Adhesion Kinase FAK Alters Remodeling Blood–Brain Barrier in Glioma

Supplementary Figure 2 from Conditional Deletion of the Focal Adhesion Kinase FAK Alters Remodeling Blood–Brain Barrier in Glioma

Supplementary Figure 1 from Conditional Deletion of the Focal Adhesion Kinase FAK Alters Remodeling Blood–Brain Barrier in Glioma

&lt;p&gt;PDF file - 349KB, Enlarged immunostaining image of U87 cells show decrease and change Y397-FAK FAK localization in Y15-treated compared with untreated cells.&lt;/p&gt;