Highly Localized SERS Measurements Using Single Silicon Nanowires Decorated with DNA Origami-Based SERS Probe.

Surface enhanced Raman spectroscopy (SERS) measurements are conventionally performed using assemblies of metal nanostructures on a macro- to micro-sized substrate or by dispersing colloidal metal nanoparticles directly onto the sample of interest. Despite intense use, these methods allow neither the removal of the nanoparticles after a measurement nor a defined confinement of the SERS measurement position. So far, tip enhanced Raman spectroscopy is still the key technique in this regard but not adequate for various samples mainly due to diminished signal enhancement compared to other techniques, poor device fabrication reproducibility, and cumbersome experimental setup requirements.

β-Sarcoglycan Deficiency Reduces Atherosclerotic Plaque Development in ApoE-Null Mice.

Background: Smooth muscle cells are important for atherosclerotic plaque stability. Their proper ability to communicate with the extracellular matrix is crucial for maintaining the correct tissue integrity. In this study, we have investigated the role of β-sarcoglycan within the matrix-binding dystrophin-glycoprotein complex in the development of atherosclerosis.

Dystrophin deficiency reduces atherosclerotic plaque development in ApoE-null mice.

Dystrophin of the dystrophin-glycoprotein complex connects the actin cytoskeleton to basement membranes and loss of dystrophin results in Duchenne muscular dystrophy. We have previously shown injury-induced neointima formation of the carotid artery in mice with the mdx mutation (causing dystrophin deficiency) to be increased. To investigate the role of dystrophin in intimal recruitment of smooth muscle cells (SMCs) that maintains plaque stability in atherosclerosis we applied a shear stress-modifying cast around the carotid artery of apolipoprotein E (ApoE)-null mice with and without the mdx mutation.

Regulation of smooth muscle dystrophin and synaptopodin 2 expression by actin polymerization and vascular injury.

Objective: Actin dynamics in vascular smooth muscle is known to regulate contractile differentiation and may play a role in the pathogenesis of vascular disease. However, the list of genes regulated by actin polymerization in smooth muscle remains incomprehensive. Thus, the objective of this study was to identify actin-regulated genes in smooth muscle and to demonstrate the role of these genes in the regulation of vascular smooth muscle phenotype.