One promising application of nanoscale engineering is detecting mycobacteria and biomarkers of disease. We have developed highly sensitive optical probes for surface-enhanced Raman spectroscopy (SERS). Their high sensitivity is due to enhancing light scattering using gold or silver nanoparticles within the probe’s core. The particle surface can then be labeled with antibodies for specific biomarker targeting. Using labeled SERS optical probes, multiple biomarkers can be targeted and identified. Alternatively, label-free techniques which exclude the use of dyes, radioactive tags, or antibodies to identify a sample, can also be used. In these cases, identification is done by recognizing the intrinsic characteristics of the sample. Our lab uses both methods for identifying biological materials.
Cindy is using dielectrophoresis and SERS nanoprobes to concentrate and detect mycocbacteria. Nate worked on SERS nanoprobes to classify B-cell malignancies which have many clinically discrete biomarkers.
This work is supported by the Nuclear Regulatory Commission. Previous funding from a USU Research Catalyst Award (EV), a USUSA Dissertation Enhancement Award (C. Hanson), and an SPIE Scholarship (C. Hanson).
We are interested in developing in vitro models of retinal pigment epithelial cells to understand disease, test new treatments and build computer simulations to understand the role of growth factors. Farhad's primary research focus is to implement a range of experimental methods to provide new insights into the cause and progression of different retinal diseases, such as age-related retinal degeneration and diabetic retinopathy. A secondary research focus is developing new materials to mimic Bruch's membrane. Bruch's membrane supports retinal pigment epithelial cell function and forms part of the retinal-blood-barrier.
This research is supported by a Career Starter Grant from the Knights Templar Eye Foundation and a Ralph E. Powe Junior Faculty Award from ORAU (for EV).
Muscular atrophy due to disuse is a serious issue for immobilized patients on Earth and in human spaceflight, where microgravity prevents normal muscle loading. Defined as the loss of muscle tissue, muscular atrophy involves a wide variety of factors including apoptosis-inducing factor, reactive oxygen species, and N-linked glycans. The specific factors involved depend on the atrophy type, such as denervation, disuse, or muscular disease. Reducing microgravity-induced atrophy would have far-reaching benefits not limited to astronauts and space flight. Those suffering from immobilization due to aging, bone fractures, and comas would benefit from maintaining muscle mass in the absence of normal stimulation. While the cellular mechanisms behind muscular dystrophy and denervation injuries differ from those involved in disuse atrophy, a comprehensive treatment that inhibits myocyte apoptosis and promotes new growth could still alleviate some symptoms. Further uses extend past the clinical realm and into muscular enhancement for athletes and soldiers.
The goal of Charles' research is to determine which atrophy-inducing factors are released due to microgravity, how to inhibit such factors, and how to promote new muscle growth without mechanical stimuli. The hypothesis of his work is that comprehensive prevention of microgravity-induced atrophy will be needed to inhibit myocyte apoptosis as well as promote new growth via supplementation of factors typically released during mechanical stimulation.
This work is supported by the Nuclear Regulatory Commission and a Utah NASA Space Grant Consortium fellowship (C. Harding).