Radiation Brightening from Virus-like Particles

Concentration quenching is a well-known challenge in many fluorescence imaging applications. Here we show that the optical emission from hundreds of chromophores confined onto the surface of a virus particle 28 nm diameter can be recovered under pulsed irradiation. We have found that, as one increases the number of chromophores tightly-bound to the virus surface, fluorescence quenching ensues at first, but when the number of chromophores per particle is nearing the maximum number of surface sites allowable, a sudden brightening of the emitted light and a shortening of the excited state lifetime are observed. This radiation brightening occurs only under short pulse excitation; steady-state excitation is characterized by conventional concentration quenching for any number of chromophores per particle. The observed suppression of fluorescence quenching is consistent with efficient, collective relaxation at room temperature. Interestingly, radiation brightening disappears when the emitters' spatial and/or dynamic heterogeneity is increased, suggesting that the template structural properties may play a role and opening a way towards novel, virus-enabled imaging vectors that have qualitatively different optical properties than state-of-the-art biophotonic agents

Lattice QCD and Particle Physics

Contribution from the USQCD Collaboration to the Proceedings of the US Community Study on the Future of Particle Physics (Snowmass 2021).Comment: 27 pp. main text, 4 pp. appendices, 30 pp. reference

Lattice QCD and Particle Physics

Contribution from the USQCD Collaboration to the Proceedings of the US Community Study on the Future of Particle Physics (Snowmass 2021)

Radiation Brightening from Virus-like Particles

Concentration quenching is a well-known challenge in many fluorescence imaging applications. Here we show that the optical emission from hundreds of chromophores confined onto the surface of a virus particle 28 nm diameter can be recovered under pulsed irradiation. We have found that, as one increases the number of chromophores tightly-bound to the virus surface, fluorescence quenching ensues at first, but when the number of chromophores per particle is nearing the maximum number of surface sites allowable, a sudden brightening of the emitted light and a shortening of the ex- cited state lifetime are observed. This radiation brightening occurs only under short pulse excitation; steady-state excitation is characterized by conventional concentration quenching for any number of chromophores per particle. The observed suppression of fluorescence quenching is consistent with efficient, collective radiation at room temper- ature. Interestingly, radiation brightening disappears when the emitters spatial and/or dynamic heterogeneity is increased, suggesting that the template structural properties may play a role and opening a way towards novel, virus-enabled imaging vectors that have qualitatively different optical properties than state-of-the-art biophotonic agents

Toward Virus-Like Surface Plasmon Strain Sensors

The strong configuration dependence of collective surface plasmon resonances in an array of metal nanoparticles provides an opportunity to develop a bioinspired tool for sensing mechanical deformations in soft matter at the nanoscale. We study the feasibility of a strain sensor based on an icosahedral array of nanoparticles encapsulated by a virus capsid. When the system undergoes deformation, the optical scattering cross-section spectra as well as the induced electric field profile change. By numerical simulations, we examine how these changes depend on the symmetry and extent of the deformation and on both the propagation direction and polarization of the incident radiation. Such a sensor could prove useful in studies of the mechanisms of nanoparticle or virus translocation in the confines of a host cell

Mustn1 ablation in skeletal muscle results in increased glucose tolerance concomitant with upregulated GLUT expression in male mice

Abstract Glucose homeostasis is closely regulated to maintain energy requirements of vital organs and skeletal muscle plays a crucial role in this process. Mustn1 is expressed during embryonic and postnatal skeletal muscle development and its function has been implicated in myogenic differentiation and myofusion. Whether Mustn1 plays a role in glucose homeostasis in anyway remains largely unknown. As such, we deleted Mustn1 in skeletal muscle using a conditional knockout (KO) mouse approach. KO mice did not reveal any specific gross phenotypic alterations in skeletal muscle. However, intraperitoneal glucose tolerance testing (IPGTT) revealed that 2‐month‐old male KO mice had significantly lower glycemia than their littermate wild type (WT) controls. These findings coincided with mRNA changes in genes known to be involved in glucose metabolism, tolerance, and insulin sensitivity; 2‐month‐old male KO mice had significantly higher expression of GLUT1 and GLUT10 transporters, MUP‐1 while OSTN expression was lower. These differences in glycemia and gene expression were statistically insignificant after 4 months. Identical experiments in female KO and WT control mice did not indicate any differences at any age. Our results suggest a link between Mustn1 expression and glucose homeostasis during a restricted period of skeletal muscle development/maturation. While this is an observational study, Mustn1's relationship to glucose homeostasis appears to be more complex with a possible connection to other key proteins such as GLUTs, MUP‐1, and OSTN. Additionally, our data indicate temporal and sex differences. Lastly, our findings strengthen the notion that Mustn1 plays a role in the metabolic capacity of skeletal muscle

Lattice QCD and Particle Physics

Kronfeld AS, Bhattacharya T, Blum T, et al. Lattice QCD and Particle Physics. arXiv:2207.07641. 2022.Contribution from the USQCD Collaboration to the Proceedings of the US Community Study on the Future of Particle Physics (Snowmass 2021)