Spin photonics on chip based on a twinning crystal metamaterial

Two-dimensional photonic circuits with high capacity are essential for a wide range of applications in next-generation photonic information technology and optoelectronics. Here we demonstrate a multi-channel spin-dependent photonic device based on a twinning crystal metamaterial. The structural symmetry and material symmetry of the twinning crystal metamaterial enable a total of 4 channels carrying different transverse spins because of the spin-momentum locking. The orientation of the anisotropy controls the propagation direction of each signal, and the rotation of the E-field with respect to energy flow determines the spin characteristics during input/output coupling. Leveraging this mechanism, the spin of an incident beam can be maintained during propagation on-chip and then delivered back into the free space, offering a new scheme for metamaterial-based spin-controlled nano-photonic applications

Optical vortices enabled by structural vortices

The structural symmetry of solids plays an important role in defining their linear and nonlinear optical properties. The quest for versatile, cost-effective, large-scale, and defect-free approaches and materials platforms for tailoring structural and optical properties on demand has been underway for decades. We experimentally demonstrate a bottom-up self-assembly-based organic engineered material comprised of synthesized molecules with large dipole moments that are crystallized into a spherulite structure. The molecules align in an azimuthal direction, resulting in a vortex polarity with spontaneously broken symmetry leading to strong optical anisotropy and nonlinear optical responses. These unique polarization properties of the judiciously designed organic spherulite combined with the symmetry of structured optical beams enable a plethora of new linear and nonlinear light-matter interactions, including the generation of optical vortex beams with complex spin states and on-demand topological charges at the fundamental, doubled, and tripled frequencies. The results of this work are likely to enable numerous applications in areas such as high-dimensional quantum information processing, with large capacity and high security. The demonstrated spherulite crystals facilitate stand-alone micro-scale devices that rely on the unique micro-scale spontaneous vortex polarity that is likely to enable future applications for high-dimensional quantum information processing, spatiotemporal optical vortices, and a novel platform for optical manipulation and trapping

Effect of growth temperature on the morphology and phonon properties of InAs nanowires on Si substrates

Catalyst-free, vertical array of InAs nanowires (NWs) are grown on Si (111) substrate using MOCVD technique. The as-grown InAs NWs show a zinc-blende crystal structure along a < 111 > direction. It is found that both the density and length of InAs NWs decrease with increasing growth temperatures, while the diameter increases with increasing growth temperature, suggesting that the catalyst-free growth of InAs NWs is governed by the nucleation kinetics. The longitudinal optical and transverse optical (TO) mode of InAs NWs present a phonon frequency slightly lower than those of InAs bulk materials, which are speculated to be caused by the defects in the NWs. A surface optical mode is also observed for the InAs NWs, which shifts to lower wave-numbers when the diameter of NWs is decreased, in agreement with the theory prediction. The carrier concentration is extracted to be 2.25 × 1017 cm-3 from the Raman line shape analysis. A splitting of TO modes is also observed

Frequency-dependent orthotropic damping properties of Nomex honeycomb composites

In this paper, the orthotropic damping behavior of Nomex honeycomb composites and its causes are investigated. The needed specimen sizes for the measurement of the frequency-dependent transverse shear moduli (TSM) and fundamental damping coefficients of the honeycomb cores were analyzed at first. Then, the effects of cell side length and beam orientation on the orthotropic damping properties were explored. The results reveal that relatively high TSM (GLT) and damping values (ηWT) can be obtained by decreasing the cell side length without adding any additional weight. Damping mechanism analysis indicates that the difference in damping contribution of the interfacial phase to honeycomb core in different directions leads to the orthotropic damping behavior of honeycomb core. This study is helpful to guide the TSM measurement and structure design of honeycomb composites

Inhibition of Stimulator of Interferon Genes Protects Against Myocardial Ischemia-Reperfusion Injury in Diabetic Mice

Background: Although the past decade has witnessed substantial scientific progress with the advent of cardioprotective pharmacological agents, most have failed to protect against myocardial ischemia/reperfusion (I/R) injury in diabetic hearts. This study was aimed at investigating the role of stimulator of interferon genes (STING) in I/R injury in diabetic mice and further exploring the underlying mechanisms. Methods: Type 2 diabetic mice were subjected to I/R or sham operation to investigate the role of STING. STING knockout mice were subjected to 30 minutes of ischemia followed by reperfusion for 24 hours. Finally, myocardial injury, cardiac function, and inflammation levels were assessed. Results: STING pathway activation was observed in diabetic I/R hearts, as evidenced by increased p-TBK and p-IRF3 expression. STING knockout significantly decreased the ischemic area and improved cardiac function after I/R in diabetic mice. STING knockout also elicited cardio-protective effects by decreasing serum cardiac troponin T and lactate dehydrogenase levels, thus diminishing the inflammatory response in the heart after I/R in diabetic mice. In vitro , STING inhibition decreased the expression of hypoxia-re-oxygenation-induced inflammatory cytokines. Conclusions: Targeting STING inhibits inflammation and prevents I/R injury in diabetic mice. Thus, STING may be a potential novel therapeutic target against myocardial I/R injury in diabetes

Immune-based mutation classification enables neoantigen prioritization and immune feature discovery in cancer immunotherapy.

Genetic mutations lead to the production of mutated proteins from which peptides are presented to T cells as cancer neoantigens. Evidence suggests that T cells that target neoantigens are the main mediators of effective cancer immunotherapies. Although algorithms have been used to predict neoantigens, only a minority are immunogenic. The factors that influence neoantigen immunogenicity are not completely understood. Here, we classified human neoantigen/neopeptide data into three categories based on their TCR-pMHC binding events. We observed a conservative mutant orientation of the anchor residue from immunogenic neoantigens which we termed the NP rule. By integrating this rule with an existing prediction algorithm, we found improved performance in neoantigen prioritization. To better understand this rule, we solved several neoantigen/MHC structures. These structures showed that neoantigens that follow this rule not only increase peptide-MHC binding affinity but also create new TCR-binding features. These molecular insights highlight the value of immune-based classification in neoantigen studies and may enable the design of more effective cancer immunotherapies

Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice

ASXL1 is mutated/deleted with high frequencies in multiple forms of myeloid malignancies, and its alterations are associated with poor prognosis. De novo ASXL1 mutations cause Bohring-Opitz syndrome characterized by multiple congenital malformations. We show that Asxl1 deletion in mice led to developmental abnormalities including dwarfism, anophthalmia, and 80% embryonic lethality. Surviving Asxl1(-/-) mice lived for up to 42 days and developed features of myelodysplastic syndrome (MDS), including dysplastic neutrophils and multiple lineage cytopenia. Asxl1(-/-) mice had a reduced hematopoietic stem cell (HSC) pool, and Asxl1(-/-) HSCs exhibited decreased hematopoietic repopulating capacity, with skewed cell differentiation favoring granulocytic lineage. Asxl1(+/-) mice also developed mild MDS-like disease, which could progress to MDS/myeloproliferative neoplasm, demonstrating a haploinsufficient effect of Asxl1 in the pathogenesis of myeloid malignancies. Asxl1 loss led to an increased apoptosis and mitosis in Lineage(-)c-Kit(+) (Lin(-)c-Kit(+)) cells, consistent with human MDS. Furthermore, Asxl1(-/-) Lin(-)c-Kit(+) cells exhibited decreased global levels of H3K27me3 and H3K4me3 and altered expression of genes regulating apoptosis (Bcl2, Bcl2l12, Bcl2l13). Collectively, we report a novel ASXL1 murine model that recapitulates human myeloid malignancies, implying that Asxl1 functions as a tumor suppressor to maintain hematopoietic cell homeostasis. Future work is necessary to clarify the contribution of microenvironment to the hematopoietic phenotypes observed in the constitutional Asxl1(-/-) mice

Loss of Asxl1 Alters Self-Renewal and Cell Fate of Bone Marrow Stromal Cell, Leading to Bohring-Opitz-like Syndrome in Mice

De novo ASXL1 mutations are found in patients with Bohring-Opitz syndrome, a disease with severe developmental defects and early childhood mortality. The underlying pathologic mechanisms remain largely unknown. Using Asxl1-targeted murine models, we found that Asxl1 global loss as well as conditional deletion in osteoblasts and their progenitors led to significant bone loss and a markedly decreased number of bone marrow stromal cells (BMSCs) compared with wild-type littermates. Asxl1(-/-) BMSCs displayed impaired self-renewal and skewed differentiation, away from osteoblasts and favoring adipocytes. RNA-sequencing analysis revealed altered expression of genes involved in cell proliferation, skeletal development, and morphogenesis. Furthermore, gene set enrichment analysis showed decreased expression of stem cell self-renewal gene signature, suggesting a role of Asxl1 in regulating the stemness of BMSCs. Importantly, re-introduction of Asxl1 normalized NANOG and OCT4 expression and restored the self-renewal capacity of Asxl1(-/-) BMSCs. Our study unveils a pivotal role of ASXL1 in the maintenance of BMSC functions and skeletal development