Search for: All records

α-Sn and SnGe alloys are attracting attention as a new family of topological quantum materials. However, bulkα-Sn is thermodynamically stable only below 13^∘C. Moreover, scalable integration ofα-Sn quantum materials and devices on silicon is hindered by their large lattice mismatch. Here, we grow compressively strainedα-Sn doped with 2-4 at.% germanium on a native oxide layer on a silicon substrate at 300–500^∘C. Growth is found to occur by a reversedβ-Sn toα-Sn phase transformation without relying on epitaxy, with germanium-rich GeSn nanoclusters in the as-deposited material acting as seeds. The size ofα-Sn microdots reaches up to 200 nm, which is approximately ten times larger than the upper size limit forα-Sn formation reported previously. Furthermore, the compressive strain makes it a candidate 3D topological Dirac semimetal with possible applications in spintronics. This process can be further optimized to achieve optically tunable SnGe quantum material and device integration on silicon.

 

The optical conductivity of single layer graphene (SLG) can be significantly and reversibly modified when the Fermi level is tuned by electrical gating. However, so far this interesting property has rarely been applied to free-space two-dimensional (2D) photonic devices because the surface-incident absolute absorption of SLG is limited to 1%–2%. No significant change in either reflectance or transmittance would be observed even if SLG is made transparent upon gating. To achieve significantly enhanced surface-incident optical absorption in SLG in a device structure that also allows gating, here we embed SLG in an optical slot-antenna-coupled cavity (SAC) framework, simultaneously enhancing SLG absorption by up to 20 times and potentially enabling electrical gating of SLG as a step towards tunable 2D photonic surfaces. This framework synergistically integrates near-field enhancement induced by ultrahigh refractive index semimetal slot-antenna with broadband resonances in visible and infrared regimes, ~ 3 times more effective than a vertical cavity structure alone. An example of this framework consists of self-assembled, close-packed Sn nanodots separated by ~ 10 nm nanogaps on a SLG/SiO2/Al stack, which dramatically increases SLG optical absorption to 10%-25% at λ = 600–1,900 nm. The enhanced SLG absorption spectrum can also be controlled by the insulator thickness. For example, SLG embedded in this framework with a 150 nm-thick SiO2 insulating layer displays a distinctive red color in contrast to its surrounding regions without SLG on the same sample under white light illumination. This opens a potential path towards gate-tunable spectral reflectors. Overall, this work initiates a new approach towards tunable 2D photonic surfaces. 

We sought to delineate the retinal features associated with the high-fat diet (HFD) mouse, a widely used model of obesity. C57BL/6 mice were fed either a high-fat (60% fat; HFD) or low-fat (10% fat; LFD) diet for up to 12 months. The effect of HFD on body weight and insulin resistance were measured. The retina was assessed by electroretinogram (ERG), fundus photography, permeability studies, and trypsin digests for enumeration of acellular capillaries. The HFD cohort experienced hypercholesterolemia when compared to the LFD cohort, but not hyperglycemia. HFD mice developed a higher body weight (60.33 g vs. 30.17g, p < 0.0001) as well as a reduced insulin sensitivity index (9.418 vs. 62.01, p = 0.0002) compared to LFD controls. At 6 months, retinal functional testing demonstrated a reduction in a-wave and b-wave amplitudes. At 12 months, mice on HFD showed evidence of increased retinal nerve infarcts and vascular leakage, reduced vascular density, but no increase in number of acellular capillaries compared to LFD mice. In conclusion, the HFD mouse is a useful model for examining the effect of prediabetes and hypercholesterolemia on the retina. The HFD-induced changes appear to occur slower than those observed in type 2 diabetes (T2D) models but are consistent with other retinopathy models, showing neural damage prior to vascular changes.