We studied the loss compensation of surface plasmon polaritons (SPPs) with InGaAsP quantum wells at telecom wavelength. The quantum wells are buried in the vicinity of a thin Au film. The propagation length of short-range SPPs increases drastically with the gain coefficient of quantum wells, generated by a forward bias. The elongation of SPP propagation is experimentally observed via long-range SPPs, which strongly couple with the short-range SPPs. This study paves a way for electrically manipulated amplification of SPPs in plasmonic circuits.

The Surface Plasmon Polariton (SPP) planar waveguide with amorphous silicon (α-Si) cladding is studied, for empowering the device modulation response. The device is fabricated with multiple quantum wells (MQWs) as the gain media electrically pumped for compensating SPP propagation loss on Au film waveguide. The SPP propagation greatly benefits from the modal gain for the long-range hybrid mode, which is optimized by adopting an α-Si cladding layer accompanied with minimal degradation of mode confinement. The proposed structure presented more sensitive response to electrical manipulation than the one without cladding in experiment.

We have investigated the propagation of the long-range mode (LRSP) and the short-range mode (SRSP) surface plasmon polaritons (SPPs) along the waveguide made from Au film and quantum wells (QWs) gain medium. Influenced by the gain spectral nonuniformity, the SRSP showed narrower spectrum than the LRSP in output, denoting that the SRSP propagation was supported by stimulated amplification (SA) in electrically-pumped QWs. An SRSP output power as large as 1.6 times of that of the LRSP was obtained over a travelling distance of 80 μm. The mechanism of SA-supported SRSP propagation can be adopted for electrical modulation of SPPs.

No abstract

Sickle cell disease (SCD) is a genetic hematological disease in which the hemoglobin molecule in red blood cells is abnormal. It is closely associated with many symptoms, including pain, anemia, chest syndrome and neurocognitive impairment. One of the most debilitating symptoms is elevated risk for cerebro-vascular accidents. The corpus callosum (CC), as the largest and most prominent white matter (WM) structure in the brain, can reflect the chronic cerebrovascular damage resulting from silent strokes or infarctions in asymptomatic SCD patients. While a lot of studies have reported WM alterations in this cohort, little is known about the shape deformation of the CC. Here we perform the first surface morphometry analysis of the CC in SCD patients using four different shape metrics on T1-weighted magnetic resonance images. We detect regional surface morphological differences in the CC between 11 patients and 10 healthy control subjects. Differences are located in the genu, posterior midbody and splenium, potentially casting light on the anatomical substrates underlying neuropsychological test differences between the SCD and control groups.