Sub-optimal Deep Pipelined Implementation of MIMO Sphere Detector on FPGA

Sphere detector (SD) is an effective signal detection approach for the wireless multiple-input multiple-output (MIMO) system since it can achieve near-optimal performance while reducing significant computational complexity. In this work, we proposed a novel SD architecture that is suitable for implementation on the hardware accelerator. We first perform a statistical analysis to examine the distribution of valid paths in the SD search tree. Using the analysis result, we then proposed an enhanced hybrid SD (EHSD) architecture that achieves quasi-ML performance and high throughput with a reasonable cost in hardware. The fine-grained pipeline designs of 4 × 4 and 8 × 8 MIMO system with 16-QAM modulation delivers throughput of 7.04 Gbps and 14.08 Gbps on the Xilinx Virtex Ultrascale+ FPGA, respectively

Professional Standards Review Organizations and Health Maintenance Organizations: Are They Compatible?

In freestanding n-type 4H-SiC epilayers irradiated with low-energy (250 keV) electrons at room temperature, the electron paramagnetic resonance (EPR) spectrum of the negative carbon vacancy at the hexagonal site, V-C(-)(h), and a new signal were observed. From the similarity in defect formation and the spin-Hamiltonian parameters of the two defects, the new center is suggested to be the negative C vacancy at the quasi-cubic site, V-C(-)(k). The identification is further supported by hyperfine calculations

Safety and efficacy of fluoxetine on functional outcome after acute stroke (AFFINITY): a randomised, double-blind, placebo-controlled trial

Background Trials of fluoxetine for recovery after stroke report conflicting results. The Assessment oF FluoxetINe In sTroke recoverY (AFFINITY) trial aimed to show if daily oral fluoxetine for 6 months after stroke improves functional outcome in an ethnically diverse population. Methods AFFINITY was a randomised, parallel-group, double-blind, placebo-controlled trial done in 43 hospital stroke units in Australia (n=29), New Zealand (four), and Vietnam (ten). Eligible patients were adults (aged ≥18 years) with a clinical diagnosis of acute stroke in the previous 2–15 days, brain imaging consistent with ischaemic or haemorrhagic stroke, and a persisting neurological deficit that produced a modified Rankin Scale (mRS) score of 1 or more. Patients were randomly assigned 1:1 via a web-based system using a minimisation algorithm to once daily, oral fluoxetine 20 mg capsules or matching placebo for 6 months. Patients, carers, investigators, and outcome assessors were masked to the treatment allocation. The primary outcome was functional status, measured by the mRS, at 6 months. The primary analysis was an ordinal logistic regression of the mRS at 6 months, adjusted for minimisation variables. Primary and safety analyses were done according to the patient's treatment allocation. The trial is registered with the Australian New Zealand Clinical Trials Registry, ACTRN12611000774921. Findings Between Jan 11, 2013, and June 30, 2019, 1280 patients were recruited in Australia (n=532), New Zealand (n=42), and Vietnam (n=706), of whom 642 were randomly assigned to fluoxetine and 638 were randomly assigned to placebo. Mean duration of trial treatment was 167 days (SD 48·1). At 6 months, mRS data were available in 624 (97%) patients in the fluoxetine group and 632 (99%) in the placebo group. The distribution of mRS categories was similar in the fluoxetine and placebo groups (adjusted common odds ratio 0·94, 95% CI 0·76–1·15; p=0·53). Compared with patients in the placebo group, patients in the fluoxetine group had more falls (20 [3%] vs seven [1%]; p=0·018), bone fractures (19 [3%] vs six [1%]; p=0·014), and epileptic seizures (ten [2%] vs two [<1%]; p=0·038) at 6 months. Interpretation Oral fluoxetine 20 mg daily for 6 months after acute stroke did not improve functional outcome and increased the risk of falls, bone fractures, and epileptic seizures. These results do not support the use of fluoxetine to improve functional outcome after stroke

Investigation on origin of Z[1/2] center in SiC by deep level transient spectroscopy and electron paramagnetic resonance

The Z[1/2] center in n-type 4H-SiC epilayers—a dominant deep level limiting the carrier lifetime—has been investigated. Using capacitance versus voltage (C-V) measurements and deep level transient spectroscopy (DLTS), we show that the Z[1/2] center is responsible for the carrier compensation in n-type 4H-SiC epilayers irradiated by low-energy (250 keV) electrons. The concentration of the Z[1/2] defect obtained by C-V and DLTS correlates well with that of the carbon vacancy ( Vc ) determined by electron paramagnetic resonance, suggesting that the Z[1/2] deep level originates from Vc

Quantitative comparison between Z1∕2 center and carbon vacancy in 4H-SiC

In this study, to reveal the origin of the Z(1/2) center, a lifetime killer in n-type 4H-SiC, the concentrations of the Z(1/2) center and point defects are compared in the same samples, using deep level transient spectroscopy (DLTS) and electron paramagnetic resonance (EPR). The Z(1/2) concentration in the samples is varied by irradiation with 250 keV electrons with various fluences. The concentration of a single carbon vacancy (V-C) measured by EPR under light illumination can well be explained with the Z(1/2) concentration derived from C-V and DLTS irrespective of the doping concentration and the electron fluence, indicating that the Z(1/2) center originates from a single V-C

Quantitative comparison between Z1∕2 center and carbon vacancy in 4H-SiC

In this study, to reveal the origin of the Z(1/2) center, a lifetime killer in n-type 4H-SiC, the concentrations of the Z(1/2) center and point defects are compared in the same samples, using deep level transient spectroscopy (DLTS) and electron paramagnetic resonance (EPR). The Z(1/2) concentration in the samples is varied by irradiation with 250 keV electrons with various fluences. The concentration of a single carbon vacancy (V-C) measured by EPR under light illumination can well be explained with the Z(1/2) concentration derived from C-V and DLTS irrespective of the doping concentration and the electron fluence, indicating that the Z(1/2) center originates from a single V-C