Journey towards tiny perceptual super-resolution

Recent works in single-image perceptual super-resolution (SR) have demonstrated unprecedented performance in generating realistic textures by means of deep convolutional networks. However, these convolutional models are excessively large and expensive, hindering their effective deployment to end devices. In this work, we propose a neural architecture search (NAS) approach that integrates NAS and generative adversarial networks (GANs) with recent advances in perceptual SR and pushes the efficiency of small perceptual SR models to facilitate on-device execution. Specifically, we search over the architectures of both the generator and the discriminator sequentially, highlighting the unique challenges and key observations of searching for an SR-optimized discriminator and comparing them with existing discriminator architectures in the literature. Our tiny perceptual SR (TPSR) models outperform SRGAN and EnhanceNet on both full-reference perceptual metric (LPIPS) and distortion metric (PSNR) while being up to 26.4 × more memory efficient and 33.6 × more compute efficient respectively

The Unreasonable Effectiveness of Texture Transfer for Single Image Super-resolution

While implicit generative models such as GANs have shown impressive results in high quality image reconstruction and manipulation using a combination of various losses, we consider a simpler approach leading to surprisingly strong results. We show that texture loss alone allows the generation of perceptually high quality images. We provide a better understanding of texture constraining mechanism and develop a novel semantically guided texture constraining method for further improvement. Using a recently developed perceptual metric employing "deep features" and termed LPIPS, the method obtains state-of-the-art results. Moreover, we show that a texture representation of those deep features better capture the perceptual quality of an image than the original deep features. Using texture information, off-the-shelf deep classification networks (without training) perform as well as the best performing (tuned and calibrated) LPIPS metrics. The code is publicly available.Comment: 19 pages, 14 figure

Primary tuberculosis appendicitis with mesenteric mass

Tuberculosis primarily affecting the appendix is extremely rare and the diagnosis is difficult. Here, we report the case of a 14-year-old healthy boy presenting with right lower quadrant abdominal pain. On computed tomography, the distended appendix with 3.3 × 2.7 cm mass located at the right side of the right iliac artery was detected. There was neither bowel wall thickening nor active lung lesion. After laparoscopic appendectomy with mass excision, histopathological examination revealed chronic granulomatous inflammation, with caseous necrosis of the appendix. We made a diagnosis of primary tuberculosis of appendix and administrated anti-tuberculosis medication

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.