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Due to their short wavelength, X-rays can in principle be focused down to a few nanometres and below. At the same time, it is this short wavelength that puts stringent requirements on X-ray optics and their metrology. Both are limited by today’s technology. In this work, we present accurate at wavelength measurements of residual aberrations of a refractive X-ray lens using ptychography to manufacture a corrective phase plate. Together with the fitted phase plate the optics shows diffraction-limited performance, generating a nearly Gaussian beam profile with a Strehl ratio above 0.8. This scheme can be applied to any other focusing optics, thus solving the X-ray optical problem at synchrotron radiation sources and X-ray free-electron lasers. X-ray optics are notoriously challenging to fabricate due to the strict tolerances that result from the short wavelength of radiation. Here, Seiboth et al . carefully quantify aberrations in complex X-ray lenses and correct them with an easy-to-fabricate broadband phase plate.

Study Objectives: The purpose of this study was to determine whether a wearable sleep-tracker improves perceived sleep quality in healthy participants and to test whether wearables reliably measure sleep quantity and quality compared with polysomnography. Methods: This study included a single-center randomized crossover trial of community-based participants without medical conditions or sleep disorders. A wearable device (WHOOP, Inc.) was used that provided feedback regarding sleep information to the participant for 1 week and maintained sleep logs versus 1 week of maintained sleep logs alone. Self-reported daily sleep behaviors were documented in sleep logs. Polysomnography was performed on 1 night when wearing the wearable. The Patient-Reported Outcomes Measurement Information System sleep disturbance sleep scale was measured at baseline, day 7 and day 14 of study participation. Results: In 32 participants (21 women; 23.8 ± 5 years), wearables improved nighttime sleep quality (Patient-Reported Outcomes Measurement Information System sleep disturbance:B = −1.69; 95% confidence interval, −3.11 to −0.27; P =.021) after adjusting for age, sex, baseline, and order effect. There was a small increase in self-reported daytime naps when wearing the device (B = 3.2; SE, 1.4; P =.023), but total daily sleep remained unchanged ( P =.43). The wearable had low bias (13.8 minutes) and precision (17.8 minutes) errors for measuring sleep duration and measured dream sleep and slow wave sleep accurately (intraclass coefficient, 0.74 ± 0.28 and 0.85 ± 0.15, respectively). Bias and precision error for heart rate (bias, −0.17%; precision, 1.5%) and respiratory rate (bias, 1.8%; precision, 6.7%) were very low compared with that measured by electrocardiogram and inductance plethysmography during polysomnography. Conclusions: In healthy people, wearables can improve sleep quality and accurately measure sleep and cardiorespiratory variables. Clinical Trial Registration: Registry: ClinicalTrials.gov ; Name: Assessment of Sleep by WHOOP in Ambulatory Subjects; Identifier:NCT03692195. Citation: Berryhill S, Morton CJ, Dean A, et al. Effect of wearables on sleep in health individuals: A randomized crossover trial and validation study. J Clin Sleep Med . 2020;16(5):775–783.

The role of myocardial viability assessment in identifying patients with ischemic cardiomyopathy who will benefit from surgical revascularization is controversial. This study assessed myocardial viability and its relationship to long-term outcomes in 601 patients with ischemic cardiomyopathy who were assigned to surgical revascularization plus medical therapy or medical therapy alone.

In a trial involving participants with HIV infection receiving antiretroviral therapy, the use of pitavastatin resulted in a lower risk of a major adverse cardiac event than placebo at a median of 5.1 years.

Excess caloric intake can lead to insulin resistance. The underlying reasons are complex but likely related to ectopic lipid deposition in nonadipose tissue. We hypothesized that the inability to appropriately expand subcutaneous adipose tissue may be an underlying reason for insulin resistance and beta cell failure. Mice lacking leptin while overexpressing adiponectin showed normalized glucose and insulin levels and dramatically improved glucose as well as positively affected serum triglyceride levels. Therefore, modestly increasing the levels of circulating full-length adiponectin completely rescued the diabetic phenotype in ob/ob mice. They displayed increased expression of PPARgamma target genes and a reduction in macrophage infiltration in adipose tissue and systemic inflammation. As a result, the transgenic mice were morbidly obese, with significantly higher levels of adipose tissue than their ob/ob littermates, leading to an interesting dichotomy of increased fat mass associated with improvement in insulin sensitivity. Based on these data, we propose that adiponectin acts as a peripheral \"starvation\" signal promoting the storage of triglycerides preferentially in adipose tissue. As a consequence, reduced triglyceride levels in the liver and muscle convey improved systemic insulin sensitivity. These mice therefore represent what we believe is a novel model of morbid obesity associated with an improved metabolic profile.

The tripartite motif (TRIM) family of E3 ubiquitin ligases is well known for its roles in antiviral restriction and innate immunity regulation, in addition to many other cellular pathways. In particular, TRIM25-mediated ubiquitination affects both carcinogenesis and antiviral response. While individual substrates have been identified for TRIM25, it remains unclear how it regulates diverse processes. Here we characterized a mutation, R54P, critical for TRIM25 catalytic activity, which we successfully utilized to “trap” substrates. We demonstrated that TRIM25 targets proteins implicated in stress granule formation (G3BP1/2), nonsense-mediated mRNA decay (UPF1), nucleoside synthesis (NME1), and mRNA translation and stability (PABPC4). The R54P mutation abolishes TRIM25 inhibition of alphaviruses independently of the host interferon response, suggesting that this antiviral effect is a direct consequence of ubiquitination. Consistent with that, we observed diminished antiviral activity upon knockdown of several TRIM25-R54P specific interactors including NME1 and PABPC4. Our findings highlight that multiple substrates mediate the cellular and antiviral activities of TRIM25, illustrating the multi-faceted role of this ubiquitination network in modulating diverse biological processes.