BackgroundEffects of extreme sleep duration on risk of mortality and cardiovascular outcomes remain controversial. We aimed to quantify the dose‐response relationships of sleep duration with risk of all‐cause mortality, total cardiovascular disease, coronary heart disease, and stroke.Methods and ResultsPubMed and Embase were systematically searched for prospective cohort studies published before December 1, 2016, that examined the associations between sleep duration and at least 1 of the 4 outcomes in generally healthy populations. U‐shaped associations were indicated between sleep duration and risk of all outcomes, with the lowest risk observed for ≈7‐hour sleep duration per day, which was varied little by sex. For all‐cause mortality, when sleep duration was <7 hours per day, the pooled relative risk (RR) was 1.06 (95% CI, 1.04–1.07) per 1‐hour reduction; when sleep duration was >7 hours per day, the pooled RR was 1.13 (95% CI, 1.11–1.15) per 1‐hour increment. For total cardiovascular disease, the pooled RR was 1.06 (95% CI, 1.03–1.08) per 1‐hour reduction and 1.12 (95% CI, 1.08–1.16) per 1‐hour increment of sleep duration. For coronary heart disease, the pooled RR was 1.07 (95% CI, 1.03–1.12) per 1‐hour reduction and 1.05 (95% CI, 1.00–1.10) per 1‐hour increment of sleep duration. For stroke, the pooled RR was 1.05 (95% CI, 1.01–1.09) per 1‐hour reduction and 1.18 (95% CI, 1.14–1.21) per 1‐hour increment of sleep duration.ConclusionsOur findings indicate that both short and long sleep duration is associated with an increased risk of all‐cause mortality and cardiovascular events.

ACL reconstruction with HT autografts or BPTB autografts achieved similar postoperative effects in terms of restoring knee joint function. HT autografts were inferior to BPTB autografts for restoring knee joint stability, but were associated with fewer postoperative complications.

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In higher plants, many mitochondrial genes contain group II-type introns that are removed from RNAs by splicing to produce mature transcripts that are then translated into functional proteins. However, the factors involved in the splicing of mitochondrial introns and their biological functions are not well understood in maize. Here, we isolated an empty pericarp 10 (emp10) mutant and identified the underlying gene by map-based cloning. Emp10 encodes a P-type mitochondria-targeted pentatricopeptide repeat (PPR) protein with 10 PPR motifs. Loss of Emp10 function results in splicing defect of the first intron of nad2, a gene encoding subunit 2 of NADH dehydrogenase (also called complex I). The emp10 mutant has undetectable activity of complex I and has arrested development of embryo and endosperm, and thus defective seeds with empty pericarp. Additionally, the basal endosperm transfer layer cells were severely affected, indicating the deficiency of cell wall ingrowths in the emp10 kernels. Moreover, the alternative respiratory pathway involving alternative oxidase was significantly induced in the emp10 mutant. These results suggest that EMP10 is specifically required for the cis-splicing of mitochondrial nad2 intron 1, embryogenesis and endosperm development in maize.

Controversies existing over resurfacing the patella in total knee arthroplasty remain in the literature. The purpose of this review was to evaluate the effectiveness of resurfacing versus nonresurfacing the patella in total knee arthroplasty. We searched the Cochrane Library, MEDLINE and EMBASE for published randomised clinical trials relevant to patellar resurfacing. The relative risk of reoperation was significantly lower for the patellar resurfacing group than for the nonresurfacing group (relative risk 0.57, 95% confidence interval 0.38-0.84, P=0.004). The overall incidence of postoperative anterior knee pain of the 1,421 knees included was 12.9% in the patellar resurfacing group and 24.1% in the nonresurfacing group. The existing evidence indicates that patellar resurfacing can reduce the risk of reoperation with no improvement in postoperative knee function or patient satisfaction over total knee arthroplasty without patellar resurfacing. Whether it can decrease the incidence of anterior knee pain remains uncertain.

Smart molecular crystals with light‐driven mechanical responses have received interest owing to their potential uses in molecular machines, artificial muscles, and biomimetics. However, challenges remain in control over both the dynamic photo‐mechanical behaviors and static photonic properties of molecular crystals based on the same molecule. Herein, we show the construction of isostructural co‐crystals allows their light‐induced cracking and jumping behaviors (photosalient effect) to be controlled. Hydrogen‐bonded co‐crystals from 4‐(1‐naphthylvinyl)pyridine (NVP) with co‐formers (tetrafluoro‐4‐hydroxybenzoic acid (THA) and tetrafluorobenzoic acid (TA)) crystallize as isostructural crystals, but have different static and dynamic photo‐mechanical behaviors. These differences are due to alternations in the orientation of NVP and hydrogen‐bonding modes of the co‐formers. After light activation, the 1D NVP‐TA crystal splits and shears off within 1 s. For NVP‐THA, its photostability and high quantum yield give novel photonic properties, including low optical waveguide loss, highly polarized anisotropy, and efficient up‐conversion fluorescence.

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