Observation of mHz-level cooperative Lamb shifts in an optical atomic clock

We report on the direct observation of resonant electric dipole-dipole interactions in a cubic array of atoms in the many-excitation limit. The interactions, mediated by single-atom couplings to the shared electromagnetic vacuum, are shown to produce spatially-dependent cooperative Lamb shifts when spectroscopically interrogating the mHz-wide optical clock transition in strontium-87. We show that the ensemble-averaged shifts can be suppressed below the level of evaluated systematic uncertainties for state-of-the-art optical atomic clocks. Additionally, we demonstrate that excitation of the atomic dipoles near a Bragg angle can enhance these effects by nearly an order of magnitude compared to non-resonant geometries. Given the remarkable precision of frequency measurements and the high accuracy of the modeled response, our work demonstrates that such a clock is a novel platform for studies of the quantum many-body physics of spins with long-range interactions mediated by propagating photons

Disentangling Pauli blocking of atomic decay from cooperative radiation and atomic motion in a 2D Fermi gas

The observation of Pauli blocking of atomic spontaneous decay via direct measurements of the atomic population requires the use of long-lived atomic gases where quantum statistics, atom recoil and cooperative radiative processes are all relevant. We develop a theoretical framework capable of simultaneously accounting for all these effects in a regime where prior theoretical approaches based on semi-classical non-interacting or interacting frozen atom approximations fail. We apply it to atoms in a single 2D pancake or arrays of pancakes featuring an effective A level structure (one excited and two degenerate ground states). We identify a parameter window in which a factor of two extension in the atomic lifetime clearly attributable to Pauli blocking should be experimentally observable in deeply degenerate gases with~103 atoms. Our predictions are supported by observation of a number-dependent excited state decay rate on the 1S0 - 3P1 transition in 87Sr atoms.Physic

Development and validation of a nomogram model for predicting unfavorable functional outcomes in ischemic stroke patients after acute phase

IntroductionPrediction of post-stroke functional outcome is important for personalized rehabilitation treatment, we aimed to develop an effective nomogram for predicting long-term unfavorable functional outcomes in ischemic stroke patients after acute phase.MethodsWe retrospectively analyzed clinical data, rehabilitation data, and longitudinal follow-up data from ischemic stroke patients who underwent early rehabilitation at multiple centers in China. An unfavorable functional outcome was defined as a modified Rankin Scale (mRS) score of 3–6 at 90 days after onset. Patients were randomly allocated to either a training or test cohort in a ratio of 4:1. Univariate and multivariate logistic regression analyses were used to identify the predictors for the development of a predictive nomogram. The area under the receiver operating characteristic curve (AUC) was used to evaluate predictive ability in both the training and test cohorts.ResultsA total of 856 patients (training cohort: n = 684; test cohort: n = 172) were included in this study. Among them, 518 patients experienced unfavorable outcomes 90 days after ischemic stroke. Trial of ORG 10172 in Acute Stroke Treatment classification (p = 0.024), antihypertensive agents use [odds ratio (OR) = 1.86; p = 0.041], 15-day Barthel Index score (OR = 0.930; p < 0.001) and 15-day mRS score (OR = 13.494; p < 0.001) were selected as predictors for the unfavorable outcome nomogram. The nomogram model showed good predictive performance in both the training (AUC = 0.950) and test cohorts (AUC = 0.942).ConclusionThe constructed nomogram model could be a practical tool for predicting unfavorable functional outcomes in ischemic stroke patients underwent early rehabilitation after acute phase

Draft genome sequence of the Tibetan antelope

The Tibetan antelope (Pantholops hodgsonii) is endemic to the extremely inhospitable high-altitude environment of the Qinghai-Tibetan Plateau, a region that has a low partial pressure of oxygen and high ultraviolet radiation. Here we generate a draft genome of this artiodactyl and use it to detect the potential genetic bases of highland adaptation. Compared with other plain-dwelling mammals, the genome of the Tibetan antelope shows signals of adaptive evolution and gene-family expansion in genes associated with energy metabolism and oxygen transmission. Both the highland American pika, and the Tibetan antelope have signals of positive selection for genes involved in DNA repair and the production of ATPase. Genes associated with hypoxia seem to have experienced convergent evolution. Thus, our study suggests that common genetic mechanisms might have been utilized to enable high-altitude adaptation

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Regulation of neuronal axon specification by glia-neuron gap junctions in C. elegans.

Axon specification is a critical step in neuronal development, and the function of glial cells in this process is not fully understood. Here, we show that C. elegans GLR glial cells regulate axon specification of their nearby GABAergic RME neurons through GLR-RME gap junctions. Disruption of GLR-RME gap junctions causes misaccumulation of axonal markers in non-axonal neurites of RME neurons and converts microtubules in those neurites to form an axon-like assembly. We further uncover that GLR-RME gap junctions regulate RME axon specification through activation of the CDK-5 pathway in a calcium-dependent manner, involving a calpain clp-4. Therefore, our study reveals the function of glia-neuron gap junctions in neuronal axon specification and shows that calcium originated from glial cells can regulate neuronal intracellular pathways through gap junctions