Two-photon laser spectroscopy of antiprotonic helium and the antiproton-to-electron mass ratio

Physical laws are believed to be invariant under the combined transformations of charge, parity and time reversal (CPT symmetry). This implies that an antimatter particle has exactly the same mass and absolute value of charge as its particle counterpart. Metastable antiprotonic helium (pHe(+)) is a three-body atom consisting of a normal helium nucleus, an electron in its ground state and an antiproton (p) occupying a Rydberg state with high principal and angular momentum quantum numbers, respectively n and l, such that n?≈?l?+?1?≈?38. These atoms are amenable to precision laser spectroscopy, the results of which can in principle be used to determine the antiproton-to-electron mass ratio and to constrain the equality between the antiproton and proton charges and masses. Here we report two-photon spectroscopy of antiprotonic helium, in which p(3)He(+) and p(4)He(+) isotopes are irradiated by two counter-propagating laser beams. This excites nonlinear, two-photon transitions of the antiproton of the type (n, l)?→?(n?-?2, l?-?2) at deep-ultraviolet wavelengths (λ = 139.8, 193.0 and 197.0?nm), which partly cancel the Doppler broadening of the laser resonance caused by the thermal motion of the atoms. The resulting narrow spectral lines allowed us to measure three transition frequencies with fractional precisions of 2.3-5 parts in 10(9). By comparing the results with three-body quantum electrodynamics calculations, we derived an antiproton-to-electron mass ratio of 1,836.1526736(23), where the parenthetical error represents one standard deviation. This agrees with the proton-to-electron value known to a similar precision.     

Reversing EphB2 depletion rescues cognitive functions in Alzheimer model

Amyloid-β oligomers may cause cognitive deficits in Alzheimer's disease by impairing neuronal NMDA-type glutamate receptors, whose function is regulated by the receptor tyrosine kinase EphB2. Here we show that amyloid-β oligomers bind to the fibronectin repeats domain of EphB2 and trigger EphB2 degradation in the proteasome. To determine the pathogenic importance of EphB2 depletions in Alzheimer's disease and related models, we used lentiviral constructs to reduce or increase neuronal expression of EphB2 in memory centres of the mouse brain. In nontransgenic mice, knockdown of EphB2 mediated by short hairpin RNA reduced NMDA receptor currents and impaired long-term potentiation in the dentate gyrus, which are important for memory formation. Increasing EphB2 expression in the dentate gyrus of human amyloid precursor protein transgenic mice reversed deficits in NMDA receptor-dependent long-term potentiation and memory impairments. Thus, depletion of EphB2 is critical in amyloid-β-induced neuronal dysfunction. Increasing EphB2 levels or function could be beneficial in Alzheimer's disease.     

A novel forecasting model for the Baltic dry index utilizing optimal squeezing

Marine transport has grown rapidly as the result of globalization and sustainable world growth rates. Shipping market risks and uncertainty have also grown and need to be mitigated with the development of a more reliable procedure to predict changes in freight rates. In this paper, we propose a new forecasting model and apply it to the Baltic Dry Index (BDI). Such a model compresses, in an optimal way, information from the past in order to predict freight rates. To develop the forecasting model, we deploy a basic set of predictors, add lags of the BDI and introduce additional variables, in applying Bayesian compressed regression (BCR), with two important innovations. First, we include transition functions in the predictive set to capture both smooth and abrupt changes in the time path of BDI; second, we do not estimate the parameters of the transition functions, but rather embed them in the random search procedure inherent in BCR. This allows all coefficients to evolve in a time-varying manner, while searching for the best predictors within the historical set of data. The new procedures predict the BDI with considerable success.     

基于穷举法的鄱阳湖叶绿素a浓度高光谱反演模型与应用研究——以GF-5卫星AHSI数据为例

光学特性复杂的浑浊水体叶绿素a浓度反演一直是水环境遥感研究的难点，高光谱以其波宽窄、谱段多、获取地物信息近似连续等优势，有望成为解决该难题的有效手段.该文以鄱阳湖为研究水域，利用2009年10月、2011年7月及2016年10月获取的实测高光谱及叶绿素a浓度数据，基于穷举法建立了针对高分五号(Gaofen-5， GF-5)卫星可见短波红外高光谱相机(Advanced HyperSpectral Imager， AHSI)的叶绿素a浓度三波段反演模型(决定系数R2＝0.82；均方根误差RMSE＝1.468 μg·L－1).通过与2018年10月7日Sentinel-2A卫星多光谱成像仪(MultiSpectral Instrument， MSI)的叶绿素a浓度反演结果对比分析，两者的空间分布具有较高的一致性，超过80%的研究水域相对偏差小于8%，在一定程度上证明了GF-5卫星高光谱数据在浑浊水体叶绿素a浓度反演中的潜力.     

Composition,characteristics and long-term variability of the freshwater microcrustacean fauna of the Faroe Islands

ABSTRACT

Despite the accessibility of the Faroe Islands, faunistic research on their numerous lakes and ponds is quite rare. The biota of Faroese freshwaters is still underexplored, and its specific traits raise many questions. In the present survey, 32 microcrustacean species were observed, 8 of which were new to the Faroese fauna. The obtained species list shows that Cladocera species prevail over Copepoda here, which is not typical of northern territories. This fact is due to (1) the extraordinarily warm climate of the Faroe Islands compared to other areas at similar latitudes because of the heating effect of the surrounding North Atlantic Current and (2) the lack of calanoid species, which have never been found in the freshwaters of the Faroe Islands. The diachronic analysis of the species diversity and composition over the centuries of research on the archipelago showed no evidence of the impact of global climate change on the fauna.     

Gerodermia osteodysplastica is caused by mutations in SCYL1BP1, a Rab-6 interacting golgin

Gerodermia osteodysplastica is an autosomal recessive disorder characterized by wrinkly skin and osteoporosis. Here we demonstrate that gerodermia osteodysplastica is caused by loss-of-function mutations in SCYL1BP1, which is highly expressed in skin and osteoblasts. The protein localizes to the Golgi apparatus and interacts with Rab6, identifying SCYL1BP1 as a golgin. These results associate abnormalities of the secretory pathway with age-related changes in connective tissues.     

Mutations in the pre-replication complex cause Meier-Gorlin syndrome

Meier-Gorlin syndrome (ear, patella and short-stature syndrome) is an autosomal recessive primordial dwarfism syndrome characterized by absent or hypoplastic patellae and markedly small ears1?3. Both pre- and post-natal growth are impaired in this disorder, and although microcephaly is often evident, intellect is usually normal in this syndrome. We report here that individuals with this disorder show marked locus heterogeneity, and we identify mutations in five separate genes: ORC1, ORC4, ORC6, CDT1 and CDC6. All of these genes encode components of the pre-replication complex, implicating defects in replication licensing as the cause of a genetic syndrome with distinct developmental abnormalities.     

Common variants in ZNF365 are associated with both mammographic density and breast cancer risk

High-percent mammographic density adjusted for age and body mass index is one of the strongest risk factors for breast cancer. We conducted a meta analysis of five genome-wide association studies of percent mammographic density and report an association with rs10995190 in ZNF365 (combined P = 9.6 × 10(-10)). Common variants in ZNF365 have also recently been associated with susceptibility to breast cancer.     

Exome sequencing identifies MAX mutations as a cause of hereditary pheochromocytoma

Hereditary pheochromocytoma (PCC) is often caused by germline mutations in one of nine susceptibility genes described to date, but there are familial cases without mutations in these known genes. We sequenced the exomes of three unrelated individuals with hereditary PCC (cases) and identified mutations in MAX, the MYC associated factor X gene. Absence of MAX protein in the tumors and loss of heterozygosity caused by uniparental disomy supported the involvement of MAX alterations in the disease. A follow-up study of a selected series of 59 cases with PCC identified five additional MAX mutations and suggested an association with malignant outcome and preferential paternal transmission of MAX mutations. The involvement of the MYC-MAX-MXD1 network in the development and progression of neural crest cell tumors is further supported by the lack of functional MAX in rat PCC (PC12) cells and by the amplification of MYCN in neuroblastoma and suggests that loss of MAX function is correlated with metastatic potential.