The Large Hadron-Electron Collider at the HL-LHC

The Large Hadron-Electron Collider (LHeC) is designed to move the field of deep inelastic scattering (DIS) to the energy and intensity frontier of particle physics. Exploiting energy-recovery technology, it collides a novel, intense electron beam with a proton or ion beam from the High-Luminosity Large Hadron Collider (HL-LHC). The accelerator and interaction region are designed for concurrent electron-proton and proton-proton operations. This report represents an update to the LHeC's conceptual design report (CDR), published in 2012. It comprises new results on the parton structure of the proton and heavier nuclei, QCD dynamics, and electroweak and top-quark physics. It is shown how the LHeC will open a new chapter of nuclear particle physics by extending the accessible kinematic range of lepton-nucleus scattering by several orders of magnitude. Due to its enhanced luminosity and large energy and the cleanliness of the final hadronic states, the LHeC has a strong Higgs physics programme and its own discovery potential for new physics. Building on the 2012 CDR, this report contains a detailed updated design for the energy-recovery electron linac (ERL), including a new lattice, magnet and superconducting radio-frequency technology, and further components. Challenges of energy recovery are described, and the lower-energy, high-current, three-turn ERL facility, PERLE at Orsay, is presented, which uses the LHeC characteristics serving as a development facility for the design and operation of the LHeC. An updated detector design is presented corresponding to the acceptance, resolution, and calibration goals that arise from the Higgs and parton-density-function physics programmes. This paper also presents novel results for the Future Circular Collider in electron-hadron (FCC-eh) mode, which utilises the same ERL technology to further extend the reach of DIS to even higher centre-of-mass energies.Peer reviewe

Gender disparities in science and engineering in Chinese universities

Gender disparities in science and engineering majors in Chinese universities have received increasing attention from researchers and educators in China in recent years. Using data from a national survey of college students who graduated in 2005, this study documents gender disparities in enrollment and academic performance in science and engineering majors, and explores gender disparities in initial employment experiences of science and engineering graduates. It finds that females lag far behind males in enrollment in science and engineering majors overall. However, females actually are more represented than males in some majors such as mathematics and chemistry though the reverse is true for other science and engineering majors. Also, in science and engineering majors, females perform better than males in both general course grades and in English competency tests. Male science and engineering graduates have a clear advantage over their female counterparts in initial employment after graduation: they have a high employment rate, a higher starting salary, and are more likely to be employed in such jobs as business management and technical specialist. The male advantage in employment rate and starting salary persists even after controlling for other factors.Gender inequality Science and engineering Higher education China

Data from: Characterization of cytoplasmic viscosity of hundreds of single tumor cells based on micropipette aspiration

Background: Cytoplasmic viscosity (μc) is a key biomechanical parameter for evaluating the status of cellular cytoskeletons. Previous studies focused on white blood cells, but the data of cytoplasmic viscosity for tumor cells were missing. Methodology: Tumor cells (H1299, A549 and drug-treated H1299 with compromised cytoskeletons) were aspirated continuously through a micropipette at a pressure of -10 kPa or -5 kPa where aspiration lengths as a function of time were obtained and translated to cytoplasmic viscosity based on a theoretical Newtonian fluid model. Quartile coefficients of dispersion were quantified to evaluate the distributions of cytoplasmic viscosity within the same cell type while neural network based pattern recognitions were used to classify different cell types based on cytoplasmic viscosity. Results: The single-cell cytoplasmic viscosity with three quartiles and the quartile coefficient of dispersion were quantified as 16.7 Pa•S, 42.1 Pa•S, 110.3 Pa•S and 74% for H1299 cells at -10 kPa (ncell=652), 144.8 Pa•S, 489.8 Pa•S, 1390.7 Pa•S, and 81% for A549 cells at -10 kPa (ncell=785), 7.1 Pa•S, 13.7 Pa•S, 31.5 Pa•S, and 63% for CD-treated H1299 cells at -10 kPa (ncell=651) and 16.9 Pa•S, 48.2 Pa•S, 150.2 Pa•S, and 80% for H1299 cells at -5 kPa (ncell=600), respectively. Neural network based pattern recognition produced successful classification rates of 76.7% for H1299 vs. A549, 67.0% for H1299 vs. drug-treated H1299 and 50.3% for H1299 at -5 kPa and -10 kPa. Conclusion: Variations of cytoplasmic viscosity were observed within the same cell type and among different cell types, suggesting the potential role of cytoplasmic viscosity in cell status evaluation and cell type classification

Extensive germline-somatic interplay contributes to prostate cancer progression through HNF1B co-option of TMPRSS2-ERG

Abstract Genome-wide association studies have identified 270 loci conferring risk for prostate cancer (PCa), yet the underlying biology and clinical impact remain to be investigated. Here we observe an enrichment of transcription factor genes including HNF1B within PCa risk-associated regions. While focused on the 17q12/HNF1B locus, we find a strong eQTL for HNF1B and multiple potential causal variants involved in the regulation of HNF1B expression in PCa. An unbiased genome-wide co-expression analysis reveals PCa-specific somatic TMPRSS2-ERG fusion as a transcriptional mediator of this locus and the HNF1B eQTL signal is ERG fusion status dependent. We investigate the role of HNF1B and find its involvement in several pathways related to cell cycle progression and PCa severity. Furthermore, HNF1B interacts with TMPRSS2-ERG to co-occupy large proportion of genomic regions with a remarkable enrichment of additional PCa risk alleles. We finally show that HNF1B co-opts ERG fusion to mediate mechanistic and biological effects of the PCa risk-associated locus 17p13.3/VPS53/FAM57A/GEMIN4. Taken together, we report an extensive germline-somatic interaction between TMPRSS2-ERG fusion and genetic variations underpinning PCa risk association and progression