Objectives To appraise the causal effect of systemic lupus erythematosus (SLE) for risk of Coronary heart disease (CHD). Methods We selected single nucleotide polymorphisms (SNPs) associated with SLE as instrumental variables (IVs) from three independent genome-wide association studies (GWAS), the three largest to date for SLE of European ancestry. Then we conducted two-sample Mendelian randomization (2SMR) analyses to estimate the effects of IVs on the odds of CHD and traditional coronary risk factors (including high LDL cholesterol levels, low HDL cholesterol levels, Apolipoprotein A-I, Apolipoprotein B, diabetes mellitus, and hypertension). Additionally, we searched for common risk loci between SLE and premature coronary atherosclerosis. Furthermore, we retrospectively reviewed the lipid profile of treatment-naive SLE patients and age-matched healthy controls. Results Genetically predicted SLE did not increase the odds of CHD. Nevertheless, we found mild causal relationships between SLE and decreased HDL cholesterol levels, and between SLE and decreased apolipoprotein A-I. There was one common risk locus (rs597808) between SLE and premature coronary atherosclerosis at a genome-wide significance level (P<5 x10-8). Retrospective analysis showed decreased HDL-cholesterol (0.98{+/-}0.516mmol/L vs. 1.46{+/-}0.307mmol/L in female, 0.76{+/-}0.199mmol/L vs. 1.19{+/-}0.257mmol/L in male; both P<0.001) and apolipoprotein A-I (1.06{+/-}0.314g/L vs. 1.37{+/-}0.205g/L in female, 0.87{+/-}0.174g/L vs. 1.24{+/-}0.200g/L in male; both P<0.001) in naive SLE patients. Conclusion SLE may accelerate coronary atherosclerosis in young patients by reducing HDL cholesterol and apolipoprotein A-I intrinsically, but it seems not to play a predominant role in CHD development in old patients.

Recently, ultra-high dose rate (> 40Gy/s) radiotherapy (FLASH RT) has gained widespread interest among researchers and clinicians owing to its remarkable normal tissue sparing as well as efficient tumor control compared to conventional radiotherapy (CONV RT) with dose rates around 0.03 Gy/s. As radiobiology modeling has been the foundation of the contemporary clinical practice in radiation oncology, the urgent need for robust mathematical modeling of this paradigm-shifting treatment, FLASH RT, is difficult to overstate. This work proposes a phenomenological model as a potential candidate to explain the observed phenomena. In this study, we combined the oxygen depletion hypothesis and Curtis' Lethal and Potentially Lethal (LPL) model. Following the oxygen depletion hypothesis on FLASH-induced normal tissue sparing, we introduced a flipped sigmoid shape function to explicitly model the time-dependent component of the radiation-induced lethal and potentially lethal lesion production rates when cells experience oxygen depletion. We conducted both numerical and analytic analyses after we selected a Logistic-type function for demonstration. Parameters from Curtis' LPL model fitting of the C3H 10T 1/2 mouse cell survival data, a generic oxygen enhancement ratio, and two newly introduced parameters describing the time scale and transition width for radiation-induced oxygen depletion were employed in our model. Both numerical and analytical tools were used to obtain the cell survival probability prediction for our modified LPL model. We demonstrated that our modified LPL model would generate asymptotical cell survival probability that decreases exponentially as the radiation dose increases in FLASH RT. Also, the numerical study indicated that our modified LPL model could produce significantly reduced normal tissue cell killings in FLASH RT. For tumor cells, since their cell environment is typically hypoxic, the mechanism mentioned above will have limited impact, and hence tumor cell death will remain at the level similar to that from CONV RT with the same total dose. We also provided an approximated analytical solution of our model's cell radiation survival prediction for future FLASH RT study. Our modified LPL model predicts that, for normal tissue cells, the difference in the logarithm of surviving fraction between FLASH RT and CONV RT is asymptotically proportional to the radiation dose, and the cell's oxygen enhancement ratio minus one. This modified LPL model has the potential to explain the prominent normal tissue sparing effect of FLASH RT, with interpretable parameters. Future studies are necessary to quantitatively validate the model predictions in systematically conducted FLASH RT experiments.

We present measurements of azimuthal correlations of charged hadron pairs in sNN=200 GeV Au+Au collisions for the trigger and associated particle transverse-momentum ranges of 14GeV/c) correlations is suppressed compared with that of correlations measured in p+p collisions. At the lowest associated particle pT(0.5

The cross section of atomic electron Compton scattering gamma + e -> gamma' + e' was measured in the 4.400-5.475 GeV photon beam energy region by the PrimEx collaboration at Jefferson Lab with an accuracy of 2.6% and less. The results are consistent with theoretical predictions that include next-to-leading order radiative corrections. The measurements provide the first high precision test of this elementary QED process at beam energies greater than 0.1 GeV. (C) 2019 The Author(s). Published by Elsevier B.V.

To find out whether hepatitis B viral infection pose risk to patients with Epstein-Barr virus (EBV)-associated nasopharyngeal carcinoma (NPC) in the intensity-modulated radiotherapy (IMRT) era. A total of 864 patients with non-metastatic, newly diagnosed NPC who received detection of pre-treatment plasma EBV DNA load and treated with IMRT were retrospectively reviewed. 74 patients had hepatitis B infection (hepatitis B surface antigen [HBsAg] seropositive). 204 HBsAg-negative patients and 68 HBsAg-positive patients were selected after using the propensity score matching method. The survival rates were evaluated by Kaplan—Meier analysis and the survival curves compared by Log-rank test. Prognostic factors were explored by multivariate analysis. No significant survival differences were observed between HBsAg-negative group and HBsAg-positive group (5-year overall survival, 85.5% vs 78.8%, P=0.224; locoregional failure-free survival, 89.9% vs 88.8%, P=0.719; distant metastasis-free survival, 84.4% vs 84.5%, P=0.973; and progression-free survival, 74.1% vs 74.3%, P=0.922). Subgroup analysis based on pre-treatment plasma EBV DNA load (cutoff, 1500 copy/ml) still failed to confirm the adverse effect of hepatitis B viral infection. After adjusting for known prognostic factors in multivariate analysis, HBsAg status (negative or positive) was not an independent prognostic factor for any outcome (all P>0 .05). In NPC patients treated with IMRT, higher pre-treatment EBV DNA accounts for poorer survival outcomes whether HBsAg is positive or not, while hepatitis B infection leads to similar survival outcomes compared to negative HBsAg status regardless of pre-treatment EBV DNA load.