A Multi-Scale Simulation Study of Irradiation Swelling of Silicon Carbide.

Silicon carbide (SiC) is a promising structural and cladding material for accident tolerant fuel cladding of nuclear reactor due to its excellent properties. However, when exposed to severe environments (e.g., during neutron irradiation), lattice defects are created in amounts significantly greater than normal concentrations. Then, a series of radiation damage behaviors (e.g., radiation swelling) appear. Accurate understanding of radiation damage of nuclear materials is the key to the design of new fuel cladding materials. Multi-scale computational simulations are often required to understand the physical mechanism of radiation damage. In this work, the effect of neutron irradiation on the volume swelling of cubic-SiC film with 0.3 mm was studied by using the combination of molecular dynamics (MD) and rate theory (RT). It was found that for C-vacancy (CV), C-interstitial (CI), Si-vacancy (SiV), Si-interstitial (SiI), and Si-antisite (SiC), the volume of supercell increases linearly with the increase of concentration of these defects, while the volume of supercell decreases linearly with the increase of defect concentration for C-antisite (CSi). Furthermore, according to the neutron spectrum of a certain reactor, one RT model was constructed to simulate the evolution of point defect under neutron irradiation. Then, the relationship between the volume swelling and the dose of neutrons can be obtained through the results of MD and RT. It was found that swelling typically increases logarithmically with radiation dose and saturates at relatively low doses, and that the critical dose for abrupt transition of volume is consistent with the available experimental data, which indicates that the rate theory model can effectively describe the radiation damage evolution process of SiC. This work not only presents a systematic study on the relationship between various point defect and excess volume, but also gives a good example of multi-scale modelling through coupling the results of binary collision, MD and RT methods, etc., regardless of the multi-scale modelling only focus on the evolution of primary point defects.

[Analysis on clinical characteristics of patients undergoing CPR in department of emergency and factors influencing the success of resuscitation].

OBJECTIVE: To analyze the clinical data and characteristics of patients undergoing cardiopulmonary resuscitation (CPR) in the emergency department and the factors affecting the success of resuscitation, so as to allocate medical resources in emergency department, improve the CPR process and increase the success rate of CPR. METHODS: 538 patients with cardiac arrest who were registered by Utstein in the emergency department of the Third Central Hospital of Tianjin from December 2009 to December 2019 were selected as study subjects. The clinical data and characteristics were analyzed. According to whether the resuscitation was successful, the patients were divided into successful group and failed group, and the factors influencing success of resuscitation were analyzed. RESULTS: A total of 538 patients were enrolled in this study, with an average age of (65.53±15.56) years old. The number of patients aged 71-80 years old was the largest (145 cases, 27.0%), followed by those aged 61-70 years old (105 cases, 19.5%) and 51-60 years old (99 cases, 18.4%). The main causes of cardiac arrest were acute myocardial infarction in 203 cases (37.7%), unknown causes in 77 cases (14.3%) and other cardiac causes in 61 cases (11.3%). The initial types of heart rhythm were no pulse electrical activity (215 cases, 40.0%) and cardiac arrest (179 cases, 33.3%). In this study, 195 patients were resuscitated successfully, and the success rate of recovery was 36.2%. Compared with the successful group, the time of onset to resuscitation (minutes: 14.94±1.03 vs. 9.02±1.05), start time of epinephrine application (minutes: 8.50±0.02 vs. 4.21±0.16), time of onset to endotracheal intubation success (minutes: 9.56±1.87 vs. 5.86±0.84) and total duration of CPR (minutes: 48.75±1.73 vs. 35.39±2.51) in the failed group were significantly prolonged (all P < 0.05), and the cumulative epinephrine dosage was significantly increased (mg: 8.48±4.81 vs. 6.31±4.86, P < 0.05). There were significant differences in the location of onset and main causes of cardiac arrest between the two groups (both P < 0.05), but there were no significant differences in gender, age, initial heart rate type and the proportion of defibrillation (all P > 0.05). Binary Logistic analysis showed that the time from onset to resuscitation [odds ratio (OR) = 1.763, 95% confidence interval (95%CI) was 1.713-1.804, P = 0.000], cumulative dosage of epinephrine (OR = 1.759, 95%CI was 1.708-1.765, P = 0.000), time of onset to endotracheal intubation success (OR = 1.023, 95%CI was 0.988-1.047, P = 0.008) and start time of epinephrine use (OR = 1.819, 95%CI was 1.785-1.946, P = 0.002) were risk factors for successful resuscitation (all P < 0.05). CONCLUSIONS: Cardiogenic disease is the main cause of cardiac arrest, and the time from onset to resuscitation, cumulative dosage of epinephrine, success time of endotracheal intubation and time of epinephrine application are independent factors influencing the success of resuscitation in department of emergency.

[Preparation of paraoxonase liposomes and their pharmacokinetics in rats].

OBJECTIVE: To prepare paraoxonase 1 (PON1) liposomes, and investigate pharmacokinetics of common PON1 liposomes (L-PON1) and polyethylene glycol-modified PON1 long circulating liposomes (PEG-PON1-LCL) in rats after intravenous administration. METHODS: L-PON1 and PEG-PON1-LCL were prepared by film dispersion method. The entrapment efficiency, mean diameter and Zeta potential of the liposomes were measured, and the stability was evaluated. Thirty-six Wistar rats were divided into three groups according to random number table, with 12 rats in each group. The rats were intravenously administrated with PON1, L-PON1 or PEG-PON1-LCL 700 U/kg, respectively. The activity of PON1 in serum was determined by phenyl acetate method, the activity of PON1 at different time points after drug administration was compared with that before drug administration, and the difference value was considered as the activity of exogenous PON1, and PON1 activity-time curve was plotted. The pharmacokinetic parameters were calculated and analyzed by DAS 2.0 pharmacokinetic program and SPSS 17.0. RESULTS: The entrapment efficiencies of L-PON1 and PEG-PON1-LCL were above 85%, the mean diameter was about 126 nm, and Zeta potential was -14.35 mV. After 2 weeks of preservation, the above parameters showed no obvious change, indicating that liposomes had good stability and the properties of preparations were basically stable. Compared with purified PON1 administration, after L-PON1 and PEG-PON1-LCL administration, the activity of PON1 was increased, the half-life of PON1 activity in rats was significantly prolonged [the half-life of distribution (T1/2α, hours): 0.142±0.018, 0.147±0.021 vs. 0.126±0.022; the half-life of clearance (T1/2ß, hours): 3.877±1.010, 4.520±1.117 vs. 1.226±0.422], the area under PON1 activity-time curve (AUC) was significantly increased [AUC from 0 hour to 24 hours (AUC0-24, U×h-1×L-1): 499.305±64.710, 563.576±70.450 vs. 18.053±2.190; AUC from the immediate injection to the disappearance of PON1 activity (AUC0-∞, U×h-1×L-1): 516.256±60.940, 587.801±76.210 vs. 21.044±3.250], the apparent volume of distribution (Vd) and clearance (CL) were significantly decreased [Vd (L): 0.140±0.065, 0.144±0.064 vs. 0.493±0.032, CL (L/h): 0.039±0.008, 0.034±0.006 vs. 0.952±0.082, all P < 0.05]. There was no significant difference in pharmacokinetics between L-PON1 and PEG-PON1-LCL. CONCLUSIONS: The film dispersion method prepared PON1 liposomes have high entrapment efficiency and small particle size with a good stability. Both liposomes can raise PON1 activity in vivo, change the pharmacokinetics of PON1 in vivo, prolong the resident time of PON1 in the blood circulating system, and compensate for the short half-life of PON1 in vivo.