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In recent years, ultra-fine-grained Fe–C alloy have received widespread attention because of their high levels of strength, hardness, and wear resistance. However, these alloy have strict requirements on control of the process parameters during production to meet product specifications. This study was aimed at designing a prediction model for their mechanical properties, which could ultimately promote the industrial development of ultra-fine-grained Fe–C alloy. The effect of process parameters on the mechanical properties of ultra-fine-grained Fe–C alloy was analyzed by electron backscatter diffraction (EBSD) and scanning electron microscope (SEM). By fusing experimental combinations of alloy composition, rolling process, annealing process, and resultant mechanical properties into a dataset for training and verification, a machine-learning-based prediction model of mechanical properties of ultra-fine-grained Fe–C alloy was constructed and tested. When choosing the machine learning algorithm, the best network model was obtained for this application by optimizing a conventional backpropagation (BP) network structure: a three-layer network structure, with a learning rate of 0.5, 18 hidden layer neurons, and activation functions of the hidden and output layers, namely Tansig and Purelin (MATLAB functions), respectively. Finally, the sample data was divided into training set and verification set, and the prediction accuracy, efficiency and generalization ability of BP neural network (BPNN), genetic neural network (GA-BP) and support vector machine (SVM) were compared and analyzed. The superiority of BPNN in the prediction of mechanical properties of ultrafine grained Fe–C alloy was determined, and the mean absolute percentage error (MAPE) of the BPNN for tensile strength, yield strength and uniform elongation are 3.02%, 4.47% and 6.47% respectively, and the number of training steps is 412, which are less than the other two models. The result lays a foundation for the production of high stability and high performance steel products.

A novel missense variant (NM_005327.7: c.99CG, p.Ile33Met) was discovered in 3-hydroxyacyl-CoA dehydrogenase (HADH), which is involved in congenital hyperinsulinism (CHI). This variant may be damaging or deleterious, as assessed using protein prediction software. This study aimed at the impact of this variant on islets and if it caused the leu-sensitive insulin secretion. The adenoassociated virus containing the HADH missense variant (p.Ile33Met), wild-type (WT) HADH or empty vector (EV) was constructed, and the rats were infected with it. Three weeks after the transfection, 15 rats were dissected to observe the effect of the variant on the islet tissue. Then we treated the remaining rats with leucine or sodium carboxymethyl cellulose (CMC-Na) by gavage and drew blood from the rat tail vein to detect the variations in blood glucose, serum insulin and serum glucagon. Further, we dissected the rats to observe the fluctuation of insulin and glucagon contents in pancreatic islets under the combined action of leucine and p.Ile33Met. Insulin and glucagon were observed in the islet tissue under an inverted fluorescence microscope, serum insulin and glucagon were detected by ELISA, and the blood glucose value was determined using a Roche glucometer. The positive area and average gray value of islet fluorescence pictures were analysed using the software Image J (USA). Rats expressing p.Ile33Met showed significantly higher insulin and glucagon content, as well as the islet area, compared to WT and EV rats. Moreover, after intragastric administration of leucine, the serum insulin content of the variant rats increased but the blood sugar level decreased significantly. Meanwhile, there was an appreciable decrease in the insulin content in rat pancreatic islet tissues. Our results suggest that the variant NM_005327.7: c.99CG promotes the proliferation of pancreatic islets, enhances the secretion of insulin, and induces leu-sensitive hyperinsulinaemia.

Computed tomography (CT) examination is the major measure for detecting and diagnosis of foreign bodies in human body. Although CT has high sensitivity in diagnosis of foreign body, some interference factors may still lead to missed diagnosis or misdiagnosis. Here we report a rare case that a bamboo stick accidentally pierced into the left chest of a young man who was drunk and unware of this hurt. The patient experienced cough, chest pain, fever, hemoptysis, and was misdiagnosed as primary and secondary tuberculosis based on chest CT examinations at a local hospital, although no tubercular bacillus detected by sputum smear. He subsequently received anti-tuberculous treatments in the following three years, but no improvement of his symptoms was observed. Until one month before his death, the bamboo stick was detected by spiral CT examination as well as three-dimensional image reconstruction at another hospital. Postmortem examination revealed pneumonia, pulmonary infarction, and abscess as the causes of his death. We analyze the potential reasons of misdiagnosis in this case, aiming to provide reference for the diagnosis and treatment of pulmonary inflammation associated with foreign body in the future.

In order to investigate the mode of action of Yimu Shenghuasan preparation in endometrial cells of dairy cows, the primary cultured endometrial cells in cows were isolated and the inflammatory models were made by lipopolysaccharide (LPS) induction. The inflammatory cells were treated with gradient concentration of herbal medicine preparation, Yimu Shenghuasan for 48 and 72 h. The expression of cytochrome P450 (CYP450) was detected by Western blot. The amounts of IgG and IgA in sera were also detected in the endometritis of dairy cows. The expression level of CYP450 in the endometrial cells of dairy cow was increased gradually, and the amounts of IgG, IgA were increased significantly as compared with those in the control group. The expression level of CYP450 in the inflammatory cells was increased significantly in the treatment of 2 000 μg mL −1 of Yimu Shenghuasan after 48 h of treatment.

Grass carp hemorrhage is an acute contagious disease caused by grass carp reovirus (GCRV). The pathogenesis of GCRV and the relationship between GCRV and the host cells remain unclear. The aim of the present study was to investigate the relations among apoptosis, intracellular oxidative stress and virus replication in GCRV infected-cells. The results showed that GCRV induced activation of caspase proteases as early as 12 h, and reached maximum activities at 24 h or 48 h post-infection in a grass carp kidney cell line (CIK cells). Meanwhile, the levels of tumor necrosis factor (TNF-α) and interleukin-1β (IL-1β) also were increased in GCRV-infected CIK cells and showed a statistically significant difference from 24 h to 96 h post-infection. The infection of GCRV caused the destruction of entire monolayer and the death of host cells. Accompanied by the infection, a severe oxidative stress occurred, which led to extensive loss of antioxidants and formation of lipid peroxidation after 48 h post-infection. These data suggested that the apoptosis which was triggered at an early stage (12-24 h) in the viral infection cycle, might be independent of virus replication, while the oxidative stress induced by GCRV was mostly related to the virus replication.

In the present study, the cellular and molecular mechanism of carbon tetrachloride (CCl4)-induced hepatotoxicity in fish was investigated by studying the effects of CCl4 on the oxidative stress, inflammatory response and hepatocyte apoptosis. Common carp were given an intraperitoneal injection of 30% CCl4 in arachis oil (0.5ml/kg body weight). At 72h post-injection, blood were collected to measure glutamate pyruvate transaminase (GPT), glutamate oxalate transaminase (GOT), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione (GSH), total antioxidant capacity (T-AOC) and malondialdehyde (MDA), liver samples were taken to analyze toll-like receptor 4 (TLR4), cytochrome P450 2E1 (CYP2E1) and gene expressions of inflammatory cytokines and nuclear factor-κB (NF-κB/cREL). Cell viability and apoptosis were analyzed after treatment of the primary hepatocytes with CCl4 at 8mM. The results showed that CCl4 significantly increased the levels of GPT, GOT, MDA, TLR4 and CYP2E1, reduced the levels of SOD, GPx, CAT, GSH and T-AOC, and up-regulated the gene expressions of NF-κB/cREL and inflammatory cytokines including tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), IL-1β, IL-6 and IL-12. In vitro, CCl4 caused a dramatic loss in cell viability and induced hepatocyte apoptosis. Overall results suggest that oxidative stress lipid peroxidation, and TNF-α/NF-κB and TRL4/NF-κB signaling pathways play important roles in CCl4-induced hepatotoxicity in fish.