Object To study the glycosides from Swertia erythrosticta Maxim Methods The glycosides were isolated on silica gel column and purified by Sephadex LH20, their structures were identified by spectral data and chemical properties Results Seven compounds were obtained from aqueous extract and identified as swertianolin (Ⅰ), norswertianolin (Ⅱ), norswertiaglucoside (Ⅲ), isoorientin (Ⅳ), loganic acid (Ⅴ), gentiopicroside (Ⅵ) and ? gentiobiose (Ⅶ) Conclusion Compounds Ⅲ, Ⅳ, Ⅴ, and Ⅶ were first obtained from this plant

Objective:To investigate the effects of microwave radiation on associative learning and memory function and hippocampal structure of mice.Methods:C57BL/6N mice were ramdomly divided into sham-radiated group ( n=27) and radiation group ( n=2). The radiation group was exposed to microwave at 2.856 GHz, 8 mW/cm 2 for 15 min, then their spatial and associative learning and memory function were examined with the morris water maze and shuttle box behavior experiment. The pathological changes of hippocampal tissue were observed by HE staining and light microscope, the ultrastructural changes of hippocampal tissue were observed by transmission electron microscope. Results:After microwave radiation, the times of mice crossing the platform for the reverse space exploration decreased from(3.60±0.79) times to (2.55±0.47) times( t=2.21, P=0.046), the average active escape rate decreased significantly ( t = 2.70, P<0.05), and the average active latency and the total shock time was significantly prolonged ( t = -3.09, -3.02, P < 0.05). At 8 d after microwave radiation, the nuclei of some neurons in the CA3 and DG regions of the hippocampus were pyknosis. The neurons were apoptotic, the synaptic spaces blurred, the glial cells swollen, and the perivascular spaces widened in the CA3 region of the hippocampus. Conclusions:Microwave radiation can decline the spatial reference memory ability and associative learning and memory ability of mice. The morphological and pathological changes of hippocampus are the structural basis of this dysfunction.

Objective To develop a new type of electric stapler, so as to solve the problems of insufficient rotation angle, inconvenient operation and difficulty in controlling the pressing strength of existing products. Methods An electric stapler was designed and manufactured. The motion trajectory curve of the prototype was measured by using the three-coordinate imaging instrument to build functional test platform of the prototype, and the goodness of fit was used to evaluate consistency between the theoretical curve and the measured curve. The small intestine tissues of fresh pig were anastomosed at different bending angles of the front end, and the forming rate of the anastomotic stoma was measured. Results The goodness of fit between the test curve and the theoretical curve for both turning motion and shooting motion was ideal, while the goodness of fit between the test curve and the theoretical curve for pressing motion was not ideal when the turning joint was bent at 0°-30°, and was ideal when it was bent at 45°-60°. In performance test, the deformity rate of the nail was smaller than 1.14%, indicating that the bending angle had no significant impacts on the anastomotic effect. Conclusions The kinematics curves of shooting motion and turning motion are consistent with the theoretical curves. The pressing motion curves fluctuate at different bending angles, which will not affect the anastomotic effect, and the effect of the electric stapler meets the clinical requirements.

With the continuous development of society, a large number of new chemicals are continuously emerging, which presents a challenge to current risk assessment and safety management of chemicals. Traditional toxicology research methods have certain limitations in quickly, efficiently, and accurately assessing the toxicity of many chemicals, and cannot meet the actual needs. In response to this challenge, computational toxicology that use mathematical and computer models to achieve the prediction of chemical toxicity has emerged. In the meantime, as researchers increasingly pay attention to understanding the interaction mechanisms between exogenous chemical substances and the body from the system level, and multiomics technologies develop rapidly such as genomics, transcriptomics, proteomics, and metabolomics, huge amounts of data have been generated, providing rich information resources for studying the interactions between chemical substances and biological molecules. System toxicology and network toxicology have also developed accordingly. Of these, network toxicology can integrate these multiomics data to construct biomolecular networks, and then quickly predict the key toxicological targets and pathways of chemicals at the molecular level. This paper outlined the concept and development of network toxicology, summarized the main methods and supporting tools of network toxicology research, expounded the application status of network toxicology in studying potential toxicity of exogenous chemicals such as agricultural chemicals, environmental pollutants, industrial chemicals, and foodborne chemicals, and analyzed the development prospects and limitations of network toxicology research. This paper aimed to provide a reference for the application of network toxicology in other fields.

Nowadays potential preclinical drugs for the treatment of nonalcoholic steatohepatitis (NASH) have failed to achieve expected therapeutic efficacy because the pathogenic mechanisms are underestimated. Inactive rhomboid protein 2 (IRHOM2), a promising target for treatment of inflammation-related diseases, contributes to deregulated hepatocyte metabolism-associated nonalcoholic steatohepatitis (NASH) progression. However, the molecular mechanism underlying Irhom2 regulation is still not completely understood. In this work, we identify the ubiquitin-specific protease 13 (USP13) as a critical and novel endogenous blocker of IRHOM2, and we also indicate that USP13 is an IRHOM2-interacting protein that catalyzes deubiquitination of Irhom2 in hepatocytes. Hepatocyte-specific loss of the Usp13 disrupts liver metabolic homeostasis, followed by glycometabolic disorder, lipid deposition, increased inflammation, and markedly promotes NASH development. Conversely, transgenic mice with Usp13 overexpression, lentivirus (LV)- or adeno-associated virus (AAV)-driven Usp13 gene therapeutics mitigates NASH in 3 models of rodent. Mechanistically, in response to metabolic stresses, USP13 directly interacts with IRHOM2 and removes its K63-linked ubiquitination induced by ubiquitin-conjugating enzyme E2N (UBC13), a ubiquitin E2 conjugating enzyme, and thus prevents its activation of downstream cascade pathway. USP13 is a potential treatment target for NASH therapy by targeting the Irhom2 signaling pathway.