Metabolic reprogramming is a key characteristic of hepatocellular carcinoma， and abnormal fatty acid metabolism is closely associated with tumor immune escape. This article systematically reviews the molecular mechanisms of fatty acid metabolic reprogramming in hepatocellular carcinoma， focusing on key enzymes and their transcriptional regulatory networks within de novo lipogenesis and fatty acid oxidation pathways. This article also analyzes the metabolic heterogeneity between β-catenin-mutant hepatocellular carcinoma and AXIN1-mutant hepatocellular carcinoma and their therapeutic implications， summarizes the multidimensional mechanisms by which the lipid microenvironment regulates immune cell function， and reviews the targeted therapeutic strategies for different molecular subtypes of hepatocellular carcinoma.

Objective To study the unqualified items in the reported quality control tests of linear accelerators, analyze the issues in quality control tests, and propose the key points and development directions for accelerator quality control test in China. Methods A literature review was conducted using the CNKI database to analyze the qualified rates of test items and the issues in quality control tests. Results In the literature on the quality control tests of linear accelerators, except for a few provinces where the qualified rates of all test items were 100%, unqualified items were reported in most of the literature. There were unqualified items related to X-ray and electron beam in different reports. Error of dose indication was the unqualified item with the highest occurrence rate in X-ray test, and the item with the lowest qualified rates in X-ray and electron beam tests. The lowest qualified rate of X-ray dose indication error was 73.5% in 2016, and the lowest qualified rate of electron beam dose indication error was 46.2% in 2017. Conclusion Tests should be carried out strictly according to the items and intervals specified by the quality control test standards. Hospitals, radiation health technology service institutions, and health administrative departments should each fulfill their respective responsibilities, work together, and place emphasis on ensuring effective quality control tests of linear accelerators to further enhance the overall quality control standards for these devices.

Objective To investigate the expression of SLC35A2 and PFDN2 in breast cancer and their relationship with clinical indicators and prognosis.Methods TCGA database and TIMER 2.0 database were used to analyze the differences of SLC35A2 and PFDN2 expression in breast cancer tissues and paracancerous tissues;K-M database was used to create the survival curves of patients in the high and low expression groups of the two.qRT-PCR and immunohistochemistry were used to detect the expression of SLC35A2 and PFDN2 in the cancerous and paracancerous tissues,and the expression differences,the relationship between their expression levels and the clinical observation indexes were statistically analyzed,and the independent prognostic factors of breast cancer were screened out;K-M survival analysis was used to compare the prognostic differences between the groups and create the survival curves.Results The expression levels of SLC35A2 and PFDN2 in breast cancer tissues were significantly higher than those in paracancerous tissues according to the results of biopsy,qRT-PCR and immuno-histochemistry,and the expression levels of SLC35A2 were significantly correlated with lymph node metastasis,while the expression of PFDN2 was significantly correlated with the diameter of the tumor and the metastasis of lymph nodes,and the expression of SLC35A2 and PFDN2 was an independent prognostic factor for breast cancer.patients had the worst prognosis.Conclusion The expression of SLC35A2 and PFDN2 in breast cancer tissues was closely related to clinical indicators and prognosis of breast cancer,and could be used as a potential target for breast cancer treatment.

Objective:To evaluate the effects of electroacupuncture (EA) on mitochondrial fusion and fission during intestinal injury in mice with endotoxemia and the role of heme oxygenase-1 (HO-1).Methods:Fifty SPF-grade healthy male C57BL/6 mice, aged 8 weeks, weighing 18-22 g, were divided into 5 groups ( n=10 each) using a random number table method: control group (group C), endotoxemia group (group E), endotoxemia plus EA group (group E+ EA), endotoxemia plus EA plus hemin group (group E+ EA+ H) and endotoxemia plus EA plus Znpp-Ⅸ group (group E+ EA+ Znpp-Ⅸ). Lipopolysaccharide (LPS) was intraperitoneally injected to develop the model of endotoxemia.Before LPS injection, the HO-1 inducer hemin 100 mg/kg was intraperitoneally injected in group E+ EA+ H, and the HO-1 inhibitor zinc protoporphyrin Ⅸ 10 μmol/kg was intraperitoneally injected in group E+ EA+ Znpp-Ⅸ.At 4, 3, 2 and 1 days and 30 min prior to development of the model, Zusanli and Hegu acupoints were stimulated with electric stimulator (disperse-dense wave, frequency 2 Hz/15 Hz, at a voltage of 1 mA) for 30 min, retaining the needle until the end of the experiment on the day of development of the model.Mice were sacrificed at 6 h after development of the model, and the small intestinal tissue was obtained from the terminal ileum for examination of the pathological results (with a light microscope) and ultrastructure of mitochondria (with an electron microscope) and for determination of the levels of reactive oxygen species (ROS), ATP and diamine oxidase (DAO) and expression of dynamin-related protein 1 (Drp1), mitofusin 1 (Mfn1) and HO-1 (by Western blot). Results:Compared with group C, the level of ROS was significantly increased, ATP content and DAO activity were decreased, the expression of HO-1 and Drp1 was up-regulated, the expression of Mfn1 was down-regulated ( P<0.05), and pathological damage to small intestine tissues was found in group E. Compared with group E, the level of ROS was significantly decreased, ATP content and DAO activity were increased, the expression of HO-1 and Mfn1 was up-regulated, the expression of Drp1 was down-regulated ( P<0.05), and pathological damage to small intestine tissues was significantly attenuated in group E+ EA.Compared with group E+ EA, the level of ROS was significantly decreased, ATP content and DAO activity were increased, the expression of HO-1 and Mfn1 was up-regulated, the expression of Drp1 was down-regulated ( P<0.05), and pathological damage to small intestine tissues was significantly attenuated in group E+ EA+ H, and the level of ROS was significantly increased, ATP content and DAO activity were decreased, the expression of HO-1 and Mfn1 was down-regulated, the expression of Drp1 was up-regulated ( P<0.05), and pathological damage to small intestine tissues was accenuated in group E+ EA+ Znpp-Ⅸ. Conclusions:EA can promote mitochondrial fusion, inhibit mitochondrial fission, and alleviate intestinal damage in mice with endotoxemia, and the mechanism is related to the up-regulation of HO-1 expression.

Objective To explore the mechanism of phlegm-resolving and stasis- removing herbals on NAFLD by observing expressions of PGC1α mRNA and insulin resistance. Methods A total of 60 male SD rats were randomly divided into the normal group, model group, positive medication control group, high-dose, middle-dose and low-dose group. The rats were fed with high-fat forage for 8 weeks. The positive medication control group were gavaged with Dongbao-Gantai liquid (0.9 g/kg/day), the high-dose, middle-dose and low-dose group were gavaged with Xiaotan-Huayu liquid (43.34、32.50、21.67 g/kg/day), and normal group, model group were gavaged with equal volume of distilled water. The drugs were given by 1 ml/100 g and last for 8 weeks. The levels of TC, TG, FFA, ALT, AST, FBG, FINS, and HOMA-IR in serum, and levels of TC, TG, and PGC-1α mRNA and pathological morphological changes in hepatic tissue were observed after 8 weeks. Results The levels of TG (0.55 ± 0.10 mmol/L, 0.58 ± 0.09 mmol/L, 0.67 ± 0.11 mmol/L vs. 1.18 ± 0.15 mmol/L), TC (1.48 ± 0.24 mmol/L, 1.69 ± 0.27 mmol/L, 1.74 ± 0.27 mmol/L vs. 3.29 ± 0.26 mmol/L), FFA (251.08 ± 48.18 μmol/L, 277.53 ± 56.73 μmol/L, 291.82 ± 48.67 μmol/L vs. 432.19 ± 67.83 μmol/L), ALT (29.32 ± 4.17 U/L, 31.26 ± 4.74 U/L, 33.56 ± 5.18 U/L vs. 47.21 ± 8.67 U/L), AST (11.05 ± 2.18 U/L, 12.15 ± 2.67 U/L, 12.96 ± 2.93 U/L vs. 19.43 ± 3.68 U/L), FBG (5.68 ± 1.22 mmol/L, 6.86 ± 1.36 mmol/L, 7.94 ± 1.82 mmol/L vs. 11.88 ± 2.54 mmol/L), FINS (8.48 ± 1.22 mmol/L, 9.55 ± 1.95 mmol/L, 9.96 ± 1.74 mmol/L vs. 12.96 ± 2.67 mmol/L), HOMA-IR (1.91 ± 0.26, 2.91 ± 0.65, 3.52 ± 0.58 vs. 6.89 ± 1.21) in serum of high-dose, middle-dose and low-dose groups were decreased than model group. Levels of FFA (242.19 ± 35.13 μmol/L, 259.78 ± 29.33 μmol/L, 277.62 ± 34.29 μmol/L vs. 436.48 ± 52.15 μmol/L), TG (23.65 ± 3.28 mmol/L, 24.41 ± 3.15 mmol/L, 25.37 ± 3.59 mmol/L vs. 15.98 ± 2.37 mmol/L), TC (7.15 ± 0.82 mmol/L, 8.60 ± 0.95 mmol/L, 8.86 ± 1.04 mmol/L vs. 36.98 ± 4.28 mmol/L) were in hepatic tissue of high-dose, middle-dose and low-dose groups were significantly lower than the model group. The levels of PGC-1α mRNA (1.24 ± 0.06, 1.02 ± 0.07, 0.99 ± 0.08 vs. 0.43 ± 0.06) in hepatic tissue of high-dose, middle-dose and low-dose groups were significantly higher than model group. Conclusions The phlegm-resolving and stasis-removing herbals may improve lipid metabolism by regulating the expression of PGC-1α mRNA, inhibiting gluconeogenesis and liver sugar output, correcting disturbance of lipid metabolism and improving insulin resistance.

Objective To evaluate the effects of artemisinin on proliferation,cell cycle and apoptosis of gallbladder cancer cells.Methods Gallbladder carcinoma cell lines (GBC-SD and NOZ) were cultured in vitro.The effects of artemisinin in different concentration on proliferation of the two cell lines in vitro were examined using MTT assay.The cell cycle distribution of GBC-SD and NOZ cells 24 h after treatments with artemisinin(20 μ mol/L) were examined using flow cytometry.The apoptosis of GBC-SD and NOZ cells 24 h after treatments with artemisinin (20 μ mol/L) were examined using Annexin V/PI staining.The expressions of p-ERK1/2,CDK4,cyclin D1,p16,cytochrome C and caspase-3 were examined by Western blot assay.t-test and one way ANOVA were used to evaluate the differences between two groups and more than two groups,respectively.Results The cell proliferation was significantly inhibited by artemisinin,the ICS0 of artemisinin against GBC-SD and NOZ cells were 14.05 μmol/L and 12.42 μmol/L,respectively.Artemisinin induced cycle arrest,and G1 population of GBC-SD and NOZ cells increased to 74.60％ and 78.86％.Cell apoptosis and apoptotic population of GBC-SD and NOZ cells were increased to 15.67％ and 16.51％ after dealt with artemisinin,respectively.In addition,expression of pl6 was increased,and expressions of p-ERK1/2,CDK4 and cyclin D1 were down-regulated by artemisinin(all P ＜0.05).Cytochrome C was released from mitochondria to cytoplasm leading to the activation of caspase-3 and PARP after dealt with artemisinin (P ＜ 0.05).Conclusion The inhibition effect of artemisinin on the proliferation gallbladder cancer cells is accompanied by down-regulation of ERK1/2 signaling pathway,G1 phase arrest and triggering caspase-3-mediate apoptosis.

Objective To evaluate the effects of artemisinin on proliferation,cell cycle and apoptosis of gallbladder cancer cells.Methods Gallbladder carcinoma cell lines (GBC-SD and NOZ) were cultured in vitro.The effects of artemisinin in different concentration on proliferation of the two cell lines in vitro were examined using MTT assay.The cell cycle distribution of GBC-SD and NOZ cells 24 h after treatments with artemisinin(20 μ mol/L) were examined using flow cytometry.The apoptosis of GBC-SD and NOZ cells 24 h after treatments with artemisinin (20 μ mol/L) were examined using Annexin V/PI staining.The expressions of p-ERK1/2,CDK4,cyclin D1,p16,cytochrome C and caspase-3 were examined by Western blot assay.t-test and one way ANOVA were used to evaluate the differences between two groups and more than two groups,respectively.Results The cell proliferation was significantly inhibited by artemisinin,the ICS0 of artemisinin against GBC-SD and NOZ cells were 14.05 μmol/L and 12.42 μmol/L,respectively.Artemisinin induced cycle arrest,and G1 population of GBC-SD and NOZ cells increased to 74.60％ and 78.86％.Cell apoptosis and apoptotic population of GBC-SD and NOZ cells were increased to 15.67％ and 16.51％ after dealt with artemisinin,respectively.In addition,expression of pl6 was increased,and expressions of p-ERK1/2,CDK4 and cyclin D1 were down-regulated by artemisinin(all P ＜0.05).Cytochrome C was released from mitochondria to cytoplasm leading to the activation of caspase-3 and PARP after dealt with artemisinin (P ＜ 0.05).Conclusion The inhibition effect of artemisinin on the proliferation gallbladder cancer cells is accompanied by down-regulation of ERK1/2 signaling pathway,G1 phase arrest and triggering caspase-3-mediate apoptosis.

This paper proposed a rehabilitation training system with electromyography (sEMG) feedback for stroke patients based on ARM embedded system and LabVIEW. The system can achieve real-time acquisition, processing and dualview of multi-channel sEMGs and compute related sEMG parameters including iEMG, RMS, MPF and co-contraction ratio. The system was detected by clinical experiments and related inspection department. The result showed that the system is functional, interactive and in accordance with the relevant standards for medical devices so that it can fully satisfy the clinical demands. In addition, the system can help doctors to master the training state of the patient more effectively in a real-time and quantitative way that is direct to improve the training programs of stroke patients.
Electromyography ; Humans ; Neurofeedback ; Stroke Rehabilitation

Based on the theory of cancer stem cells (CSCs),people have been searching for the treatments of malignant cancers.Gastric cancer side population cells (SP) have the characteristics of CSCs.Searching for the molecular targeted therapy strategy of gastric cancer which embarks from the gastric cancer SP and is based on the theory of CSCs provides a new direction for the treatment,early diagnosis,therapeutic effect and prognosis of gastric cancer.