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Objective To investigate the effects of C-type lectin domain family 5,member A(CLEC5A)on the proliferation, apoptosis, and cell cycle of leukemia cell lines THP-1 and K562,and the underlying mechanism. Methods The expression ofCLEC5Ain leukemia patients was investigated in the GEPIA database.Recombined plasmid containingCLEC5Awas transfected into THP-1 and K562 cells for overexpression ofCLEC5A.Small interfering RNA(siRNA)was used to knock down the endogenousCLEC5Ain leukemia cells.CCK-8 and EdU assays were used to assess the leukemia cells proliferation.Flow cytometry was used to assess cell cycle.Flow cytometry was used to assess cell apoptosis under hydrogen peroxide(H2O2)stress.The RNA sequencing(RNA-seq)and pathway enrichment analysis were used to analyze the signal pathways of significant enrichment of up-regulated or down-regulated genes after knocking downCLEC5Agene.Protein expression levels of several members in AKT1/mTOR and p53 signaling pathways were detected by Western blot assays. Results CLEC5Awas significantly up-regulated in bone marrow tissues of leukemia patients compared to the matched non-tumor tissues of healthy individuals.Knockdown ofCLEC5Asignificantly reduced the proliferation(allP<0.01) and S phase progression(allP<0.05),and increased the apoptosis(allP<0.001) under H2O2stress, in THP-1 and K562 cells.Conversely, overexpression ofCLEC5Asignificantly increased the proliferation(allP<0.001) and S phase progression(allP<0.01),and reduced the apoptosis(allP<0.01) under H2O2stress, in THP-1 and K562 cells.The up-regulated genes were significantly enriched in AKT1-mTOR and other signal pathways after knocking downCLEC5A,while the down-regulated genes were significantly enriched in cell cycle signal pathways.CLEC5Ain leukemia cells significantly reduced the genes expression levels of BAX and p53,and significantly induced the gene expression levels of BCL-2 and phosphorylation levels of AKT1 and mTOR proteins. Conclusion CLEC5Aincreases the cell cycle and proliferation and inhibits cells apoptosis in THP-1 and K562 cells, and the mechanism may be related to activating the AKT/mTOR and p53 signaling pathways.

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Objective To evaluate the effect of maternal hypothyroidism on lipid metabolism in the early life offemale offspring by constructing a murine model during pregnancy. Methods Female mice C57BL/6J were randomly divided into normal control group(NC0),hypothyroidism complicated with pregnancy group(PH0) and pregnancy complicated with hypothyroidism group(GH0).Firstly, PH0 group was given 0.15% propylthiouracil diet for 28 days, while NC0 and GH0 groups were given normal diet.After the successful modeling of PH0 was confirmed, female mice in GH0 and PH0 groups were given 0.15% propylthiouracil diet during pregnancy, and NC0 group was still given normal diet.After delivery, the levels of free triiodothyronine(FT3),free thyroxine(FT4),thyroid stimulating hormone(TSH) and total cholesterol(TC),triglyceride(TG) in each group were detected at 3 weeks of age for female offspring.The pathological changes of thyroid and liver were observed by HE staining.Western blot detected the levels of proteins associated with lipid metabolism. Results Compared with the NC0 group, the levels of serum FT3 and FT4 decreased, the levels of serum TSH,serum TC,hepatic TC and TG increased in the female offspring of the PH0 and GH0 groups, and lipid deposition was observed in their livers.The expression levels of HMGCR,FAS and CD36 related to lipid metabolism in livers increased, while the expressions of CPT1A and LDL-R were down-regulated. Conclusion Hypothyroidism during pregnancy may lead to the disturbance of lipid metabolism in the early life of female offspring mice.

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Objective To compare acute ulcerative colitis(UC) model induced by dextran sulfate sodium(DSS) at 1.5% and 3.0% concentrations and obtain a cost-effective modeling scheme with low mortality. Methods C57BL/6J mice were randomly divided into control group, 1.5% and 3.0%DSS group.The mice in control group drank sterilized water and the mice in each group of DSS drank the corresponding concentration of DSS solution, all mice were treated for 7 days.And all mice drank sterilized water on day 8 to 14.The blood stool of mice was observed and the disease activity index, the percentage of body weight loss and the percent of survival of mice were calculated on day 1 to 14.Mice were sacrificed on day 8.The spleen index was calculated and the length of colon was measured; HE staining was used to observe the histopathological changes of colon; The expressions of tight junction protein Claudin-1 and Occludin in colon tissue were detected by immunohistochemistry; Immunofluorescence detected the ratio of macrophage in colon tissue; Levels of tumor necrosis factor-α(TNF-α) in serum and colon tissue homogenates were detected by ELISA. Results Compared with the control group, both mice of 1.5%DSS group and mice of 3.0%DSS group showed similar clinical and pathological features to human UC;The colon lengths were both shortened(P<0.01);The expressions of Claudin-1 and Occludin in colon tissue both decreased(P<0.01);Spleen index increased(P<0.01);The proportion of macrophages in colon tissue increased(P<0.01);Levels of TNF-α in serum and colon tissue homogenates both increased(P<0.01).The percent of survival of 1.5%DSS mice within 14 days was higher than that of 3.0%DSS mice. Conclusion The acute UC model can be established efficiently and economically by giving 1.5% concentration of DSS solution in mice for 7 days.

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Objective To investigate the effect of sinomenine on proliferation and migration of multiple myeloma(MM) cells by regulating STAT3 and NF-κB signaling pathway. Methods The cultured U266 cells were treated with different concentrations of sinomenine(0,0.5,1,2 mmol/L).The control group was added DMSO with 0.5% concentration.CCK-8 assay was used to detect the proliferation of U266 cells.Flow cytometry was used to detect the apoptosis of U266 cells.Western blot assay was used to detect the expression levels of apoptosis-related proteins, STAT3 and NF-κB signaling pathway proteins in the each group. Results Compared with CON group, the apoptosis of U266 cells increased after Sinomenine treatment, the proliferation was inhibited; B lymphoma-2(Bcl-2) myeloid and cell leukemia-1(Mcl-1) expression level decreased; activated Caspase-3(cleaved Caspase-3) and PARP(Cleaved Caspase-3) expression levels increased; the activity of STAT3 and NF-κB signaling pathway decreased. Conclusion Sinomenine can down-regulate the activity of STAT3 and NF-κB signaling pathway, promote the apoptosis of U266 cells and inhibit the proliferation of U266 cells.

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Objective To investigate the expression of N6-methyladenosine modification(m6A) and related enzymes FTO, METTL3 and YTHDF2 in gastric epithelial cells infected withHelicobacter pylori(Hp), and to analyze its expression and clinical significance in gastric cancer by using online websites. Methods Gastric epithelial cells GES-1 and AGS were infected with Hp GZ7 strain, and the multiplicity of infection was 30 ∶1.Total RNA and total protein were collected after infecting 24 h, and the m6A modification level of total RNA was detected by RNA dot hybridization. The mRNA and protein expressions of FTO, METTL3 and YTHDF2 were detected by q-PCR and Western blot. The expression difference of FTO, METTL3 and YTHDF2 in gastric cancer tissues and normal tissues and their expression in Stage classification were analyzed by GEPIA, and the relationship between the expression of FTO,METTL3 and YTHDF2 and prognosis was analyzed by Kaplan-Meier Plotter. Results Compared with the uninfected group, the m6A modification level of total RNA in both Hp-infected GES-1 and AGS cells significantly decreased, the mRNA and protein expression levels of FTO increased, and the mRNA and protein levels of METTL3 and YTHDF2 decreased, with statistical significance(P<0.05). The expression level of FTO in gastric cancer tissues was higher than that in normal tissues, with statistical significance(P<0.05), YTHDF2 was higher than that in normal tissues, with no statistical significance, and the expression level of METTL3 was lower than that in normal tissues, with no statistical significance. Patients with high expression of FTO and METTL3 had a lower survival rate, while patients with high expression of YTHDF2 had a higher survival rate. The expression of FTO was significantly correlated with Stage classification(P<0.05), while the expression of METTL3 and YTHDF2 was not significantly correlated with Stage classification. Conclusion Hp infection can change the level of m6A and the expression of related enzymes FTO, YTHDF2 and METTL3, suggesting that m6A methylation may play a role in the occurrence and development of Hp-induced gastric cancer.

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Objective To investigate the impact of SOX4 on ovarian granulosa cells, stable overexpression of SOX4 was achieved in human KGN cell line, followed by analysis of its effects on proliferation, migration and apoptosis. Methods The recombinant lentiviral plasmid pLV-EF1a-GFP/Puro-SOX4 was generated through homologous recombination with linearized pLV-EF1a-GFP/Puro vector.Human ovarian granulosa cells(KGN cell line) were transduced with Lentiviral expression vectors.KGN cells infected with pLV-EF1a-GFP/Puro-NC were served as the LV-CON group, while those infected with pLV-EF1a-GFP/Puro-SOX4 were designated as the LV-SOX4 group.Following transfection, puromycin selection was employed to establish stable SOX4-expressing KGN cells.The expression levels of SOX4 m RNA and protein in KGN cells from the LV-CON and LV-SOX4 groups were assessed using RT-qPCR and Western blot analysis.Cell proliferation was assessed using the CCK-8 assay in both LV-CON and LV-SOX4 groups.Cell migration ability was evaluated by means of a cell scratch test in these two groups.The proportion of apoptotic cells was determined via flow cytometry analysis in both LV-CON and LV-SOX4 groups. Results The sequencing results of pLV-EF1a-GFP/Puro-SOX4 indicated a complete match between the inserted gene sequence and the SOX4 mRNA sequence.The lentiviral titers were 7×108TU/ml in the LV-CON group and 1×108TU/ml in the LV-SOX4 group.The recombinant plasmid was successfully transfected into KGN cells with a transfection efficiency of over 90% under fluorescence inverted microscopy.The results of RT-qPCR and Western blot tests demonstrated a significant increase in the expression level of SOX4 in KGN cells of LV-SOX4 group compared to that of LV-CON group(t=3.10,P<0.05;t=14.20,P<0.05).The CCK-8 assay results demonstrated that the LV-SOX4 group exhibited a significant increase in cell proliferation(24 h:t=45.92,P<0.01; 72 h:t=25.60,P<0.01) compared to the LV-CON group.The cell scratch assay indicated that the migratory capacity of KGN cells in the LV-SOX4 group was significantly enhanced(t=7.65,P<0.01) compared to that in the LV-CON group.The LV-SOX4 group exhibited a significant reduction in apoptosis ratio(t=25.84,P<0.01) compared to the LV-CON group. Conclusion SOX4-overexpressing KGN cell line was successfully established, and the overexpression of SOX4 facilitated proliferation and migration while inhibiting apoptosis in human ovarian granulosa cells.

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Objective To investigate the role of Epac1/CaMK Ⅱ signaling pathway in myocardial ischemia reperfusion injury(MIRI) in mice, and to investigate the protective effect of vitexin(VT) on acute MIRI. Methods C57/BL mice were randomly divided into 5 groups: Sham surgery group(Sham),ischemia reperfusion group(I/R),and ischemia reperfusion+vitexin group(function 3,6,12 mg/kg groups).Ligation of the left anterior descending coronary artery(LAD coronary artery) in mice resulted in ischemia of part of the heart tissue for 30min and reperfusion of the blood for 120min.Mouse myocardial ischemia reperfusion injury(MIRI) model was established.In the sham operation group, only the LAD was not ligated.Serum LDH levels of mice were detected.Hematoxylin-eosin(H&E) staining was performed on the left ventricular myocardium of mice to observe the histopathological changes.The expression level of Epac1 in myocardial tissue was observed by immunohistochemistry.The protein expressions of Epac1,Rap1,CaMK Ⅱ and ERK/p-ERK were determined by Western Blot. Results Compared with Sham group, serum LDH level of mice in I/R group was significantly increased, protein expressions of Epac1,Rap1 and CaMK Ⅱ in myocardial tissue were significantly up-regulated, and ERK1/2 phosphorylation level was decreased.Compared with I/R group, vitexin(3,6,12 mg/kg) pretreatment group decreased serum LDH level, inhibited Epac1,Rap1 and CaMK Ⅱ protein expression in mouse myocardial tissue, and promoted ERK1/2 phosphorylation(P<0.05 orP<0.01).The histopathological results showed that the myocardial fibers in the I/R group were disordered and broken, with increased gaps and obvious inflammatory cell infiltration.In the vitexin treatment group, the myocardial fibers were arranged more neatly and inflammatory cells were infiltrated less. Conclusion Vitexin may regulate Epac1/CaMK Ⅱ signaling pathway, down-regulate CaMK Ⅱ protein expression, increase ERK phosphorylation, and effectively reduce MIRI.

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Objective To explore the method of using high-fat diet combined with angiotensin-Ⅱ(Ang-Ⅱ) and β-aminopropionitrile(BAPN) to establish the model of aortic dissection in mice. Methods 24 C57BL/6J mice(4 weeks old, male) were randomly divided into control group[intraperitoneal injection of 0.9% sodium chloride solution 10 ml/(kg·d)] and experimental groups[Ang-Ⅱ 4 mg/(kg·d) group, Ang-Ⅱ 4 mg/(kg·d)+BAPN 0.33 g/(kg·d) group],each group with 8 mice; all mice were given a high-fat diet and the mice weights were measured at the same time point and administered according to the weight standard.The dead mice were dissected immediately and the aorta was taken out for pathological section, then observed under the microscope.The morphology of aorta was detected by small animal ultrasound and the mice with obvious dissection were killed and dissected directly. Results After administration, the activity and appetite of mice in the high-fat diet combined with Ang-Ⅱ+BAPN group decreased most significantly, and the mortality rate of aortic dissection rupture and the success rate of modeling in this group were higher than those in the high-fat diet combined with Ang-Ⅱ group, while there was no significant change in the control group.Under the ultrasound of small animals, compared with the other two groups, the mice in the high-fat diet combined with Ang-Ⅱ+BAPN group showed the formation of abdominal aortic vascular false lumen and vascular enlargement.The mice that died during the administration were dissected immediately, and a large number of blood clots in the abdominal cavity and around the blood vessels could be seen.The mice with aortic dissection or aortic aneurysm could be seen under ultrasound in small animals, and severe adhesion between the vascular wall and the surrounding tissues could be found when dissected, while no obvious abnormalities were found in the blood vessels of the control group.The results of the staining showed that the false lumen of blood vessel wall was formed and the arrangement of elastin and collagen was disordered in the mice of high fat diet combined with Ang-Ⅱ+BAPN group.The thickness of blood vessel wall in each group was statistically analyzed, and it was found that the blood vessels in the two experimental groups were thicker than those in the control group, which was statistically significant(P<0.001).The vascular wall of Ang-Ⅱ+BAPN+high-fat diet group showed severe elastin degradation. Conclusion High-fat diet combined with Ang-Ⅱ 4 mg/(kg·d) and BAPN 0.33 g/(kg·d) can establish an efficient model of aortic dissection in mice.

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Objective To investigate the effect of miR-135a-5p on the expression levels of insulin-like factor 3(INSL3) and testosterone in the testicular tissues of flutamide-induced cryptorchidism mouse. Methods A model of flutamide-induced cryptorchidism in mouse was constructed, and the experiment was divided into normal control group, flutamide group, flutamide + miR-135a-5p knockdown group and flutamide + miR-135a-5p overexpression group.RT-qPCR was used to detect the expression levels of miR-135a-5p and INSL3 mRNA.Western blot was employed to assess the protein expression level of INSL3.ELISA was performed to measure the expression level of testosterone. Results The expression levels of miR-135a-5p, INSL3 mRNA and protein and testosterone were significantly down-regulated in the testis of cryptorchid mice by flutamide(P<0.05).Knockdown of miR-135a-5p could downregulate the expression of INSL3 mRNA,INSL3 protein and testosterone(P<0.01),while overexpression of miR-135a-5p had the opposite result. Conclusion miR-135a-5p decreased in flutamide-induced cryptorchidism mouse testicular tissues, and overexpression of miR-135a-5p could restore the expression levels of INSL3 and testosterone.

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Objective To investigate the effects and mechanism of small ubiquitin-like modifier(SUMO) specific proteinase-1(SENP-1) on chronic intermittent hypoxia(CIH) induced myocardial injury in rats.Methods 32 male SD rats were randomly divided into: control group, CIH group, negative control adeno-associated virus intervention group(AAV-shNC) and SENP-1 shRNA adeno-associated virus intervention group(AAV-shSENP-1),with 8 rats in each group.After 6 weeks of CIH induction, echocardiography was performed.The levels of cardiac troponin I(cTNI),creatine kinase MB isoenzyme(CKMB),myoglobin(Mb),lactate dehydrogenase(LDH) in serum and malondialdehyde(MDA),uperoxide dismutases(SOD),glutathione(GSH),interleukin(IL)-1β,IL-6 and tumor necrosis factor-α(TNF-α) in myocardial tissue were detected by ELISA.The pathological changes of myocardial tissue was observed by HE staining.The reactive oxygen species(ROS) level in myocardial tissue was detected by DCFH-DA fluorescence probe labeling.The small ubiquitin-like modifier(SUMO) level of hypoxia inducible factor-1α(HIF-1α) protein in myocardial tissue was detected by kit.The mRNA and protein levels of SENP-1 and HIF-1α in myocardial tissue were detected by qRT-PCR and Western blot.Results Compared with the control group, the pathological damage of myocardial tissue in CIH group was serious, the levels of left ventricular end diastolic diameter(LVEDD),left ventricular end systolic dimension(LVESD) and serum cTNI,CKMB,Mb and LDH significantly increased(P<0. 05),and the levels of ROS,MDA,IL-1β,IL-6,TNF-α and the mRNA and protein levels of SENP-1 and HIF-1α in myocardial tissue also significantly increased(P<0. 05),while the levels of LVEF,LVFS,serum GSH and SOD significantly decreased(P<0. 05),and the SUMOylates level of HIF-1α protein in myocardial tissue also significantly decreased(P<0. 05). Compared with CIH group,AAV-shSENP-1 group had less myocardial pathological damage,the levels of LVEDD,LVESD and serum cTNI,CKMB,Mb and LDH significantly decreased(P<0. 05),and the levels of ROS,MDA,IL-1β,IL-6,TNF-α and the mRNA and protein levels of SENP-1 and HIF-1α in myocardial tissue also significantly decreased(P<0. 05),the levels of LVEF,LVFS,serum GSH and SOD significantly increased(P<0. 05),and the SUMOylates level of HIF-1α protein in myocardial tissue also significantly decreased(P<0. 05). Conclusion Inhibition of SENP-1 expression can alleviate CIH induced myocarditis and oxidative stress in rats,improve myocardial injury and cardiac dysfunction,and its mechanism may be related to the improvement of HIF-1α SUMOylates level,thus inhibiting HIF-1α expression.

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Objective To establish myeloid(including macrophage and granulocyte) specific knockout mice of mammalian sterile line 20-like kinase 1(MST1) gene for furtherinvestigating the role and the mechanism of MST1 in macrophages in related clinical diseases. Methods Mst1 flox / flox LysM-Cre(referred to asMst1 ΔM / ΔM hereafter) mice were generated by crossingMst1 flox / flox with lysozyme(Lysm-Cre) mice. The loxP site and Cre gene were amplified by PCR for genotyping.The knockdown efficiency of MST1 in macrophages was verified by quantitative PCR and immunofluorescence.The main immune cell populations in the livers were detected by flow cytometry. Results Mst1 flox / flox LysM-Cre(Mst1 ΔM / ΔM ) was the genotype of macrophage specific knockout MST1 mice.The results of qPCR and immunofluorescence showed that the knock-out efficiency of MST1 was more than 70% in bone marrow-derived macrophages and peritoneal macrophages.Flow cytometry showed that macrophage knockout of MST1 had no significant effect on the main immune cell populations in the liver of mice. Conclusion Macrophage-specific knockout of MST1 mouse model is successfully established, which lays a foundation for further investigation on the role and mechanism of macrophage MST1 in clinical related disease.

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Objective By observing the changes of interleukin-22(IL-22),signal transduction and transcriptional activator 3(STAT3), fasting blood glucose(FBG)and fasting insulin(FINS) of rats under the circumstance of chronic intermittent hypoxia and reoxygenation, to explore the role of IL-22/STAT3 pathway in insulin resistance induced by chronic intermittent hypoxia.Methods 24 SD rats were randomly divided into control group(NC group) and intermittent hypoxia group(CIH group),with 12 rats in each group.NC group was placed in normoxia environ-ment for 12 weeks, while CIH group was first given intermittent hypoxia for 8 weeks and then resumed normoxia feeding until 12 weeks. FBG,FINS,IL-22 and p-STAT3/STAT3 levels were measured at baseline,week 8 and week 12 in both groups,and insulin resistance index(HOMA-IR) was calculated. The differences between the two groups were compared. Results(1) There was no significant difference of the observation indexes between the two groups at baseline(P>0. 05). At 8 weeks,the levels of FBG,FINS and HOMA-IR in CIH group were higher than those in NC group(P<0. 05),and the levels of IL-22 were lower than those in NC group(P<0. 05). p-STAT3/STAT3 showed a decreasing trend,but not statistically significant. At 4 weeks of reoxygenation,there were no significant differences in FBG,FINS,HOMA-IR and IL-22 levels between the two groups(P>0. 05). p-STAT3/STAT3 in CIH group was significantly higher than that in NC group(P<0. 05).(2) Spearman rank correlation analysis showed that HOMA-IR was negatively correlated with IL-22 and p-STAT3/STAT3( all P<0. 05). Conclusion Chronic intermittent hypoxia can inhibit the expression of IL-22/STAT3 signaling pathway,IL-22/STAT3 signaling pathway may mediate insulin resistance induced by chronic intermittent hypoxia.

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Objective To study the expression of QSOX1 in osteosarcoma tissues and cells and its role in proliferation, migration and invasion. Methods Western blot and immunohistochemistry were used to verify the expression of QSOX1 in osteosarcoma tissues and cells, and the cell line MG63 with the highest expression was selected.Slow virus knocked down and selected stable strains shQSOX1 group and shCtrl group.Western blot was used to detect the expression level of QSOX1 protein in MG63 after transfection.CCK-8 assay was used to detect the level of cell proliferation.Scratch test verified the level of cell migration.Transwell test was used to detect the invasion ability of cells; Western blot was used to detect the mRNA expression level of NF-κB signal pathway in shCtrl group and shQSOX1 group. Results Western blot and immunohistochemistry showed that QSOX1 was low expressed in human osteoblast line hFOB1.19 and adjacent tissues, but high expressed in osteosarcoma tissue and osteosarcoma cells(P<0.001).CCK-8 experiment showed that the proliferation ability of shQSOX1 group was inhibited compared with shCtrl group(P<0.05);In the scratch test, the migration ability of shQSOX1 group decreased(P<0.001);Transwell proved that the invasive ability of shQSOX1 group was affected(P<0.001);NF-κB was highly expressed in shCtrl group and low expressed in shQSOX1 group(P<0.001). Conclusion QSOX1 is highly expressed in osteosarcoma.Knockout of QSOX1 gene can inhibit the proliferation, migration and invasion of osteosarcoma.Knockout of QSOX1 makes NF-κB signal pathway is deactivated.

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Objective To investigate the improvement effect and possible mechanism of cornus officinalis glycosides on MRL/lpr lupus nephritis. Methods Forty mice lupus-prone MRL/lpr mice were divided into model group, cornus officinalis glycosides low-dose, medium-dose, high-dose group(27.5,55,110 mg/kg),with 10 mice in each group, and 10 C57BL/6 mice were taken as the control group.Gastric administration was carried out 1 time/day for 4 weeks.24-hour urine was collected before drug intervention and 2 and 4 weeks after intervention to determine the content of urine protein.After the drug intervention, mouse serum and kidney tissues were taken and the levels of serum creatinine(Scr),urea nitrogen(BUN) and anti-double-stranded DNA(dsDNA) antibodies were detected by kits.The levels of interleukin-6(IL-6),tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) in serum were detected by ELISA.The changes in peripheral blood T lymphocyte subsets were detected by Flow cytometry; The changes of renal histopathology were observed by HE staining; The protein expression levels of toll-like receptor 4(TLR4),myeloid differentiation factor-88(MyD88),nuclear transcription factor(NF-κB) p65,and p-NF-κB p65 in kidney tissue were detected by Western blotting. Results Compared with the control group, the changes of renal histopathology of the model group was severe, and the levels of 24-hour urine protein, Scr, BUN and anti-dsDNA antibodies, IL-1β,IL-6 and TNF-α significantly increased(P<0.01),the peripheral blood CD4+T/CD8+T lymphocyte ratio was significantly reduced(P<0.01),and the protein expression levels of TLR4,MyD88 and p-NF-κB p65 in kidney tissue were significantly up-regulated(P<0.01);Compared with the model group, the changes of renal histopathology of each dose group of cornus officinalis glycosides were significantly improved, the levels of 24-hour urine protein, Scr, BUN and anti-dsDNA antibodies, IL-1β,IL-6 and TNF-α were significantly reduced(P<0.01),the peripheral blood CD4+T/CD8+T lymphocyte ratio significantly increased(P<0.01),and the protein expression levels of TLR4,MyD88 and p-NF-κB p65 in renal tissue were significantly down-regulated(P<0.01).Among them, the high-dose group had the most significant changes in each index.While there was no significant difference in the expression of NF-κB p65 protein in the groups. Conclusion Cornus officinalis glycosides have a certain effect on renal inflammatory response in mice lupus-prone MRL/lpr mice, and the mechanism may be related to the inhibition of TLR4/NF-κB signaling pathway.

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Objective To study the effect of lipopolysaccharide(LPS)-induced immune system activation on synaptic structure andDISC1gene expression in the cortex of rats with schizophrenia. Methods 40 rats were divided into 4 groups, which were PBS group, PBS+MK-801 group, LPS group and LPS+MK-801 group.The rats in LPS group and LPS+MK-801 group were administrated with LPS solution(0.2 mg/kg, i.p.BIW) for 6 times in total, the rats in PBS group and PBS+MK801 group were administrated with PBS.At the third time when the rats were administrated with LPS solution, the rats in PBS+MK-801 group and LPS+MK-801 group were administrated with MK-801 solution(0.5 mg/kg, i.p.BIW) for a total of 4 times, the rats in PBS group and LPS group were administrated with saline.The head shaking and the open field tests were then evaluated in the rats.Immediately, the rats were sacrificed, and their brain were saved for testing.RT-qPCR,Golgi staining, immunohistochemistry and ELISA kits were used to detectDISC1gene expression, dendritic spine status, microglia activation and inflammatory cytokine content in cortex, respectively. Results Compared with the PBS group, the expression ofDISC1gene of the rats in the PBS+MK-801 group increased(P<0.01),the score of head shaking increased(P<0.01),and the distance of the open field increased(P<0.000 1);As well as the LPS+MK-801 group, compared with the LPS group, the expression ofDISC1gene increased(P<0.000 1),the head shaking score and the distance of the open field increased(P<0.000 1).In addition, compared with the PBS+MK-801 group, the expression ofDISC1gene, the shaking head score and the open field distance of the LPS+MK-801 group further improved(P<0.000 1).Furthermore, compared with PBS group and PBS+MK-801 group, the content of iba1 in the cortex of LPS group and LPS+MK-801 group significantly increased(P<0.05),the content of inflammatory cytokines significantly increased(P<0.05),and the length and density of dendritic spines significantly decreased(P<0.05). Conclusion The activation of the immune system induced by LPS can contribute to the susceptibility of schizophrenia model, and the possible mechanism is that it cooperates with MK-801 to increase the expression ofDISC1gene, which ultimately leads to abnormal mental behavior in rats.

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Objective Based on the expression of NFATc1 and prognosis in colorectal cancer, we interfered NFATc1 via shRNA transfection, analyzed the effect of NFATc1 on colorectal cancer cell proliferation, and further explored potential mechanisms.Methods We explored the correlation between NFATc1 expression and the prognosis of colorectal cancer using the TCGA database.Thereafter, we compared the expression of NFATc1 in colorectal cancer tissues and adjacent normal tissues by immunohistochemical staining of postoperative samples from clinical colorectal cancer patients.We analyzed the effect of NFATc1 on colorectal cancer cell proliferation by measuring CCK-8 after NFATc1 interfered using shRNA transfection; Tumorigenic potential of colorectal cancer cells was measured with clone formation assay; Cell cycle distribution was measured by flow cytometry after propidium iodide staining. The effect of NFATc1 on the transcriptional activity of cell-cycle-related factors was measured by qPCR. Results Based on the TCGA data,we found that high NFATc1 expression in colorectal cancer patients was associated with poor prognosis. The expression of NFATc1 in clinical colorectal cancer tissues was significantly higher than that in adjacent normal tissues. Additionally,interference with NFATc1 inhibited the proliferation rate of colorectal cancer cells in vitro,and the clonogenic capacity of cells was impaired. As expected,the cell cycle was arrested at the G0/G1 phase. The qPCR results indicated that the knockdown of NFATc1 increased the transcriptional activity of multiple key cell cycle inhibitors. Conclusion NFATc1 promotes cell cycle progression by inhibiting the transcriptional activity of cell cycle regulatory factors,thereby promoting the proliferation and tumorigenic ability of colorectal cancer cells.

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Objective To investigate the effects of luteolin on invasion and migration of endometriosis stromal cells and whether its mechanism is related to the regulation of 15-hydroxyprostaglandin dehydrogenase(HPGD) expression. Methods The endometrial stromal cells HEM15A were divided into control group(cells were cultured in normal medium),luteolin group(cells were treated with different concentrations of luteolin),si-HPGD group(cells were transfected with si-HPGD),si-NC group(cells were transfected with si-NC),luteolin + si-HPGD Group(cells were transfected with si-HPGD and treated with 20 μmol/L luteolin),Luteolin + si-NC Group(cells were transfected with si-NC and treated with 20 μmol/L luteolin).Real-time quantitative PCR was used to detect mRNA level of HPGD.Cell proliferation was detected by CCK-8 assay, Transwell and scratch assays were used to detect cell invasion and migration.The protein expression of proliferating cell nuclear antigen(PCNA),matrix metalloproteinase(MMP-2),MMP-9 and HPGD were detected by Western blot, and the level of prostaglandin E2(PGE2) was detected by ELISA. Results Compared with 0 μmol/L luteolin, luteolin at 20,50 and 100 μmol/L significantly inhibited the proliferation activity of hEM15A cells, and reduced PCNA expression(allP<0.05).Compared with the control group, 20 μmol/L of luteolin significantly inhibited cell invasion and migration(P<0.05),decreased the expressions of MMP-2 and MMP-9(P<0.05),and up-regulated the mRNA and protein levels of HPGD(P<0.05),while inhibited cellular PGE2 level(P<0.05).Compared with the luteolin group, the luteolin + si-HPGD group increased cell invasion and migration(P<0.05),increased the expressions of MMP-2 and MMP-9(P<0.05). Conclusion Luteolin regulates HPGD/PGE2 signaling pathway to inhibit the invasion and migration of endometrial stromal cells.

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Objective Angiotensin Ⅱ Type 2 receptor(AT2R) is a major receptor of angiotensin Ⅱ,which has a protective effect on damage to various tissues and organs.In this study, an overexpression plasmid of AT2R was constructed to explore the effect of overexpression of AT2R on lipopolysaccharide(LPS)-induced inflammatory response in mouse hepatocytes(AML12 cells).Methods Mice tissues and organs were used as samples to amplify the gene of interest(AT2R) fragments containing EcoR Ⅰ and Hind Ⅲ restriction sites, and then the final product was obtained by digestion and ligation.The final positive clones were sequenced and identified.The pCMV-Flag-N-AT2R plasmid was transfected into HEK 293T cells, and the expression of Flag protein was detected by the Western blot method after 24 h.AT2R expression on AML12 cells was observed by Western blot and laser confocal microscopy.AML12 cells were treated differently and divided into control group, LPS treatment group, pCMV-Flag-N-AT2R group and pCMV-Flag-N-AT2R+LPS group, and cell viability was detected by CCK8.Western blot detected PCNA proteins and observed cell proliferation; Cytoinflammatory factor levels were detected by qPCR;Western blot detected the expression level of nuclear transcription factor NF-кB(p65) in cells.Results The identification and sequencing results of EcoR Ⅰ and Hind Ⅲ double restriction showed that pCMV-Flag-N-AT2R plasmid was successfully constructed, and the detection results of the Western blot method showed successful expression of AT2R protein.Laser confocal observed that there were AT2R receptors on AML12 cells, and AT2R recombinant plasmids could be expressed on AML12;Compared with the control group, the viability and proliferation ability of LPS-treated AML12 cells were weakened, while the levels of IL-6 and TNF-α increased, and the expression level of nuclear transcription factor NF-кB(p65) increased.Compared with the LPS group, the viability and proliferation of cells in AML12 cells treated with pCMV-Flag-N-AT2R and LPS were enhanced, while the levels of IL-6 and TNF-α decreased.The expression of the nuclear transcription factor NF-кB(p65) decreased.Conclusion AT2R overexpression plasmids were successfully constructed and successfully expressed on AML12 cells, and AT2R could inhibit the inflammatory response of LPS-induced AML12 cells.

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Objective To study the protective effect and mechanism of remimazolam on cognitive function in septic mice. Methods Fifty-four C57BL/6 mice were randomly divided into saline group(NS group),simple remimazolam group(RM group),sepsis model group[lipopolysaccharide(LPS)group] and sepsis groups with different doses of remimazolam injection(RM10,RM15and RM20groups).The sepsis model was established by intraperitoneal injection of 1 mg/kg LPS;the RM group was injected intraperitoneally with 15 mg/kg remimazolam solution; the RM10,RM15and RM20groups were respectively injected with 10,15 and 20 mg/kg remimazolam solution 30 mins before LPS injection.The number of times the mice crossed the platform and the percentage of time they stayed in the first quadrant were recorded in the Morris water maze experiment; the levels of tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) in peripheral blood and hippocampus were measured by enzyme-linked immunosorbent assay(ELISA);the levels of malondialdehyde(MDA),glutathione(GSH) and superoxide dismutase(SOD) activity in hippocampus were measured by chemical colorimetric assay; and the pathological changes of neurons in CA1 area of hippocampus were observed by Hematoxylin-eosin(HE) staining. Results In the LPS group, the number of platform crossing times, the percentage of staying time in the first quadrant, GSH level and SOD activity significantly decreased, and TNF-α,IL-1β and MDA levels significantly increased.In addition, the arrangement of neurons in CA1 area of hippocampus was disturbed; cytoplasmic staining was deepened; and the nucleus was solidly stained.Comparing RM10,RM15and RM20groups with the LPS group, the number of platform crossing times, the staying time in the first quadrant, GSH level and SOD activity increased, and the levels of TNF-α,IL-1β and MDA decreased.And the results of hippocampal staining showed a decrease in degenerated neuronal cells.When it came to the comparision in the groups with different doses of remimazolam injection, septic mice in the RM20group showed less improvement in cognitive dysfunction and inflammatory oxidative stress than the RM10and RM15groups. Conclusion Remimazolam has a protective effect on cognitive dysfunction in septic mice, and its mechanism may be related to its binding of translocator protein(TSPO) to inhibit macrophage polarization and thus reduce neuroinflammation and oxidative stress damage.It also reflects that dose of 10 mg/kg and 15 mg/kg has more significant protective effect than that of 20 mg/kg.

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Objective To investigate the effect and signaling mechanism of terpinen-4-ol(T4O) on vascular oxidative stress injury in mice with chronic kidney disease(CKD). Methods A CKD mice model was prepared using high phosphorus diet combined with adenine, and the normal group was given an equal volume of saline gavage.The CKD model with low expression of SIRT1 in vivo was established by tail vein injection of lentiviral SIRT1 RNAi for the study of signaling mechanism.The administration groups were given T4O at low and high doses(10 mg/kg and 20 mg/kg) for 6 weeks by continuous gavage.Serum was collected to detect urea nitrogen(BUN) and creatinine(CRE) levels, and HE staining was used to observe the morphology of blood vessels in the thoracic aorta of mice expression. Results T4O reduced serum BUN and CRE levels in CKD mice to improve renal function, improved kidney and thoracic aortic vascular morphology, reduced vascular tissue MDA content, increased SOD content, and reduced ROS levels; T4O intervention promoted Nrf2 nuclear translocation and upregulated HO-1,NQO-1 and SIRT1 protein expression; LV-SIRT1 RNAi+T4O group was able to inhibit the effect of T4O on CKD-induced MDA and SOD levels, partially counteracting the effect of T4O in upregulating Nrf2 nuclear translocation and the protein expression levels of SIRT1,HO-1 and NQO-1. Conclusion T4O has a protective effect against oxidative stress injury in the thoracic aorta of CKD mice, and its molecular signaling mechanism may be related to the level of drug-regulated SIRT1/Nrf2 cascade signaling.

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Objective To investigate the protective effect of caffeine on oxidative stress injury induced by hyperoxia in neonatal SD rats with bronchopulmonary dysplasia(BPD) and its related mechanism.Methods Neonatal SD rats were randomly divided into air control group(N group),caffeine air control group(NC group),model group(H group) and caffeine intervention group(HC group).The high oxygen induction method was used to establish the BPD model.Blood and lung tissue of six samples were collected from each group on day 3,7,14 and 21.Each group was divided into four subgroups according to four days of age.The 21-day panel of four groups measured their body weights.The upper lobe of the right lung was used to measure wet-dry weight ratio(W/D) of lung tissue in each group; the lower lobe of the right lung was sliced after paraffin embedding and stained with hematoxylin-eosin(HE) to observe morphological changes and calculate radial alveolar count(RAC) values; the levels of malondialdehyde(MDA) and superoxide dismutase(SOD) in blood and lung tissues were determined to evaluate the imbalance of oxidative and antioxidant homeostasis in neonatal rats; real-time fluorescence quantitative reverse transcription polymerase chain reaction(RT-qPCR) was used to detect the relative expression level of nuclear factor-erythroid 2-related factor 2(Nrf2) mRNA in lung tissues.Results(1) H group showed a gradual decline in activity after 3 days and an increasing trend in body weight after 14 days.(2) W/D value of H group reached its peak at day 14,and the trend of HC group was similar to that of H group.(3) The lung tissue structure of H group was irregular,RAC value of which decreased significantly after 7 days of peak,and the difference between H group and HC group was statistically significant( P<0. 01).(4) The MDA value of H group increased on day 7 and gradually decreased on day 14,while the SOD activity decreased obviously on day 7,and there were significant differences in MDA and SOD activity between H group and HC group at 14 days and 21 days( P<0. 05).(5) The expression of Nrf2 mRNA in H group was significantly enhanced at day 7 and stabilized at day 14,and there were statistically significant differences between H and HC groups at day 3,day 7 and day 14( P<0. 05).(6) The relative expression level of Nrf2 mRNA was positively correlated with MDA and negatively correlated with SOD. Conclusion Caffeine can regulate oxidative stress response through Nrf2 pathway and alleviate lung oxidative stress injury induced by hyperoxia in neonatal rats with BPD.

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Objective This work mainly studied the effects of acute sleep deprivation(SD) on anxiety and depression behavior in mice, and explored possible molecular mechanisms. Methods 33 male 8-week-old C57BL/6 mice were randomly divided into environment control(EC) group and a SD group.The open field test and elevated plus maze test were used to evaluate their spontaneous and anxiety behavior, while the forced swimming test and tail suspension test were used to detect depression behavior in mice.The expression of neuroinflammatory proteins and the levels of autophagy-related proteins were detected by Western blot method. Results Behavioral results showed that comparing to the EC group, the total distance traveled by mice in the SD group significantly increased in the open field test(P<0.01),while the number of crossings and time spent in the central area did not show significant differences.Results from the forced swimming test showed that immobility time significantly increased in the SD group mice(P<0.01),but there were no significant differences in tail suspension and elevated plus maze test.Western blot results showed that comparing to the EC group, the levels of NLRP1,TNF-α,IL-1β,IL-18,and autophagy protein p62 in the hippocampus of the SD group mice significantly increased, while the levels of Atg5,Atg7 decreased significantly, and the phosphorylation level of AMPK also decreased significantly. Conclusion SD may induce depression-like behavior in mice by inhibiting the AMPK-autophagy signaling pathway in the hippocampus and upregulating neuroinflammatory levels.

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Objective To investigate the effect and mechanism of ARRB1 on Armillariella tabescens polysaccharides reversal of 5-fluorouracil(5-FU)-induced chemotherapeutic intestinal mucosal injury. Methods Twelve ARRB1 knockout(ARRB1-/-) and wild-type(WT) C57BL/6 mice were randomly divided into Control, Model and ATPS groups(200 mg/kg),respectively.5-FU(50 mg/kg) was injected intraperitoneally for 7 days to establish a model of chemotherapeutic intestinal mucosal injury.The histopathological damage of jejunum was evaluated by HE staining; the activity of serum superoxide dismutase(SOD) and diamine oxidase(DAO) was measured by kits; the expression of tight junction protein(TJ) markers ZO-1,Occludin, Claudin-1 and proliferation-associated protein Ki-67 was detected by immunohistochemistry.Crypt isolation and organoid culture were used to detect the growth status of small intestinal organoids. Results 5-FU chemotherapy reduced body weight, aggravated histopathological damage in small intestine, decreased SOD level, TJ protein and Ki-67 protein expression, increased serum DAO level, decreased spherical structure formation rate and organoid formation rate; compared with the model group, after ATPS treatment, WT mice recovered body weight, decreased pathological damage, increased serum SOD level, TJ protein and Ki-67 protein expression, DAO levels decreased, and the rates of spherical structure formation and organoid formation were significantly higher.However, ARRB1-/-mice failed to reverse the effect of 5-FU after ATPS treatment. Conclusion ATPS reverses 5-FU-induced intestinal mucositis through the protective effects of ARRB1 on intestinal barrier and organoid growth.

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Objective To investigate the expression of circular RNA(circRNA) circPRKDC in serum of patients with new-onset type 2 diabetes and its protective effect on palmitic acid-induced islet cell injury and its mechanism. Methods Fifty patients with new-onset type 2 diabetes and 50 healthy individuals who underwent physical examination during the same period were selected, and the expression of circPRKDC in serum was detected by real-time quantitative polymerase chain reaction(qRT-PCR).The mouse pancreatic β cell line MIN6 was treated with 110 μmol/L palmitic acid for 24 h to establish cell injury model.Negative control lentivirus or circPRKDC overexpression lentivirus were transfected, namely control group and circPRKDC group, respectively.Flow cytometry was used to determine the apoptosis and intracellular reactive oxygen species(ROS) levels of cells in each group.Bioinformatics software predicted miRNA with binding sites for circPRKDC.The dual-luciferase reporter gene experiment verified the direct binding of circPRKDC to downstream miRNA.The expression of miRNA in each group of cells was detected by qRT-PCR.Western blot was used to detect the expressions of apoptosis-related factors(Bax, Bcl-2,caspase 8) and inflammation-related proteins(NF-κB,p65) in each group of cells. Results Compared with healthy subjects, the expression of circPRKDC in serum of patients with type 2 diabetes was significantly lower(P<0.01).Compared with the control group, the expression of circPRKDC in the circPRKDC group increased(P<0.01),the level of apoptosis decreased(P<0.01),and the content of intracellular ROS decreased(P<0.01).circPRKDC directly bound miR-375(P<0.01).Compared with the control group, the expression of miR-375 in cells in the circPRKDC group decreased(P<0.01),the protein expression of Bcl-2 was up-regulated(P<0.01),and the protein expressions of Bax, caspase 8,NF-κB and p65 were down-regulated(allP<0.01). Conclusion The expression of circPRKDC is down-regulated in the serum of patients with new-onset type 2 diabetes, and it reduces palmitic acid-induced oxidative stress in islet cells by targeting miR-375,thereby inhibiting apoptosis and inflammatory responses.

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Objective To investigate the influences of circ＿WBSCR17 on high glucose-induced fibrosis and inflammation in human mesangial cells by regulating the miR-30a-5p/JAK1 axis. Methods Human mesangial cells HMCL were grouped into: NG group(5.5 mmol/L glucose-treated HMCL cells),HG group(30 mmol/L glucose-treated cells),si-NC group(30 mmol/L glucose+transfected with si-NC),si-circ＿WBSCR17 group(30 mmol/L glucose+transfected with si-circ＿WBSCR17),si-circ＿WBSCR17+inhibitor-NC group(30 mmol/L glucose+co-transfected with si-circ＿WBSCR17 and inhibitor-NC),and si-circ＿WBSCR17+miR-30a-5p inhibitor group(30 mmol/L glucose+co-transfected with si-circ＿WBSCR17 and miR-30a-5p inhibitor);RT-qPCR was performed to detect the expression of circ＿WBSCR17 and miR-30a-5p in cells; CCK-8 assay was performed to detect cell proliferation; flow cytometry was performed to detect apoptosis; ELISA was performed to detect the expression levels of tumor necrosis factor-α(TNF-α),interleukin(IL)-6 and IL-8;Western blot was performed to detect the expression of JAK1,proliferating cell nuclear antigen(PCNA),Bax, transforming growth factor-β1(TGF-β1),fibronectin(FN),collagen IV,and α-smooth muscle actin(α-SMA);distribution of WBSCR17 was detected by fluorescence in situ hybridization(FISH);dual-luciferase reporter gene experiment was performed to verify the relationship between circ＿WBSCR17 and miR-30a-5p, miR-30a-5p and JAK1,respectively. Results Compared with the NG group, the HMCL cell proliferation ability of the HG group decreased, the levels of TNF-α,IL-6 and IL-8,the protein expressions of p-JAK1/JAK1,p-STAT1/STAT1,p-STAT3/STAT3,TGF-β1,FN,collagenIV and α-SMA,and the apoptosis ability increased(P<0.05);compared with HG group and si-NC group, the expression of miR-30a-5p, OD450value and PCNA expression in HMCL cells of si-circ＿WBSCR17 group increased, the levels of TNF-α,IL-6 and IL-8,the expressions of circ＿WBSCR17,p-JAK1/JAK1,p-STAT1/STAT1,p-STAT3/STAT3,Bax, TGF-β1,FN,collagenIV and α-SMA decreased(P<0.05);inhibition of miR-30a-5p attenuated the promoting effect of knockdown of circ＿WBSCR17 on proliferation of HMCL cells, and enhanced apoptosis, cellular fibrosis and inflammatory responses; FISH experiment confirmed that WBSCR17 was mainly distributed in the cytoplasm; dual-luciferase reporter gene experiment confirmed that circ＿WBSCR17,JAK1 and miR-30a-5p had a targeted regulatory relationship. Conclusion Knockdown of circ＿WBSCR17 can reduce high glucose-induced fibrosis and inflammation in human mesangial cells by regulating the miR-30a-5p/JAK1 axis.

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Objective To analyze the epidemiological characteristics and pathogen spectrum of hand, foot mouth disease(HFMD) in Anhui province from 2015 to 2022,and to provide scientific evidence for prevention and control measures of HFMD. Methods The surveillance data of hand, foot and mouth disease in Anhui province from 2015 to 2022 were analyzed by descriptive epidemiology.Real-time PCR was used to detect and classify HFMD samples. Results A total of 650 590 HFMD cases were reported in Anhui province from 2015 to 2022,including 1 406 severe cases and 17 deaths. The annual reported incidence was 131.45/100 000.The epidemic features of “low incidence in odd years and high incidence in even years” were presented from 2015 to 2019.The incidence showed a continuous decline from 2020 to 2022.The monthly distribution showed the characteristics of bimodal epidemic, and the main peak was not obvious in 2020.Hefei, Fuyang, Bozhou, Chuzhou and Suzhou ranked the top five cities in terms of cumulative incidence.The age of onset was mainly distributed in children aged 5 years and below, accounting for 89.26% of the total cases.The male to female ratio was 1.48 ∶1.A total of 28 657 laboratory-confirmed cases had been reported from 2015 to 2022.EV71 cases accounted for 10.57%,Cox A16 cases accounted for 24.90%,and other enterovirus cases accounted for 64.53%.The dominant pathogens showed dynamic changes in different years.Since 2018,the proportion of EV71 decreased significantly, and the proportion of other enteroviruses gradually increased to become the dominant pathogens.Among other enteroviruses, Cox A6 strain was dominant(80.48%). Conclusion This study suggests that the prevention and control of HFMD in Anhui province should be paid more attention from April to July and from October to December.The focus areas are the cities in northern Anhui and Hefei where the floating population is large.The focus of prevention and control is on children aged 5 years and below.Other enteroviruses have become the dominant pathogens of hand-foot-mouth disease in Anhui province, Cox A6 strain is dominant.

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Objective To explore the difference of serum inflammatory cytokines level in depression patients with non-suicidal self-injury(NSSI),depression patients without NSSI and normal control group, and to analyze the correlation between inflammatory cytokine level and impulsive characteristics of patients in NSSI group. Methods 40 depression patients with NSSI( NSSI group),45 depression patients without NSSI( non-NSSI group) and 40 cases of normal control group were selected, and enzyme-linked immunosorbent assay(ELASA) was used to detect serum IL-2、IL-6、IL-10、IL-15 and TNF-α levels.The Hamilton Depression Scale(HAMD) was used to evaluate the condition.The patient′s impulsivity was evaluated with Barratt Impulsive-ness Scale(BIS-11). Results The levels of serum IL-2、IL-6、IL-10、IL-15 and TNF-α in the NSSI group were significantly higher than those in the non-NSSI group and the normal control group(P<0.01),and the difference was statistically significant.The score of BIS-11 motor impulsiveness, nonplanning impulsiveness and total score in NSSI group were higher than those in non-NSSI group, with statistically significant difference(P<0.01).The levels of serum IL-2、IL-6、IL-10、IL-15 and TNF-α in NSSI group were positively correlated with BIS-11 motor impulsiveness score, nonplanning impulsiveness score and total score. Conclusion The levels of inflammatory cytokines in depression patients with NSSI increase significantly, and the patients have more obvious impulsive personality characteristics.The levels of inflammatory cytokines is positively correlated with the impulsivity of patients.

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Objective To explore the frontal EEG characteristics of elderly patients with postoperative delirium(POD) after spinal surgery under conscious and general anesthesia. Methods The inclusion criteria were patients aged≥65 years who underwent elective spinal surgery.POD was evaluated using The Confusion Assessment Method(CAM) 1-7 days after surgery.Patients were divided into two groups based on whether POD occurred: Postoperative Delirium Group(POD group) and Non Postoperative Delirium Group(Non POD group).The raw EEG data of two groups of patients in the EEG monitoring instrument were extracted, and the data of two time periods of wakefulness and anesthesia were intercepted for spectral analysis.The EEG data that did not meet the requirements were excluded, and ultimately 80 patients were included, including 32 in the POD group and 48 in the Non-POD group. Results Compared with the Non-POD group, patients in the POD group were found to be under anesthesia the power of θ、α、β waves(5-18 Hz) significantly decreased, the peak α frequency of the wave was slower(P=0.038),the peak power of α(P<0.001) and the total power were lower(P<0.001).Comparing the EEG changes between two groups from wakefulness to anesthesia, the study found that the increase of α power in POD group was not significant. Conclusion The characteristic electroencephalograms associated with POD in elderly patients during the perioperative period can help anesthesiologists to identify high-risk patients with POD in the early.

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Objective To evaluate the effect of Arthroscopic Treatment of Popliteal Cyst through the modified double posteromedial portal. Methods A total of 210 patients who diagnosed with popliteal cyst between April 2019 and June 2021 were chosen.62 patients underwent surgical treatment, include open excision and arthroscopic surgery.At the same time, 31 patients with conservative treatment were included as conservative treatment group.The Visual Analogue Score(VAS score),Lysholm knee function score, and Knee Society Score(KSS) scores were assessed before and 3 months after the operation. Results In the open excision group, preoperative VAS score was 3.69±0.93,Lysholm score was 63.75±4.76,KSS score was 60.87±5.85,and postoperative VAS score was 2.04±1.04,Lysholm score was 76.81±6.35,KSS score was 70.42±4.87.In the arthroscopic surgery group, preoperative VAS score was 3.81±0.84,Lysholm score was 62.84±4.85,KSS score was 58.95±4.79,and postoperative VAS score was 1.47±0.85,Lysholm score was 82.35±7.34,KSS score was 78.52±5.67.In conservative treatment group, preoperative VAS score was 3.92±1.02,Lysholm score was 61.39±3.92,KSS score was 62.42±6.78,and postoperative VAS score was 3.94±1.14,Lysholm score was 61.85±7.48,KSS score was 60.52±6.37.Significant improvement was observed in all the measurements after the operation compared to before the operation(P<0.001).Compared with the open excision group, the arthroscopic surgery group improved better(P<0.05). Conclusion Arthroscopy through the modified double posteromedial portal in the treatment of popliteal cyst has satisfactory results.

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Objective To explore the association of time in range(TIR) and glucose management indicator(GMI) with the risk of type 2 diabetic nephropathy(DN). Methods The clinical data of 215 patients with type 2 diabetes mellitus(T2DM) were collected and analyzed. According to the results of estimated glomerular filtration rate(eGFR) and urinary albumin to creatinine ratio(UACR),they were divided into 117 patients with T2DM and 98 patients with DN. The clinical data,biochemical indicators and continuous glucose monitoring(CGM) indicators of the two groups were compared. Logistic regression was used to analyze the influencing factors of DN risk. The predictive value of TIR and GMI on the risk of DN was evaluated by receiver operating characteristic(ROC) curve. Results There were significant differences in age,duration of diabetes,systolic blood pressure,glycosylated hemoglobin(HbA1c),fasting plasma glucose(FPG),2 hour postprandial plasma glucose(2hPG),creatinine(Cr),UACR,eGFR between the two groups(P<0. 05). There were statistically significant differences between the two groups in the CGM indexes of GMI,mean absolute difference of mean of daily differences(MODD),glucose above target range time(TAR) and TIR(P<0. 05). The results of logistic regression analysis showed that TIR was a protective factor of DN. In the ROC curve analysis of TIR prediction DN,the area under the ROC curve was 0. 718(95% CI =0. 648 ～ 0. 789,P<0. 001),and the Yoden index was 0. 38. At this time,the sensitivity was 66. 7%,and the specificity was 71. 3%. In the ROC curve analysis of GMI prediction DN,the area under the ROC curve was 0. 701(95% CI = 0. 629 ～ 0. 774,P<0. 001),and the Yoden index was 0. 368. At this time,the sensitivity was 63. 3%,and the specificity was 73. 5%. Conclusion TIR and GMI are significantly associated with the risk of DN. Specifically,lower TIR and higher GMI increase the risk of DN.

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Objective To investigate the effects of different occlusal veneer preparation designs and fiber posts on the fracture load and failure mode of endodontically treated maxillary premolars with pulp-piercing wedge-shaped defect. Methods 60 maxillary first premolars were randomly divided into group A and group B after Root Canal Therapy(RCT)and severe defects(n=30).Group A was filled with glass fiber post and resin core, and group B was filled with resin core only.Then the occlusal veneer(G2),buccal-occlusal veneer(G3)and buccal-proximal-occlusal veneer(G4)were applied to the isolated teeth.The teeth filled with composite resin(G1)and full crown(G5)were set as negative and positive control respectively, with 6 samples in each group.The sample was subjected to 5 000 hot and cold cycles and 20 000 vertical compression load aging.Finally, all the samples were loaded with static load until the sample broke at the speed of 0.5mm/min.The fracture load and failure mode of each sample were recorded. Results Both the fracture load in group A and B was G5>G3>G2>G4>G1,and the fracture load in G2,G3,G4,G5 was significantly higher than that in G1(P<0.05),and there was no significant difference between group A and B(P>0.05).The fracture form of G3 was mostly unbonding of the repair body, which was conducive to re-repair. Conclusion Buccal(occlusal) veneer is the most effective in repairing pulp-piercing wedge-shaped defects.The fiber post could not significantly enhance the fracture load of the pulp-piercing wedge-shaped defects teeth.