Objective To discuss the protective effect of dexmedetomidine （DEX） on intestinal function in rats with enterogenous sepsis， and to clarify its potential mechanism based on E2F transcription factor 1 （E2F1）/nuclear factor kappa B （NF-κB） signaling pathway. Methods Sixty SD rats were selected， among which 50 rats were used to establish enterogenous sepsis models by cecal ligation and puncture （CLP）， and the remaining 10 rats were used as sham operation group （only cecal separation without ligation or puncture）. The 40 successfully modeled rats were randomly divided into model group， low dose of DEX group， medium， doses of DEX group， and high dose of DEX group， with 10 rats in each group. The rats in low， medium， and high dose of DEX groups were intraperitoneally injected with 20， 40 and 60 μg·kg^-1 DEX immediately after modeling， while the rats in sham operation group and model group were intraperitoneally injected with the same volume of saline. After 24 h of administration， the intestinal myoelectric activities of the rats in various groups were detected； the colony counts of Escherichia coli， Lactobacillus and Bifidobacterium in cecal contents of the rats in various groups were detected； the pathomorphology of small intestinal tissue of the rats was observed by HE staining； the levels of secretory immunoglobulin A （sIgA） in supernatant of small intestinal tissue homogenate and the levels of diamine oxidase （DAO） and D-lactic acid in serum of the rats in various groups were detected by kit； real-time fluorescence quantitative PCR （RT-qPCR） method was used to detect the mRNA expression levels of macrophage polarization markers in small intestinal tissues of the rats in various groups； Western blotting method was used to detect the protein expression levels of macrophage polarization markers， E2F1， phosphorylated NF-κB p65 （p-NF-κB p65）， and NF-κB p65 in small intestinal tissue of the rats in various groups. Results Compared with sham operation group， the slow wave frequency and amplitude of intestinal smooth muscle of the rats in model group were decreased （P<0.05）； compared with model group， the slow wave amplitude of intestinal smooth muscle of the rats in low dose of DEX groups was increased （P<0.05）， the slow wave frequency and amplitude of intestinal smooth muscle of the rats in medium and high doses of DEX groups were increased （P<0.05）； compared with low dose of DEX group， the slow wave frequency and amplitude of the rats in medium and high doses of DEX groups were increased （P<0.05）； compared with medium dose of DEX group， the slow wave frequency and amplitude of intestinal smooth muscle of the rats in high dose of DEX group were increased （P<0.05）. Compared with sham operation group， the colony count of Escherichia coli in intestinal tract of the rats in model group was increased （P<0.05）， while the colony counts of Bifidobacterium and Lactobacillus were decreased （P<0.05）； compared with model group， the colony count of Bifidobacterium in intestinal tract of the rats in low dose of DEX group was decreased （P<0.05）， the colony count of Escherichia coli in intestinal tract of the rats in medium， and high doses of DEX groups was decreased （P<0.05）， while the colony counts of Bifidobacterium and Lactobacillus were increased （P<0.05）； compared with low dose of DEX group， the colony count of Escherichia coli in intestinal tract of the rats in medium and high dose of DEX groups was decreased （P<0.05）， while the colony counts of Bifidobacterium and Lactobacillus were increased （P<0.05）； compared with medium dose of DEX group， the colony count of Escherichia coli in intestinal tract of the rats in high dose of DEX group was decreased （P<0.05）， while the colony counts of Bifidobacterium and Lactobacillus were increased （P<0.05）. The HE staining results showed that the small intestinal mucosal structure in sham operation group was normal and intact； the small intestinal mucosal epithelial cells in model group were necrotic， with damaged， collapsed and disordered villi； Compared with model groups， the pathological changes of small intestinal tissues in low， medium， and high doses of DEX groups were improved. Compared with sham operation group， the level of sIgA in supernatant of small intestinal tissue homogenate of the rats in model group was decreased （P<0.05）， while the protein expression levels of DAO and D-lactic acid in serum were increased （P<0.05）； compared with model group， the level of DAO in serum of the rats in low dose of DEX groups was decreased （P<0.05）， the level of sIgA in supernatant of small intestinal tissue homogenate of the rats in medium and high doses of DEX groups was increased （P<0.05）， while the protein expression levels of DAO and D-lactic acid in serum were decreased （P<0.05）； compared with low dose of DEX group， the level of sIgA in supernatant of small intestinal tissue homogenate of the rats in medium and high doses of DEX groups was increased （P<0.05）， while the protein expression levels of DAO and D-lactic acid in serum were decreased （P<0.05）； compared with medium dose of DEX group， the level of sIgA in supernatant of small intestinal tissue homogenate of the rats in high dose of DEX group was significantly increased （P<0.05）， while the protein expression levels of DAO and D-lactic acid in serum were decreased （P<0.05）. The RT-qPCR results and Western blotting results showed that compared with sham operation group， the mRNA and protein expression levels of CD86， monocyte chemoattractant protein-1 （MCP-1）， and CD80 in small intestinal tissue of the rats in model group were increased （P<0.05）， while the mRNA and protein expression levels of CD206， interleukin-4 （IL-4） and， CD163 were decreased （P<0.05）； compared with model group， the expression levels of CD80 mRNA， CD86 protein and MCP-1 protein in small intestinal tissue of the rats in low dose of DEX group were decreased （P<0.05）， and the expression levels of IL-4 mRNA， CD163 mRNA， CD206 protein， and CD163 protein were decreased （P<0.05）， the mRNA and protein expression levels of CD86， MCP-1， and CD80 in small intestinal tissue of the rats in medium and high doses of DEX groups were decreased （P<0.05）， while the mRNA and protein expression levels of CD206， IL-4 and CD163 were increased （P<0.05）； compared with low dose of DEX group， the mRNA and protein expression levels of CD86， MCP-1， and CD80 in small intestinal tissue of the rats in medium and high doses of DEX groups were decreased （P<0.05）， while the mRNA and protein expression levels of CD206， IL-4， and CD163 were increased （P<0.05）； compared with medium dose of DEX group， the mRNA and protein expression levels of CD86， MCP-1， and CD80 in small intestinal tissue of the rats in high dose of DEX group were decreased （P<0.05）， while the mRNA and protein expression levels of CD206， IL-4， and CD163 were increased （P<0.05）. The Western blotting results showed that compared with sham operation group， the protein expression level of E2F1 in small intestinal tissue of the rats in model group was decreased （P<0.05）， while the ratio of p-NF-κB p65/NF-κB p65 was increased （P<0.05）； compared with model group， the protein expression levels of E2F1 and ratio of p-NF-κB p65/NF-κB p65 in small intestinal tissue of the rats in low， medium and high doses of DEX groups were decreased （P<0.05）； compared with low dose of DEX group， the protein expression level of E2F1 in small intestinal tissue of the rats in medium and high doses of DEX groups was increased （P<0.05）， while the ratio of p-NF-κB p65/NF-κB p65 was decreased （P<0.05）； compared with medium dose of DEX group， the protein expression level of E2F1 in small intestinal tissue of the rats in high dose of DEX group was increased （P<0.05）， while the ratio of p-NF-κB p65/NF-κB p65 was decreased （P<0.05）. Conclusion DEX can improve the small intestinal mucosal injury in the rats with enterogenous sepsis and promote the polarization of macrophages to M2 type in small intestinal tissues， and its mechanism may be related to the regulation of E2F1/NF-κB signaling pathway by DEX.

Objective To discuss the effect of long non-coding RNA（lncRNA） LINC00973 on the migration， invasion， and distant metastasis of epithelial ovarian cancer， and to clarify its molecular mechanism. Methods The human ovarian cancer SKOV3 and OVCAR3 cells were divided into EF1a-FH empty vector control group （control group）， LINC00973 overexpression group （LINC00973 OE group）， U6-shRNA empty vector control group （SHV group）， and LINC00973 knockdown group （LINC00973 KD group）， and were transfected with lentivirus containing nonsense sequence （pLent-EF1a-FH-CMV-copGFP-P2A-Puro）， LINC00973 overexpression， nonsense sequence （pLent-U6-shRNA-CMV-copGFP-P2A-Puro） and LINC00973 shRNA， respectively， followed by puromycin screening to obtain stably transfected SKOV3 and OVCAR3 cells. Real-time fluorescence quantitative PCR（RT-qPCR） method was used to detect the mRNA expression levels of target genes in the cells in various groups； wound healing assay was used to detect the migration rate of the cells in various groups； Transwell chamber assay was used to detect the number of transmembrane cells in various groups； The mice were divided into control group （WT group）， LINC00973 OE group， and LINC00973 KD group， with 4 mice in each group. SKOV3 wild-type cells， LINC00973 OE cells， and LINC00973 KD cells were intraperitoneally injected into the mice in various groups， respectively， to establish the epithelial ovarian cancer intraperitoneal implantation and metastasis model； HE staining was used to observe the morphology of the colon and liver tissues of the mice in various groups； RNA-secquencing （RNA-seq） was used to analyze the differentially expressed genes between SHV and LINC00973 KD groups in the SKOV3 cell line； RT-qPCR method was used to detect the mRNA expression levels of LINC00973 in the normal ovarian epithelial cells IOSE-80 and epithelial ovarian cancer cells SKOV3， A2780 and OVCAR3， the mRNA expression levels of LINC00973， Vimentin， Snail family transcriptional repressor 1 （Snail）， Twist family basic helix-loop-helix transcription factor 1 （Twist）， zinc finger E-box binding homeobox 1 （ZEB1）， zinc finger E-box binding homeobox 2 （ZEB2）， CXCL8 and matrix metalloproteinase （MMP） 16 in the cells in various groups， and the mRNA expression levels of LINC00973， Vimentin and Twist in liver and colon tissues of the mice in various groups. Results Compared with normal ovarian epithelial cells IOSE-80， the expression level of LINC00973 mRNA in the epithelial ovarian cancer cells SKOV3， OVCAR3 and A2780 was significantly increased （P<0.01）， with the highest expression level of LINC00973 in SKOV3 and OVCAR3 cells， which were therefore selected for subsequent experiments. In SKOV3 and OVCAR3 cells， compared with control group， the expression level of LINC00973 mRNA in the cells in LINC00973 OE group was increased （P<0.01）； compared with SHV group， the expression level of LINC00973 mRNA in the cells in LINC00973 KD group was decreased （P<0.05 or P<0.01）， indicating successful construction of LINC00973 overexpression and knockdown cell lines. In SKOV3 cells， compared with control group， the mRNA expression levels of Vimentin and Twist in LINC00973 OE group were increased （P<0.05 or P<0.01）， while no significant difference was observed in Snail mRNA expression level（P>0.05）； compared with SHV group， the mRNA expression levels of Vimentin， Snail and Twist in LINC00973 KD group were decreased （P<0.01）. In OVCAR3 cells， compared with control group， the mRNA expression levels of Vimentin， Snail and Twist in LINC00973 OE group were increased （P<0.01）； compared with SHV group， the expression levels of Vimentin， Snail， and mRNA Twist in LINC00973 KD group were decreased （P<0.01）. The wound healing assay results showed that compared with control group， the wound healing rates of the SKOV3 and OVCAR3 cells in LINC00973 OE group were significantly increased （P<0.01）； compared with SHV group， the wound healing rates of the cells in LINC00973 KD group were significantly decreased （P<0.01）. The Transwell chamber assay results showed that compared with control group， the numbers of transmembrane cells of the SKOV3 and OVCAR3 cells in LINC00973 OE group were significantly increased （P<0.01）； compared with SHV group， the numbers of transmembrane cells in LINC00973 KD group were significantly decreased （P<0.01）. Compared with WT group， the number of peritoneal nodules in LINC00973 OE group was increased， with rough liver surface and multiple nodules formed on mesentery and colon surface， and the expression levels of LINC00973， Vimentin， and Twist mRNA in colon tissue were increased （P<0.01）； compared with WT group， no nodules were formed in the peritoneal cavity of LINC00973 KD group， with smooth liver surface， no nodules in liver tissue， and decreased expression levels of LINC00973， Vimentin， and Twist mRNA， and no nodules were observed on mesentery and colon surface. The HE staining results showed that compared with WT group， the multiple lesions were observed in liver and colon tissues in LINC00973 OE group， manifested as uneven cell size， irregular shape， unclear cell boundaries， increased nuclear division， and uneven red staining in cytoplasm， while in LINC00973 KD group， the cells in liver and colon tissues were arranged neatly with regular shape， and uniform distribution of nuclei and cytoplasm. The RNA-seq results showed that compared with SHV group， no key signaling pathways related to tumor metastasis were enriched in LINC00973 KD group， and the transcription levels of metastasis-related genes CXCL8， MMP16， ZEB1， and ZEB2 were decreased. The RT-qPCR results showed that compared with control group， the expression levels of ZEB1， ZEB2， CXCL8， and MMP16 mRNA in the cells in LINC00973 OE group were significantly increased （P<0.01）； compared with SHV group， the expression levels of ZEB1， ZEB2， CXCL8， and MMP16 mRNA in the cells in LINC00973 KD group were significantly decreased （P<0.01）. Conclusion LINC00973 can up-regulate the expression of metastasis-related factors Vimentin， Snail， Twist， ZEB1， ZEB2， CXCL8， and MMP16， and promote the migration， invasion， and distant metastasis of epithelial ovarian cancer.

Objective To discuss the role of changes of serum total bile acid （TBA） levels induced by long-term high-fat diet in the occurrence of supraventricular arrhythmia （SVA） in the apolipoprotein E knockout （ApoE^-/-） mice， and to clarify its mechanism. Methods Twenty ApoE^-/- mice were randomly divided into normal diet group and high-fat diet （HFD） group （n=10）； after 20 weeks of feeding， surface electrocardiogram was used to detect cardiac electrophysiology of the mice in various groups； echocardiography was used to detect cardiac systolic function and structure in the mice in various groups； enzyme-linked immunosorbent assay （ELISA） was used to detect serum levels of blood lipids， total bile acid （TBA） and inflammatory factors in the mice in various groups； hematoxylin-eosin （HE） staining was used to detect cardiac inflammatory response in the mice in various groups； Masson staining was used to observe myocardial fibrosis degree in the mice in various groups. Results Compared with normal diet group， 4 cases of junctional premature beat （JPB）/junctional tachycardia （JT）， 1 case of premature atrial contraction （PAC） and 1 case of premature ventricular contraction （PVC） were found in HFD group， while only 1 case of JPB/JT and 1 case of PAC were found in normal diet group. Compared with normal diet group， the heart rate of the mice in HFD group was significantly decreased （P<0.05）； the QRS and QT intervals were significantly prolonged（P<0.05）； the ejection fraction （EF） and fractional shortening （FS） were significantly decreased （P<0.05）； the end-diastolic volume （EDV） was increased （P<0.05）， but there was no significant difference in end-systolic volume（ESV） between groups （P>0.05）； the left ventricular internal diameter at end-diastole （LVIDd） and left ventricular internal diameter at end-systole （LVIDs） were significantly increased （P<0.05）. There were no significant differences in plasma total cholesterol （TC）， triglyceride （TG）， high-density lipoprotein （HDL-c） and low-density lipoprotein （LDL-c） levels and body weight between normal diet group and HFD group （P>0.05）. Compared with normal diet group， the TBA level of the mice in HFD group was significantly increased （P<0.05）. There were no significant differences in interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， monocyte chemoattractant protein-1 （MCP-1）， and C-X-C motif chemokine ligand 1 （CXCL-1） levels between HFD group and normal diet group. Compared with normal diet group， the interleukin-1β （IL-1β） level in HFD group showed an increasing trend， but there was no significant difference between groups （P>0.05）.The HE staining results showed that the inflammatory cell infiltration was similar between HFD group and normal diet group.The Masson staining results showed that compared with normal diet group， the fibrosis of the mice in HFD group showed an increasing trend， but there was no significant difference in myocardial fibrosis area between groups （P>0.05）. Conclusion Long-term high-fat diet may increase serum TBA level in ApoE^-/- mice， which may induce SVA.

Objective To investigate the preventive and therapeutic effects of iridoid glycosides from Boschniakia rossica （IGBR） on precancerous lesions of liver cancer in rats， and to clarify its possible mechanism. Methods Thirty Wistar rats were selected and the precancerous liver lesion model was established using the modified Solt-Faber method. The rats were randomly divided into sham operation group， model group， and IGBR group， and there were 10 rats in each group. The morphology of liver tissue of the rats in various groups were observed； the liver weights， liver indexes and liver regeneration degrees of the rats in various groups were measured； HE staining was used to observe the pathomorphology of liver tissue of the rats in various groups； immunohistochemistry method was used to detect the expression of glutathione-S-transferase（GST）-Pi protein in liver tissue of the rats in various groups； colorimetric method was used to detect the activities of γ-glutamyl transpeptidase （γ-GT）， catalase （CAT）， superoxide dismutase （SOD）， glutathione peroxidase （GSH-Px） and glutathione S-transferase （GST）， and the level of malondialdehyde （MDA） in liver tissue and mitochondria of the rats in various groups； Western blotting method was used to detect the expression levels of α-smooth muscle actin （α-SMA）， collagen type Ⅰ alpha 1 chain （ColⅠα1）， matrix metalloproteinase （MMP） 13， MMP2， tissue inhibitor of metalloproteinase （TIMP） 1， TIMP2， transforming growth factor β1 （TGF-β1）， TGF-β1 receptor （TβR）， mothers against decapentaplegic homolog （Smad） 2/3， Smad4， and Smad7 proteins in liver tissue of the rats in various groups. Results Compared with sham operation group， the liver weight， liver index and degree of liver regeneration of the rats in model group were increased （P<0.05）； compared with model group， the liver weight and liver index of the rats in IGBR group showed a decreasing trend， but the difference was not statistically significant （P>0.05）. The HE staining results showed that the liver lobule structure in sham operation group was intact and clear， with large hepatocytes， abundant eosinophilic cytoplasm， and hepatocytes arranged in single cords radiating from the central vein； there were irregular hepatic sinusoids between plates， with only a small amount of collagen fibers and inflammatory cell infiltration in the portal area， and no degeneration or necrosis of hepatocytes. In model group， the normal arrangement of hepatocytes disappeared， the liver lobule structure was disrupted， small cell hyperplasia （mainly oval cells） was observed in the portal area， with massive collagen deposition and significant fibrous tissue hyperplasia in the fibrous septum； hepatocytes showed extensive degenerative edema， hydropic degeneration or even ballooning degeneration and focal necrosis； basophilic hepatocytes formed proliferative areas with clear cytoplasm， centrally located nuclei and 1-2 prominent nucleoli； glassy hepatocytes with enlarged nuclei and pale transparent cytoplasm were also observed. In IGBR group， the liver lobule structure was basically preserved， with reduced inflammatory lesions， mild edema， and scattered spotty or focal necrosis； nuclear atypia and pathological mitotic figures or binucleation were observed. The immunohistochemistry results showed GST-Pi protein positive foci with brown-yellow cytoplasmic staining in round or oval nodules. The GST-Pi protein positive foci were observed in liver tissue of the rats in model group， indicating successful establishment of precancerous liver lesion model. The scattered GST-Pi protein positive foci were observed in IGBR group， which were significantly reduced compared with model group. Compared with sham operation group， the activity of γ-GT in liver tissue of the rats in model group was increased （P<0.05）； compared with model group， the activity of γ-GT in liver tissue of the rats in IGBR group was decreased （P<0.05）. Compared with sham operation group， the GST activity and MDA level in liver tissue and liver mitochondria of the rats in model group were increased （P<0.05）， while the activities of SOD， CAT， and GSH-Px were decreased （P<0.05）； compared with model group， the GST activity and MDA level in liver tissue and liver mitochondria of the rats in IGBR group were decreased （P<0.05）， while the activities of SOD， CAT， and GSH-PX were increased （P<0.05）. The Western blotting results showed that compared with sham operation group， the expression levels of α-SMA， ColⅠα1， TIMP1， and TIMP2 proteins in liver tissue of the rats in model group were increased （P<0.05）， while the expression levels of MMP13 and MMP2 proteins were decreased （P<0.05）， and the ratios of TIMP1/MMP13 and TIMP2/MMP2 were increased （P<0.05）； compared with model group， the expression levels of α-SMA， ColⅠα1， and TIMP2 proteins in liver tissue of the rats in IGBR group were decreased （P<0.05）， while the expression levels of MMP13 and MMP2 proteins were increased （P<0.05）， and the ratios of TIMP1/MMP13 and TIMP2/MMP2 were decreased （P<0.05）. Compared with sham operation group， the expression levels of TGF-β1 and Smad2/3 proteins in liver tissue of the rats in model group were increased （P<0.05）； compared with model group， the expression levels of TGF-β1， Smad2/3 and Smad 4 proteins in liver tissue of the rats in IGBR group were decreased （P<0.05）. Conclusion IGBR can inhibit precancerous liver lesions and liver fibrosis in rats， and its mechanism may be related to enhancing the antioxidant capacity of liver tissue， inhibiting TGF-β/Smad signaling pathway and regulating TIMP/MMP balance.

Objective To investigate the impact of ginseng alcohol extract （GEE） on improving sleep quality in the aged Drosophila model by regulating the redox balance， and to elucidate its associated mechanism. Methods Thirty-two male drosophila melanogaster （7-days-old） were randomly selected as young group， while 64 male Drosophila melanogaster flies （35-days-old） were randomly assigned to aged model group （n=32） and GEE group （n=32）. The sleep parameters， including total sleep duration， daytime sleep duration， night sleep duration， 0-4 h of sleep duration after lights off （ZT0-4 sleep duration）， deep sleep duration， sleep episodetimes， sleep fragmentation， and the activity parameters such as the total number of locomotor activity daytime locomotor activity amount and nighttime locomotor activity amount were analyzed using the DAM2 Drosophila behavioral analysis system 7 d after administration. The grouping of the drosophila was as above， and there were 100 drosophila ineach group. The differentially expressed proteins in drosophila brain tissue were screened， identified， and functionally analyzed using two-dimensional fluorescence difference gel electrophoresis（2D-DIGE） and matrix-assisted laser desorption/ionization time of flight mass spectrometry（MALDI-TOF/TOF-MS） proteomic methods. The grouping of the drosophila was as above， and there were 100 drosophila in each group.The activities of superoxide dismutase （SOD）， catalase （CAT）， and glutathione peroxidase （GSH-Px） and the levels of lipid peroxidation product （MDA） in brain tissue of the drosophila were determined using assay kits. Results Compared with young group， the total sleep duration daytime sleep duration and night sleep cluration of the drosophila in agaed group were decreased（P<0.05 or P<0.01）； and the sleep rhythm amplitude was shortened. Compared with aged group， the total sleep duration and daytime and nighttime sleep durations of the drosphila in GEE group were lengthened （P<0.01）. Compared with young group， the ZT0-4 sleep duration deep sleep duration and sleep fragment of the drosophila in aged group were decreased （P<0.05 or P<0.01）， and the sleep rhythm amplitude was shortened. Compared with young group， the ZT0-4 sleep duration， deep sleep duration， and single sleep fragment of the drosphila in GEE group were significantly prolonged （P<0.01）， and the sleep amplitude was increased.Compared with young group， there was no significant difference in diurnal spontaneous activity or total spontaneous activity of the drosophila in aged group（P>0.05）， while the nocturnal spontaneous activity was significantly increased （P<0.05）. Compared with aged group， the diurnal spontaneous activity， nocturnal spontaneous activity， and total spontaneous activity of the drosophila in GEE group were significantly decreased （P<0.05 or P<0.01）. A total of 47 differentially expressed proteins were selected in the 2D-DIGE electrophoretic mapping. Compared with young group， the expressions of 47 differentially expressed protein sites in aged group were down-regulated mainly including glutathione S-transferase， peroxiredoxin 1 and dihydrolipoic dehydrogenase， which were related to redox balance. Compared with young group， the activities of SOD， CAT and GSH-Px in brain tissue of the drosophila in aged group were decreased （P<0.05 or P<0.01）， and the level of MDA was increased （P<0.01）； compared with aged group， the activities of SOD， CAT and GSH-Px in brain tissue of the drosphila in GEE group were increased （P<0.05 or P<0.01）， and the MDA level was decreased （P<0.05）. Conclusion GEE has improvement effect on the sleep quality of aged drosophila， and its possible mechanism may be related to upregulating the activities of antioxidant enzymes， inhibiting the accumulation of lipid peroxidation products， and maintaining redox balance.

? Objective To prepare novel dental composite resins using zinc（Zn）- and nitrogen（N）- modified titanium dioxide （TiO?） nanoparticles （NPs） and mesoporous alumina （Al?O?，r type， 20 mm） NPs as reinforcing fillers， systematically evaluating their antibacterial activity， mechanical strength， basic performance， and biosafety to obtain the dental composite resins with excellent antibacterial activity and mechanical strength. Methods Zn-N-TiO? NPs and mesoporous Al?O? NPs were added into a resin matrix at varying mass ratios to prepare five composite resins： control group （no filler）， group 0 （Zn-N-TiO?∶Al?O?=1∶0）， group 1 （Zn-N-TiO?∶Al?O? = 1∶1）， group 2 （Zn-N-TiO?∶Al?O?=1∶2）， and group 3 （Zn-N-TiO?∶Al?O?=1∶3）. Plate colony counting method was used to detect the number of adhered bacteria on composite resin surfaces in various groups and calculate the antibacterial rate； scanning electron microscope （SEM） was used to observe the morphology of adhered bacteria in various groups； universal testing machine was used to measure flexural strength （FS） and elastic modulus （EM） of composite resins in various groups； SEM was used to observe fracture surface morphology of composite resins in various groups； microhardness tester was used to determine Vickers microhardness of the composite resins in various groups； Fourier transform infrared spectroscope was used to detect double bond conversion rate （DC） after 20 s photocuring and calculate curing depth； water contact angle meter was used to measure water contact angle （WCA）， water sorption property （WSP）， and water solubility level （WSL） of composite resins in various groups； cell counting kit-8 （CCK-8） method was used to evaluate relative growth rate （RGR） of the mouse fibroblast L-929 cells cultured in composite resin extracts on days 1， 3， and 5 and determine in vitro cytotoxicity grade. Results The plate colony counting results showed that compared with control group， the colony counts on agar plates in the other groups were significantly reduced， with group 1 showing the lowest count. The SEM images results showed densely distributed and morphologically intact Streptococcus mutans in control group； small clusters of bacteria with depressed cell membranes in group 0 and group 3； sparsely distributed bacteria with obvious membrane shrinkage and cytoplasmic leakage in group 1 and group 2. No statistically significant difference in colony counts was found between group 1 and group 2 （P>0.05）， but both were lower than the other groups （P<0.05）. All the composite resins in experimental groups exhibited >85% antibacterial rates， with group 1 and group 2 exceeding 99%.The composite resins in group 0 showed the lowest FS. With addition of mesoporous Al?O?， the FS of the composite resin in group 1 and group 2 were significantly increased， with the composite resin in group 2 showing the highest FS among all groups. Although the FS of the composite resin in group 3 was lower than that in group 2， but it remained higher than other groups （P<0.05）. The SEM images results showed that in control group， the smooth-surfaced sillicon dioxide （SiO?） particles exhibited clear fracture interfaces with resin matrix， with >50% particle exposure； the composite resin in group 0 showed similar morphology and large Zn-N-TiO? agglomerates with tight filler-matrix bonding； the composite resin in group 1， 2， and 3 showed resin adhesion to SiO? surfaces （<50% particle exposure） and uneven fracture surfaces. Fractured SiO? spheres were observed in group 2. Filler distribution was uniform in group 1 and group 2， while the minor NP agglomeration occurred in group 3. The composite resin in control group showed the lowest EM. The EM was significantly improved in experimental groups， with group 3 having the highest value. Group 0 exhibited the lowest Vickers microhardness， showing statistically significant differences among other groups （P<0.05）. The Vickers microhardness of the composite resion was gradually increased with the rising of Al?O? content.The resins in group 2 and group 3 achieved >45 HV hardness， representing increases of 29.73% and 33.82% compared with control group， and 51.34% and 56.28% compared with group 0. No significant differences in DC of the composite resin were found among groups （P>0.05）. The depth of cure for all composite resin groups exceeded 4 mm， with no significance differences observed between various groups （P>0.05）. The composite resin in group 0 showed the smallest WCA. The hydrophobicity of the composite resion was increased with the rising of Al?O? content， but all the WCA values remained <80°. The composite resin in group 3 had the largest WCA without statistical significance compared with group 2 （P>0.05）. Filler incorporation reduced the water sorption/solubility. The composite resin in the CCK-8 assay results showed the composite resins in all groups had RGR>75%， meeting in vitro safety standards. Conclusion Reinforcing fillers impart superior antibacterial activity and mechanical properties to composite resins. Under experimental conditions， group 2 composite resin achieves optimal comprehensive performance in antibacterial efficacy and mechanical strength， demonstrating promising clinical application potential.

Objective To observe the effects of recombinant human growth hormone （rh-GH） on depressive-like behavior in mice with chronic restraint stress （CRS）， and to discuss its possible mechanism. Methods The CRS method was used to establish an animal model of depression； a total of 45 mice were didided into control group （non-modeled， n=15）， and CRS model group （modeled， n=30） the sucrose preference test （SPT） was used to detect the sucrose preference rate of the mice； the tail suspension test （TST） was used to detect the immobility time of the mice； the open field test （OFT） was used to detect the total moving distance of the mice within 5 min and the time spent in the central area. The CRS mice were randomly divided into CRS model+saline group and CRS model+rh-GH group（n=10）； the mice in CRS model+saline group were injected with normal saline； the mice in CRS model+rh-GH group were subcutaneously injected with rh-GH daily for 1 month； the peripheral blood of the mice was collected before and after intervention to detect the expression levels of growth hormone （GH） and insulin-like growth factor Ⅰ （IGF-Ⅰ） proteins in serum； after all behavioral experiments， the hippocampus tissue was taken to detect the expression level of synapsin-1 （SYN-1） protein in the tissue of the mice. Results Compared with control group， the body weight of the mice in CRS model group was significantly decreased （P<0.01）， the sucrose preference rate in SPT was significantly decreased （P<0.01）， the immobility time in TST was significantly prolonged （P<0.01）； in OFT， the total moving distance of mice showed no significant change （P>0.05）， while the time spent in the central area was significantly shortened （P<0.05）. Compared with control group， the expression levels of GH and IGF-Ⅰ proteins in serum of the mice in CRS model group were significantly decreased （P<0.01）. Compared with CRS model+saline group， the sucrose preference rate in SPT of the mice in CRS model+rh-GH group was significantly increased （P<0.01）， the immobility time in TST was significantly shortened （P<0.05）， the total moving distance in OFT showed no significant difference （P>0.05）， and the time spent in the central area was significantly increased （P<0.01）. Compared with model+saline group， the expression levels of GH and IGF-I proteins in serum of the mice in CRS model+rh-GH group were significantly increased （P<0.01）. Compared with model group， the expression level of SYN-1 protein in hippocampus tissue of mice in drug-treated model group was significantly increased （P<0.05）. Conclusion rh-GH has ameliorative effects on depressive-like behavior induced by chronic restraint stress in mice， and its mechanism may be associated with regulation of the GH/IGF-Ⅰ axis and increased expression of SYN-1 in hippocampus tissue.

Objective To discuss the effect of quorum sensing-related gene expression on biofilm formation and drug resistance in clinically multidrug-resistant Pseudomonas aeruginosa， and to clarify the mechanism of enhacing drug resistance. Methods A total of 77 strains of Pseudomonas aeruginosa were collected. Based on drug resistance， the strains were divided into multidrug-resistant group and sensitive group. The optimal biofilm formation conditions were determined using the microtiter plate method； biofilm formations of the stains in both groups was observed under an optical microscope； crystal violet staining was used to semiquantitatively detect biofilm formation ability of P. aeruginosa in both groups； microbroth dilution method was used to determine the minimal inhibitory concentration （MIC） values of the quorum sensing inhibitor （C-30） against Pseudomonas aeruginosa in both groups； RNA was extracted from two groups using a commercial kit， while RNA from planktonic state and biofilm state of multidrug-resistant strains was extracted using modified TRIzol method； real-time fluorescence quantitative PCR （RT-qPCR） method was used to detect the mRNA expression levels of quorum sensing-related genes （lasR/I， RhlR/I， PqsR/A） of the stains in multidrug-resistant group and sensitive group， as well as before and after adding the quorum sensing inhibitor C-30. Results Among 77 strains of Pseudomonas aeruginosa， 56 were multidrug-resistant （multidrug-resistant group） and 21 were fully sensitive（sensitive group）. Optimal biofilm formation occurred at a bacterial concentration of 1.5×10⁸ CFU·mL^-1 with 48 h incubation. The biofilm positivity rate was 91%， with strongly positive， moderately positive， weakly positive， and negative biofilms accounting for 16%， 34%， 41%， and 9%， respectively. The biofilm positivity rate in multidrug-resistant strains was 96%， and biofilm formation ability in multidrug-resistant group was higher than that in sensitive group （P<0.05）. When the concentration of C-30 was 8 mg·L^-1 the biofilm formation in most Pseudomonas aeruginosa was inhibited， with enhanced suppression at higher concentrations. The absorbtion （A） value of both planktonic-state and biofilm-state RNA ranged from 1.8 to 2.0. The RT-qPCR results showed that compared with planktonic state， the expression levels of lasR/I， RhlR/I， and PqsR/A mRNA of the stains in biofilm state were significantly increased （P<0.01）. Compared with non-inhibitor group， the expression levels of lasR/I， RhlR/I， and PqsR/A mRNA in biofilm state of inhibitor-treated group were significantly decreased （P<0.01）. Conclusion High expression of quorum sensing-related genes in multidrug-resistant P. aeruginosa promotes biofilm formation， thereby enhancing drug resistance.

Objective To discuss the ameliorative effect of total flavonoids from corn silk （TFCS） on kidney injury in the rats with urate nephropathy， and to clarify the possible mechanism. Methods Sixty male Wistar rats were randomly divided into control group， model group， positive control group ［benzbromarone（BZM） group， 5 mg·kg^-1·d^-1］， low dose of TFCS group （20 mg·kg^-1·d^-1）， medium dose of TFCS group （40 mg·kg^-1·d^-1）， and high dose of TFCS group （80 mg·kg^-1·d^-1）， and there were 10 rats in each group. Except for control group， the rats in the other groups were administered potassium oxonate （350 mg·kg^-1） and adenine （70 mg·kg^-1） by gavage for 4 weeks to establish the hyperuricemic nephropthy models. The rats in different doses of TFCS groups were treated with TFCS for 2 weeks. Speckle blood flow imager was used to detect the renal blood perfusion of the rats in various groups and the kidney coefficients of the rats in various groups were caculated； HE staining and Masson staining were used to observe the pathomorphology and fibrosis degrees of kidney tissue of the rats in various groups and enzyme-linked immunosorbent assay（ELISA） method was used to detect the levels of uric acid （UA）， creatinine （Cr）， blood urea nitrogen （BUN）， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） in the serum and levels of β2-microglobulin （β₂-MG） and microalbumin （ALB） in the urine of the rats in various groups； Western blotting method was used to detect the expression levels of urate transporter 1 （URAT1）， glucose transporter 9 （GLUT9）， and ATP-binding cassette transporter G2 （ABCG2） proteins in kidney tissue of the rats in various groups. Results Compared with control group， the renal blood perfusion volume of the rats in model group was significantly decreased （P<0.01）. Compared with model group， the renal blood perfusion volumes of the rats in BZM group and low， medium， and high doses of TFCS groups were significantly increased （P<0.05 or P<0.01）. Compared with control group， the kidney weight of the rats in model group was increased， with visible white granular spots on the surface， absence of blood color， and kidney volume was increased. Compared with model group， the kidney volumes of the rats in BZM group and medium and high doses of TFCS groups were decreased， with color tending toward that in control group， and the white granular spots on the surface were significantly reduced. Compared with model group， the kidney coefficients of the rats in BZM group and medium and high doses of TFCS groups were decreased （P<0.01）. The HE staining results showed there were no abnormalities in kidney tissue structure in control group， while there were a small amount of brown-yellow urate crystal deposition and interstitial connective tissue hyperplasia in model group； compared with model group， the kidney tissue damage and inflammatory infiltration were alleviated to varying degrees in BZM group and different doses of TFCS groups. The Masson staining results revealed no obvious collagen fiber deposition in control group， whereas significant blue collagen fiber deposition in kidney tissue of the rats was found in model group， and the collagen volume fraction （CVF） was increased compared with control group （P<0.01）； compared with model group， the CVFs of the rats in BZM group and different doses of TFCS groups were decreased （P<0.01）. The ELISA results showed that compared with control group， the levels of UA， Cr， BUN， IL-6， and TNF-α in serum of the rats in model group were increased （P<0.01）； compared with model group， the levels of UA， Cr， BUN， IL-6， and TNF-α in serum of the rats in BZM group and medium and high doses of TFCS groups were decreased （P<0.01）. Compared with control group， the levels of β₂-MG and ALB in urinary in model group were increased （P<0.01）； compared with model group， the levels of β₂-MG and ALB in urinary of the rats in different doses of TFCS groups were decreased （P<0.05 or P<0.01）. The Western blotting results showed that compared with control group， the expression levels of URAT1 and GLUT9 proteins in kidney tissue of the rats in BZM group and model group were increased （P<0.01）， while the expression level of ABCG2 protein was decreased （P<0.01）. Compared with model group， the expression levels of URAT1 and GLUT9 proteins in kidney tissue of the rats in different doses of TFCS groups were decreased （P<0.05 or P<0.01）， and the expression level of ABCG2 protein was increased （P<0.01）. Conclusion TFCS can significantly alleviate the kidney injury in the rats with urate nephropathy model， and its mechanism may be related to the downregulation of expression of URAT1 and GLUT9 proteins and upregulation of ABCG2 protein expression in kidney tissue.

Objective To discuss the effect of microRNA-34a-5p （miR-34a-5p） on the neuron apoptosis in hippocampus tissue of the rats with temporal lobe epilepsy， and to clarify its mechanism. Methods Fifty-two male SD rats were randomly divided into control group， model group， miR-34a-5p inhibitor group， and inhibitor negative control group， and there were 13 rats in each group. The PONEMAH 6.X experimental animal telemetry platform was used to record the electroencephalogram （EEG） of the rats in various groups； real-time fluorescence quantitative PCR （RT-qPCR） was used to detect the expression levels of miR-34a-5p in hippocampus tissue of the rats in various groups； HE staining was used to observe the morphology of hippocampus tissue of the rats in various groups； TUNEL method was used to detect the apoptotic rates of neurons in hippocampus tissue of the rats in various groups； immunohistochemistry method was used to determine the positive expression rates of CDK6， p-Rb， and E2F1 proteins in hippocampus tissue of the rats in various group； Western blotting method was used to detect the expression levels of cyclin-dependent protein kinase 6 （CDK6）， phosphorylated retinoblastoma protein （p-Rb）， and E2F transcription factor 1 （E2F1） proteins in hippocampus tissue of the rats in various groups. Results No abnormalities were observed in the rats in control group； the rats in model group， miR-34a-5p inhibitor group， and inhibitor negative control group exhibited varying degrees of drooling， trembling， bloody tears， staring， chewing tremors， followed by nodding and blinking， and finally forelimb convulsions， standing upright， and falling. Compared with control group， the total duration of epileptic seizures of the rats in model group was significantly prolonged （P<0.01）； compared with model group， the total duration of epileptic seizures of the rats in miR-34a-5p inhibitor group was shortened （P<0.01）； compared with miR-34a-5p inhibitor group， the total duration of epileptic seizures of the rats in inhibitor negative control group was prolonged （P<0.01）. The RT-qPCR results showed that compared with control group， the expression level of miR-34a-5p in hippocampus tissue of the rats in model group was increased （P<0.01）； compared with model group， the expression level of miR-34a-5p in hippocampus tissue of the rats in miR-34a-5p inhibitor group was increased （P<0.05）； compared with miR-34a-5p inhibitor group， the expression level of miR-34a-5p in hippocampus tissue of the rats in inhibitor negative control group was increased （P<0.01）. The HE staining results showed that compared with control group， the cell arrangement in model group was disordered； compared with model group， the cell arrangement in miR-34a-5p inhibitor group was orderly； compared with miR-34a-5p inhibitor group， the cell morphology in inhibitor negative control group was irregular. The TUNEL staining results showed that compared with control group， the apoptotic rate of neurons in CA1 region of hippocampus tissue of the rats in model group was increased （P<0.01）； compared with model group， the apoptotic rate of neurons in CA1 region of hippocampus tissue of the rats in miR-34a-5p inhibitor group was decreased （P<0.05）； compared with miR-34a-5p inhibitor group， the apoptotic rate of neurons in CA1 region of hippocampus tissue of the rats in inhibitor negative control group was increased （P<0.05）. The immunohistochemistry results showed that compared with control group， the positive expression rates of CDK6， p-Rb and E2F1 proteins in hippocampus tissue of the rats model group were increased （P<0.05 or P<0.01）； compared with model group， the positive expression rates of CDK6， p-Rb and E2F1 proteins in hippocampus tissue of the rats in miR-34a-5p inhibitor group were decreased （P<0.05）； compared with miR-34a-5p inhibitor group， the positive expression rates of CDK6， p-Rb and E2F1 proteins in hippocampus tissue of the rats in inhibitor negative group were increased （P<0.05 or P<0.01）.The Western blotting results showed that compared with control group， the expression levels of CDK6， p-Rb， and E2F1 proteins in hippocampus tissue of the rats in model group were increased （P<0.01）； compared with model group， the expression levels of CDK6， p-Rb， and E2F1 proteins in hippocampus tissue of the rats in miR-34a-5p inhibitor group were decreased （P<0.05 or P<0.01）； compared with miR-34a-5p antagomir group， the expression levels of CDK6， p-Rb， and E2F1 proteins in hippocampus tissue of the rats in inhibitor negative control group were increased （P<0.05 or P<0.01）. Conclusion The expression of miR-34a-5p is upregulated in the hippocampal tissue of temporal lobe epilepsy rats， and hippocampal neuron apoptosis is increased. Inhibition of miR-34a-5p expression can reduce the hippocampal neuron apoptotic rate， and its mechanism may be related to the regulation of CDK6， p-Rb， and E2F1 protein expressions in the hippocampus tissue by miR-34a-5p.

Objective To discuss whether safranal affects the proliferation， migration， and phenotypic transformation of the vascular smooth muscle cells （VSMCs） in a high-glucose environment and to clarify the function of safranal in the prevention and treatment of diabetic （DM） vascular complications.? Methods The SD rats were selected as experimental subjects； primary VSMCs were cultured from rat thoracic aortas and divided into control group， 25 mmol·L^-1 high glucose （HG） group， HG+ 20 μmol·L^-1 safranal group， HG+40 μmol·L^-1 safranal group， and HG+80 μmol·L^-1 safranal group. The cells in control group received no treatment； the cells in 25 mmol·L^-1 HG group were pretreated with 25 mmol·L^-1 HG； the cells in HG+20， 40， and 80 μmol·L^-1 safranal groups were further treated with 20， 40， and 80 μmol·L^-1 safranal respectively for 48 h on the basis of 25 mmol·L^-1 HG group. Cell counting kit-8 （CCK-8） method was used to determine the appropriate concentration of safranal and detect the viabilities of the VSMCs in various groups； cell scratch healing assay was used to detect the scratch healing rates of the VSMCs in various groups； Transwell chamber assay was used to detect the numbers of the migration VSMCs in various groups； immunofluorescence method was used to detect the fluorescence intensities of alpha-smooth muscle actin （α-SMA） and rabbit anti-osteopontin （OPN） in the VSMCs in various groups； Western blotting method was used to detect the expression levels of OPN， α-SMA， and proliferating cell nuclear antigen （PCNA） in the VSMCs in various groups. Results Under microscope， on the 4th day of in vitro culture， the spindle-shaped or triangular cells crawled out from the edge of the thoracic aorta tissue blocks， with long spindle being the most common morphology. On the 14th， the cells gradually covered the bottom of the dish； when cell density reached 80%-90%， the characteristic “hills and valleys” growth pattern appeared. Third-generation cells were taken for immunofluorescence identification； immunofluorescence staining with VSMC-specific marker α-SMA showed positive expression of α-SMA protein in the primarily cultured VSMCs. The CCK-8 assay results showed that compared with control group， the cell viability of the cells in 160 μmol·L^-1 safranal group was significantly decreased （P<0.01）， indicating toxic damage to the cells. Under the conditions of safranal concentrations at 20， 40， and 80 μmol·L^-1 respectively， after 48 h intervention on VSMCs， no significant adverse effect on cell viability was observed； considering both the effect and toxicity of safranal， these three concentrations were used in subsequent cell experiments. After 48 h intervention， compared with control group， the activity of the VSMCs in 25 mmol·L^-1 HG group was increased （P<0.001）； compared with 25 mmol·L^-1 HG group， the activities of the VSMCs in HG+20， 40， and 80 μmol·L^-1 safranal groups were gradually decreased （P<0.05）. The cell scratch healing assay and Transwell assay results showed that after 48 h intervention， the scratch healing rate of the VSMCs in 25 mmol·L^-1 HG group was significantly higher than that in control group （P<0.01）， and the number of transmembrane cells through the Transwell chamber was significantly increased （P<0.05）； compared with 25 mmol·L^-1 HG group， the scratch healing rates of the VSMCs in HG+20， 40， and 80 μmol·L^-1 safranal groups were gradually decreased （P<0.05）， and the number of transmembrane cells was decreased （P<0.05）. The immunofluorescence staining results showed that compared with control group， the fluorescence intensity of α-SMA protein in the VSMCs in 25 mmol·L^-1 HG group was significantly weakened（P<0.001）， while the fluorescence intensity of OPN protein was significantly enhanced （P<0.001）； compared with 25 mmol·L^-1 HG group， the fluorescence intensities of α-SMA protein in the VSMCs in HG+20， 40， and 80 μmol·L^-1 safranal groups were gradually increased （P<0.05）， and the fluorescence intensities of OPN were gradually weakened （P<0.05）. The Western blotting method results showed that compared with control group， the expression level of α-SMA protein in the VSMCs in 25 mmol·L^-1 HG group was decreased （P<0.05）， and the expression levels of PCNA and OPN proteins were increased （P<0.01）； compared with 25 mmol·L^-1 HG group， the expression level of α-SMA protein in the VSMCs in HG+20， 40， and 80 μmol·L^-1 safranal groups were increased （P<0.05）， and the expression levels of PCNA and OPN proteins were decreased （P<0.05）. Conclusion Safranal can inhibit the proliferation， migration， and phenotypic transformation of the VSMCs induced by high glucose.

Objective To discuss the effect of long non-coding RNA （lncRNA） DUXAP8 in exosomes （Exo） derived from the lung cancer A549 cells on the growth and immune escape of the lung cancer cells， and to clarify the mechanism. Methods The human lung cancer cell line A549 was cultured， and its exosomes were extracted and identified. The A549 cells were treated with PKH67-labeled Exo to observe the uptake of Exo by A549 cells. Real-time fluorescence quantitative PCR （RT-qPCR） method was used to detect the expression level of lncRNA DUXAP8 in A549 cells before and after Exo treatment. The A549 cells were divided into control group （no treatment）， Exo group （A549 cells treated with Exo）， Exo+sh-NC group （A549 cells treated with Exo and then transfected with sh-NC）， and Exo+ sh-DUXAP8 group （A549 cells treated with Exo and then transfected with sh-DUXAP8）. RT-qPCR method was used to detect the expression level of lncRNA DUXAP8 in A549 cells in various groups； colony formation assay was used to detect the colony formation abilities of the A549 cells in various groups； 5-ethynyl-2'-deoxyuridine （EdU） staining method was used to detect the proliferation abilities of the A549 cells in various groups. After co-culturing A549 cells in various groups with human peripheral blood lymphocytes， flow cytometry was used to detect the percentages of activated CD8+ T lymphocytes in the human peripheral blood lymphocytes in various groups； 3-（4，5-dimethylthiazol-2-yl）-2， 5-diphenyltetrazolium bromide （MTT） method was used to detect the killing rates of human peripheral blood lymphocytes on the A549 cells in various groups. Results The diameter of Exo vesicles was 50-150 nm， and the exosome-specific marker proteins cluster of differentiation 63（CD63）， cluster of differentiation 9（CD9）， tumor susceptibility gene 101（TSG101）， and heat shock protein 70（HSP70） were positively expressed， indicating successful exosome extraction. A549 cells efficiently took up PKH67-labeled Exo. The RT-PCR results showed that compared with A549 cells cultured alone， the expression level of lncRNA DUXAP8 in the A549 cells was increased after treatment with Exo derived from A549 cells （P<0.05）. compared with control group， the expression level of lncRNA DUXAP8 in the A549 cells in Exo group was increased （P<0.05）； compared with Exo group， the expression level of lncRNA DUXAP8 in the A549 cells in Exo+sh-DUXAP8 group was decreased （P<0.05）， while there were no significant difference in the expression level of IncRNA DUXAP8 in the cells in Exo+sh-NC group （P>0.05）. The colony formation assay results showed that compared with control group， the number of colony formation of the A549 cells in Exo group was increased （P<0.05）； compared with Exo group， the number of colony formation of the A549 cells in Exo+sh-DUXAP8 group was decreased （P<0.05）， while there was no significant difference in the number of colony formation of the A549 cells in Exo+sh-NC group （P>0.05）. The EdU staining results showed that compared with control group， the EdU-positive rate of the A549 cells in Exo group was increased （P<0.05）； compared with Exo group， the EdU-positive rate in A549 cells in Exo+sh-DUXAP8 group was decreased （P<0.05）， while there was no significant difference in the EDU-positive rate in the cells in Exo+sh-NC group （P>0.05）. The flow cytometry results showed that compared with control group， the percentage of activated CD8+T lymphocytes in the human peripheral blood lymphocytes in Exo group was decreased （P<0.05）； compared with Exo group， the percentage of activated CD8+T lymphocytes in the human peripheral blood lymphocytes in Exo+ sh-DUXAP8 group was increased （P<0.05）， while there was no significant difference in the percentage of activated CD8+T lymphaytes in Exo+sh-NC group （P>0.05）. The MTT assay results showed that compared with control group， the killing rate of human peripheral blood lymphocytes on the A549 cells in Exo group was decreased （P<0.05）； compared with Exo group， the killing rate of human peripheral blood lymphocytes on A549 cells in Exo+sh-DUXAP8 group was increased （P<0.05）， while no significant difference was observed in Exo+sh-NC group （P>0.05）. Conclusion The lncRNA DUXAP8 in exosomes derived from the lung cancer A549 cells promotes the proliferation of lung cancer cells and tumor immune escape.

Objective To discuss the protective effect of TUG-891 on ischemic stoke（IS） induced by ischemia-hypoxia， and to clarify its potential mechanism. Methods A total of 60 healthy male C57BL/6 mice were randomly divided into sham operation group（ n=20）， model group ［distal middle cerebral artery occlusion（dMCAO） group， n=20］， and model+TUG-891 group （dMCAO+TUG-891 group， n=20）. After modeling， the mice were intraperitoneally injected with TUG-891 solution （35 mg·kg?1·d?1） for 3 consecutive days. Modified neurological severity score （mNSS） and rotarod test were used to evaluate the neurological function of the mice in various groups； 2，3，5-triphenyltetrazolium chloride （TTC） staining was used to observe the cerebral infarction volumes of the mice in various groups； biochemical method was used to detect the malondialdehyde （MDA） level and superoxide dismutase （SOD） activity in the supernatant of brain tissue of the mice in various groups； Hematoxylin-Eosin （HE） and NISSL staining were used to observe the pathomerphology of brain tissue of the mice in various groups； terminal deoxynucleotidyl transferase dUTP nick-end labeling （TUNEL） staining was used to detect the apoptotic indexes of neuronal cells in brain tissue of the mice in various groups； Western blotting method was used to detect the expression levels of glucose-regulated protein 78 （GRP78）， protein kinase R-like endoplasmic reticulum kinase （PERK）， phosphorylated PERK （p-PERK）， and C/EBP homologous protein （CHOP） proteins in brain tissue of the mice in various groups. Results The mNSS and rotarod test results shoued that compared with sham operation group， the mNSS of the mice in dMCAO group was significantly increased （P<0.01）， and the time on the rod was significantly decreased （P<0.01）； compared with dMCAO group， the mNSS of the mice in dMCAO+TUG-891 group was decreased （P<0.05）， and the time on the rod was increased （P<0.05）. The TTC staining results shoued that compared with sham operation group， the volume of white infarct foci in the cerebral cortex of the mice in dMCAO group was increased （P<0.01）； compared with dMCAO group， the cerebral infarction volume of the mice in dMCAO+TUG-891 group was significantly decreased （P<0.01）. The HE staining results showed that compared with sham operation group， the cortex of the mice in dMCAO group was severely damaged， manifested by disordered arrangement of neuronal cells and obvious nuclear pyknosis in the infarct area， and the morphology of cortical infarct area of the mice in dMCAO+TUG-891 group was improved； the NISSL staining results showed that the Nissl bodies in the cortical infarct area of the mice in dMCAO group became thinner， elongated， and lost more. The pathological damage of brain tissue of the mice in dMCAO+TUG-891 group was significantly improved. Compared with sham operation group， the MDA level in brain tissue of the mice in model group was significantly increased （P<0.01）， and the SOD activity was decreased （P<0.01）； compared with model group， the MDA level in brain tissue of the mice in TUG-891 group was significantly decreased （P<0.01）， and the SOD activity was significantly increased （P<0.01）. The TUNEL staining results showed that compared with sham operation group， the apoptotic index of neuronal cells in brain tissue of the mice in dMCAO group was increased （P<0.01）； compared with dMCAO group， the apoptotic index of neuronal cells in brain tissue of the mice in dMCAO+TUG-891 group was decreased （P<0.01）. Compared with sham operation group， the expression levels of GRP78， p-PERK， and CHOP proteins in brain tissue of the mice in dMCAO group were increased （P<0.05）； compared with dMCAO group， the expression levels of GRP78， p-PERK， and CHOP proteins in brain tissue of the mice in dMCAO+TUG-891 group were decreased （P<0.05）. Conclusion TUG-891 can alleviate neurological injury caused by ischemic stroke， and its mechanism may be related to the inhibition of endoplasmic reticulum stress and apoptosis.

Objective To discuss the regulatory effect of lutein on the phosphatidylinositol-3-kinase （PI3K）/protein kinase B （AKT） signaling pathway and chondrocyte autophagy in mandibular joint cartilage tissue of rabbits with traumatic temporomandibular joint ankylosis （TMJA）， and to clarify its mechanism. Methods Thirty-two male New Zealand white rabbits were divided into sham operation group， model group， lutein group， and 3-MA （PI3K/AKT signaling pathway inhibitor） + lutein group， and there were 8 rabbits in each group. The rabbit model of TMJA was established in model group， lutein group， and 3-MA+lutein group， while the rabbits in sham operation group only underwent tissue exposure without surgery. The rabbits in lutein group were administered 10 mg·kg^-1 lutein， and those in 3-MA+lutein group were administered 15 mg·kg^-1 3-MA and 10 mg·kg?1 lutein. All the drugs were injected via the marginal ear vein starting 24 h after surgery， once a week for 3 consecutive months. After completion， the cartilage tissue on the surgical side was collected. HE staining was used to evaluate the patho morphology of the mandibular joint cartilage tissue of the rabbits in various groups； Western blotting method was used to detect the expression levels of PI3K， AKT， phosphorylated AKT （p-AKT）， Beclin-1， autophagy-related protein 5 （ATG5）， microtubule-associated protein 1 light chain 3-Ⅰ （LC3-Ⅰ）， microtubule-associated protein 1 light chain 3-Ⅱ（LC3-Ⅱ）， autophagy receptor protein （P62）， matrix metalloproteinase 13 （MMP-13）， a disintegrin and metalloproteinase with thrombospondin motifs-5 （ADAMTS-5）， aggrecan， and type Ⅱ collagen （Col Ⅱ） proteins in temporomandibular joint cartilage tissue of the rabbits in various groups； transmission electron microscopy was used to detect the numbers of autophagosomes in temporomandibular joint cartilage tissue of the rabbits in various groups. Results Compared with sham operation group， the pathological score of mandibular joint cartilage tissue of the rabbits in model group was increased （P<0.05）. The Western blotting results showed that compared with sham operation group， the expression levels of PI3K， p-AKT， aggrecan， and Col Ⅱ proteins in mandibular joint cartilage tissue of the rabbits in model group were decreased （P<0.05）， while the expression levels of Beclin-1， ATG5， P62， MMP-13， ADAMTS-5 proteins and ratio of LC3-Ⅱ/LC3-Ⅰ were increased （P<0.05）. Compared with model group， the expression levels of PI3K， p-AKT， aggrecan， and Col Ⅱ proteins in mandibular joint cartilage tissue of the rabbits in lutein group were increased （P<0.05）， while the expression levels of Beclin-1， ATG5， P62 protein and ratio of LC3-Ⅱ/LC3-Ⅰ were decreased （P<0.05）. Compared with lutein group， the expression levels of PI3K， p-AKT， Beclin-1， ATG5， and ratio of LC3-Ⅱ/LC3-Ⅰ， and P62 proteins in mandibular joint cartilage tissue of the rabbits in 3-MA+ lutein group were decreased （P<0.05）， while the expression levels of MMP-13 and ADAMTS-5 proteins were increased （P<0.05）， and the expression levels of aggrecan and Col Ⅱ proteins were decreased （P<0.05）. The transmission electron microscope observation results showed that compared with sham operation group， the number of autophagosomes in temporomandibular joint cartilage tissue of the rabbits in model group was increased （P<0.05）； compared with model group， the number of autophagosomes in temporomandibular joint cartilage tissue of the rabbits in lutein group was decreased （P<0.05）； compared with lutein group， the number of autophagosomes in temporomandibular joint cartilage tissue of the rabbits in 3-MA+lutein group was decreased （P<0.05）. Conclusion Lutein improves the mandibular joint cartilage tissue damage in the TMJA rabbits by regulating the PI3K/AKT signaling pathway and chondrocyte autophagy.

Objective To discuss the promotive effect of nerve growth factor （NGF）， which is highly expressed in the adipose-derived stem cell （ADSC）-induced Schwann-like cells （SCLCs）， on the growth of dorsal root ganglion （DRG） cell processes in the rats， and to clarify its mechanism. Methods The ADSCs were extracted from the epididymal adipose tissue of the SD rats， and their multidirectional differentiation potential was identified through osteogenic， adipogenic， and chondrogenic induction. The ADSCs were induced to differentiate into the SCLCs， and the expression levels of glial fibrillary acidic protein （GFAP） and S100 calcium-binding protein β （S100β） protein in the ADSCs and SCLCs were detected by immunofluorescence staining and Western blotting methods. The DRG cells were isolated and cultured， and immunofluorescence staining was used to detect the βⅢ-tubulin expression in the DRG cells for identification. The SCLCs were co-cultured with the DRG cells（co-culture group）， the single-culture DRG cells were regared as DRG group and toluidine blue staining was used to observe and measure the length of DRG cell processes under the optical microscope in co-culture group and DRG group. Small interfering RNA （siRNA） transfection was used to knock down NGF， and plasmid transfection was used to over-express NGF. Real-time fluorescence quantitative PCR （RT-qPCR） method was used to detect the NGF mRNA expression levels in the cells in various groups； enzyme-linked immunosorbent assay （ELISA） method was used to detect the NGF protein levels in the cell supernatants. The transfected SCLCs were co-cultured with DRG cells and divided into control group， siNC/vector group， NGF knockdown group （si-NGF group）， and NGF over-expression group （oe-NGF group）. The lengths of DRG cell processes in various groups were observed. Results The primary ADSCs adhered within 24 h after seeding， with a small number of lipid droplets remaining. After 3 d of culture， the cells were mostly short spindle-shaped， fusiform， or polygonal， growing rapidly in a vortex pattern. After passaging， the cells exhibited a uniform morphology， appearing as long spindles arranged in a fish-school pattern. After 14 d of adipogenic induction， the cell morphology changed from spindle-shaped to flat-round， with translucent lipid droplets forming in the cytoplasm， which were stained red by Oil Red O. After 28 d of osteogenic induction， the cells appeared sand-like with blurred morphology， and calcified nodules were observed， which were stained red by Alizarin Red and deposited in the extracellular matrix. After 28 d of chondrogenic induction in a 3D culture system， millet-sized chondrogenic spheres formed. Frozen sections of the spheres were stained with Alcian Blue， and acidic mucopolysaccharides in the cartilage tissue were stained blue under the microscope. Under the fluorescence microscope， the third-passage purified ADSCs showed positive expression of CD29 ［fluorescein isothiocy anate（FITC）-labeled green fluorescence］ and CD44 （Cy3-labeled red fluorescence）. The immunofluorescence staining results showed that GFAP was labeled with FITC （green fluorescence）， and S100β was labeled with Cy3 （red fluorescence）. The Western blotting results showed that compared with ADSCs， the expression levels of S100β and GFAP proteins in the SCLCs were increased （P<0.05）. The primary DRG cells began to adhere 6 h after conventional culture， and after 3 d， the cell bodies appeared round and bright， with two linear processes extending from them. Under fluorescence microscope， the cells positively expressed the neuron-specific marker βⅢ-tubulin， confirming that the isolated cells were DRG cells. Compared with the ADSCs， the NGF protein expression level in the SCLCs was increased （P<0.05）. Compared with DRG group， the length of DRG cell processes in co-culture group was the highest when DRG cells and SCLCs were co-cultured at a 1∶2 ratio （P<0.05）. The RT-qPCR results showed that compared with si-NC group， the expression levels of NGF mRNA in the cell supernatant in si-NGF-1， si-NGF-2， and si-NGF-3 groups were significantly decreased （P<0.05）， with si-NGF-1 showing the highest knockdown efficiency， which was selected for subsequent experiments. The ELISA results showed that compared with si-NC group， the NGF levels in the cell supernatant of si-NGF-1， si-NGF-2， and si-NGF-3 groups were decreased （P<0.05）. Compared with Vector group， the expression level of NGF mRNA and NGF protein level in the supernatant in oe-NGF group were increased （P<0.05）. Compared with control group and siNC/vector group， the length of DRG cell processes in si-NGF group was decreased （P<0.05）， while the length of DRG cell processes in oe-NGF group was increased （P<0.05）. Conclusion ADSCs can be directionally differentiated into SCLCs， and the differentiated cells highly express NGF. Knockdown or overexpression of NGF can affect the growth of DRG cell processes.

Objective To discuss the effect of KH-type splicing regulatory protein（KHSRP） on the malignant biological behaviors of colorectal cancer （CRC） by activating the Janus kinase（JAK）/signal transducer and activator of transcription（STAT） signaling pathway， and to clarify its possible mechanism. Methods The CRC tissue and adjacent normal tissue from 64 CRC patients were selected. The human CRC cells （HT29， SW620， SW480， DLD-1， LOVO， and RKO） and normal human colorectal mucosal FHC cells were cultured in vitro. The total RNA from CRC tissue and cells were extracted， real-time fluorescence quantitative PCR （RT-qPCR） was used to detect the expression levels of KHSRP in the CRC tissue， adjacent normal tissue and all kinds of cells. The HT29 and SW620 cells were divided into sh-NC group （lentiviral plasmid inserted with non-targeting nucleotide sequence） and sh-KHSRP group （transfected with KHSRP knockdown lentivirus）. The SW480 and DLD-1 cells were divided into oe-NC group （lentiviral plasmid inserted with non-targeting nucleotide sequence） and oe-KHSRP group （transfected with KHSRP overexpression lentivirus）. Immunohistochemistry （IHC） staing in method was used to analyze the expressions of KHSRP in CRC tissue and adjacent normal tissue； CCK-8 method was used to detect the proliferation activities of the CRC cells in various groups； Transwell assay was used to detect the numbers of migration and invasion cells in various groups； Western blotting method was used to detect the expression levels of KHSRP， JAK1， phosphorylated JAK1（p-JAK1）， JAK2， phosphorylated JAK2（p-JAK2）， STAT1， STAT2， STAT3， and STAT5 proteins in the CRC cells in various groups. The subcutaneous xenograft tumor models in the nude mice were used to measure the tumor volumes and weights of the mice in various groups. Results Compared with adjacent normal tissue， the expression level of KHSRP in the CRC tissue was increased （P<0.05）. Compared with FHC cells， the expression levels of KHSRP in the CRC cells were increased （P<0.05）. Therefore， the HT29 and SW620 cells were selected for knockdown of KHSRP， while the SW480 and DLD-1 cells were selected for over-expression of KHSRP. The Western blotting results showed that the expression amounts of KHSRP protein in the CRC tissue and cells were higher than those in adjacent normal tissue and FHC cells. The IHC results showed that compared with adjacent normal tissue， the expression level of KHSRP protein in CRC tissue was increased （P<0.01）. The RT-qPCR results showed that compared with sh-NC group， the expression levels of KHSRP mRNA in the HT29 and SW620 cells in sh-KHSRP group were decreased （P<0.01）； compared with oe-NC group， the expression levels of KHSRP mRNA in the SW480 and DLD-1 cells in oe-KHSRP group were increased （P<0.01）， indicating successful transfection. The CCK-8 results showed that compared with sh-NC group， the proliferation activities of the HT29 and SW620 cells in sh-KHSRP group after knockdown of KHSRP were decreased （P<0.05 or P<0.01）； compared with oe-NC group， the proliferation activities of the SW480 and DLD-1 cells in oe-KHSRP group after over-expression of KHSRP were increased （P<0.05 or P<0.01）. Compared with sh-NC group， the numbers of migration and invasion cells in the HT29 and SW620 cells in sh-KHSRP group after knockdown of KHSRP were decreased （P<0.05）； compared with oe-NC group， the numbers of migration and invasion cells in the CRC cells in oe-KHSRP group after over-expression of KHSRP were increased （P<0.05）. After knockdown of KHSRP， the tumor volume and weight in sh-KHSRP group were smaller than those in sh-NC group （P<0.05 or P<0.01）， while the tumor volume andweight in oe-KHSRP group were larger than those in oe-NC group after over-expression of KHSRP （P<0.05 or P<0.01）. Compared with sh-NC group， the expression levels of JAK1， p-JAK1， and STAT3 proteins in the CRC cells in sh-KHSRP group were significantly decreased （P<0.05 or P<0.01）； compared with oe-NC group， the expression levels of JAK1， p-JAK1， and STAT3 proteins in the CRC cells in oe-KHSRP group were significantly increased （P<0.05 or P<0.01）. Conclusion High expression of KHSRP promotes the proliferation， migration， and invasion of the CRC cells and enhances the growth of subcutaneous xenograft tumors in the mice； its mechanism may be associated with its activation of the JAK1/STAT3 signaling pathway.

Objective To analyze and identify the expression profiles of oxidative stress-related genes and circular RNAs （circRNAs） in ricin toxin （RT）-induced pyroptosis of mouse mononuclear macrophages （RAW264.7） using transcriptome sequencing and bioinformatics technology， and to preliminarily analyze their potential functions. Methods The macrophages （RAW264.7 cells） were treated with RT to establish a cell pyroptosis model and divided into control group， 40 μg·L^-1 RT group， and 80 ng/mL RT group. Transmission electron microscope （TEM） was used to observe the morphology of the RAW264.7 cells in various groups； Western blotting method was used to detect the expression levels of the pyroptosis pathway-related proteins in the cells in various groups； 80 μg·L^-1 RT was selected for subsequent experiments. Transcriptome sequencing （RNA-Seq） was performed to obtain the circRNA and mRNA expression profiles in the RAW264.7 cells in control group and RT-treated group， followed by bioinformatics analysis. Results Compared with control group， the cells in 40 and 80 μg·L^-1 RT groups underwent morphological changes； the cells in RT groups showed obvious pyroptosis-like morphological changes， characterized by significant swelling of dying cells and the appearance of characteristic large bubbles on the plasma membrane. Compared with control group， the expression level of gasdermin DN-terminal fragment （GSDMD-N） protein in 40 and 80 μg·L^-1 RT groups was increased （P<0.05）； compared with 40 μg·L^-1 RT group， the expression level of GSDMD-N protein in the cells in 80 μg·L^-1 RT group was increased （P<0.05）； therefore， the subsequent experiments used the RT concentration of 80 μg·L^-1. A total of 2930 differentially expressed messenger RNAs （mRNAs） and 24 differentially expressed circRNAs were identified. The constructed circRNA-microRNA （miRNA）-mRNA competing endogenous RNA （ceRNA） regulatory network consisted of 7 circRNAs， 12 miRNAs and 13 mRNAs. Gene Ontology （GO） functional enrichment analysis showed that in biological process （BP）， the functions regulated by differentially expressed genes mainly included immune response and oxidative stress response； in cellular component （CC）， differentially expressed genes were mainly localized to the external side of plasma membrane and cell leading edge； in molecular function （MF）， they were mainly involved in transporter transmembrane activity and hormone receptor binding. Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis showed that differentially expressed genes were mainly enriched in Toll-like receptor signaling pathway， Forkhead box O（FoxO） signaling pathway and nuclear factor kappa-light-chain-enhancer of activated B cells （NF-κB） signaling pathway. In the protein-protein interaction （PPI） network， the top 10 hub genes with the highest connectivity were screened by CytoHubba， including matrix metalloproteinase 9 （MMP9）， superoxide dismutase 2 （SOD2）， and v-src sarcoma viral oncogene homolog （Src）. Conclusion The expression profiles of oxidative stress-related genes and circRNAs in RAW264.7 cells are altered after RT treatment. The screened differentially expressed circRNAs and mRNAs may serve as potential targets to regulate RT-induced pyroptosis in RAW264.7 cells through oxidative stress pathways.

Objective To discuss the expression of Rh family C glycoprotein （RHCG） in the esophageal squamous cell carcinoma （ESCC） tissue and its effect on the malignant biological behavior of ESCC cells， and to clarify the value of RHCG as a diagnostic and prognostic marker for the ESCC patients. Methods A total of 143 ESCC tissue samples and 105 adjacent normal tissue samples were collected. Using immunohistochemical staining method， 141 ESCC samples were divided into two groups： RHCG low expression group （immunohistochemistry score ≤6） and RHCG high expression group （immunohistochemistry score >6）. Immunohistochemical method was used to detect the RHCG protein expression in 143 ESCC tissues and 105 normal tissues， and the relationship between the clinicopathological characteristics of the ESCC patients was analyzed. Receiver operating characteristic （ROC） curve and Kaplan-Meier survival analysis were used to evaluate the value of RHCG in diagnosis and prognosis of the ESCC patients； univariate and multivariate COX regression analysis were used to determine the independent risk factors affecting the prognosis of the ESCC patients. Gene Expression Profiling Interactive Analysis （GEPIA2） database was used to analyze the expression of RHCG mRNA in various tumor tissues. The ESCC TE-1 cells were cultured and transfected in to 6-well cell culture plates with different Lipofectamine2000∶RHCG ratios； the cells in RHCG transfection group were transfected with weights of 2.0， 2.5， and 3.0 μg for 24 and 48 h， respectively， and the cells in NC group transfected with empty vector as control. Western blotting method was used to detect the RHCG protein expression level in the TE-1 cells in various groups after transfection at different concentrations and verify the optimal transfection conditions； cell counting kit-8 （CCK-8） assay was used to detect the proliferation activities of the TE-1 cells； plate clone formation assay was used to detect the colony formation numbers of the TE-1 cells； Transwell chamber assay was used to detect the numbers of migrating TE-1 cells. Results Compared with adjacent normal tissue， the RHCG gene expression level in various cancer tissues including ESCC， glioblastoma multiforme， and head and neck squamous cell carcinoma was significantly decreased （P<0.05）. RHCG protein was mainly located on the cell membrane of normal esophageal squamous epithelial cells； the RHCG protein expression intensity in ESCC tissues was lower than that in adjacent normal esophageal tissue （χ2=109.373， P<0.001）， and the patients in RHCG low expression group had poorer differentiation than those in RHCG high expression group （P=0.041）. The area under the curve （AUC） value of RHCG for diagnosing ESCC was 0.86， with sensitivity and specificity of 95.1% and 75.0%， respectively； the Kaplan-Meier survival analysis results showed that compared with high RHCG expression group， the patients in low RHCG expression group had shorter survival time and poorer prognosis ［harard ratio（HR）=0.269，95% confidence interval（CI）： 0.113-0.639， P=0.020］； the COX regression analysis results showed that low RHCG expression could serve as an independent risk factor affecting the prognosis of ESCC ［HR=4.569， 95%CI=1.315-15.877， P=0.017）］. The Western blotting results verified that the optimal transfection condition was 3.0 μg RHCG plasmid for 48 h， at which time RHCG overexpression was optimal and RHCG protein expression level was highest. The CCK-8 assay results showed that compared with control group， the proliferation activity in RHCG overexpression group was decreased on the 4th day after cell seeding （P<0.001）. In the TE-1 cells， the colony formation number of the TE-1 cells in RHCG over-expression group was lower than that in control group （t=17.70， P<0.001）. The Transwell chamber assay results showed that compared with control group， the number of migrating cells in RHCG over-expression group was decreased （t=23.74， P<0.001）. Conclusion RHCG expression is decreased in ESCC tissues and associated with poor prognosis in ESCC patients； overexpression of RHCG can inhibit the proliferation and migration of the TE-1 cells， providing a theoretical basis for RHCG as a novel diagnostic and prognostic marker and therapeutic target for ESCC.

Objective To discuss the influencing factors of angina pectoris in the patients with diabetes mellitus （DM）， to construct a Bayesian network model to explore the network relationships among the influencing factors， and to predict the risk of angina pectoris in the patients with DM. Methods Based on the UK Biobank（UKB） database， the Logistic regression aralysis model was used to screen the influencing factors of angina pectoris in the patients with DM. The taboo search algorithm was used for structure learning， and the Bayesian parameter estimation method was used for parameter learning to construct the Bayesian network model. Results A total of 22 712 DM patients were included. The influencing factors of angina pectoris in the patients with DM included 14 variables： gender， age， body mass index （BMI）， triglycerides （TG）， total cholesterol （TC）， glycated hemoglobin （HbA1c）， hypertension， maternal smoking around delivery， smoking status， alcohol consumption， regular exercise， insomnia， sleep duration， and childhood relative body size （P<0.05）. A Bayesian network model was constructed with 15 nodes and 22 directed edges. Among them， age， HbA1c， hypertension， regular exercise， BMI， and sleep duration were directly associated with the occurrence of angina pectoris in the patients with DM， while gender， smoking status， alcohol consumption， TC， TG， insomnia， childhood relative body size， and maternal smoking around delivery were indirectly associated with the occurrence of angina pectoris in the patients with DM. Conclusion Age， HbA1c， hypertension， regular exercise， BMI， and sleep duration are direct influencing factors of angina pectoris in the patients with DM. Controlling HbA1c， blood pressure， and BMI levels， engaging in regular exercise， and maintaining appropriate sleep duration are beneficial for reducing the risk of angina pectoris in the patients with DM.

Objective To screen the Alzheimer’s disease（AD）-related genes and construct its diagnostic model using bioinformatics technology and machine learning （ML） algorithms， to discuss the immunological characteristics of AD patients， and to provide novel biomarkers for AD diagnosis. Methods The AD-related gene expression dataset GSE125583 was downloaded from the Gene Expression Omnibus （GEO） database. Differentially expressed genes （DEGs） were identified through differential analysis. Gene Ontology （GO） functional enrichment and Kyoto Encyclopedia of Genes and Genomes （KEGG） signaling pathway enrichment analyses were performed to explore the biological functions and signaling pathways of DEGs. A protein-protein interaction （PPI） network was constructed， and hub genes were screened using Cytoscape software combined with three ML algorithms： Least Absolute Shrinkage and Selection Operator （LASSO）， eXtreme Gradient Boosting （XGBoost）， and Random Forest （RF）. The screened hub genes were utilized to build an AD diagnostic model via RF， followed by feature importance ranking. The model’s efficacy and key genes were evaluated using a test set. Single-sample gene set enrichment analysis （ssGSEA） was used for immune cell infiltration analysis between AD group and control group. Results Differential analysis identified 1 287 DEGs. The GO functional enrichment analysis results revealed that DEGs were primarily involved in biological functions related to neural signaling， synapses， and vesicles. KEGG signaling pathway enrichment analysis indicated significant enrichment of DEGs in ion transport， neurotransmitter， and ligand-gated channel pathways. Nine overlapping hub genes were screened by the three ML algorithms. In the AD diagnostic model， the top four key genes with highest diagnostic performance were adenylate cyclase-activating polypeptide 1 （ADCYAP1）， brain-derived neurotrophic factor （BDNF）， platelet-derived growth factor receptor β （PDGFRB）， and C-X-C motif chemokine receptor 4 （CXCR4）， with corresponding area under the curve （AUC） values of 0.852， 0.795， 0.820， and 0.756， respectively. The model achieved an AUC of 0.828， accuracy of 81.25%， sensitivity of 84.40%， and specificity of 71.43%. The immune cell infiltration analysis results demonstrated higher infiltration of macrophages， monocytes， natural killer（NK） cells， and lymphocytes in AD tissue. Among these， NK/natural killer T（NKT） cells and plasmacytoid dendritic cells showed significant correlations with the four key genes（P<0.05）. Conclusion The feature genes screened based on bioinformatics and ML exhibit diagnostic potential for AD. Genes such as ADCYAP1 may serve as potential biomarkers for AD diagnosis， offering significant implications for early prevention and treatment.

Objective To evaluate the potential causal relationship between tinnitus and the risk of Alzheimer’s disease （AD） onset using the two-sample Mendelian randomization （MR） method and to clarify its mechanism of action， so as to provide new ideas for early warning of AD. Methods Genome-wide association study （GWAS） database was used to search the keywords “tinnitus” and “Alzheimer” to obtain the related datasets of exposure factor tinnitus and outcome AD； the tinnitus datasets included ukb-d-4803_11， ukb-d-4803_12， ukb-d-4803_13， ukb-b-14254 and ukb-a-384； the AD datasets included ieu-b-5067， ieu-b-2， ieu-a-297， ebi-a-GCST90027158 and ebi-a-GCST002245. The single nucleotide polymorphisms （SNPs） closely and independently associated with tinnitus were screened as instrumental variables （IVs）， and the SNPs associated with AD were used as outcomes. Inverse variance weighted （IVW） method was used to conduct MR analysis to evaluate its odds ratio （OR） value， 95% confidence interval （CI） and P value； P<0.05 indicated significant causal relationship. Sensitivity detection used Cochran’s Q test to detect the heterogeneity of IVs to evaluate its Q value， df value and P value； when IVW method P>0.05， it indicated no significant heterogeneity； MR-Egger intercept was used to detect horizontal pleiotropy； when the intercept was 0 or close to 0 and P>0.05， it indicated no significant horizontal pleiotropy； meanwhile， leave-one-out method was used for sensitivity analysis. Finally， visualization results were performed using forest plot， scatter plot， funnel plot and leave-one-out plot. Results A total of 286 SNPs were screened as IVs. All instrumental variables satisfied F>10， suggesting no weak instrumental variable； after screening by PhenoScanner web tool， all SNPs were unrelated to confounding factors. When the tinnitus and AD datasets were ukb-d-4803 and ebi-a-GCST90027158 respectively， there was a significant positive correlation between tinnitus and the risk of AD onset （IVW： OR=1.842， 95%CI：1.065-3.188， P=0.029）； Cochran’s Q test suggested no significant heterogeneity of IVs （Q=9.788， df=10.000， P=0.459）； MR-Egger intercept indicated no horizontal pleiotropy （Egger intercept=-0.006， P=0.147）； leave-one-out method showed stable results， and no SNP with significant influence on the results was detected. Conclusion There is a positive causal relationship between tinnitus and the risk of AD onset. Neuroinflammation accompanied by persistent microglial activation to varying degrees may be the common pathogenesis of tinnitus and AD； in addition， depression may also act as an upstream factor to hyperactivate the hypothalamic-pituitary-adrenal （HPA） axis， leading to the progression of relationship between tinnitus and AD.

Objective To compare the differences in clinical characteristics among the patients at clinical high risk for bipolar disorder （CHR-BD）， the patients with bipolar disorder （BD）， and the healthy controls （HC） at low risk， and to provide the basis for the diognasis and treatment of CHR-BD. Methods For the first time， the BD risk criteria and prospective structured assessment tools were jointly used in outpatients aged 16-30 years， and 43 CHR-BD patients were included to ensure the accuracy of the assessment. Meanwhile， 33 BD patients and 32 HC subjects were also enrolled. The clinical symptoms， neurocognitive function， and global functional levels of the subjects in the three groups were evaluated using observer-rated and self-rated tools. The CHR-BD and BD groups were combined， and Logistic regression analysis was used to identify the independent influencing factors related to diagnostic status； Pearson or Spearman correlation analysis was used to analyze the correlations between the global functional levels and the symptoms or neurocognitive characteristics of the patients in CHR-BD and BD groups. Results There were statistically significant differences in the scores of symptom and global functional level scales among HC， CHR-BD， and BD groups （P<0.05）. Compared with HC group， the scores of mood symptoms （anxiety， depression， and mania/hypomania）， psychotic symptoms， total affective temperament questionnaire scores， and some dimensions （cyclothymic， depressive， irritable， and anxious temperaments） in CHR-BD and BD groups were significantly increased （P<0.001）， while the global functional levels were significantly decreased （P<0.001）. Compared with BD group， the lowest global functional level score in the past year in CHR-BD group was significantly increased （P=0.022）， while the current global functional level score was significantly decreased （P=0.005）. No significant differences were observed in neurocognitive function scores among the three groups （P>0.05）. The lowest global functional level score in the past year was an independent influencing factor for BD diagnosis ［odds ratio （OR）=0.952， 95% confidence interval（CI）：0.917-0.988，P=0.010］. In both CHR-BD and BD patients， the current global functional levels were negatively correlated with depressive （r=-0.417， P=0.005； r=-0.617， P<0.001） and anxiety symptoms （r=-0.360， P=0.018； r=-0.506， P=0.003）. In BD patients， the current global functional level was negatively correlated with lifetime manic/hypomanic symptoms （r=-0.360， P=0.039）， psychotic symptoms （r=-0.502， P=0.003）， and affective temperament scores （r=-0.479， P=0.005）， while the lowest global functional level in the past year was negatively correlated with lifetime manic/hypomanic symptoms （r=-0.391， P=0.024）. Conclusion CHR-BD patients share similar mood symptom characteristics with BD patients， and their global functional levels are negatively correlated with depressive and anxiety symptoms. BD patients exhibit worse lowest global functional levels in the past year， and their global functional levels are negatively correlated with manic/hypomanic symptoms.

Objective To screen the key genetic， diagnostic and therapeutic targets of chronic obstructive pulmonary disease （COPD） patients by using microarray datasets and Mendelian randomization （MR） method， and to provide the evidence for clinical diagnosis and treatment of COPD. Methods Four COPD gene expression profile datasets were obtained from the Gene Expression Omnibus （GEO） database. The data were processed and normalized using R software， and differentially expressed genes （DEGs） were screened. MR analysis was performed to explore the causal relationship between COPD and expression quantitative trait loci （eQTL）， intersection with DEGs was taken to identify potential key targets. Gene Set Enrichment Analysis （GSEA）， Gene Ontology （GO） functional enrichment analysis， and Kyoto Encyclopedia of Genes and Genomes （KEGG） signaling pathway enrichment analysis were conducted to investigate the functional roles and pathways of the key targets， external datasets were used to validate their expression. Results A total of 1 571 DEGs were screened， including 820 upregulated genes and 751 downregulated genes. MR analysis identified 286 COPD-related genes， and intersection with DEGs revealed 3 upregulated genes： diacylglycerol kinase gamma （DGKG）， neurofilament heavy polypeptide （NEFH）， and Fc receptor like B （FCRLB）； and 6 downregulated genes： STEAP4 metalloreductase （STEAP4）， pleckstrin homology domain containing family F member 2 （PLEKHF2）， CD3d molecule （CD3D）， transgelin 2 （TAGLN2）， tripartite motif containing 22 （TRIM22）， and ribosomal protein L9 （RPL9）. The biological function analysis results indicated that these genes were mainly involved in pathways such as iron ion transport into the cells， oxidoreductase activity， primary immunodeficiency， and Th1 and Th2 cell differentiation. The MR analysis results confirmed the causal relationship between these targets and COPD. The external validation results showed that compared with healthy controls， the expression level of FCRLB in COPD samples was significantly increased （P<0.01）， while the expression levels of CD3D and RPL9 were significantly decreased （P<0.05 or P<0.01）， which was consistent with the MR analysis results， highlighting the reliability of this study. Conclusion DGKG， NEFH， FCRLB， STEAP4， PLEKHF2， CD3D， TAGLN2， TRIM22， and RPL9 may serve as important regulatory factors and clinical diagnostic/therapeutic targets in the pathogenesis of COPD， providing clues for early screening， diagnosis， and targeted treatment of COPD.

Objective To discuss the causal association between sterol esters and intrahepatic duct， biliary tract， and gallbladder malignancies using two-sample Mendelian randomization （MR） analysis， and to clarify the biological mechanisms of sterol esters， and to provide the a basis for early prevention and treatment of these malignancies. Methods The instrumental variable data for 15 different types of sterol ester traits were obtained from the Finnish database （FinnGen）. The genome-wide association study （GWAS） data for intrahepatic duct， biliary tract， and gallbladder malignancies were retrieved from the GWAS database using the keywords “sterol ester” and “intrahepatic duct， biliary tract， and gallbladder malignancies”（accession numbers： ICD-O-3 and GCST90277238-GCST9027725）. The inverse-variance weighted （IVW） method， MR-Egger regression， and weighted median （WM） method were used to assess the causal association between sterol esters and the risk of these malignancies. Pleiotropy was tested using the MR-Egger intercept method； heterogeneity was evaluated using Cochran’s Q test； and sensitivity analysis was performed using the leave-one-out approach to comprehensively assess the reliability and robustness of the results. Results The IVW analysis results showed that Sterol ester （27：1/14：0） odds ratio（OR）=2.349， 95% confidence interval （CI）=1.371-4.025， P=0.002）， Sterol ester（27：1/16：0） （OR=1.248， 95%CI=1.018-1.523， P=0.033）， Sterol ester （27：1/18：2） （OR=1.361， 95%CI=1.078-1.718， P=0.009）， and Sterol ester （27：1/22：6） （OR=1.339， 95%CI=1.001-1.791， P=0.049） were associated with an increased risk of intrahepatic duct， biliary tract， and gallbladder malignancies. The MR-Egger regression analysis results indicated that Sterol ester （27：1/18：2） （OR=2.038， 95%CI=1.337-3.105， P=0.011） was a risk factor for these malignancies. The WM analysis results revealed that Sterol ester （27：1/14：0） （OR=2.786， 95%CI=1.419-5.468， P=0.003） and Sterol ester （27：1/18：2） （OR=1.548， 95%CI=1.148-2.088， P=0.004） were also risk factors. The MR-Egger intercept analysis and Cochran’s Q test results indicated no significant horizontal pleiotropy or heterogeneity. The leave-one-out sensitivity analysis did not identify any influential outlier single nucleotide polymorphism （SNPs）， confirming the reliability of the study. Conclusion Sterol ester （27：1/14：0）， Sterol ester （27：1/16：0）， Sterol ester （27：1/18：2）， and Sterol ester （27：1/22：6） exhibit causal associations with intrahepatic duct， biliary tract， and gallbladder malignancies and may promote their development.

Objective To discuss the changes of adenosine deaminase 2 （ADA2） activity in the serum of the systemic lupus erythematosus （SLE） patients， and to clarify its clinical value in the diagnosis and disease assessment of the SLE patients. Methods According to the inclusion and exclusion criteria， 69 SLE patients （SLE group） and 69 healthy controls （control group） were enrolled as study subjects. The disease activity of SLE patients was evaluated by SLE Disease Activity Index （SLEDAI）. The ADA2 activity in the serum of the subjects in both groups was detected. The patients were further divided into subgroups based on the presence or absence of the following clinical symptoms： arthritis， myositis， hematuria， proteinuria， pyuria， alopecia， new rash， mucosal ulcer， pleuritis， hypocomplementemia， elevated anti-double-stranded DNA （anti-dsDNA） antibody， thrombocytopenia， and leukopenia. The differences in serum ADA2 activity between joint symptomatic group and joint asymptomatic group were analyzed. The diagnostic efficacy of serum ADA2 activity was evaluated by receiver operating characteristic （ROC） curve analysis. The correlation between ADA2 activity and disease activity in the SLE patients was analyzed by Spearman correlation analysis. Results Compared with control group， the ADA2 activity in the serum of the patients in SLE group was significantly increased （P<0.01）. The ROC analysis results showed that when the cut-off value of ADA2 activity was set at 8.5 U·L^-1， the diagnostic performance was optimal， with an area under the curve （AUC） of 0.879 （95%CI： 0.817-0.940）， the specificity was 89.86%， and the sensitivity was 75.36%. The serum ADA2 activity was positively correlated with disease activity in the SLE patients （r=0.32， P=0.007）. The subgroup analysis of clinical symptoms results showed that the serum ADA2 activity in the SLE patients with symptoms was significantly higher than that in the SLE patients without symptoms （P<0.01）. No significant differences were observed in serum ADA2 activity between the SLE patients with and without myositis， hematuria， proteinuria， pyuria， alopecia， new rash， mucosal ulcer， pleuritis， hypocomplementemia， elevated anti-dsDNA antibody， thrombocytopenia， or leukopenia （P>0.05）. Conclusion The serum ADA2 activity is increased in the SLE patients and can serve as a diagnostic marker for SLE. Serum ADA2 activity is positively correlated with disease activity and is associated with arthritis in the SLE patients， suggesting its potential as an indicator for disease assessment and monitoring.

Objective To discuss the characteristics of pulmonary function changes in the pediatric patients with Mycoplasma pneumoniae pneumonia （MPP）， the effect of inhaled corticosteroids during the recovery phase on pulmonary function， and the improvement effects of different aerosolized medications on pulmonary function， and to clarify the significance of inhaled corticosteroids in the treatment of MPP pediatric patients during the recovery phase. Methods A retrospective study was conducted. Sixty-nine MPP children who received inhaled corticosteroids after discharge were selected as treatment group. According to the different medications used after discharge， they were divided into steroid group （receiving inhaled corticosteroids alone， n=42） and combination group （receiving inhaled corticosteroids combined with inhaled long-acting bronchodilators，n=27）. Additionally， 30 children who did not receive aerosol therapy after discharge during the same period were selected as control group. The general data of the pediatric patients in various groups were collected. The pulmonary function parameters， including forced vital capacity （FVC）， forced expiratory volume in the first second （FEV1）， ratio of forced expiratory volume in 1 second to forced vital capacity （FEV1/FVC）， peak expiratory flow （PEF）， and maximal mid-expiratory flow （MMEF）， were detected using pulmonary function equipment at the time of entering the recovery phase and 1 month after entering the recovery phase. The changes in pulmonary function of the pediatric patients between control group and treatment group were analyzed. Results The pulmonary ventilation dysfunction in the MPP pediatric patients was mainly restrictive， followed by mixed. The pulmonary function could be normal or only show small airway dysfunction in some children. In both teatment and control groups， the second pulmonary function parameters including FVC， FEV1， PEF， maximal expiratory flow at 25% of forced vital capacity（MEF25）， maximal expiratory flow at 50% of forced vital capacity（MEF50）， maximal expiratory flow at 75% of forced vital capacity（MEF75）， and MMEF of the pediatric patients were significantly increased compared with the first measurement （P<0.05）. Compared with control group， the increase in FEV1/VC at the second measurement of the pediatric patients in treatment group was not significant （P>0.05）. The differences in pulmonary function parameters showed an increasing trend in treatment group and control group. The differences in MEF25 and MMEF of the pediatric patients in the treatment group were higher than those in control group （P<0.05）. The differences in pulmonary function parameters of the pediatic patients in both steroid group and the combination group showed an overall increasing trend. The differences in FVC， FEV1， FEV1/VC， MEF25， MEF50， and MMEF of the pediatric patients in steroid group were slightly higher than those in combination group. Compared with steroid group， the differences in PEF and MEF75 of the pediatric patients in combination group were slightly higher， but the differences were not statistically significant （P>0.05）. The differences in MEF25， MEF50， and MMEF of the pediatric patients in steroid group were higher than those in control group （P<0.05）. Conclusion Both large and small airway functions can be affected in the pediatric patients with MPP， with restrictive ventilation dysfunction being predominant. Airway function can improve during the disease recovery phase. Inhaled corticosteroids during the recovery phase may have a positive therapeutic significance in promoting the recovery of pulmonary function， especially small airway function. The bronchodilators showed no significant effect on improving the pulmonary function during the recovery phase. Therefore， inhaled corticosteroids alone during the recovery phase may promote the recovery of pulmonary function in children with MPP.

The patients with skeletal Class Ⅱ high-angle malocclusion are frequently complicated by idiopathic condylar resorption （ICR）， which may lead to temporomandibular joint （TMJ） dysfunction and dentofacial deformities. This article reports the diagnosis and treatment process of a 24-year-old female patient with skeletal Class Ⅱ high-angle malocclusion accompanied by ICR. The patient’s chief complaints were anterior open bite and TMJ pain， and was diagnosed with ICR through clinical examination and imaging. After stabilizing condylar resorption with occlusal splint therapy， combined orthodontic-orthognathic treatment was performed. The 42-month follow-up revealed： well-aligned dentition with complete closure of diastemas， significant improvement of protrusive facial profile （ANB angle reduced by 4.2°）， complete resolution of TMJ pain and clicking， and establishment of stable Class Ⅰ occlusion. Three-dimensional CT demonstrated satisfactory condylar bone remodeling and normalized joint space. Through multidisciplinary treatment， both occlusal function and facial aesthetics were significantly improved. This case demonstrates that orthodontic-orthognathic treatment should be performed after condylar stabilization in ICR patients， and occlusal splint therapy serves as an effective preoperative intervention.

Ovarian sclerosing stromal tumor （OSST） is a benign tumor originating from the ovarian sex cord-stroma， accounting for only 2%-6% of ovarian stromal tumors. It predominantly occurs in young women， and cases of OSST concurrently presenting with Meigs syndrome are extremely rare. This study reports a case of OSST， summarizes its clinical manifestations， and reviews relevant literature. The patient， a 22-year-old female， was admitted due to abdominal distension for 2 months， worsening over the past week. The physical examination results revealed abdominal distension， shifting dullness， mild tenderness， and no muscle tension or rebound tenderness. A mass measuring approximately 16.0 cm×14.0 cm×8.0 cm was palpated in the pelvic and abdominal cavity， with a firm texture， moderate mobility， and no tenderness. The gynecological ultrasound results showed a mixed cystic-solid echo of about 15.3 cm×14.0 cm×8.4 cm above the left side of the uterus， with clear boundaries， and fluid-filled dark areas in the pelvic and abdominal cavity， with a maximum anteroposterior diameter of about 11.9 cm. The-CT results revealed a cystic-solid mixed-density mass in the lower abdomen and right adnexal area， suggestive of a neoplastic lesion， with increased glucose metabolism in the solid portion， leaning toward malignancy. Carbohydrate antigen 125 （CA125） was >800 U·mL^-1， and pelvic puncture cytology indicated no cancer cells. The findings suggested a benign or borderline ovarian tumor， requiring differentiation from ovarian malignant tumors. Based on intraoperative observations and rapid pathological results， a left ovarian tumor enucleation was performed. Postoperative pathology confirmed ovarian sclerosing stromal tumor. Follow-up over 2 years showed no abnormalities. As a benign ovarian tumor， the clinical manifestations of OSST often mimic those of malignant tumors， leading to frequent misdiagnosis. Early diagnostic accuracy should be improved to develop the optimal treatment plan for patients.

Malignant pleural effusion （MPE） is a common complication in patients with advanced malignant tumors，which not only significantly reduces their quality of life but also shortens their survival duration. Despite the widespread use of traditional treatment methods such as thoracentesis and pleurodesis，their efficacy is limited accompanied by high recurrence rates. Therefore，exploring novel therapeutic strategies becomes particularly urgent. In recent years， immunotherapy has attracted extensive attention for its potential in cancer treatment. This article systematically reviews the roles of CD4+T cell subsets，including regulatory T cells （Treg）， T helper cell（Th）17， Th9， and Th22 cells， within the immunosuppressive microenvironment of MPE. These cell subsets are involved in the formation of the immunosuppressive state of MPE through various mechanisms and play key roles in the occurrence and development of the disease. In addition，the article discusses in detail the role of immune checkpoint molecules， such as programmed death protein 1 （PD-1）， PD-1 ligand（PD-L1）， and cytotoxic T-lymphocyte-associated protein 4 （CTLA-4）， in the immune evasion of MPE. The abnormal expressions of these molecules provide opportunity for tumor cells to evade immune system surveillance. At the same time， this article also summarizes the application prospects of novel immunotherapy strategies， such as adoptive cell therapy （ACT） and chimeric antigen receptor T cell （CAR-T） therapy，in the treatment of MPE. These innovative therapies offer possibilities for improving the prognosis of MPE patients through activating and enhancing the anti-tumor immune response.

Nanometal materials have been extensively studied due to their non-toxic， stable， and efficient biological properties. Among them， nano-zinc oxide （ZnO-NPs）， which exhibits good biocompatibility， is considered a promising antibacterial material for medical applications due to its broad-spectrum antibacterial effects and photocatalytic activity. The antibacterial mechanism of ZnO-NPs is not yet fully understood， but two widely recognized modes have been proposed： one is a non-contact mechanism dominated by reactive oxygen species （ROS） generated by ZnO-NPs and the release of Zn²⁺， and the other is a direct contact antibacterial mechanism involving the interaction between ZnO-NPs and bacterial cell wall components. These two distinct antibacterial mechanisms are attributed to the physicochemical properties of ZnO-NPs. As a wide-bandgap semiconductor， the antibacterial efficacy of ZnO-NPs is influenced not only by light exposure but also by factors such as particle size， concentration， morphology， as well as the type and structure of the target bacteria. Therefore， understanding the precise mechanisms is crucial for elucidating the antibacterial functions of ZnO-NPs against bacteria and fungi. This review summarizes the latest research progress on the antibacterial mechanisms of ZnO-NPs and their influencing factors， and provides an overview of the factors affecting the antibacterial performance of ZnO-NPs， offering a basis for a deeper understanding and application of ZnO-NPs in antibacterial therapy.

Peripheral nerve injury （PNI） is a common neurological disorder. As the primary constituent cells of the myelin sheath， Schwann cells （SCs） play a crucial role in the repairment process after PNI. After PNI， the SCs are activated and rapidly migrate to the injury site， forming a neural bridge that connects the proximal and distal stumps in conjunction with the endothelial cells， the extracellular matrix（ECM）， and the fibroblasts. This bridge provides a pathway for axonal regrowth and guides axonal regeneration. The ability of SCs to migrate quickly to the damaged nerve site is a key factor influencing the formation of the neural bridge. The ECM， NT， non-coding RNAs， particularly long non-coding RNAs （lncRNA） and microRNA （miRNA）， and various transcription factors regulate the migratory capacity of the SCs through multiple signaling pathways， thereby affecting the repair of PNI. However， to date， there has been no systematic study on the factors influencing the migration of SCs in PNI or their underlying mechanisms. This article comprehensively reviews the various factors affecting the migration of SCs after PNI， including the ECM， NT， non-coding RNAs， and transcription factors， as well as the related signaling pathways. It aims to provide the basis for systematically understanding the role of SCs in PNI repairment and to offer the reference for comprehensive analysis of the repairment mechanisms after PNI.

Epithelial-mesenchymal transition （EMT） is a critical process in the development of various cancers， including glioma. In glioma cells， the activation of hypoxia-inducible factors （HIFs） can influence the occurrence of EMT， promoting cell migration and invasion. This review aims to explore the role of HIF in the EMT process of glioma cells， focusing on its impact on cell migration and invasion， including regulation of angiogenesis， metabolic reprogramming， glycolysis， and the immune system in the tumor microenvironment. Additionally， this review summarizes the role of HIF in EMT-related signaling pathways， such as Wnt/β-catenin （β-catenin）， Notch， and transforming growth factor-β （TGF-β）， and provides new insights and directions for further understanding the mechanisms of HIF in the EMT process of glioma cells.