Mucosal-associated invariant T (MAIT) cells are evolutionarily conservative and non-conventional innate T cell subsets, having the characteristics of both innate and adaptive immune cells. They have antibacterial and tissue repair functions,and are the important part of the immune system. MAIT cells are highly abundant in human liver and play a complex role in various liver diseases. Current studies have shown that the markedly reduced number of MAITs and the dysfunction of immunomodulatory effect in various liver diseases were closely related to the occurrence and progression of liver diseases. This paper mainly reviews the characteristics of MAIT cells and their latest progress in chronic viral hepatitis, autoimmune liver disease, non-alcoholic fatty liver disease, alcoholic liver disease and hepatocellular carcinoma, and further discuss the potential mechanisms underlying the loss of MAIT cells, so as to provide some references for follow-up research.

Chronic hepatitis C virus (HCV) is a worldwide epidemic and the main cause of liver cirrhosis and hepatocellular carcinoma (HCC). The anti-HCV treatment has gone through two eras of pegylated interferon-α plus ribavirin (PR therapy) and direct-acting antiviral agent (DAA). Generally, achieving a sustained virological response (SVR) can reduce the incidence of HCC through antiviral treatment. In recent years, increasing researchers pay more attention to the issue whether DAA treatment might increase the risk of HCC occurrence or recurrence. This article aims to review the related studies on the risk of HCC after PR therapy and DAA treatment, summarize the risk factors, and explore the mechanism of HCC and its impact on the efficacy of DAA, in order to help clinicians to determine the timing of initiation of antiviral therapy and provide clinical evidence for individualized management.

Perioperative hypothermia is not rare in surgical patients, and is closely related to a variety of complications,which is not conducive to postoperative recovery of patients. At present, many studies focus on the risk factors, adverse outcomes and prevention strategies of perioperative hypothermia, and few studies analyze the changes of perioperative hypothermia from a multidimensional perspective. By summarizing and analyzing the previous research results, this paper reviews the physiology of body temperature, perioperative hypothermia, perioperative monitoring and maintenance of body temperature, and the new opinions and derived parameters of perioperative hypothermia, which is expected to bring some new perspectives for researchers and clinicians to develop better strategies for the prevention and treatment of perioperative hypothermia.

Bullet vascular embolism is a serious complication of firearm injury, which is caused by military weapons in wartime and civil guns in peacetime. However, small caliber bullets and small mass fragments are mostly used in military weapons now, which makes it more likely that bullets/fragments will be left in the body, leading to a higher incidence of bullet vascular embolism. Therefore, the incidence of bullet vascular embolism in wartime in the future would be higher than it in the past. Bullet vascular embolism after firearm injury is more harmful to human body, and more emergency treatment is needed. This article reviews the mechanism, vulnerable vessels, embolization types, diagnostic methods and treatment points of bullet vascular embolism, so as to provide reference for clinical diagnosis and treatment of bullet vascular embolism.

Fecal microbiota transplantation (FMT) is becoming a new approach for dysbiosis conditions. It means that fecal microbiota from healthy donors could be transplanted into the recipient's digestive tract, to modulate their tissue and organ function and intestinal microecology, thus gaining a therapeutic effects for dysbiosis disorders. The FMT rescue program aims to provide standard FMT technology and products to military institutions for treating antibiotic-associated diarrhea like clostridium difficile infection (CDI) and other dysbiosis conditions with the FMT indication. The program contents include the purpose, the application scope, the process and technology for rescue use, the composition and responsibility of institutions, etc.

Objective To investigate the role of Toll-like receptor 4 (TLR4) in cardiac function injury of rats with heat stroke disease by regulating myocardial ferroptosis. Methods (1) 24 SD rats were randomly divided into control group and heat stroke disease (HS) group (12 in each group). During heat attack, anal temperature of rats was measured by anal thermometer, heart rate and mean arterial pressure of rats were measured by BL-420F biological function experiment system. (2) 24 SD rats were randomly divided into control group, ferroptosis inhibitor (Liproxstatin-1) group, HS group and HS+Liproxstatin-1 group (6 in each group). Thirty minutes before modeling, rats in Liproxstatin-1 group and HS+Liproxstatin-1 group were intraperitoneally injected with Liproxstatin-1 (10 mg/kg). The expression of solute carrier family 7 member 11 (SLC7A11) in myocardial tissue was detected by immunofluorescence staining, and the expression levels of SLC7A11 and glutathione peroxidase 4 (GPX4) were detected by Western blotting. (3) 48 SD rats were randomly divided into control group, TLR4 inhibitor (TAK-242) group, HS group and HS+TAK-242 group (12 in each group). Thirty minutes before modeling, rats in TAK-242 group and HS+TAK-242 group were intraperitoneally injected with TAK-242 (3 mg/kg). The expression of TLR4 in myocardial tissue was detected by immunofluorescence staining, cardiac hemodynamic indexes [left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), maximum rate of increase (+dp/dt_max) and maximum rate of decrease (–dp/dt_max) of left ventricular pressure] were detected by BL-420F biological function experiment system, cardiac function indexes [cardiac output (CO), diastolic left ventricular posterior wall thickness (LVPWd) and systolic left ventricular posterior wall thickness (LVPWs)] were detected by cardiac ultrasound, the expression levels of TLR4/NF-κB-p53 signaling pathway protein [TLR4, nuclear factor kappa B (NF-κB), p53] and ferroptosis related protein (SLC7A11 and GPX4) were detected by Western blotting. Results Compared with control group, the core body temperature and heart rate of rats in HS group increased significantly after heat shock for 180 minutes (P<0.01), the mean arterial pressure decreased significantly (P<0.05). Immunofluorescence staining results showed that compared with control group, the expression of myocardial SLC7A11 in HS group significantly decreased (P<0.01); Compared with HS group, the expression of SLC7A11 in HS+TAK-242 group improved significantly (P<0.01). The results of Western blotting showed that compared with control group, the expression levels of SLC7A11 and GPX4 in myocardium of HS group decreased significantly (P<0.05); Compared with HS group, the expression levels of SLC7A11 and GPX4 in HS+Liproxstatin-1 group improved significantly (P<0.05). Immunofluorescence staining results showed that compared with control group, the expression level of myocardial TLR4 in HS group increased significantly (P<0.01); Compared with HS group, the expression level of TLR4 in HS+TAK-242 group improved significantly (P<0.01). The results of BL-420F biological function test system showed that compared with control group, LVEDP increased, LVSP decreased (P<0.01) in HS group. LVSP, LVEDP, +dp/dt_max and –dp/dt_max were improved in HS+TAK-242 group (P<0.05). Compared with control group, CO was significantly decreased, and LVPWd and LVPWs were increased in HS group (P<0.01). Compared with HS group, CO increased, and LVPWd and LVPWs decreased in HS+TAK-242 group (P<0.05). Western blotting results showed that compared with control group, the expression levels of TLR4, NF-κB and p53 in the HS group increased significantly (P<0.01), and of SLC7A11 and GPX4 decreased significantly (P<0.01); Compared with HS group, the expression levels of TLR4, NF-κB and p53 decreased significantly, and of SLC7A11 and GPX4 increased significantly (P<0.05) in HS+TAK-242 group. Conclusion Ferroptosis may exist in myocardial injury caused by heat stroke. Inhibition of TLR4 can improve cardiac function of rats with heatstroke, and the mechanism may be related to ferroptosis mediated by TLR4/NF-κB-p53/SLC7A11 signaling pathway.

Objective To investigate the effect and mechanism of up-regulating calcium-sensing receptor (CaSR) on osteogenic differentiation of complex culture with porous tantalum-bone marrow mesenchymal stem cells (BMSCs). Methods BMSCs were extracted from SD rats and cultured to the third passage, and identified by alizarin red staining and toluidine blue staining after osteogenic and chondrogenic induction. The growth and adhesion of BMSCs on porous tantalum surface were observed by fluorescence microscope. CCK-8 assay was used to detect the proliferation of BMSCs cultured at different concentrations (200, 250, 300, 350, 400 μmol/L) of GdCl₃ for 1-5 d, and the optimal concentration was selected. Confocal laser scanning microscopy was used to observe the intracellular calcium distribution after activation of CaSR. The third-generation of BMSCs were divided into control group (with osteogenic induction medium), GdCl₃ group (with osteogenic induction medium containing 300 μmol/L GdCl₃), porous tantalum group (with domestic porous tantalum material, with osteogenic induction medium) and GdCl₃+porous tantalum group (with domestic porous tantalum material, with osteogenic induction medium containing 300 μmol/L GdCl₃). At the 7th day of culturing, alkaline phosphatase (ALP) activity was measured in each group. On the 7th, 14th and 21st day of culturing, the protein secretion levels of type I collagen (ColⅠ) and osteopontin (OPN) were detected by ELISA, and the protein expression levels of ColⅠ, OPN, Runt-related transcription factor 2 (Runx2) and Homer 1 were detected by Western blotting. Results Alizarin red and toluidine blue staining showed that the isolated and extracted cells were BMSCs; CCK-8 assay showed that 300 μmol/L GdCl₃-treated cells had the highest activity (P<0.05); confocal laser scanning microscopy showed that the intracellular calcium content was significantly increased after activation of CaSR (P<0.05). ALP activity on day 7 and relative expression levels of ColⅠ, OPN, Runx2 and Homer1 protein on days 7, 14 and 21 in GdCl₃ group, porous tantalum group and GdCl₃+porous tantalum group were higher than those in control group (P<0.05). ALP activity and relative expression levels of ColⅠ, Runx2 and Homer1 protein on day 7 were higher in GdCl₃+porous tantalum group than those in GdCl₃ group and porous tantalum group; relative expression levels of ColⅠ, OPN, Runx2 and Homer1 protein on day 14 were higher than those in GdCl₃ group; relative expression levels of ColⅠ, OPN, Runx2 and Homer1 protein on day 21 were higher than those in porous tantalum group, the secretion levels of ColⅠ on days 7, 14, and 21, and OPN on days 7 and 21 were higher than those in GdCl₃ group, porous tantalum group and GdCl₃ + porous tantalum group (P<0.01). The secretion levels of ColⅠ on day 21 and OPN on day 14 in GdCl₃ group were higher than those in control group (P<0.05). The secretion of OPN protein was higher in GdCl₃ group than in control group on the 21st and 14th day of culture (P<0.05). Conclusions After co-culture of porous tantalum with BMSCs, up-regulation of CaSR may promote osteogenic differentiation of BMSCs by activating the expression of Col I, Runx2 and OPN.

Objective To investigate the effect and its mechnism of ubiquitin ligase cullin3 (CUL3) on the proliferation, migration and invasion of gastric cancer cells. Methods The expression of CUL3 in gastric cancer and adjacent tissues and its relationship with clinical prognosis were analyzed based on TCGA database. HGC-27 and BGC-823 cells were transfected with CUL3 shRNA and empty lentivirus to construct a CUL3 knockdown gastric cancer cell line group (shCUL3 group) and an empty lentivirus transfection group (Vector group). CCK-8 assay, clone formation assay, EdU staining, scratch assay and Transwell assay were used to detect the changes of proliferation, migration and invasion ability of the two groups; Western blotting was used to detect the expression of epithelial-mesenchymal transition (EMT)-related proteins and PI3K/Akt/GSK3β pathway proteins in two groups;The changes of migration and invasion ability of shCUL3 group were detected after application of PI3K agonist 740 Y-P. Results In the TCGA database, CUL3 was highly expressed in gastric cancer, and was significantly associated with poor prognosis of gastric cancer patients. Compared with Vector group, CCK-8, clone formation assay and EdU staining showed that the proliferation of gastric cancer cells in shCUL3 group was inhibited (P<0.05), and CUL3 shRNA could significantly inhibit cell migration and invasion (P<0.05); In addition, compared with Vector group, the expression of E-cadherin protein in shCUL3 group increased, and the protein levels of vimentin, β-catenin, p-PI3K, p-Akt and p-GSK-3β significantly decreased (P<0.05); In contrast, application of the PI3K agonist 740 Y-P could partially reverse the inhibitory effect of CUL3 shRNA on gastric cancer cell migration and invasion. Conclusions Knockdown of CUL3 can inhibit the proliferation, migration and invasion of gastric cancer cells, and the mechanism of action of CUL3 in gastric cancer may be related to the activation of PI3K/Akt/GSK3β signaling pathway.

Objective To investigate the targeting relationship of miR-149-5p and fibroblast growth factor 21 (FGF21), and the effect of miR-149-5p on hypoxia/reoxygenation (H/R) injury of rat`s cardiomyocytes. Methods Ten male C56BL/6J mice were used to construct the cardiac ischemia-reperfusion (I/R) models, and qRT-PCR was performed to detect the changes of miR-149-5p levels in the heart tissues of I/R mice. H9c2 cells cultured to logarithmic phase were divided into control group, H/R group, H/R+miR-149-5p inhibitor group, H/R+miR-149-5p NC group, H/R+miR-149-5p mimics group and H/R+miR-149-5p mimics+FGF21 group, and induced H/R model and transfection treatment. The activities of lactate dehydrogenase (LDH) and creatine kinase (CK) in H9c2 cardiomyocytes were detected by ELISA; Cell viability was detected by MTT assay; apoptosis was detected by flow cytometry; the level of miR-149-5p was detected by qRT-PCR; the expression levels of Bcl-2, Bax, cleaved caspase-3 and FGF21 proteins were detected by Western blotting; the targeting relationship between miR-149-5p and FGF21 were determined by dual luciferase assay. Results Compared with the sham operation group, the level of miR-149-5p in the heart tissue of I/R mice was significantly increased (P<0.05). Compared with those in control group, the apoptosis rate, LDH and CK activities and Bax, cleaved caspase-3 protein expression levels of H9c2 cells in H/R group were significantly increased (P<0.05), cell viability and FGF21, Bcl-2 protein expression levels decreased significantly (P<0.05). Compared with those in H/R group and H/R+miR-149-5p NC group, the apoptosis rate, LDH and CK activities and Bax, cleaved caspase-3 protein expression levels of H9c2 cells in H/R+miR-149-5p inhibitor group were significantly decreased (P<0.05), cell viability and FGF21, Bcl-2 protein expression levels were significantly increased (P<0.05). Compared with those in H/R group, the apoptosis rate, LDH and CK activities and Bax, cleaved caspase-3 protein expression levels of H9c2 cells in H/R+miR-149-5p mimics group were significantly increased (P<0.05), cell viability and FGF21, Bcl-2 protein expression levels decreased significantly (P<0.05). Compared with those in H/R+miR-149-5p mimics group, the apoptosis rate, and LDH and CK activities of H9c2 cells in miR-149-5p mimics+FGF21 group were significantly decreased (P<0.05), cell viability was significantly increased (P<0.05). The result of dual luciferase assay indicated the targeted regulatory relationship between miR-149-5p and FGF21. Conclusions MiR-149-5p is up-regulated significantly in the myocardial tissue of I/R mice, and negatively regulate the level of FGF21, leads to decreased cell viability and increased apoptosis of H/R-treated rat's cardiomyocytes.

Objective To investigate the effect of macrophage inflammatory protein-1α (MIP-1α) on proliferation, migration and osteo-differentiation of human periodontal stem cells (hPDLSCs) and its possible mechanism. Methods A total of 16 healthy teeth (orthodontic minus premolar or blocked third molar) extracted from patients aged 12 to 25 years attending the outpatient clinic of the Department of Stomatology, the Second Affiliated Hospital of Xinjiang Medical University from November 2020 to October 2021 were collected and primary stem cells were cultured by tissue block method combined with enzymatic digestion, and the cell phenotype was identified by flow cytometry. (1) Cell biological characteristics experiment: the 3rd generation hPDLSCs were divided into 0 (control group), 1 and 10 μg/ml MIP-1α groups, and each group was then added with α-MEM medium containing volume fraction of 10% fetal bovine serum, 100 U/ml penicillin, and 2 mmol/L glutamine, respectively, and the proliferation ability of each group was detected by CCK-8 method after 24, 48 and 72 h of intervention. The lateral migration ability of cells in each group was detected by scratch assay after 24 h of intervention. (2) Effect and possible mechanism of osteo-differentiation: 3rd generation hPDLSCs were divided into 0 (control group) 1 and 10 μg/ml MIP-1α groups, and osteogenic induction solution was added to each group, and osteogenic ability of cells was detected by alkaline phosphatase (ALP) staining and semi-quantitative analysis 7 d after intervention and by alizarin red staining and semi-quantitative analysis 14 d after intervention;osteogenic ability of cells was detected by qRT-PCR and Western blotting. The mRNA and protein expression of osteogenic genes Runt-related transcription factor 2 (Runx2), bone bridge protein (OPN) and transcription factor SP7 (Osterix) and Notch1 receptor,Jagged 1 ligand and downstream factor Hey1 were detected by qRT-PCR and Western blotting 7 d after intervention. Results Flow cytometry results showed that hPDLSCs STRO-1 and CD146 showed positive expression, and CD34 showed negative expression.(1) In the experiment of cell biological characteristics, the results of CCK-8 method showed that the differences in OD values of hPDLSCs were not statistically significant (P>0.05) in 1 μg/ml and 10 μg/ml MIP-1α groups at 24 h and 48 h compared with control group; at 72 h, the differences in OD values of hPDLSCs were not statistically significant (P>0.05) in 1 μg/ml MIP-1α group compared with control group, while the differences in OD values of hPDLSCs in 10 μg/ml MIP-1α group were significantly higher (P<0.05). The results of scratch assay showed that the difference of scratch healing rate of cells in 1 μg/ml MIP-1α group was not statistically significant compared with that in control group (P>0.05), while the scratch healing rate of 10 μg/ml MIP-1α group was significantly higher (P<0.05). (2) In the experiments of the effect of osteo-differentiation and possible mechanism, ALP staining and semi-quantitative results showed that the ALP activity was obviously lower in 1 μg/ml and 10 μg/ml MIP-1α groups than that in control group (P<0.05). The results of alizarin red staining and semi-quantification showed that the number of mineralized nodules in 1 μg/ml and 10 μg/ml MIP-1α groups were significantly less than that in control group (P<0.05). qRT-PCR and Western blotting results showed that the osteogenesis-related genes Runx2, OPN and Osterix mRNA and protein expression levels in 1 μg/ml MIP-1α group of hPDLSCs were not statistically significant compared with control group, while those in the 10 μg/ml MIP-1α group were significantly lower (P<0.05). Notch1 mRNA and protein expression levels in 1 μg/ml and 10 μg/ml MIP-1α groups were significantly lower than those in control group (P<0.05); Jagged1 and Hey1 mRNA and protein expression levels in 10 μg/ml MIP-1α group were lower than those in control group (P<0.05). while the differences were not statistically significant in the 1 μg/ml MIP-1α group (P>0.05). Conclusion MIP-1α can promote proliferation and inhibit the osteo-differentiation of hPDLSCs, and the mechanism may be related to the inhibition of Notch signaling pathway activation.