The incidence rate of vascular dementia is increasing year by year, and there is still no effective treatment at present, so it is very important to reduce the risk of developing vascular dementia. Research shows that diabetes is associated with vascular dementia. Based on the research literature related to diabetes and vascular dementia from January 1995 to April 2023, This article reviews the relationship between diabetes and vascular dementia, pathological mechanism and prevention and control strategies. It is found that diabetes can promote the occurrence and development of vascular dementia by inducing cerebrovascular disease, oxidative stress and inflammatory reaction, using hypoglycemic drugs, removing the incentives of cerebrovascular disease, maintaining the stability of blood-brain barrier and adhering to a healthy lifestyle are the main measures for the prevention and control of vascular dementia at this stage. Future research needs to further explore the mechanism of vascular dementia induced by diabetes, and seek economic and effective prevention targets.

Objective To investigate the mechanism of acquisition of HLA-G1 antigen by NK cells.Methods K562 cells stably expressing HLA-G1 antigen (K562-G1) were constructed.K562-G1 cells, K562 cells and shed HLA-G1 were respectively co-cultured with NK-92MI cells to observe the acquisi-tion of HLA-G by NK cells.To further investigate the mechanism , NK-92MI cells with blockage HLA-G re-ceptors were further co-cultured with K562-G1 cells and HLA-G1 proteins expressing on K 562-G1 cells were blocked and then co-cultured with NK-92MI cells. Acquisition of HLA-G 1 by NK-92MI cells was analyzed by flow cytometry and fluorescence microscopy .The effects of HLA-G1 expression on the cytotoxicity of NK-92MI cell were evaluated by flow cytometry analysis based on CD 107a labeling.R esults NK-92MI cells could quickly acquire HLA-G1 from K562-G1 cells in co-culture experiments .Blockade of HLA-G1 or its re-ceptors KIR2DL4 and ILT2 with specific mAbs did not affect the acquisition of HLA-G1 by NK-92MI cells. Moreover, HLA-G1 could significantly inhibit the cytotoxicity of NK cell ( P<0.01).Conclu sion NK-92MI cells acquire HLA-G1 from K562-G1 cells via trogocytosis , which is not associated with affinity be-tween receptor and ligand , extracellular domain of HLA-G1 or passive adhesion .

AIM: To investigate effect of naringenin on ADP-induced platelet aggregation and its possible mechanism.METHODS: The levels of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) were measured in the platelets with ADP stimulation using ELISA in the presence or absence of different concentrations of naringenin.The effect of naringenin at different concentrations on the change of phosphodiesterase (PDE) activity was measured by high efficiency liquid chromatography.The effects of naringenin at different concentrations on phosphorylation of vasodilator-stimulated phosphoprotein (VASP) at positions Ser157 and Ser239 in washed platelets with ADP stimulation were analyzed by Western blot.The phosphorylation of VASP at Ser239 was also analyzed in the presence of protein kinase A (PKA), protein kinase G (PKG), or protein kinase C (PKC) inhibitors before incubation with naringenin.The platelet aggregation was measured in the presence of PKA or PKG inhibitors before incubation with naringenin.RESULTS: Naringenin elevated cGMP levels significantly but not cAMP levels in the platelets with ADP stimulation in a dose-dependent manner.Naringenin inhibited PDE activity.Naringenin increased the phosphorylation of VASP at Ser239 in a dose-dependent manner in the platelets with ADP stimulation but only modest changes in the phosphorylation at position Ser157.The phosphorylation level of VASP at Ser239 position was inhibited when the platelets were treated with PKA inhibitor before incubation with naringenin.Incubation of platelets with neither PKG nor PKC inhibitors before treatment with naringenin affect the phosphorylation of VASP at Ser239.Pretreatment with PKA inhibitor but not PKG inhibitor significantly reversed the antiplatelet aggregation by naringenin in ADP-stimulated platelets.CONCLUSION: Naringenin may inhibit platelet activation through the elevation of cGMP-and PKA-mediated VASP phosphorylation.

AIM: To investigate the antiplatelet aggregation of naringenin and its possible mechanism . METHODS:The effects of naringenin at different concentrations on adenosine diphosphate ( ADP)-induced platelet aggre-gation and platelet spreading on immobilized fibrinogen were detected by aggregational detector and observed under fluores -cence microscope, respectively.The expression of phosphoinositide 3-kinase (PI3K) and the phosphorylation of Akt were analyzed by Western blot .RESULTS:Naringenin significantly inhibited ADP-induced platelet aggregation in a dose-de-pendent manner in vitro and in vivo, and inhibited platelet ' s spreading on immobilized fibrinogen in vitro.Further studies indicated that naringenin inhibited platelet activation accompanied by attenuating not only the activation of PI 3K, but also the phosphorylation of Akt .Moreover, naringenin combined with LY294002 additively inhibited the ADP-induced platelet aggregation.CONCLUSION:Naringenin may inhibit platelet activation by regulation of PI 3K/Akt signaling pathway.

Objective To study the clinical significances of CD14bright CD16bright cell subset in pe-ripheral blood of patients with gastric cancer (GC). Methods The CD14bright CD16bright cells in peripheral blood samples collected from 124 patients with gastric cancer ( GC), 130 patients with chronic gastritis (CG) and 80 normal healthy controls (HC) were measured by using flow cytometry. Differences in the CD14bright CD16bright cells between different groups were analyzed with the Mann-Whitney U test. The feasibili-ty of using CD14bright CD16bright cells as a potential biomarker for differentiating GC patients from CG was as-sessed by using the receiver operating characteristic ( ROC) curve analysis. Correlations between the CD14bright CD16bright cells and clinicopathologic parameters of GC were analyzed with multivariate correlation analysis. Results The percentages of CD14bright CD16bright cells in peripheral blood samples and in CD14bright monomuclear cells collected from the patients with GC [median: 0. 38% (0. 23% -0. 52% ) and 6. 61%(4. 23% -9. 56% )] were significantly higher than those of the CG and HC groups [ median: 0. 11%(0. 07% -0. 15% ) and 5. 08% (3. 35% -6. 42% ); median: 0. 05% (0. 03% -0. 07% ) and 5. 09%(4. 20% -7. 40% )] (P<0. 01). The area under the ROC curve for CD14bright CD16bright cells in the peripher-al blood was 0. 934 (95% CI: 0. 900-0. 968) indicating that the value of CD14bright CD16bright cells in the di-agnosis of GC was much higher than that of alpha fetoprotein (AFP), cacino-embryonic antigen (CEA) and carbohydrate antigen CA199. The area under the ROC curve for combined multi-markers by using logistic model (CD14bright CD16bright cell subset and serum tumor markers) was 0. 947 (95% CI: 0. 920-0. 973). The CD14bright CD16bright cells were closely associated with lymphocyte cells ( P < 0. 01). Conclusion The CD14bright CD16bright cells were dramatically increased in the peripheral blood of patients with gastric cancer, which could be used as a biomarker in the diagnosis of gastric cancer.

In this article we analyzed the current development of moxibustion treating rheumatoid arthritis from the usefulness, advancement, synergistic effect as well as the variance between different kind of moxibustion. We concluded that moxibustion was an effective intervention for treating RA, and the methods used in moxibustion were searched in clinic. But the clinical tralls has a long way to go, we should pay more attention to the critical issues while in the use of moxibustion.

Objective To systematically assess the clinical efficacy and security of Wendan Decoction in the treatment of dyslipidemia. Methods Retrieved from CNKI, CBM, VIP database, Wanfang Database, and PubMed, articles of RCTs about Wendan Decoction in the treatment of dyslipidemia were included. The searching range was from the establishment of the database to April, 2016. NoteExpress3.2.0 was used to establish database. Two researchers independently screened the articles and extracted the data. Cochrane Systematic Review Manual 5.1.0 was used for quality evaluation. Meta-analysis was performed with RevMan5.3 software. Results 12 articles involving 848 patients were included. Results of Meta-analysis showed that compared with the western medicine treatment, Wendan Decoction group was more capable of significantly improving clinical effective rate of dyslipidemia [OR=2.46, 95%CI (1.41, 4.30), P=0.001], lowering the level of TG [WMD=-0.31, 95%CI (-0.46, -0.15), P=0.0001] and LDL-C [WMD=-0.25, 95%CI (-0.30, -0.20), P=0.00001], but there was no statistical significance in regulating TC [WMD=-0.14, 95%CI (-0.35, -0.08), P=0.49] and HDL-C [WMD=0.04, 95%CI (-0.01, -0.1), P=0.13] between the two groups; compared with the western medicine group, Wendan Decoction combined with western medicine group was more capable in the clinical effective rate of dyslipidemia (P<0.05), regulating the level of TG [WMD=0.30, 95%CI (-0.37, -0.23), P=0.00001], TC [WMD=0.65, 95%CI (-0.80, -0.69), P=0.00001], LDL-C (P<0.05, P<0.01) between the two groups; Wendan Decoction combined with western medicine group had low rate of adverse reactions. Conclusion Wedan Decoction can effectively regulate dyslipidemia, with good safety. High quality RCTs in large-scale and multi-center are necessary for further evidence due to the poor methodological quality of included trials with few samples and other limitations.

Objective:To explore the effects of exosomes derived from bone-marrow endothelial progenitor cells(EPCs-Exos)on the angiogenesis and collagen deposition in vitro,and to illustrate the possible mechanism for EPCs-Exos to accelerate the cutaneous deficiency repair.Methods:The endothelial progenitor cells (EPCs) were isolated, cultivated and identified;at the same time, the EPCs-Exos were also isolated and identified.The EPCs-Exos uptake in EPCs was observed and analyzed.16 rats were randomly divided into 4 groups, and then the models of skin defect were established, respectively.The equal volume of PBS and 50, 100, 150 mg·L-1 EPCs-Exos were injected into the area around skin defect of the rats in 4 groups.The wound closed sizes on the 0, 3rd, 7th and 14th days were measured, and Masson''s trichrome staining and CD31 immunofluorescence staining were performed on the 14th day for evaluating the tissue healing efficacy after EPCs-Exos treatment.In vitro,the mediums containing PBS and 50, 100, 150 mg·L-1 EPCs-Exos were used to culture the human umbilical vein endothelial cells (HUVECs), respectively.Scratch test and tubule formation assay were used to detect the migration and capillary network formation of HUVECs.At the same time, Western blotting was used for analyzing the expression level of angiogenesis related gene vascular endothelial growth factor A (VEGFA) in HUVECs.Results: The primary EPCs were isolated and identified successfully, and EPCs-Exos were purified and characterized.The CD31 immunofluorescence staining and double staining of DiL-ac-LDL and FITC-UEA-I of EPCs were positive.The electron microscope results showed that EPCs-Exos were nearly spheroidal, with the diameter about 40-100 nm.For the models of rat skin injury treated by EPCs-Exos, with the increasing of injection doses, the sizes of skin defect scar were gradually reduced, the degrees of scar healings were gradually increased,and the differences between various groups were statistically significant (P< 0.05).EPCs-Exos promoted the collagen maturity of healing skin in a dose-dependent manner;on the 14th day, the effect in 150 mg·L-1 EPCs-Exos group was the most significant.In vitro, EPCs-Exos promoted the migration and capillary network formation of HUVECs and increased the expression level of VEGFA;the migration rate,the net number of branches and the expression level of VEGFA in 150 mg·L-1 EPCs-Exos group were significantly higher than those in 50 mg·L-1 EPCs-Exos group and PBS group (P< 0.05).Conclusion: EPCs-Exos can promote the repair of traumatic skin defect of the rats by positively regulating the vascular endothelial cell function.

AIM: To investigate the multidrug resistance(MDR),reversal activity of 2-[4-(2-pyridin-2-yl-vinyl) henyl]-4,5-bis-(4-N,N-diethylaminophenyl)-1(H)-imidazole(FG020318) in a retinoblastoma subline SO-Rb50/VCR,which is resistant to vincristine.METHODS: The procedure of stepwise increase in drug concentrations was used to obtain SO-Rb50/VCR,which was resistant to 200 ?g/L vincristine. The chemosensitivity of this drug resistant cell line with and without FG020318 or cyclosporine A(CSA) were detected by MTT assay and the function of p-glycoprotein(P-gp) was examined by rhodamine 123 accumulation detected with flow cytometry(FCM).RESULTS: FG020318(2.5 ?mol/L) significantly reduced IC50 and increased the rhodamine accumulation in a concentration-dependent manner. It was much stronger than the positive control CSA in reversal of MDR.CONCLUSION: A new tumor MDR modulator FG020318 partly reverses MDR in SO-Rb50/VCR.It may be a promising new drug to tackling MDR.

BACKGROUND:The structure of tissue engineering carrier affects the bio-action of cells greatly.OBJECTIVE: To investigate the biological characteristics of bone marrow stem cells (MSCs) in different concentrations of alginate combined with de-antigen bone xenograft (DBX).DESIGN: Observational trial.SETTING: PLA Institute of Trauma and Orthopedics, the Fourth Military Medical University of Chinese PLA.MATERIALS: Alginate, calcium chloride, MSCs, bone xenograft.METHODS: Bovine cancellous bone was out into cubes, which were degreased, deproteinized and then lyophilized.Cubes in pore size within 300-500 μm were selected for use after ethylene oxide sterilization. The purified sodium alginate was dissolved in DMEM cell culture medium of concentrations as different as 0.5%, 2%, 8% and 16%; 1×1012 L-1 induced MSCs were blended with isopyknic alginate-DMEM and compounded with DBX at a status of 0.5 Mpa negative pressure for 5 minutes in order to make a cell suspension fully fill into the pores of the cancellous bone. Then alginate was crosslinked with 50 g/L calcium gluconic acid for 30 seconds. The complex was put into a CO2 incubator and cultured for 4 days. The gel compound and cell growth in the pores of the complex were grossly observed with an inverted microscope. Status of cell growth in the complex with different concentrations of alginate was observed with scanning electron microscopeMAIN OUTCOME MEASURES: Compound status of alginate and bone xenograft, cell growth status and matrix secretion in compound carries.RESULTS: When the concentration of alginate was 0.25% or 1%, alginate was equally combined in DBX, while that of 4% and 8% only combined on the surface of cancellous bone. After in vitro cultured for 4 days, alginate of 0.25% were broken off from DBX surface. But alginate of 1% was equally combined with DBX pores with cells secreting well in alginate. Development of cells in alginate of 4% was restricted and no cells were seen in alginate of 8%.CONCLUSION: Alginate of 1% is suitable for constructing the carrier of bone tissue engineering with bone xenograft.