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Objective To investigate the correlation of glucose and blood lipid metabolism in elderly patients with Helicobacter pylori (Hp) infection complicated with metabolic syndrome (MS), and to provide theoretical basis for clinical diagnosis and treatment of MS patients. Methods A total of 176 elderly MS patients treated in our hospital from February 2020 to February 2021 were selected. Uremic [13C] tablet breath test kit was used to determine Hp infection. According to Hp infection, they were divided into Hp positive group (n=59) and Hp negative group (n=117). Glucose metabolism indexes (FBG, 2hPG, HbA1c, FINS) and serum lipid metabolism indexes (TC, HDL-C, LDL-C) were determined in all subjects. Risk factors of Hp infection in MS patients were analyzed by multivariate logistic regression. Pearson correlation analysis was conducted between sreum LDL-C, HbA1c and FINS levels and DOB value in MS patients. Results The levels of FBG, 2hPG, HbA1c, FINS and LDL-C in Hp positive group were significantly higher than those in Hp negative group (P0.05). It showed that LDL-C, HbA1c and FINS were independent risk factors for Hp infection in MS patients (P<0.05). Pearson correlation analysis showed that There was a positive correlation between DOB and LDL-C, HbA1c and FINS levels in MS patients (r=0.475,0.512,0.459,P<0.05). Conclusion Hp infection can affect glucose and lipid metabolism in elderly MS patients, and there is a close relationship between Hp infection and ldL-C, HbA1c and FINS levels in elderly MS patients.
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Objective:To preliminarily investigate the mechanism of MMP-9 blocking CD73 detachment from RPE cells surface and preventing and treating experimental autoimmune pigment membranitis(EAU).Methods:RPE cells isolated from wild-type C57BL/6 and CD73 gene knockout (CD73 -/-) mice were cultured in vitro, and treated with lipopolysaccharide and TNF-α to induce CD73 detachment from RPE surface. According to whether MMP-9 inhibitor CTK8G1150 was added at the same time (the final concentration was 5.0 mol/L) or not, RPE cells cultured in the two types of mice were respectively set as MMP-9 inhibitor intervention group and non-intervention control group. The cells in each group were treated with the intervention of a solvent, 1 μmol/Ladenosine monophosphate (AMP), 1 μmol/L AMP, and 3 μmol/L 5' -α,β-methylene adenosine diphosphate (APCP) (AMP+APCP). The stimulating effect of RPE cells in different groups on CD4 + T cell proliferation was detected by tritiated thymidine incorporation. Adoptive immune induced EAU in wild-type B6 mice and CD73 -/- mice, respectively. The receptor mice were randomly divided into the MMP-9 inhibitor intervention group and the non-intervention control group, and CTK8G1150 or the solvent were injected into the subretinal cavity 4, 7 and 10 days after adoptive immunity. CD73 mRNA and protein expression in RPE cells of recipient mice were detected by real-time quantitative PCR (RT-PCR) and Western blot. One-way ANOVA was used to analyze all experimental data. Results:When the stimulation mode was AMP, the proliferation of CD4 + T cells in the C57BL/6 MMP-9 inhibitor intervention group decreased significantly compared with the nonintervention group ( F=13.28, P<0.01). When the stimulation mode was solvent and AMP+APCP, there was no statistically significant difference in the proliferation capacity of CD4 + T cells between the two groups ( F=7.78, 6.58; P>0.05). There was no statistically significant difference in the proliferation capacity of CD4 + T cells between the CD73 -/- MMP-9 inhibitor intervention group and the non-intervention group ( F=5.24, 6.12, 7.04; P>0.05). RT-PCR results showed that there was no statistically significant difference in the relative expression of CD73 mRNA in RPE cells between the MMP-9 inhibitor group and the non-intervention control group( F=6.54, P>0.05). Western blot results showed that the expression of CD73 protein in RPE cells in the MMP-9 inhibitor group of B6 receptor mice was significantly increased compared with the control group ( F=15.24, P<0.01). Conclusion:MMP-9 inhibitor blocks CD73 detachment from RPE cells surface and has a protective effect on EAU.
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Objectives:To investigate the prevalence of depressive emotion and related factors among rural elderly living in urban-rural fringe zones and traditional villages.Methods:Totally 1135 rural elderly were surveyed in Fuding,Fujian Province.The 10-item CES-D Scale was adopted to assess depressive emotion (score 10 or higher as having depression problem),and a self-made questionnaire was used to investigate other relevant demographical information.Results:Rural elderly lived in traditional villages had significantly higher ratio of depression than the elderly lived in urban-rural fringe zones (49.6％ vs.30.3％,P ＜0.001).Logistic regression analysis showed that the ratio of depression in elderly of traditional villages was 1.40 times that of urban-rural fringe zone after control ling other factors.Other important factors (P ＜ 0.001) related to depression were poorer self-rated health (OR =7.52),financial strain (OR =4.41),negative life event (OR =2.91),and living alone (OR =2.72) in elderly of urban-rural fringe zone,but only financial strain (OR =8.52) in elderly of traditional villages.Conclusion:Depression is more prevalently identified among rural elderly living in traditional villages,and urbanization could effectively reduce depression in rural elderly.Public policies should improve the financial and medical security,social support and so on to promote the emotional well-being among rural elderly during urbanization.
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Objective To study how CD73 is shed from the retinal pigment epithelium (RPE) surface. Methods CD73 shedding was induced by treating RPE with lipopolysaccharides (LPS) and TNF-α. After Phospholipase C (PLC) or pan matrix metalloproteinase (MMP) inhibitors were added, surface amount of CD73 was evaluated by flow cytometry (FACS). Then selective inhibitors or their corresponding siRNAs of MMP-2 and MMP-9 were applied to the treatments of RPE; and their effects on induced CD73 shedding were evaluated by FACS. By site directed mutagenesis, mutations were introduced to Lys547-Phe548 coding sites of CD73 cDNA, which was cloned in a pcDNA mammalian expression vector. Both wt-CD73 and mutated-CD73 were over expressed in CD73-/- RPE and their induced shedding was compared. Results LPS and TNF-α induced CD73 shedding from RPE was completely blocked by the addition of pan MMP inhibitor but not PLC inhibitor. Selective MPP-9, but not MMP-2, inhibitor or its siRNA blocked CD73 shedding. In CD73-/- RPE induced CD73 shedding was happened to overexpressed wt-CD73 but not Lys547-Phe548 sites mutant CD73. Conclusion MMP-9 is responsible for shedding CD73 from RPE through hydrolyzing its Lys547 -Phe548 sites.
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Objective To study how CD73 is shed from the retinal pigment epithelium (RPE) surface. Methods CD73 shedding was induced by treating RPE with lipopolysaccharides (LPS) and TNF-α. After Phospholipase C (PLC) or pan matrix metalloproteinase (MMP) inhibitors were added, surface amount of CD73 was evaluated by flow cytometry (FACS). Then selective inhibitors or their corresponding siRNAs of MMP-2 and MMP-9 were applied to the treatments of RPE; and their effects on induced CD73 shedding were evaluated by FACS. By site directed mutagenesis, mutations were introduced to Lys547-Phe548 coding sites of CD73 cDNA, which was cloned in a pcDNA mammalian expression vector. Both wt-CD73 and mutated-CD73 were over expressed in CD73-/- RPE and their induced shedding was compared. Results LPS and TNF-α induced CD73 shedding from RPE was completely blocked by the addition of pan MMP inhibitor but not PLC inhibitor. Selective MPP-9, but not MMP-2, inhibitor or its siRNA blocked CD73 shedding. In CD73-/- RPE induced CD73 shedding was happened to overexpressed wt-CD73 but not Lys547-Phe548 sites mutant CD73. Conclusion MMP-9 is responsible for shedding CD73 from RPE through hydrolyzing its Lys547 -Phe548 sites.
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Objective To investigate whether toll like receptor ( TLR) signaling pathways can in-crease the expression of IL-17 R in neuralglial cells , and if they can whether the increased IL-17 R is func-tional.Methods Experimental autoimmune encephalomyelitis (EAE) was induced in B6 mice by immuni-zation with an emulsion of myelin oligodendrocyte glycoprotein 35-55 ( MOG35-55 ) in complete Freund's adju-vant (CFA).The expression of Il17ra and Il17rc in the brains and spinal cords of mice with EAE were de-tected by real-time PCR.Luxol fast blue ( LFB) staining was performed to the spinal cord sections to detect tissue demyelination.Immunohistological staining against IL-17RA and CD3 were undertook to visualize IL-17RA+and CD3 + cells.Same approaches were also applied to immunized Rag1 -/- mice to figure out whether T cells infiltration is necessary for increasing IL-17RA expression in the central nervous system ( CNS) .Then B6 mice were immunized with incomplete Freund′s adjuvant ( IFA) plus different TLRs ago-nists to measure the expression of Il17ra in the brains and spinal cords by qPCR .The purified astrocytes , microglia and oligodendrocytes isolated from neonatal mice brains were cultured in vitro for two weeks , and then treated with different TLRs agonists .The expression of Il17ra at mRNA and protein levels in the cells were determined by qPCR and Western blot respectively .The astrocytes were treated with IL-17A and LPS individually or in the combination to detect the level of CCL 2, CXCL8 and IP-10 in the supernatant by ELISA.Results B6 mice with induced EAE showed significantly increased Il17ra expressions in the brain and spinal cord , which was also detected in immunized Rag1 -/-mice.Although no spinal cord demyeliza-tion and CD3 cells infiltration were detected in Rag1 -/-mice, significantly increased number of IL-17RA positive cells could still be visualized .In vivo TLRs agonist participated immunization and in vitro treatment of purified neuroglial cells demonstrated that TLRs agonists could directly evoke IL -17RA expression in the CNS or cultured astrocytes , microglia and oligodendrocytes with high efficiency .Both IL-17 A and LPS could stimulate astrocytes to secrete CCL2, CXCL8 and IP-10, however, a combined use of IL-17A and LPS fur-ther augmented the production of these chemokines to a large extend .Conclusion Taken together , we con-cluded that TLRs agonists could directly stimulate neuroglial cells to express IL -17RA which functionally re-spond to IL-17A by secreting chemokines .
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Objective To investigate the expression of adenosine receptor (ADOR) subtypes (A2A and A2B subtypes) in the mucosal dendritic cells (DCs) from patients with Crohn's disease and their pathogenic roles.Methods Mucosal DCs (mDCs) were isolated from resected intestine of patients with or without Crohn's disease.Some of the mDCs were cultured in vitro and others were used to extract RNA.The expression of ador-a2a and ador-a2b were detected by real-time qPCR.mDCs in culture were treated with selective ADOR-A2A and ADOR-A2B agonists (CGS 21680 and BAY 60-6583) and then the concentration of IL-1,IL-6 and IL-12 in the medium were measured by ELISA.The binding affinities of ADOR-A2A and ADOR-A2B to adenosine were determined by 3H-adenosine in combination with selective ADOR-A2A and A2B antagonists (SCH58261 and MRS1706).Na(i)ve CD4+ cells were collected from human umbilical cord blood and co-cultured with mDCs treated by different ADOR agonists to observe T cell responses.The production of cytokines in culture was measured by ELISA.The polarization of CD4+ cells was analyzed by intracellular cytokine staining and FACs analysis.Peripheral blood mononuclear cells (PBMCs) were treated with IL-4 and GMCSF to induce the expression of monocyte-derived DCs (Mo-DCs).Mo-DCs were treated with different toll-like receptor ligands to investigate their effects on the expression of ador-a2a and adora2b.Moreover,Mo-DCs were treated with LPS and BAY 60-6583 individually or in the combination to stimulate CD4+ cells.Then the production of cytokines and the polarization of CD4+ cells were evaluated.Results Compared with patients without Crohn's disease,patients with Crohn's disease showed no change in the expression of ador-a2a but a significantly increased expression of ador-a2b in mCDs (CD-mDCs),enabling to bind more adenosines.Activated ADOR-A2B signaling pathway induced CD-mDCs to secret more proinflammatory cytokines and to promote polarization of CD4+ cells toward Th1 and Th17 cells.Toll-like receptor ligands,pam3csk4 and LPS could intensively augment the expression of ador-a2b in Mo-DCs.The pathogenicity of Mo-DCs was strengthened upon a combined stimulation with BAY 60-6583 and LPS.Conclusion The significantly increased expression of ador-a2b in mDCs might be involved in the pathogenesis of Crohn's disease by promoting mDCs to secret more pro-inflammatory cytokines and enhancing the polarization of CD4+ cells.Moreover,the expression of ador-a2b in DCs could be regulated by certain toll like receptors.
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Objective To investigate the effect of propofol on the cerebral injury induced by ketamine in neonatal rats. Methods Eighty 7-day-old SD rats of both sexes, weighing 12-20 g, were randomly divided into 4 groups (n = 20 each): normal saline (NS) group, ketamine-induced cerebral injury group (group K), propofol group (group P) and propofol combined with ketamine group (group PK). Group NS received intraperitoneal NS 1 ml. In groups K, P and PK, ketamine 70 mg/kg, propofol 70 mg/kg and propofol 70 mg/kg + ketamine 70 mg/kg were injected intraperitoneally once every 2 h for 3 times respectively. Ten rats in each group were selected and sacrificed at 24 h after emergence from anesthesia and the hippocampi obtained to determine the neuronal apoptosis (by TUNEL) and Bcl-2 and Bax protein expression(by immunohitochemistry). The apoptosis rate was calculated.The other 10 rats in each group were selected at 21 days after the intraperitoneal injection and the learning and memory functions (escape latency and frequency of crossing the original platform) were evaluated using Morris water maze. Results Compared with group NS, the apoptosis rate was significantly increased in group K, Bcl-2 protein expression was up-regulated in groups P and PK, and Bax protein expression was up-regulated, the escape latency was significantly prolonged and the frequency of crossing the original platform was significantly decreased in the other groups (P ＜ 0.05 .or 0.01 ). Compared with group K, the apoptosis rate was significantly decreased in group PK, Bax protein expression was down-regulated in group P, and Bcl-2 protein expression was up-regulated,the escape latency was significantly shortened and the frequency of crossing the original platform was significantlyincreased in groups P and PK ( P ＜ 0.05). Conclusion Propofol can reduce the cerebral injury induced by ketamine in neonatal rats, and the regulation of the Bcl-2 and Bax protein expression and inhibition of the neuronal apoptosis in hippocampus may be involved in the mechanism.
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Objective To investigate the effect of propofol on ketamine-induced cognitive dysfunction and neuronal apoptosis in hippocampus in aged rats. Methods Thirty-two male SD rats aged 18-24 months weighing 380-470 g were randomly divided into 4 groups ( n = 8 each) :control group (group C);propofol group (group P);ketamine group (group K) and propofol + ketamine group (group PK). Propofol 30 mg·kg-1·h-1 or/and ketamine 40 mg· kg-1·h-1 were infused for 2 h once a day for 7 consecutive days. After the last day of drug administration cognitive function was assessed using Morris water maze (escape latency and the number of animals' swimming across the platform). The animals were sncrificed after water naze test and their hippocampi were removed for determination of neuronal apoptosis (by TUNEL) and caspase-3 expression (by immuno-histochemistry) in hippocampal CA1 region. Results There was no significant difference in escape latency and the number of the animals,swimming across the platform, the neuronal apoptotic rate (the number of apoptotic neurons/the number of total neurons) and caspase-3 expression between group C and P. In group K and PK the escape latency was prolonged,the number of animals' swimming across the platform was decreased, neuronal apoptotic rate increased and the caspase-3 expression up-regulated as compared with group C. The ketamine-induced changes were significantly attenuated by coadministration of propofol in group PK. Conclusion Coadministration of propofol can ameliorate ketamine-induced cognitive dysfunction and hippocampal neuronal apoptosis.
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Objective: To study the relationship between the depth and width of cavity design and to analyze the tendency of breaking load in preparations. Methods:Plaster models of mandibular first molar were prepared and magnified by 150%. Cavity on occlusal surface was designed and prepared in a cylinder shape with the depth(mm) of 3.0,4.5 and 6.0,and diameter(mm) of 3.0,4.5 and 6.0,respectively. 8 cavity samples were prepared for each design. The breaking load of the tooth models before and after restoration with self-curing resin was measured by Instron tester.Mechanical model static load test and two variable regression analysis were applied to study the mechanical property of the cavity design. Results:Before restoration, with the increase of depth and diameter, the incidence rate of tooth fracture increased. The width was the main factor. After restoration, the load was undertaken by restoration directly, and could be transfered to tooth and periodontal tissue through restoration uniformly. When the diameter of the cavity increased, the diameter of restoration also increased, and thus decreased the load on local structure of the tooth. With two-regression analysis, the regression equation and regression curve were obtained. Conclusion: The fracture of tooth before and after restoration is related to the diameter and depth of cavity design in cylinder shape. The regression equations of changing tendency of breaking load (Y) in preparation caused by the change of depth(X 1) and diameter(X 2) of cavity obtained by two-regression analysis are presented as follows: Before restoration: Y=1593.317-51.178 X 1-79.489X 2.After restoration:Y=1802.928 -192.461X 1+225.128X 2.