Objective To explore the effects of environmental lead exposure on immune system in preschool children. Methods The blood lead levels of 217 preschool children were determined by graphite furnance atomic absorption spectrophotometry. The distribution of T_lymphocyte subsets: CD 3+,CD 3+CD 4+,CD 3+CD 8+, B cells (CD 3- CD 19+), NK cells (CD 3-CD 16+CD 56-) were analyzed by flow cytometer, the levels of serum immunoglobulin G and immunoglobulin M were determined by scattering turbidimetry, the levels of serum immunoglobulin E were examined with ELISA. Results The mean level of blood lead of 217 preschool children was (0.46?0.27)?mol/L(range:0.11～2.71 ?mol/L). The blood lead levels of 63 preschool children were ≥0.48 ?mol/L. 38 preschool children among 63 preschool children with blood lead level of ≥0.48 ?mol/L were selected as the high_blood_lead group, 35 preschool children with blood lead levels of 0.05). Condusion The blood lead levels of ≥0.48 ?mol/L presented adverse effects on the T_lymphocyte subsets.

Objective To evaluate the effect of azithromycin on mycoplasmal pneumonia (MP).Methods We divided 90 MP cases into azithromycin and erythromycin treatment groups. In azithromycinThe pyretolysis time, cough improvement time, the disappearing time and the mean length of hospitalization of azithromycin group were shorter than that of erythrornycin group. The local ache, stomach and intestinal tract adverse reaction, and damage of hepar function were less than these in erythromycin group. ConclusionAzithromycin is an effective and safe drug to MP.

Adult ; Female ; Humans ; Middle Aged ; Posture ; Pregnancy ; Pregnancy Outcome ; Retrospective Studies ; Sedentary Lifestyle ; Surveys and Questionnaires ; Work ; Young Adult

AIM:To investigate the effect of fluvastatin on the expression of serum and glucocorticoid inducible kinase 1 ( SGK1) and connective tissue growth factor ( CTGF) induced by aldosterone ( Ald) in rat mesangial cells (GMCs). METHODS:GMCs were divided into (1) control group; (2) aldosterone group with different concentrations and times; (3) Ald (10 -7 mol/L) + spironolactone (10 -9 mol/L) group; (4) Ald (10 -7 mol/L) + LY294002 (20 ?mol/L) group; (5) Ald (10-7mol/L) +SB203580 (20 mmol/L) group; (6) the group of Ald (10-7mol/L) + fluvas-tatin at different concentrations (10-7,10-6,10-5 mol/L); (7) Ald (10 -7mol/L) + fluvastatin (10 -5mol/L) + mevalonate (10 -4 mol/L) group; (8) Ald (10 -7 mol/L) + fluvastatin (10 -5 mol/L) + FPP (farnesyl pyrophosphate,10-4 mol/L) group; (9) Ald (10 -7mol/L) + fluvastatin (10 -5 mol/L) + GGPP (geranylgerany pyrophosphate,10 -4 mol/L) group. The protein levels of SGK1 and CTGF were determined by Western blotting. The levels of fibronection (FN),monocyte chemoattractant protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1) in the supernatants were determined by enzymelinked immunosorbant assay (ELISA). RESULTS:Aldosterone stimulated the protein expression of SGK1 and CTGF in cultured mesangial cells in a dose-dependent manner (P

Chromosomes, Human, Pair 14 ; Humans ; Ring Chromosomes ; Syndrome

Objective It remains a controversy whether 5-lipoxygenase (5-LOX) is associated with colon cancer stem cells.This study was to investigate the effect of the 5-LOX inhibitor MK886 in maintaining the stemness of the human colon cancer cell line HT-29.Methods Using CCK-8 assay, we examined the inhibitory effects of different concentrations of MK886 (12.5, 25, 50, 75, 100, and 200 μmol/L) on the colon cancer HT-29 cells cultured in vitro and calculated its half-inhibitory concentration (IC50).Then, we detected the effects of MK886 IC50 on the clone-and sphere-forming abilities of the cells, determined the mRNA expressions of the stemness markers CD133, Lgr5, Oct4 and Ascl2 by real-time PCR after 24 and 48 hours of MK886 IC50 intervention, and measured their protein expressions by Western blotting after 24, 48 and 72 hours of MK886 IC50 intervention.Results The inhibition rates of MK886 on the HT-29 cells at 24 and 48 hours were significantly increased in a time-and dose-dependent manner ([14.99±3.06] and [19.98±0.57]％ at 12.5 μmol/L, [20.46±1.14] and [34.97±6.02]％ at 25 μmol/L, [50.76±5.94] and [66.90±5.74]％ at 50 μmol/L, [66.84±1.77] and [73.11±2.48]％ at 75 μmol/L, [72.67±2.36] and [77.78±3.30]％ at 100 μmol/L, [83.67±0.24] and [84.69±2.24] ％ at 200 μmol/L) as compared with the blank control (0％ and 0％) (P<0.05).The clone-forming rate and number of spheres formed were remarkably lower in the MK886 intervention than in the control group ([10.60±1.71] vs [44.67±3.21]％, P<0.05;6.00±1.60 vs 19.07±2.89, P<0.05).After 24 and 48 hours of MK886 intervention, the mRNA expression of CD133 in the HT-29 cells was markedly up-regulated in comparison with that at 0 hour (0.72±0.10 and 0.39±0.07 vs 1.66±0.33, P<0.05), and so were those of Lgr5, Oct4 and Ascl2 (P<0.05).Conclusion The 5-LOX inhibitor MK886 can inhibit the proliferation and clone-and sphere-forming abilities of human colon cancer HT-29 cells by down-regulating the expressions of the stemness markers and thus suppressing the stemness of the colon cancer stem cells.

OBJECTIVETo study the anti-immune inflammation efficacy and toxicity of Tripterygium wilfordii decoction, in order to provide experimental basis for studies on its "efficacy-toxicity" correlation.

METHODThe delayed hypersensitivity model was established by dinitrofluorobenzene in mice. Different doses of T. wilfordii decoction was administered for 5 consecutive days. The ear swelling inhibition ratio and the toxic action were observed. After the final administration, the biochemical indexes of PGE2, TNF-α, IL-2, ALT, AST, PA, TBA, TBIL in serum were detected, and the visceral indexes of heart, liver, spleen and kidney were measured.

RESULTThe DNFB-induced ear swelling could be notably inhibited by multiple oral administration of T. wilfordii decoction, with the ED50 and its 95% confidence limit of 0.34 (0.21-0.42) g x kg(-1). The contents of PGE2, TNF-α, IL-2 in serum decreased in a dose-dependent manner. The activities of serum AST, ALT, TBA, TBIL and the PA content reduced.

CONCLUSIONT. wilfordii decoction shows a significant anti-immune inflammation efficacy within the dosage range between 0.59 and 2.34 g x kg(-1) in a dose-dependent manner. With a certain hepatotoxicity, high dose (2.34-4.68 g x kg(-1)) of T. wilfordii decoction can cause substantial liver injury, with a dose dependence in liver function index. Therefore, the efficacy and toxicity of T. wilfordii is dose dependent, which provides reference for preventing adverse drug reactions in clinic and developing early-warning schemes and ensure the clinical medication safety of T. wilfordii.

Animals ; Anti-Inflammatory Agents ; administration & dosage ; chemistry ; toxicity ; Drug Dosage Calculations ; Drug Evaluation, Preclinical ; Drugs, Chinese Herbal ; administration & dosage ; chemistry ; toxicity ; Edema ; drug therapy ; genetics ; immunology ; Humans ; Interleukin-2 ; genetics ; immunology ; Male ; Mice ; Tripterygium ; chemistry ; toxicity ; Tumor Necrosis Factor-alpha ; genetics ; immunology

AIM:To investigate the effect of 18 alpha-glycyrrhetinic acid (18α-GA) on delaying the senescent progress and promoting the proliferation in late-passage bone marrow mesenchymal stem cells ( BMSCs ) .METHODS:Late-passage BMSCs were incubated with 2.0 mg /L 18α-GA or the same volume of DMSO for 30 d, and the cells were harvested to determine the proteasome activity .The expression of senescence-related proteins p53, p21 and p16 was detec-ted by senescence-associated β-galactosidase ( SA-β-Gal) staining and Western blot .The cell proliferation , the expression level of cell cycle-related proteins and cell cycle distribution of the cells were measured by CCK -8 assay, BrdU incorpora-tion, Western blot and flow cytometry.RESULTS:Compared with DMSO group, the proteasome activity in 18α-GA group increased significantly by about 0.2 times (P<0.01).SA-β-Gal-positive cells in 18α-GA group decreased, and cell stai-ning was lighter.The contents of p53 and p21 in 18α-GA group were decreased (P<0.05).The results of CCK-8 assay showed that the A value in 18α-GA group was 0.3 times higher than that in DMSO group (P<0.01).BrdU incorporation showed the increased proliferation in 18α-GA group compared with DMSO group ( P<0.05).The cells in G1 phase in 18α-GA group decreased significantly compared with DMSO group , while the cells in S phase increased significantly ( P<0.05).The expression level of cyclin D1 in 18α-GA group was 2.8 times higher than that in DMSO group (P<0.01), and the CDK4 level was 1.4 times higher than that in DMSO group (P<0.05).CONCLUSION:Activation of the pro-teasome activity by 18α-GA delays the aging process in the BMSCs and promotes the cell proliferation via up -regulation of the cell cycle-related proteins .

Objective To investigate the role and possible mechanism of P120 catenin involving in the hemodynamic changes by inducing vascular endothelial cells injury through an in vitro experiment. Methods The hemodynamic environment under the different hemodynamic conditions at the vascular bifurcations was simulated through a T-shaped flow chamber system designed by ourselves. The human umbilical vein endothelial cells (HUVEC)cultured in vitro were stimulated and used the HUVEC cells of the small interfering RNA (SiRNA)after P120ctn gene fragments being knocked out. After loading flow rate of 250 and 500 ml/ min respectively and acting on for 12 h,the HUVEC morphology,growth pattern,and expression of P120ctn and other proteins were observed. Results (1)Normal HUVEC:500 ml/ min was loaded for 12 h,the cells were fused excessively at the impinging point,the cell gaps became narrowed,the cell density decreased and the morphology was elongated in the high wall shear stress (WSS)and wall
shear stress gradient (WSSG)regions. A part of cells migrated downstreamly,and their arrangement direction was consistent with the direction of impinging flow. Compared with the unloaded impinging flow field,after the 2 kinds of impinging flows being loaded for 12 h,the expression levels of P120ctn,vascular endothelial calcium (VEC),Kaiso,α-catenin,and other proteins were decreased. The expression level of matrix metalloproteinase 2 (MMP-2)was increased. There were significant differences (all P < 0. 05). (2)HUVEC after P120ctn being knocked out:Under the impact of the impinging flow,the cell growth time was reduced to 60 min. 250 ml/ min being loaded for 60 min,the impinging point and its surrounding cells still maintained the polygon,but some cells in the high WSS and high WSSG regions began to move downstreamly and aggregated,the cell arrangement mode partly arranged along with the direction of the flow;500 ml / min being loaded for 60 min,the cell density in the high WSS and high WSSG regions were decreased significantly and the morphology was elongated. A large number of cells migrated downstreamly and aggregated. The arrangement mode was parallel and consistent with the direction of the impinging flow. Compared with the unloaded impinging flow field,after the 2 kinds of velocities being loaded for 60 min,the expression levels of VEC,Kaiso,α-catenin proteins were decreased. The expression level of MMP-2 was increased,There were significant differences (all P < 0. 05) Conclusions The hemodynamic change may induce the changes in vascular endothelial cell morphology,growth pattern,and expression of P120ctn and other related proteins, leading to the decrease of vascular endothelial cell adhesion connection stability and the expression changes of related proinflammatory factors. The knockout of P120ctn may result in a further decrease of the vascular endothelial cell adhesion connection stability.