Alzheimer's disease (AD) is a most common neurodegenerative disease. The mechanisms underlying AD, especially late-onset AD, remain elusive. In the past few years, results from genome-wide association studies (GWAS) and systems approaches indicated that innate immune responses mediated by microglia played critical roles in AD. Functional analysis on animal models also showed that immune receptors or proteins expressed in microglia mediated Abeta-induced inflammation, or Abeta phagocytosis by microglia. Microglia plays double sword roles in AD. More work is warranted to elucidate the exact roles of microglia in AD, which will facilitate our better understanding of the mechanisms underlying AD.
Alzheimer Disease ; pathology ; Animals ; Disease Models, Animal ; Genome-Wide Association Study ; Humans ; Inflammation ; pathology ; Microglia ; physiology ; Phagocytosis ; Receptors, Immunologic ; physiology

Objective To study the impact of sodium arsenite(NaAsO2) exposure on melanoma cells A375 (hereinafter referred to as the A375) and G361 (hereinafter referred to as the G361) pigment production and tyrosinase (TYR) activity and the differences of pigment metabolism capacity between the cell lines.Methods A375 and G361 cells were exposed to sodium arsenite at concentrations of 0.0(control),0.1 and 1.0 μmol/L for 72hours.Cell viability was measured by Alamar Blue assay.Melanin levels and TYR activity were measured at the same time.Results After exposure for 72 hours,the cells of 0.1 μmol/L dose groups of both of the two cell lines [A375:(103.32 + 1.26)％; G361:(104.10 + 1.76)％] showed a slightincrease of proliferation without significant differences compared with those of the control[A375:(100.00 ± 1.08)％; G361:(100.00 + 1.79)％,all P ＜ 0.05] ;while cell viability of the 1.0 μmol/L dose group of both of the two cell lines[A375:(75.32 ± 1.59)％; G361:(78.26 ± 2.10)％] were significantly lower than those of the control (all P ＜ 0.05).Melanin levels of G361 cell line [(7.19 ± 0.35),(7.34 ± 0.83),(8.19 ± 0.86)pg/cell] were significantly higher than that of A375[(4.35 ± 0.72),(4.54 ± 0.01),(4.60 + 0.59)pg/cell,all P ＜ 0.05] in all the three groups.TYR activity of G361 cell line [(54.13 ± 1.21),(54.56 ± 0.21),(56.25 ± 0.85)Bq] were also markedly higher than that of A375 cell[(42.00 ±0.21),(42.90 ± 0.54),(42.91 ± 0.01)Bq,all P ＜ 0.05] in all the three groups.The melanin levels and TYR activities of both of the two cells lines showed an increase tendency along with increased doses of arsenic exposure,but without significant differences when compared with those of the three groups (all P ＞ 0.05).Conclusions Arsenic related pigment disorder may be associated with increased melanin levels and TYR activities induced by arsenic exposure; individual difference of pigment metabolism may be associated with different basal melanin levels and TYR activity between different individuals.

Drug-Eluting Stents ; adverse effects ; Humans ; Middle Aged ; Myocardial Infarction ; etiology ; Sirolimus ; administration & dosage ; Thrombosis ; etiology

Adolescent ; Adult ; Arthroscopy ; methods ; Humans ; Knee Injuries ; surgery ; Male ; Menisci, Tibial ; surgery ; Middle Aged ; Tibial Meniscus Injuries ; Young Adult

ATP Binding Cassette Subfamily B Member 11 ; ATP Binding Cassette Transporter, Sub-Family G, Member 2 ; ATP-Binding Cassette Transporters ; physiology ; ATP-Binding Cassette, Sub-Family B, Member 1 ; physiology ; Animals ; Bile ; metabolism ; Biliary Tract ; physiology ; Drug Interactions ; Drug Resistance, Multiple ; Humans ; Liver ; physiology ; Multidrug Resistance-Associated Proteins ; physiology ; Neoplasm Proteins ; physiology ; Organic Anion Transporters ; physiology ; Organic Anion Transporters, Sodium-Dependent ; physiology ; Organic Cation Transport Proteins ; physiology ; Symporters ; physiology

ObjectiveTo study the protective effects of tert-butylhydroquinone(tBHQ) on sodium arsenite (NaAsO2)-induced cytotoxicity and oxidative injuries. Methods Chang liver cells were pretreated with tBHQ[0(control), 5, 25 μmol/L]for 24 h, and then co-treated with tBHQ(5 μmol/L) together with NaAsO2[0(control),30, 40, 50, 60 μmol/L] for another 24 h, and Alamar blue reduction rates were used to evaluate cell viability,the results were expressed as the relative ratio of Alamar blue reduction rates between the experimental group and the control group. On the other hand, Chang liver cells were pretreated with tBHQ[0(control), 5, 25 μmol/L] for24 h,and then co-treated with tBHQ(5 μmol/L) together with NaAsO2[0(control), 40, 50 μmol/L] for another 24 h,and the levels of cellular reactive oxygen species(ROS) were detected by staining cells with 2',7'-dichlorofluorescin diacetate(DCFH-DA), the results were expressed as the relative ratio of mean fluorescence intensity between the experimental group and the control group. ResultsCell viability decreased dramatically by treatment with NaAsO2(30, 40, 50, 60 μmol/L), while relieved to some extent by pretreatment with 5, 25 μmol/L tBHQ, the main effects of NaAsO2 and tBHQ, as well as their interaction were all statistically significant(F =566.57, 55.09, 14.50,all P ＜ 0.05) ; the cell viability of NaAsO2(30, 40, 50, 60 μmol/L) pretreated with tBHQ(5, 25 mol/L) were 0.75 ±0.02, 0.70 ± 0.04, 0.59 ± 0.03, 0.43 ± 0.03 and 0.75 ± 0.02, 0.73 ± 0.03, 0.65 ± 0.02, 0.50 ± 0.02, respectively,all significantly higher than corresponding NaAsO2 alone groups(0.70 ± 0.03, 0.64 ± 0.03, 0.43 ± 0.03, 0.33 ±0.01, all P ＜ 0.05), the cell viability of NaAsO2(50, 60 μmol/L) pretreated with 25 μmol/L tBHQ was higher than corresponding 5 μmol/L tBHQ pretreatment groups(all P ＜ 0.05). On the other hand, 40, 50 μmol/L of NaAsO2 significantly induced hepatocellular ROS generation, while tBHQ(5, 25 μ mol/L) pretreatment significantly decreased NaAsO2-induced intracellular ROS levels, the main effects of NaAsO2 and tBHQ, as well as their interaction were all statistically significant (F =181.78, 60.55, 4.93, all P ＜ 0.05) ; the ROS levels of NaAsO2(40, 50 μ mol/L) pretreated with tBHQ(5, 25 μmol/L) were 1.87 ± 0.09, 1.80 ± 0.07 and 1.36 ± 0.11, 1.44 ± 0.12,all significantly decreased than corresponding NaAsO2 alone groups(2.30 ± 0.18, 2.18 ± 0.17, all P ＜ 0.05),the ROS levels of NaAsO2(40, 50 μmol/L) pretreated with 25 μmol/L tBHQ decreased than corresponding 5 μmol/L tBHQ pretreatment groups (all P ＜ 0.05). ConclusiontBHQ has a certain antagonism on arsenic induced cytotoxicity and oxidative injuries.

Objective To observe whether sodium arsenite(NaAsO2)can activate the expressions of hemeoxygenase-1(HO-1)of normal human liver cell line named Chang liver.Methods Chang liver cells were exposed to NaAsO2 at 10 μmoL/L,0(contml),2,6,12,24 h and at 0(control),5,10,25,50 μmol/L in 12 h, followed by the measuring of the expressions of HO-1 protein in ceUs with western blot.Results In 10 μmol/L groups Chang liver cells exposed for 6,12,24 h cultured in vitro,the expressions of HO-l protein(3.97±0.72, 12.92±2.98,23.29±3.82)was significantly higher than that of control(1.00±0.00),and compared with the control, the difference being statistically significant(F=85.83,P＜0.01;t=-9.42,-8.95,-13.83,respectively,P＜ 0.05 or＜0.01).In 12 h,5,10,25 and 50 μmol/L groups cultured in vitro,the expressions of HO-1(16.34±0.25, 7.75±0.39,7.93±0.14,12.48±0.35)was significantly higher than that of control(1.00±0.00).and compared with the control,the difference being statistically significant(F=85.83,P＜0.01;t=-36.25,-30.19,-86.40, -56.40,respectively,all P＜0.01).Conclusion Inorganic arsenic call induce the activation of HO-1,promote the expression of protein in a time-and dose-dependent manner.

The objective was to observe the effect of G-CSF as a mobilizer of hematopoitic stem cells on the absolute counts of T-cell subsets in peripheral blood and their relevance with the mobilized CD34(+) cells. The examples of peripheral blood from 26 patients performed of autologous stem cell transplantation were taken before and after mobilization by G-CSF. Flow cytometry was used for detecting CD3(+), CD3(+)CD4(+), CD3(+)CD8(+), CD3(+)CD4(+)CD8(+) and CD3(+)CD4(-)CD8(-) cells. Concurrently, their correlations with mobilized CD34(+) cells in peripheral blood were compared. The results showed that after the mobilization by G-CSF, the amounts of CD3(+), CD3(+)CD4(+), CD3(+)CD4(+)CD8(+) and CD3(+)CD4(-)CD8(-) cells in peripheral blood increased by 2.23, 2.62, 2.99 and 10.96 fold respectively, but that of CD3(+)CD4(-)CD8(+) cells was nearly no changed (P = 0.243). The correlation coefficient of CD3(+)CD4(-)CD8(-) cells and mobilized CD34(+) cells was 0.796, (P = 0.000) and no correlation with other T-cell subsets. It was concluded that when CD34(+) cells were mobilized by G-CSF from bone marrow to peripheral blood, the absolute counts of the peripheral T-cell subsets got changed. The increase of CD3(+)CD4(-)CD8(-) cells had correlated with mobilization effect of CD34(+) cells into peripheral blood.
Adolescent ; Adult ; Antigens, CD34 ; analysis ; Female ; Granulocyte Colony-Stimulating Factor ; pharmacology ; Hematopoietic Stem Cell Mobilization ; Humans ; Male ; Middle Aged ; T-Lymphocyte Subsets ; drug effects

OBJECTIVETo study the possible relationship between serum zinc levels and attention deficit hyperactivity disorder (ADHD) in Chinese children.

METHODSFollowing a systematic search for case-control studies on the serum zinc levels in Chinese children with ADHD published between 2000 and 2015, a Meta analysis was conducted using Stata 12.0 software.

RESULTSA total of 17 studies, including 2 177 children with ADHD and 2 900 normal children, were enrolled. The Meta analysis showed that serum zinc levels in children with ADHD were lower than normal children (SMD= -1.33; 95%CI: -2.22, -0.44; P=0.003). The sensitivity analysis indicated that the results were reliable. Eggerγs test did not find the existence of publication bias.

CONCLUSIONSSerum zinc levels may be associated with susceptibility to ADHD in children.

Attention Deficit Disorder with Hyperactivity ; blood ; Case-Control Studies ; Child ; Humans ; Zinc ; blood

OBJECTIVESTo construct an eucaryotic expression plasmid carrying the BMP7 gene and express in MSCs.

METHODSThe BMP7 gene was cloned into the eucaryotic expression vector pcDNA3.1. At the same time, mesenchymal stem cells (MSCs) were isolated and cultured in vitro. The plasmid carrying the BMP7 gene was transfected into MSCs.

RESULTSPCR and digesting demonstrated that the eucaryotic expression plasmid -pcDNA-BMP7 was obtained. RT-PCR and immunohistochemical methods showed that the BMP7 gene was expressed in MSCs.

CONCLUSIONConstruction of an eucaryotic expression plasmid carrying BMP7 gene and expression in MSCs provide a sound basis for gene therapy using the BMP7 gene and the ideal seeds for tissue engineering.

Bone Morphogenetic Protein 7 ; Bone Morphogenetic Proteins ; genetics ; Genetic Therapy ; Humans ; Mesenchymal Stromal Cells ; metabolism ; Plasmids ; Polymerase Chain Reaction ; Tissue Engineering ; Transforming Growth Factor beta