Objective To investigate the current situation of the flow maternal health management in Jinyun ,and propose in‐tervention strategies according to the results .Methods Medical records of maternal in 18 confinements hospitals in Jinyun during October 2009 to September 2013 were selected and retrospectively analyzed ,including 16 ,430 cases of household registered mater‐nal and 1 ,301 non‐household registered maternal .Maternal health management of household registered maternal and non‐household registered maternal were compared;and maternal health care management satisfaction survey were implemented for 100 cases in each group .Results The household registration book built rate ,early build rates ,system management rate ,postpartum visit rates were 99 .2% (16 297/16 430) ,96 .7% (15 882/16 430) ,95 .8% (15 733/16 430) ,and 97 .7% (16 ,057/16 430) in household regis‐tered maternal ,while which were 74 .5% (969/1 301) ,64 .0% (832/1 301) ,59 .0% (768/1 301) and 65 .5% (852/1 301) in non‐household registered maternal ,the difference was statistically significant (P<0 .05);3 cases were not satisfied during the childbirth hospitalization in household registered maternal ,the dissatisfied rate was 1 .5% ,12 cases were not satisfied during the childbirth hospitalization in non‐household registered maternal ,the dissatisfied rate was 6 .0% ,the difference was statistically significant (P<0 .05) .Conclusion There is a considerable gap in maternal Jinyun flow maternal health management and local residence ,and we should strengthen the flow of maternal health care management ,making it a fair quality of health care management and opportuni‐ties ,thus contributing to local economic and social development .

Objective To investigate the influence of murine cytomegalovirus(MCMV) infection on differentiation and differentiation gene expression of neural stem cells (NSCs) in vitro for studying the mechanisms of brain abnormalities calmed by congenital cytomegalovirns infection. Methods NSCs were separated from fetal BALB/c mouse and cultured and identified in vitro. The differentiation potency of NSCs was observed by immunnfluorescence. The NSCs infected by MCMV at dosage of multiplicity of infection (MOI) equaled to 5, I and 0. 1, respectively, were cultured in differentiation medium. The morphological changes of the cells were observed by inverted microscope. The ratios of NSCs and its differentiated cells were detected by flow cytometry. The expression changes of nestin, GFAP and NSE, markers of NSCs and its differentiated cells, were studied by immunofluorescence ( MOI = 1 ). The expression of early antigen (EA) of MCMV was detected to observe the infection process. Real-time RT-PCR method was employed to measure the expression levels of the key differentiation genes Wnt-3 and Wnt-7a in Wnt signal pathway of NSCs at early phage of differentiation culture. Results NSCs isolated from embryonic mouse brains could proliferate to form neurnspheres and strongly express Nestin and differentiate into NF-200 positive neurons or GFAP positive astrocytes. The NSCs of the infected groups couldn't adhere to the wall and appear differentia-tion growth, but showed swollen gradually after differentiation culture. The nostin expression of the infected groups downregulated slowly and was higher than that of the control groups ( P < 0.05 ). The GFAP and NSE expression of the infected groups were lower than that of the control groups (P <0.05). The EA of MCMV could be always detected in the cells of the infected groups. The ratios of nestin positive cells of the infected groups were higher than that of the control groups, but the ratios of GFAP and NSE positive cells of the for-mer were lower than that of the latter from 3rd to 9th day after differentiation culture ( P < 0.05 ). The levels of Wnt-3 mRNA and Wnt-7a mRNA of the infected groups were markedly lower than that of the control groups from 1st to 2nd clay and from 12th hour to 2nd day after differentiation culture respectively ( P < 0.05 ) . These changes of the infected groups became more obvious as MCMV MOI increased . Conclusion MCMV could inhibit significantly NSCs differentiate to neurons and astrocytes and lead to the decrease of dif-ferentiated cells. MCMV could inhibit or interfere with the gene expression of Wnt-3 and Wnt-7a in Wnt sig-nal pathway of NSCs. The effect that MCMV inhibited the differentiation and the differentiation gene expres-sion of NSCs showed dose-dependent with MCMV MOI. The inhibitory effect of MCMV on the differentiation of NSCs might be induced by interfering the differentiation gene expression of NSCs, which is possibly the one of primary causes of brain development disorders caused by congenital CMV infection.

Objective To investigate the effects of maternal long-term exposure to low-dose trichlorfon on the serum paraoxonase (PON) activity of pregnant mice and development of embryos. Methods Female ICR mice (n=120) were randomly divided into control group and trichlorfon groups of different doses,and were managed by intragastric injection with trichlorfon of 0,2,10 and 50mg/kg,respectively. All the mice were managed once a day for a consecutive of 27 days,and were subjected to mating. The pregnant mice were continued to be managed with trichlorfon for 3 days,and were sacrificed on day 3 of gestation. The serum PON and acetylcholinesterase (AchE) activities were detected,and the development of embryos was evaluated. Results The serum PON activity of 2,10 and 50mg/kg trichlorfon group were (14.15?1.22),(12.78?1.80) and (10.45?1.95)IU/mL,respectively,and that of 50mg/kg trichlorfon group was significantly lower than that of control group [(13.37?2.31)IU/mL] (P0.05),while the the percentage of abnormal embryos of 50mg/kg trichlorfon group had an increased tendency. Conclusion Long-term exposure to low-dose trichlorfon can inhibit serum PON and AchE activity in pregnant mice without obvious effect on the development of embryos.

Objective To investigate the biological function of M122 in pathogenesis of MCMV in developmental brain disorders and brain damage, screening for mouse brain cDNA library interacting with M122 was performed by a yeast two-hybrid system. Methods The reconstructed bait plasmid pGBKT7-M122 was transformed into yeast cells AH109 and screened on the nutrient deficiency medium SD/-Trp. After express of the bait protein in AH109 yeast strains was detected by Western blot analysis, yeast-two hybrid screening was performed by mating AH109 with Y187 containing mouse brain cDNA library plasmid. The diploid yeast cells were plated on the nutrient deficiency medium SD/-Trp/-Leu/-His/-Ade. The second screening was performed with SD/-Trp/-Leu/-His/-Ade containing X-α-gal. The plasmids in positive colonies were extracted and transformed into E. coli JM109 cells. After plasmid DNA in JM109 cells were extracted form positive colonies and sequenced, the results were analyzed by bioinformatic methods. The interactions between M122 protein and the protein obtained from positive colonies were further confirmed by repeating yeast-two hybrid. Then, autoactivations of the proteins obtained from positive colonies were detected.Results The reconstructed bait plasmid was transformed into yeast cells AH109 successfully. The bait protein expressed in the yeast cells AH109 stably. 24 proteins interacting with MCMV M122 were screened, including syntaxin 8 ( Stx8 ), phosphoglucomutase 2 ( Pgm2 ), potassium voltage-gated channel, shaker-related subfamily, beta member 1 ( Kcnab1 ), collagen, type ⅪⅩ, alpha 1 ( Col19a1 ), archain 1 ( Arcn1 ), cytidylate kinase( Cmpk), DnaJ(Hsp40) homolog, subfamily A, member 1 (Dnaja1), ATPase, Na+/K + transporting, beta 3 polypeptide( Atp1b3 ), SH3-domain GRB2-like ( endophilin ) interacting protein 1 ( Sgip1 ),ankyrin repeat domain 17 (Ankrd17), Smg-7 homolog, nonsense mediated mRNA decay factor(Smg7),sperm associated antigen 9 ( Spag9 ), FK506 binding protein 1a ( Fkbp1a), MYST histone acetyltransferase monocytic leukemia 4 ( Myst4), hyaluronan and proteoglycan link protein 1 ( Hapln1), autophagy-related 3 (Atg3), splicing factor, arginine/serine-rich 5 ( Sfrs5 ), zinc finger, C3HC-type containing 1 ( Zc3hc1 ),thioredoxin-related transmembrane protein 1 ( Txndc1 ), adaptor protein complex AP-1, gamma 1 subunit (Ap1g1), Cullin 1 ( Cul1 ), and so on. Three of them were formerly unknown proteins. M122 protein could interact with the proteins obtained from positive colonies in the yeast cells AH109. Ap1g1 and Cul1 were proved to have autoactivation. Conclusion A class of proteins in brain interacting with M122 has been obtained. It is presumed that these proteins are correlated with neuropathogenesis of the brain disorders caused by CMV, but the candidates still need further confirmation for the interaction.

AIM: The influence of MCMV infection on differentiation and differentiation gene expression in neural stem cells ( NSCs) in vitro were investigated for studying the mechanisms of brain abnormalities caused by congenital cytomegalovirus infection. METHODS: NSCs were separated from fetal BALB/C mouse, and cultured and identified in vitro. The differentiation potency of NSCs was observed by immunofluorescence. The NSCs infected by MCMV at dosage of MOI( multiplicity of infection) equaled to 5, 1 and 0.1 .respectively, were cultured in differentiation medium. The morphological changes of infected cells were observed under inverted microscope. The ratios of NSCs and its differentiated cells were detected by flow cytometry. The expressions of nestin, GFAP and NSE, markers of NSCs and its differentiated cells, were studied by immunofluorescence( MOI = 1). The expression of early antigen ( EA ) of MCMV was detected to observe the infection process. Real - time RT - PCR method was employed to measure the expression levels of the key genes Neurog2, Myc and Ccnd1 in Wnt signal pathway of NSCs at early stage of differentiation culture. RESULTS: NSCs isolated from embryonic mouse brains proliferated to form neurospheres, strongly expressed nestin and differentiated into NF - 200 positive neurons or GFAP positive astrocytes. The infected NSCs did not adhere to the wall and appeared differentiation growths, but showed swollen gradually after differentiation culture. The nestin expression in the infected cells downregulated slowly and was higher than that in control groups ( P < 0.05). The GFAP and NSE expressions of the infected cells were lower than those in control groups ( P <0.05). The early antigen ( EA) of MCMV was always detected in the cells in infected groups. The ratios of nestin positive cells in infected groups were higher than those in control groups, but the ratios of GFAP and NSE positive cells of former were lower than that of the latter from 3rd to 9th d after differentiation culture(P < 0.05 ). The levels of Neurog2 mRNA and Myc mRNA in infected groups were markedly lower than those in normal control groups on 1st d and from 1st to 4th d after differentiation culture, respectively( P <0.05). The levels of Ccnd1 mRNA of infected groups were obviously lower than those in normal control groups from 12th h to 1st d( P <0.05 ). These changes in infected groups became more obvious as MCMV MOI increased. CONCLUSION: MCMV significantly inhibits differentiation of NSCs to neurons and astrocytes, and leads to the decrease in differentiated cells. MCMV inhibits or interferes with the gene expression of Newog2, Myc and Ccnd1 in Wnt signal pathway of NSCs. The effect that MCMV inhibits the expressions of differentiation and the differentiation genes in NSCs shows dose - dependent with MCMV MOI. The inhibitory effect of MCMV on the differentiation of NSCs might be induced by interfering with the expression of differentiation gene in NSCs, which is possibly the one of primary causes of brain development disorders induced by congenital CMV infection.

AIM:To investigate the inhibitory effect of allicin on apoptosis and caspase-12 activation of macro-phage-derived foam cells,and to elucidate the underlying molecular mechanisms. METHODS:RAW264.7 macrophages were pretreated with allicin (12.5,25 and 50 mg/L) or 4-phenylbutyric acid(PBA,4 mmol/L) for 1 h and then treated with oxidized low-density lipoprotein(ox-LDL,100 mg/L) or tunicamycin(TM,4 mg/L) for 24 h. The cell viability and apoptosis were examined by MTT assay and flow cytometry with Annexin V-FITC/PI staining,respectively. The activities of caspase-3 in the cells and lactic dehydrogenase (LDH) in the medium were measured. The protein levels of caspase-12 were determined by Western blot. The intracellular lipid accumulation was measured with oil red O staining and the content of intracellular total cholesterol was determined by enzymatic colorimetry. RESULTS:Similar to the endoplasmic reticulum stress (ERS) inhibitor PBA, allicin inhibited ox-LDL-induced injury of RAW264.7 macrophages in a concentration-de-pendent manner,as determined by the increased cell viability and the decreased LDH leakage,apoptosis and caspase-3 ac-tivity. The decrease in cell viability and increases in LDH leakage and apoptosis induced by TM (an ERS inducer) were also suppressed by allicin. Moreover, similar to PBA, allicin remarkably inhibited ox-LDL- or TM-induced activation of caspase-12. Furthermore, allicin remarkably attenuated ox-LDL-induced lipid accumulation in the RAW264.7 cells and foam cells formation in a concentration-dependent manner. CONCLUSION:Allicin may inhibit macrophage-derived foam cell apoptosis induced by ox-LDL,and the mechanism is partially related to suppressing the activation of caspase-12.

This study was aimed to explore the single nucleotide polymorphism (SNPs) of breakpoint cluster region of bcr gene in Chinese people and the relationship between SNPs and chronic myelogenous leukemia (CML). A 3.12 kb region spanning from exon 13 to exon 15 in the bcr region were screened by DNA pooling and denaturing high performance liquid chromatography (dHPLC), and the results were verified by sequencing. The results indicated that 6 novel SNP sites and 2 bases different from reference sequence were confirmed in the region studied, and the frequency of 6 novel SNP sites in studied population was obtained, one SNP of which was found in exon 13 and caused a nonsynonymous mutation. The gene frequencies of novel SNPs had no significant difference between CML and control people. It is concluded that sequence polymorphisms in the major breakpoint cluster region of bcr gene are found, most of which are SNPs, No relationship can be confirmed between SNPs and CML disease.
Base Sequence ; Chromosome Breakage ; Fusion Proteins, bcr-abl ; genetics ; Humans ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; genetics ; Molecular Sequence Data ; Polymorphism, Single Nucleotide ; Proto-Oncogene Proteins c-bcr ; genetics

AIM:To investigate the effect of short-chain acyl-CoA dehydrogenase ( SCAD) on collagen expres-sion and proliferation of rat cardiac fibroblasts and to explore the relationship between SCAD and cardiac fibrosis . METHODS:The model of proliferation and collagen expression of rat cardiac fibroblasts induced by angiotensin II was es -tablished.After treatment with siRNA-1186, the expression of SCAD at mRNA and protein levels , fatty acids beta oxida-tion rate, ATP, the enzyme activity of SCAD and free fatty acids in the rat cardiac fibroblasts were determined . RESULTS:The mRNA and protein expression of SCAD was decreased in the rat cardiac fibroblasts induced by angiotensin II compared with the control cells , and the expression of collagen I and collagen III was significantly upregulated .Com-pared with negative control group , SCAD expression and activity , fatty acid beta-oxidation rate and ATP significantly de-creased in siRNA-1186 group, but the content of free fatty acids were obviously increased in the rat cardiac fibroblasts , and the expression of collagen I and collagen III was significantly up-regulated.CONCLUSION:The expression and synthesis disorder of collagen may be triggered by down-regulation of SCAD .SCAD may be a promising therapeutic target for myocar-dial fibrosis .

OBJECTIVETo observe the effect of GETO on expression of PSD-95 and Shank-1 protein in postsynaptic dense zone in Alzheimer disease (AD) model rats.

METHODSThe AD model rats were established by beta-amyloid protein (Abeta(1-42)) injection into hippocampus CA1 zone. They were assigned into the model group, the donepezil treated group and the GETO treated group, besides, a normal group was set for control. Four weeks after modeling, Morris water maze test was applied to determine the learning and memory function of the AD rats, the number of PSD-95 and Shank-1 protein positive neuron as well as the optical density (OD) in post-synaptic dense zone of hippocampus CA1 area were determined by using immuno-histochemical stain and computerized graphic analysis techniques.

RESULTSMorris water maze test showed that the mean escape latent period (MELP) of the model rats obviously prolonged than that of the normal rats, and the times of traversing flat roof obviously decreased (P < 0.01), while in the model rats after being treated by GETO, the two parameters were significantly shortened and increased respectively (P < 0.01), reaching the level insignificantly different to those in the donepezil group and the normal group. Immunohistochemical test showed that the number of positive stained neuron of PSD-95 and Shank-1 in hippocampus CA1 zone in the model group was significantly different to those in the normal group (P < 0.01), while in the GETO group those indexes were insignificantly different to those in the donepezil group and the normal group (P > 0.05), but showed a significant difference when compared with those in the model group (P < 0.05).

CONCLUSIONGETO can obviously improve the function of learning and memory of AD rats induced by Abeta(1-42), and the mechanism may be associated with its actions in improving expressions of PSD-95 and Shank-1 protein in hippocampus CA1 zone, and recovering the structure and function of synapse and enhancing its plasticity.

Adaptor Proteins, Signal Transducing ; metabolism ; Alzheimer Disease ; drug therapy ; metabolism ; Animals ; Drugs, Chinese Herbal ; therapeutic use ; Hippocampus ; metabolism ; Male ; Maze Learning ; Nerve Tissue Proteins ; metabolism ; Phytotherapy ; Rats ; Rats, Sprague-Dawley ; Synapses ; metabolism ; Synaptic Transmission ; drug effects

Background:X-linked inhibitor of apoptosis (XIAP) is a vital factor in the anti-apoptosis mechanism of tumors and is highly expressed in renal cell carcinoma (RCC).However,the mechanism through which XIAP regulates DNA damage repair is unknown.This study investigated the regulatory mechanism of XIAP in etoposide-induced apoptosis in two Caki-1 cell lines with high or low XIAP expression.Methods:The two cell lines were established using RNA interference technology.The differentially expressed proteins in the two cell lines were globally analyzed through an isobaric tags for relative and absolute quantitation-based quantitative proteomics approach.Proteomic analysis revealed 255,375,362,and 5 differentially expressed proteins after 0,0.5,3,and 12 h of drug stimulation,respectively,between the two cell lines.The identified differentially expressed proteins were involved in numerous biological processes.In addition,the expression of histone proteins (H1.4,H2AX,H3.1,H3.2,and H3.3) was drastically altered,and the effects of XIAP silencing were accompanied by the marked downregulation of H2AX.Protein-protein interactions were assessed and confirmed through immunofluorescence and Western blot analyses.Results:The results suggested that XIAP may act as a vital cell signal regulator that regulates the expression of DNA repair-related proteins,such as H2AX,and influences the DNA repair process.Conclusions:Given these functions,XIAP may be the decisive factor in determining the sensitivity of RCC cell apoptosis induction in response to chemotherapeutic agents.