11.0 for the pH of reaction solution,65℃～75℃for the reaction temperature,and 1:1.7 for the mass ratio of corn(dry weight)to FeCl_3?6H_2O.The corn polysaccharide-Fe(Ⅲ)complex synthesized with the optimized process was stable,with good solubility in water.The assay of Fe(Ⅲ)was 39.86%,40.20%and 40.17%,respectively for three batches of products.The RSD was

OBJECTIVETo investigate the role of p38 MAPK on ischemic postconditioning (IPO) attenuating pneumocyte apoptosis after lung ischemia/reperfusion injury (LIRI).

METHODSForty adult male SD rats were randomly divided into 5 groups based upon the intervention (n = 8): control group (C), LIR group (I/R), LIR + IPO group (IPO), IPO + solution control group (D), IPO + SB203580 group (SB). Left lung tissue was isolated after the 2 hours of reperfusion, the ratio of wet lung weight to dry lung weight (W/D), and total lung water content (TLW) were measured. The histological structure of the left lung was observed under light and electron transmission microscopes, and scored by alveolar damage index of quantitative assessment (IQA). Apoptosis index (AI) of lung tissue was determined by terminal deoxynuleotidyl transferase mediated dUTP nick end and labeling (TUNEL) method. The mRNA expression and protein levels of and Bax were measured by RT-PCR and quantitative immunohistochemistry (IHC).

RESULTSCompared with C group, W/D, TLW, IQA, AI and the expression of Bax of I/R were significantly increased, the expression of Bcl-2 and Bcl-2/Bax were significantly decreased (P < 0.05, P < 0.01), and was obviously morphological abnormality in lung tissue. Compared with I/R group, all the indexes of IPO except for the expression of Bcl-2 and Bcl-2/ Bax were obviously reduced, the expression of Bcl-2 and Bcl-2/Bax were increased (P < 0.05, P < 0.01). All the indexes between D and IPO were little or not significant( P > 0.05). The expression of Bcl-2 and Bcl-2/Bax of SB were significantly increased and other indexes were reduced than those of IPO (P < 0.05, P < 0.01).

CONCLUSIONIPO may attenuate pneumocyte apoptosis in LIRI by inactivation of p38 MAPK, up-regulating expression of Bcl-2/Bax ratio.

Alveolar Epithelial Cells ; cytology ; Animals ; Apoptosis ; Disease Models, Animal ; Ischemic Postconditioning ; Lung ; blood supply ; enzymology ; pathology ; Male ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; enzymology ; pathology ; prevention & control ; bcl-2-Associated X Protein ; metabolism ; p38 Mitogen-Activated Protein Kinases ; metabolism

In order to elucidate the function of homeobox A10 gene (HOXA10) and p57 during decidualization our present study was designed to observe the change of HOXA10 and p57 expression and subcellular localization of HOXA10 in the process of endometrial stromal cell (ESC) differentiation in vitro. Decidualization was induced by 0.5 mmol/L 8-Bromo-cAMP (8-Br-cAMP) together with 1x10(-6) mol/L medroxyprogesterone acetate (MPA). Expression of p57 and HOXA10 was detected by RT-PCR and Western blot after 1-day, 2-day, and 4-day treatment (D1, D2, D4). ESCs cultured in 2%FBS for 1 and 4 d were used as control (C1, C4). The location of HOXA10 was detected by indirect immunofluorescence and HOXA10-GFP transfection. The results are as follows: (1) The expression of HOXA10 decreased progressively during the course of decidualization, and showed significant difference compared to control group C4 after 2-day treatment (D2). (2) On the contrary, the expression of p57 increased progressively and also showed significant difference compared to the control group C4 after 2-day treatment (D2). (3) There was no significant change of HOXA10 and p57 expression after culturing ESCs in 2%FBS for 4 d (C1, C4). (4) HOXA10 located in the nucleus throughout the course. Cytoplasm and nucleus shuttle was not detected in the experiment. Our results suggest that the down-regulation of HOXA10 may contribute to the increase of p57 and that the up-regulation of p57 likely plays an important role in ESC differentiation. Progesterone receptor (PR) pathway may participate in promoting ESCs to exit cell cycle and enter differentiation.

OBJECTIVETo explore the role of Xuebijing Injection (XBJI) in inhibiting inflammatory factors associated with anoxia/reoxygenation myocardial inflammatory response of rats.

METHODSTotally 36 healthy male Sprague-Dawley rats, 280 ± 30 g were randomly divided into six groups, i.e., the normal control group (N group), the balanced perfusion group (BP group),the model group (M group),the low dose XBJI group (XBJI(L) group), the middle dose XBJI group (XBJI(M) group),and the high dose XBJI group (XBJI(H) group), 6 in each group. The myocardial anoxia/reoxygenation rat model was established by Langendorff isolated heart perfusion. The concentration of TNF-α in the myocardial tissue was detected by ELISA. The expression of nuclear factor kappa B p65 (NF-κB p65) protein and Toll like receptor 4 (TLR4) protein were detected using Western blot. The expression of NF-κB p65 mRNA and TLR4 mRNA was detected by RT-PCR. Ultrastructural changes of anoxia-reoxygenation rats' heart muscle were observed under transmission electron microscope.

RESULTSCompared with the M group,the TNF-α concentration, expression levels of NF-κB p65 protein and mRNA, TLR4 protein and mRNA decreased to various degrees in the XBJI(L) group, the XBJI(M) group, and the XBJI(H) group. The TNF-α expression level decreased most significantly in the XBJI(L), group (P < 0.01), while other indices decreased most obviously in the XBJI(M) group (P < 0.01, P < 0.05). Expression levels of NF-κB p65 and TLR4 protein were obviously lower in the XBJI(M) group than in the XBJI(L) group (P < 0.05). There was no statistical difference in other indices among the three XBJI groups (P > 0.05). Myocardial fibers were loose and broken with disappearance of transverse striation, and mitochondrial cristae was dissolved and severely damaged in the M group. The aforesaid condition was improved after treated by XBJI, with the most obvious effect obtained in the XBJI(M) group.

CONCLUSIONSDifferent doses of XBJI could attenuate inflammatory reactions after myocardial anoxia/reoxygenation rats' heart muscle through inhibiting TLR4-NF-κB-TNF-α signal transduction pathway. The best effect could be obtained by 4 mL/100 mL XBJI.

Animals ; Drugs, Chinese Herbal ; administration & dosage ; pharmacology ; therapeutic use ; Hypoxia ; Male ; Myocardium ; metabolism ; Myocytes, Cardiac ; NF-kappa B ; metabolism ; Oxygen ; metabolism ; RNA, Messenger ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Toll-Like Receptor 4 ; metabolism ; Transcription Factor RelA ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo screen the genes related with leukocyte responses in mice early after burn injury by bioinformatic analysis of the gene expression profiling data.

METHODSGene expression profiles were obtained from GEO (GSE7404, Mouse musculus, 25% TBSA, full-thickness) database. After screening of the differentially expressed genes (DEGs) through paired-sample t-test and fold-change, DAVID online tools were used to select the DEGs related to leukocyte responses to burns by GO functional enrichment analysis; the interacting genes identified through KEGG pathway enrichment analysis were transferred to STRING to construct the protein-protein interaction (PPI) network. Biological annotation of the sub-networks was executed using the software Cytoscape. Real-time PCR was used to verify the DEGs identified in mice.

RESULTSOf the 259 leukocyte response-related DEGs screened at 1 day post-burn, 118 were up-regulated and 141 were down-regulated. KEGG pathway enrichment analysis showed that the pathways were associated with the immune function, cell growth and cell death. PPI network and module analysis suggested that some of genes (such as Lck, Stat1, Myd88, Stat3, and Jun) play critical roles in the PPI network post-burn. RT-PCR results were consistent with those of bioinformatic analysis.

CONCLUSIONSLck, Stat1, Myd88, Stat3, and Jun might be critical players in the development of leukocyte response in mice early after burn injury. Our finding provides new insights into the pathogenesis of leukocyte response to burn injury and identifies several potential biomarkers for burn treatment.

Animals ; Burns ; genetics ; Computational Biology ; Down-Regulation ; Gene Expression Profiling ; Gene Regulatory Networks ; Leukocytes ; physiology ; Mice ; Real-Time Polymerase Chain Reaction ; Software ; Up-Regulation

Objective To confirm the species of multidrug-resistant Acinetobacter baumannii (MRAB)strains collected from our hospital by specific PCR amplification,and further investigate their distribution,antibiotic resistance and molecular classification characteristics.Methods We collected 47 MRAB clinical strains which had been identified by VITEK-2 system,followed by species confirmation using specific primers sp2F,sp4F and sp4R through PCR amplification.Antibiotic resistance characteristics were detected using VITEK-2 system.And the homology of MRAB isolates was analyzed using multilocus sequence typing (MLST).Results We confirmed 46 out of 47 strains as A .baumannii .All of them were multidrug-resistant strains,and the majority of them were found in sputum samples from patients in intensive care units (ICUs).MLST analysis found 4 ST types,namely ST195,ST218,ST368 and ST208.The last two types had the closest genetic relationship.Conclusion SpecificPCR amplification is a rapid and accurate method to identify A .baumannii .The MRAB strains in our hospital are mainly distributed in ICUs and are susceptible to only a few antibiotics such as tigecycline.

Aged ; Aged, 80 and over ; Carcinoma, Hepatocellular ; diagnosis ; pathology ; surgery ; Humans ; Keratin-18 ; analysis ; Keratin-19 ; analysis ; Male ; Pancreatic Neoplasms ; diagnosis ; pathology ; surgery ; alpha-Fetoproteins ; analysis

Adolescent ; Adult ; Aged ; Female ; Humans ; Laparoscopy ; Male ; Middle Aged ; Splenectomy ; methods

OBJECTIVETo investigate the effects of non-surgical periodontal therapy on serum inflammatory factors and metabolism levels in obese rats with experimental periodontitis.

METHODSSixteen obese rats with experimental periodontitis were randomly divided into treatment group and control group with non-surgical periodontal therapy and no treatment, respectively. Oral glucose tolerance test was performed before treatment and 2 weeks after the treatment. All the rats were sacrificed 2 weeks after treatment and the orbital vein blood was taken to detect fasting blood glucose, fasting insulin, and serum level of C-reactive protein (CRP). Results Two weeks after periodontal treatment, fasting blood glucose (t=2.445, P=0.034) and beta cell function index (t=-2.543, P=0.027) were significantly lower in the treatment group than in the control group. Compared with those in the control group, CRP level (t=2.388, P=0.028) and the area under the curve in the oral glucose tolerance test (t=12.053, P=0.000) decreased significantly in the treatment group.

CONCLUSIONNon-surgical periodontal treatment can reduce serum CRP level and improve glucose metabolism in obese rats.

OBJECTIVETo screen the genes related with leukocyte responses in mice early after burn injury by bioinformatic analysis of the gene expression profiling data.

METHODSThe gene expression profiles were obtained from GEO (GSE7404, Mouse musculus, 25% TBSA, full-thickness) database. T test, fold changes and GO functional enrichment analysis were used to identify the differentially expressed genes (DEGs) related to leukocyte responses to burns; the interacting genes were transferred to STRING to construct the protein-protein interaction (PPI) network. Biological annotation of the sub-networks was executed using the software Cytoscape. Real-time PCR and Western blotting were used to verify the DEGs in mice.

RESULTSIn mice at 1 day post-burn, a total of 658 genes were up-regulated and 1167 were down-regulated. PPI network and module analysis suggested that some of the genes (Stat1, Cdk1, Cd19, Lck and Jun) may play critical roles in the PPI network post-burn. Real-time PCR and Western blotting results in mice were consistent with those of bioinformatic analysis of Stat1, Cdk1 and Jun.

CONCLUSIONStat1, Cdk1 and Jun might be critical players in the development of leukocyte response in mice early after burn injury. Our finding provides new insights into the pathogenesis of leukocyte response to burn injury and identifies several biomarkers as potential targets for burn treatment.