Child, Preschool ; Female ; Humans ; Lupus Erythematosus, Systemic ; complications ; Respiratory Insufficiency ; complications

Objective To investigate the protective effect of angiotensin-converting enzyme inhibitor (ACEI) on kidney function in patients with sepsis.Methods Eighty-seven patients with sepsis were randomly (random number) divided into the routine treatment (A group,n ＝45) and the ACEI intervention group (B group,n =42).Patients were managed by international guidelines for sepsis in A group and were treated with benazepril (ACEI) 20 mg a day in addition in B group.Serum creatinine and cystatin C were detected and APACHE Ⅱ scores and urine output were recorded on the 1st,3rd and 7th day.Those laboratory findings and APACH Ⅱ score were compared between two groups.The incidence of acute kidney injury (AKI) and abnormal cystatin C levels were compared between two groups.Results In B group,serum creatinine and cystatin C of patients were lower compared with A group.The incidence of AKI and abnormal cystatin C and APACHE Ⅱ scores were reduced in B group compared with the A group.Conclusions Benazepril improved sepsis-induced AKI and patient conditions.

In order to investigate the anti-leukemia effects of gambogic acid (GA) and its relation to the regulation of nucleoporin Nup88 in U937 cells in vitro, the inhibitory effect of GA on the growth of U937 cells was examined by using MTT assay. Apoptosis was detected by Annexin-V FITC/PI double-labeled cytometry. Cell cycle regulation was studied by propidium iodide method. Both flow cytometry (FCM) and RT-PCR were employed to assess the expression of Nup88, and the localization of Nup88 was determined by confocal microscopy. The results indicated that GA had strong inhibitory effect on cell proliferation and apoptosis induction activity in U937 cells in vitro in a time-and dose-dependent manner. The 24-h IC(50) value was (1.019+/-0.134) mg/L. Moreover, GA induced arrest of U937 cells in G(0)/G(1) phase. Over-expression of Nup88 was found in U937 cells, whereas GA could significantly down-regulate both the protein and mRNA levels of Nup88. Nup88 was diffusely distributed between nucleus and cytoplasm and was located at the cytoplasmic side of nuclear rim, and occasionally in cytoplasm. It is suggested that GA exerts its anti-leukemia effects by regulating the expression and distribution of nucleoporin Nup88. It promises to be new agent for the treatment of acute leukemia.
Antineoplastic Agents, Phytogenic/*pharmacology ; Apoptosis/drug effects ; Cell Proliferation/drug effects ; Nuclear Pore Complex Proteins/genetics ; Nuclear Pore Complex Proteins/*metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; U937 Cells ; Xanthones/*pharmacology

Objective To analyze the clinical characteristics, risk factors and prevention measures of nosocomial infection in senile patients with hematologic disorders. Methods The clinical data of 581 senile patients with hematologic disorders from July 2005 to June 2007 were retrospectively analyzed. Results The nosoeomial infection rate was 30.5%(177/581). The 581cases developed nosocomial infection for 254 times [43.7% (254/581)]. Lower respiratory tract infection was the most frequent infection site, followed by intestinal infection and upper respiratory infection. The species were predominated by Gram-negative bacillus (67.1%) . The risk factors of nosocomial infection were non-remission of malignant diseases,chronic underlying diseases, long time hospitaliation, community infection, granulocytopenia, invasive manipulation and application of adrenocortical hormone and antibiotic. Conclusions The nosoeomial infection rate is high in senile patients with hematologic disorders and it can be decreased by taking prevention measures according to the risk factors.

AIM:To investigate the changes of connexin 43 (Cx43) via establishing a model of sympathomi-metic atrial fibrillation ( AF) .METHODS:The mongrels ( n=15) were randomly divided into control group , rapid atrial pacing (RAP) group and isoprenaline (ISO) perfusion+RAP group (ISO+RAP group).All mongrels’ hearts were taken out rapidly by median sternotomy to establish the cardiac model with Langendorff perfusion in vitro.The atrial effective re-fractory period ( AERP) and AF inducability were tested .The expression and distribution of tyrosine hydroxylase ( TH) were analyzed by immunohistochemistry .Total protein level of Cx 43 and phosphorylation of Cx 43 were determined by West-ern blot.The distribution of Cx43 were also observed by immunofluorescence staining .The cell apoptosis was analyzed by TUNEL staining.The generation of reactive oxygen species ( ROS) in the mitochondria was measured by fluorescence spec-trophotometry .RESULTS:No significant change of AERP was found between control group and RAP group , while that in ISO+RAP group was significantly decreased (P<0.05) and induced AF.Compared with control group, the expression of TH, apoptotic index and the generation of ROS increased gradually (P<0.05), while the content of Cx43 decreased grad-ually both in the total protein and the phosphorylation levels in RAP group and ISO +RAP group (P<0.05).The fluores-cence intensity of Cx43 was also attenuated and Cx43 were lateralized apparently in RAP group , while Cx43 were character-ized as punctate distribution in ISO +RAP group.CONCLUSION:Sympathetic nerves may activate autophagosome at in-tercalated discs and trigger cell apoptosis , resulting in remodeling and downregulation of Cx 43 via oxidative stress , thus having effects on mediating and maintaining AF .

To explore the protective effects of trimetazidine on vascular endothelial cells injury induced by hydrogen peroxide (H2O2) and its pharmacological mechanisms of anti-oxidation.Methods Human umbilical vein endothelial cells (HUVECs) were injured by H2O2.Next,the cells were treated with three different concentrations of trimetazidine (1 μmol/L,10 μmol/L,100μmol/L,respectively).The viability of cells was detected by methyl thiazoeyl tetrazolium (MTT) assay.In addition,malondialdehyde (MDA)contents,superoxide dismutase (SOD) and secretion of NO were measured.Results Trimetazidine could enhance the viability of the injured HUVECs induced by oxidation,decrease the level of MDA,enhance the SOD activity,and increase the secretion of nitrogen monoxide.These effects were in a certain dose-dependent manner and the difference was significant among the three concentrations (P＜0.05).Conclusions Our results suggest that trimctazidine may protect lipid peroxidation and prevent oxidation-induced cellular dysfunction of HUVECs (J Geriatr Cardiol 2008;5:248-251)

Objective To study the gene expression profiles of megakaryocytes(MKs) from human cord blood CD34+ cells in vitro expanded and to understand megakaryopoiesis at the molecular level. Methods CD34+ cells were isolated using density gradient centrifugation and magnetic activated cell sorting. The cells were cultured and stimulated with recombinant human TPO ( 100 ng/ml). After 12 days, the MKs fraction was separated using an anti-CD41 monoclonal antibody by immunomagnetic sorting. The gene expression profiles of MKs, non-MKs as well as meg-01 cells were studied by gene chip assay. THBSI, HOX A9,β-actin, lL-8,Annexin A6, FGF-8 were selected to validate the gene chip results by RT-PCR. Results A total of 116 genes between MKs and non-MKs cells were significantly different, 52 genes were up-regulated and 64 genes were down-regulated. In addition, 158 genes between MKs and meg-01 cells were significantly different, 71 genes were up-regulated and 87 genes were down-regulated. THBSI showed higher expression in MKs than in non-MKs. HOXA9 showed lower expression in MKs than in non-MKs. The expression of β-actin did not show any significant difference in MKs and non-MKs. IL-8 showed higher expression in MKs than in meg-01 cells, while ANXA6 showed lower expression in MKs than in meg-01 cells. The expression of FGF-8 did not show any significant difference between MKs and meg-01 cells. Conclusions MKs, non-MKs and meg-01 cells show different gene expression profiles. The regulatory genes include stress response genes,immune related genes, DNA synthesis and repair genes, metabolism genes, pro-onco genes and tumor suppressor genes.

Objective To prepare specific polyclonal antibodies to outer membrane protein (Opr) D_2 of Pseudomonas aeruginosa (PA),and explore the relationship between loss of OprD_2 and imipenem resistance.Methods The genomic DNA of PA was ex- tracted with phenol:chloroform.OprD_2 coding gene was amplified by PCR and prokaryotic expression vector pRSET-OprD_2 was constructed.OprD_2 protein was expressed by IPTG induction in E.coli BL21(DE3),and purified with SDS-PAGE.The new protein band was recovered and used as antigens to subcutaneously immunize two New Zealand rabbits to prepare poly- clonal antibody.The specificity of the antibody was determined by Western blot.The expression of OprD_2 in 32 clinical isolates of PA was detected with the prepared polyclonal antibody by Western blot.Results The vector pRSET-OprD_2 has been success- fully expressed in E.coli BL21 (DE3).The polyclonal anti-OprD_2 antibody with high specificity has been successfully pre- pared.Present results show that of the 27 imipenem-resistant PA clinical isolates,OprD2 protein was low-expressed in 5 iso- lates (18.5%) and normally expressed in 2 isolates (7.4%) but not expressed in 20 isolates (74.1%).Conclusions The loss or low-expression of OprD_2 is one of the essential mechanisms accounting for imipenem resistance in clinical isolates of PA.

Objective:Establish mass-scale purification technology of cell-derived influenza virus. Methods: A microcarrier-based process was used to produce human influenza virus in serum free-adapted Vero cells. The virus was purified in a sequence of downstream processing steps including inactivation, clarification, anion exchange chromatography, affinity chromatography and size-exclusion chromatography. Results: The recovery of HA reached 102%. 95.3% total protein, including 99.77% host cell protein, and 99.99% host cell DNA were removed during downstream processing. Conclusion: Providing a high effective purification technology for cell-derived influenza virus.

Objective To evaluate the expression and relationship of miR-100 and FZD-8, one of the major compo?nents of Wnt signaling pathway, and the correlation of their expressions with lymph node metastasis in patients with breast cancer. Methods The expression of miR-100 was determined in 50 samples of human breast cancer tissues and adjacent normal tissues by in situ hybridization. The correlation of miR-100 expression with lymph node metastasis was analyzed by Mann-Whitney U test. The expression of FZD-8 was measured in 50 samples of human breast cancer tissues and adjacent normal tissues by immunohistochemistry. The correlation of the miR-100 expression with the protein expression of FZD-8 was evaluated by Pearson rank analysis. Results The expression of miR-100 was significantly lower in human breast can?cer tissues than that in adjacent normal breast tissues [2.00 (1.00, 3.00) vs. 6.00 (3.50, 8.00)]. The miR-100 expression was lower in patients with lymph node metastasis than that in patients without lymph node metastasis [1.50 (1.00, 2.75) vs. 3.00 (2.00, 4.00)]. The expression of FZD-8 was significantly higher in human breast cancer tissues than that in adjacent normal breast tissues [8.00 (6.00, 9.00) vs. 6.00 (3.75, 9.00)]. The miR-100 expression was negatively correlated with the FZD-8 pro?tein expression in human breast cancer tissues (rs=-0.592, P<0.001). Conclusion The miR-100, as an anti-metastasis-miRNA, may involve in the metastasis of breast cancer, which may be related with the regulation of the expression of FZD-8.