Objective To investigate the diagnostic value of serum soluble transferrin receptor(sTfR) in children with iron deficiency anemia(IDA).Methods Sixty-three children with microcytic hypochromic anemia were divided into IDA and non-IDA(n-IDA)groups,on which sTfR and other iron metabolism related indexes such as serum ferritin(SF) and serum iron(SI) were measured,and(t-test) between groups and analysis of ROC curve were carried out.Results The mean concentration of sTfR in the group of IDA was above normal value and t-test difference was extremely significant compared with n-IDA group(P

Objective To evaluate the effects of ischemic postconditioning on nuclear factor kappa B (NF-κB) and intercellular adhesion molecule-1 (ICAM-1) expression during lung ischemia-reperfusion (I/R) injury in a dog model of cardiopulmonary bypass (CPB), and further investigate the pulmonary protection induced by ischemic postconditioning and the underlying mechanism.Methods Twelve adult mongrel dogs of both sexes, weighing 12-15 kg, were randomly divided into either CPB group or ischemic postconditioning group (IPO group) using a random number table, with 6 dogs in each group.CPB was established after the chest was opened in dogs anesthetized with pentobarbital sodium.Ischemic postconditioning was induced by 2 cycles of 5 min reperfusion followed by 5 min ischemia immediately after occlusion of the left pulmonary artery was released in group IPO.Before CPB (T1), before occlusion of the artery was released (T2) , and at 2 h after termination of CPB, lung specimens were obtained for examination of pathological changes which were scored (with light microscope) and for determination of the expression of NFκB and ICAM-1 (using Western blot) and wet/dry lung weight ratio (W/D ratio) in left lung tissues.Blood samples were collected from femoral arteries at T1 and T3 for blood gas analysis, and oxygenation index (OI), respiration index (RI) and dynamic lung compliance (Cdyn) were calculated.Results OI and Cdyn were significantly decreased, and RI was increased at T3 , and W/D ratio, pathological scores, and expression of NF-κB and ICAM-1 were increased at T2,3 than at T1 in the two groups.W/D ratio, pathological scores, and expression of NF-κB and ICAM-1 were significantly higher at T3 than at T2 in the two groups.Compared with group CPB, OI and Cdyn were significantly increased, and R1, W/D ratio, pathological scores, and expression of NF-κB and ICAM-1 were decreased at T3 in group IPO.Conclusion Ischemic postconditioning up-regulates the expression of ICAM-1 through inhibiting NF-κB activity, thus reducing lung I/R injury induced by CPB and improving the lung function in dogs.

Antigens, Bacterial ; immunology ; urine ; Child ; Child, Preschool ; Female ; Humans ; Legionella pneumophila ; immunology ; Legionnaires' Disease ; diagnosis ; immunology ; Male ; Respiratory Tract Infections ; immunology

Objective To study the effect of hyperbaric oxygen (HBO) on the proliferation and differentiation of neural stem cells (NSCs) in rats after middle cerebral artery occlusion (MCAO).Methods Seventy-two adult,male,Sprague-Dawley rats were randomly divided into a control (CON) group,a hyperbaric air (HBA) group,a normobaric oxygen (NBO) group and a hyperbaric oxygen (HBO) group.All were subjected to MCAO.Rats in the CON group did not receive any treatment; those in the other groups were treated with HBA,NBO or HBO daily beginning 2 hours after the operation.Western blotting was applied to detect the expression of nestin,MAP2 and GFAP at 2,3,7 and 14 days after the MCAO.Results The expression of nestin in the HBO group was significantly higher than in the other groups on the 3rd,7th and 14th days.It peaked at day 3 but remained high until day 14.Similarly,expression of MAP2 was significantly higher than in the other groups at least until day 14.GFAP expression was significantly lower than in the other groups.Conclusion HBO can increase neural stem cell proliferation and neuronal differentiation,and inhibit the proliferation of astrocytes.

Objective To investigate the expression of human macrophage metalloelastase(HME) both in gastric cancer cell lines and gastric cancer tissues,and to find the role of HME in gastric carcino genesis.Methods Fifty eight patients who were operated in our hospital during April to Aug.2003 were enrolled.The samples taken from cancer,paracancer or normal tissues of these patients and cancer cell lines(MGC-803,SGC-7901,AGS)were detected for HME protein and HME mRNA expressions by Western blot and immunohistochemistry,RT-PCR and fluorescence quantitative PCR,respectively. Results Both HME mRNA and HME protein expressions were found in all three gastric cancer cell lines.The expressions of HME mRNA and HME protein in gastric cancer tissues was increased signifi- cantly compared with that in normal tissues(P0.05).Conclusions The increased HME expression in gastric cancer tissures compared with normal tissue indicate that HME may be a potential tumor marker for gastric cancer.

Objective To systematically assess the incidence of needlestick injury in Chinese nursing interns.Methods Research articles published on China Academic Journal Electronic Retrieval Database (CNKI),Chinese Scientific Journals Full-text Database (VIP),Wanfang DATA,ISI Web of Knowledge,PUBMED,OVID,Springer and other databases before 2013 were searched,which were relevant to needlestick injury in Chinese nursing interns.Using STATA 12.0 software,pooled estimates were summarized by Meta-analysis.Results 61 articles were included in this study,which covered a total of 15 451 nursing interns.Meta-analysis showed that the pooled incidence of needlestick injury in nursing interns was 65％,95％CI=60％～71％.Although the incidence declined year by year in recent decade,it was still higher than 55％.However,the injury reporting rate was 22％,95％ CI=16％～29％.Conclusions Needlestick injury showed a high incidence in Chinese nursing interns,but declined slightly year by year.However,the injury reporting rate was still very low.

Aim To investigate the effect of genistein ( GEN) against Aβ( 25 -35 )-induced PC12 cells in regulation of Fas pathway through the activation of JNK. Methods Aβ( 25 -35 )-induced PC12 cells model was established. MTT and fluorescence activated cell sorting to analyze cell viability and apoptotic rate. Fluorescence quantitative PCR was used to detect Fas apoptotic pathways related gene Fas, FasL, caspase-3 and caspase-8 mRNA relative expression. Spectropho-tometry was used to detect caspase-3 and caspase-8 en-zyme activity. Western blot was adopted to detect JNK and p-JNK protein expression level changes. Results GEN attenuated Aβ( 25-35 )-induced upregulation of Fas and FasL, caspase-3 and caspase-8 mRNA lev-el, caspase-3 and caspase-8 enzyme activity, and sig-nificantly reduced Aβ(25-35) induced JNK phospho-rylation level. Conclusion GEN can protect PC12 cells from Aβ(25-35)-induced apoptosis via reducing Aβ( 25 -35 )-induced phosphorylation of JNK activa-tion, and then inhibit the JNK dependent Fas apoptotic pathway.

Asialoglycoprotein receptor (ASGPR) is highly expressed on the surface of parenchymal liver cells. It can specifically recognize and bind to desialylated glycoproteins which contain terminal galactose or N-acetylgalactosamine residues, and endocytosed by clathrin-mediated endocytosis, transported and then degraded in lysosome. Based on this character, ASGPR mediated liver-targeted drug delivery is likely to increase drug distribution, reduce potential side effects and lower dose. This article reviewed the expression, structure, ligand binding and endocytosis of ASGPR, and summarized the design and optimization of ASGPR ligands and the release strategies. Finally, we put forward some expects about the clinical drug development for ASGPR.

This research explored the synergistic effects and the potential mechanisms of RCE-4 and various nonsteroidal anti-inflammatory drugs (NSAIDs) on the proliferation of cervical cancer Ca Ski cells. The MTT assay and CalcuSyn V2.0 software were used to detect cell proliferation and calculate the combination index (CI); the expression levels of various proteins were analyzed using Western blot assay; mitochondrial membrane potential (MMP) was assessed using JC-1 staining; acridine orange/ethidium bromide (AO/EB) double-fluorescence staining was used to detect the apoptosis of Ca Ski cells; a co-immunoprecipitation (Co-IP) assay was used to analyze the relative content of Bcl-2-Beclin 1 complex in Ca Ski cells. The results demonstrate that the combination of RCE-4 and NSAIDs increases the inhibition of Ca Ski cells compared to the single-RCE-4 group, and celecoxib provided the best synergistic effect among the four NSAIDs tested, with a CI of 0.32. The combination of RCE-4 and celecoxib significantly down-regulated the expression of cyclooxygenase-2 (COX-2) and nuclear transcription factor-κB (NF-κB), and promoted the expression of non-steroidal anti-inflammatory drugs activity gene-1 (NAG-1). In addition, autophagy induced by RCE-4 was markedly inhibited in combination with celecoxib, which was associated with down-regulation of the expression of microtubule-associated protein 3 (LC3)-II, Beclin 1, p62 and autophagy-related gene (ATG) 3/4B/5/7/14. RCE-4-induced apoptosis was significantly enhanced by altering the depolarization of mitochondrial membrane potential and the expression of B cell lymphoma-2 (Bcl-2), B cell lymphoma-xl (Bcl-xl), Bcl-2 associated X protein (Bax), Bcl-2/Bcl-xl-associated death promoter (Bad) and cleaved cysteinyl aspartate specific proteinase (cleaved-caspase) 3/7/9. Furthermore, the formation of the Bcl-2-Beclin 1 complex was significantly inhibited in Ca Ski cells treated with RCE-4 in combination with celecoxib. Taken together, this research shows that the combination of RCE-4 and celecoxib has a significant synergistic effect on the proliferation of Ca Ski cells by promoting apoptosis, inhibiting autophagy and disturbing the formation of the Bcl-2-Beclin 1 complex, which may be a novel strategy to increase the sensitivity of anti-cervical cancer drugs.