AIM:To observe the effect of parenteral nutrition(PN)in the feeding of premature infants.METHODS:Seventy five premature infants were randomly assigned into three groups.The control group supplied glucose combined with minimal enteral nutrition and assisted with nonutrition sucking.In treatment groups:the no-fat emulsion PN group supplied amino acids and glucose combined with minimal enteral nutrition and assisted with nonutrition sucking,and the fat emulsion PN group supplied fat emulsion,amino acids and glucose combined with minimal enteral nutrition and assisted with nonutrition sucking.After 1 week,the weight,the state correlated biochemical indicator and complications were detected.RESULTS:Both of the no-fat emulsion PN therapy and the fat emulsion PN therapy could promote weight gain and lessen complications,and the clinical application was comparatively safe.CONCLUSION:The PN can improve growth and development of premature infants and elevate the clinical therapeutic efficacy.

AIM:To observe the neuroprotection effects exogenous adrenomedullin(AM) against hypoxic-ischemia reperfusion damage(HIRBD) in neonatal rat models.METHODS:Forty neonatal rats were randomly divided into Control Group(n=8,with sham operation),Hypoxic-ischemia Reperfusion(HIR) Group and Intervention Group(n=8,wth intraperitoneal AM injection 0,6 and 12 h after making model).All rats were decapitated at 48 hours after reperfusion,and the cerebral slices were made at the 2 mm level in front of the interaural line.The pathobiological changes of brain tissue were observed by the method of HE dye in light microscope,and the levels of nitrogen monoxide synthase(NOS),glutathion(GSH) and myeloperoxidase(MPO) in neonatal rats cerebral tissue were determined by using chromatometry.RESULTS:Hypoxic-ischemia reperfusion could induce obviously cerebral pathological change which could be improved by AM.The brain tissue levels of cNOS and GSH in AM 0 and 6 h Group were significantly higher than those of HIR Group(P

BACKGROUND: The epidermal growth factor receptor (EFGR) mutation was closely related to the invasion and metastasis of lung adenocarcinoma and the biological axis of CXCR4/CXCL12 (chemokine receptor 4/chemokine ligand 12) played an important role in the organ-specific metastasis of the tumor. It was a question surrounding whether there is interaction between them in the process of lung adenocarcinoma metastasis. To investigate the potential molecular mechanisms of EGFR over-expression and EFGR-mutations effects on cell proliferation, migration and invasion, we constructed EGFR over-expression and three EFGR-mutant human lung adenocarcinoma H1299 cell sublines. METHODS: EGFR over-expression and three EFGR-mutant (EGFR-E746-A750del, EGFR-T790M and EGFR-L858R) plasmid were designed and transfected H1299 cells with Lipofectamine 2000. H1299 cells transfected with empty vector were negative control (NC), and H1299 cells without transfection were set as blank control (BC). The effects of EGFR over-expression and mutations on the proliferation, migration and invasion of H1299 cells were detected by cell cloning assay, wound healing assay and Transwell assay. The mRNA and protein expression levels of MMP-2, MMP-9, CXCR4 and CXCL12 were detected by RT-PCR and Western blot. RESULTS: Compared with negative control group and blank control group, EGFR over-expression and EGFR-E746-A750 deletion have significantly higher colony formation (28±2, 28.33±4.16; respectively) (P<0.05) and the cell migration and invasion ability were significantly increased (P<0.05). RT-PCR and Western blot assay showed that the mRNA and protein expression of MMP-2, MMP-9, CXCR4 and CXCL12 in EGFR over-expression and EGFR-E746-A750 deletion group were remarkably higher than that in negative control and blank control group (P<0.05). CONCLUSIONS EGFR over-expression and 19 exon deletion can promote the expression of MMP-2 and MMP-9 by up-regulating CXCR4/CXCL12 signaling pathway, leading to the change of tumor biological characteristics such as higher proliferation, migration and invasion ability.
Adenocarcinoma ; pathology ; Adenocarcinoma of Lung ; Cell Line, Tumor ; Cell Movement ; genetics ; Chemokine CXCL12 ; metabolism ; ErbB Receptors ; genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms ; pathology ; Mutation ; Neoplasm Invasiveness ; Receptors, CXCR4 ; metabolism ; Signal Transduction ; genetics