Child ; Congresses as Topic ; Humans ; Pediatrics ; Sleep

Child ; Humans ; Nephrology ; Pediatrics

Factor V ; Factor V Deficiency ; Female ; Humans ; Infant, Newborn

Antifungal Agents ; therapeutic use ; Echinocandins ; therapeutic use ; Humans ; Infant, Newborn ; Infant, Premature ; Lipopeptides ; Mycoses ; drug therapy

AIM: To screen the binding proteins to HMGB1 promoter by phage display technique. METHODS: HMGB1 promoter was incubated with phage display library. Unbound phages were eluted and phages bound to HMGB1 promoter were amplified. Twenty individual clones were randomly selected and identified by enzyme-linked immunosorbent assay (ELISA). Positive clones were characterized by DNA sequencing and the sequences were subjected for computer analysis. RESULTS: Positive phages binding to HMGB1 promoter were enriched after 4 rounds of biopanning. Twenty phage clones were selected and eleven clones of which were identified to bind specifically to HMGB1 promoter. The sequences in full length were obtained and searched for homologous sequences from GenBank. Altogether eight coding sequences were obtained, six of which were known proteins including activator protein-1(AP-1) and two of which were uncharacterized ones. CONCLUSION: Several proteins were obtained that bind specifically with HMGB1 promoter. The results will be useful for further studying the expression and regulation mechanism of HMGB1.

Objective To investigate the role of extracellular regulated protein kinase (ERK) signal pathway in mechanical stretch induced high mobility group box 1 protein (HMGB1) expression on alveolar epithelial cells (A549). MethodsA549 cells were cultured and seeded at 1×10~5 cells/ml in 6-well Bioflex cell culture plates. Subsequently, the cells were exposed to cyclic mechanical stretch at 14% (group B) elongation for 4 hours using Flexercell 4000T cell stretching unit. In group C, cells were pretreated with PD98059 for 2 hours before mechanical stretch. Cells in group A without stretch were served as control. The expression of HMGB1 protein and mRNA in A549 cells were detected by immunocytochemisty staining and RT-PCR, respectively. ERK activity was measured by Western blotting method. Results Immunocytochemisty staining indicated that the expression of HMGB1 protein in A549 cells was increased obviously in group B (P<0.05) and decreased in group C (P<0.05). Polymerase chain reaction (RT-PCR) showed that the expression of HMGB1 mRNA was also significantly increased in group B (P<0.05) and decreased in group C (P<0.05). Western blotting analysis confirmed the activation of ERK in A549 cells by mechanical stretch (P<0.05). PD98059, an inhibitor of ERK, might significantly inhibit mechanical stretch induced HMGB1 protein and mRNA expression in A549 cells (P<0.05). Conclusion Mechanical stretch could regulate the expression of HMGB1 gene and protein in A549 cells through ERK signal pathway.

Objective To study the relationship between spinal shifting and C5 palsy after posterior approach cervical decompression surgery (PACDS).Methods Twenty-four patients underwent PACDS were examined with MRI before and one month after operation.The spinal shifting were measured.Clinical and imaging characteristics of patients with post-operative C5 palsy were observed.Analyzed the correlation between C5 palsy and spinal shifting after operation.Results The average spinal shifting was (2.41 ± 0.46) mm.Three cases developed C5 palsy,whose spinal shifting at C5 level was significantly greatert han those without C5 palsy.Conclusion Excessive posterior spinal shifting after PACDS can drag C5 nerve root leading to C5 palsy.

Child ; Congresses as Topic ; Humans ; Kidney Diseases ; Nephrology ; Pediatrics

Humans ; Infant ; Intracellular Signaling Peptides and Proteins ; genetics ; Membrane Proteins ; genetics ; Mutation ; Nephrotic Syndrome ; etiology ; genetics ; WT1 Proteins ; genetics

Aim To examine the effect of different dosages hydroxyethyl starch(HES)130/0.4 on intercellular adhesion molecule 1(ICAM-1)expression in lung tissue of acute lung injury in endotoxemic rats and explore the role of MAPKs pathway in its expression.Methods Thirty six healthy Sprague Dawley(SD)rats weighing 270~320 g were randomly divided into 6 groups with 6 animals in each group.In group H1-H4,1 min after lipopolysaccharide(LPS)5 mg?kg-1 intravenously administration,HES 130/0.4 with 3.75,7.5,15,30 ml?kg-1 were infused intravenously respectively at a rate of 0.2 ml?min-1.In group L,saline instead of HES 130/0.4 was administered.Group N served as control by giving the same volume of saline.The animals were anesthetized with pentobarbital.Right external jugular vein was injected with LPS.The animals were killed 4 hours after LPS injection for determination of total protein,WBC,MPO,W/D,ICAM-1 protein and mRNA and MAPKs activity.Results Compared with control group,total protein,WBC,MPO,W/D,expression of ICAM-1 protein and mRNA and MAPKs activity were increased significantly in group L.Compared with group L,total protein,WBC,MPO,W/D,expression of ICAM-1 protein and mRNA and MAPKs activity were decreased significantly in group H1 and H2,especially at the dosage of 7.5 ml?kg-1.Conclusion HES 130/0.4(7.5 ml?kg-1)can attenuate inflammatory response of acute lung injury induced by LPS,which may be related with inhibiting the expression of ICAM-1 protein and mRNA through MAPKs signal pathway.