Effect of glucocorticoid receptor function on the behavior of rats with attention deficit hyperactivity disorder / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the ideal animal models for attention deficit hyperactivity disorder (ADHD) subtypes and the effect of glucocorticoid receptor (GR) function on the behavior of ADHD rats by comparing behavioral differences between spontaneously hypertensive rats (SHRs), Wistar Kyoto (WKY) rats, and Sprague-Dawley (SD) rats.</p><p><b>METHODS</b>A total of 24 male SHRs aged 21 days were randomly divided into GR agonist group, GR inhibitor group, and SHR group, with 8 rats in each group. Eight male WKY rats and 8 male SD rats, also aged 21 days, were enrolled as WKY group and SD group respectively. The GR agonist group was treated with intraperitoneal injection of dexamethasone (0.5 mg/kg daily); the GR inhibitor group was treated with intraperitoneal injection of mifepristone (RU486) (54 mg/kg daily); the SHR, WKY, and SD groups were treated with intraperitoneal injection of normal saline (0.5 mL/kg daily). The course of treatment was 14 days for all groups. The open field test and Lat maze test were used to evaluate spontaneous activity and non-selective attention.</p><p><b>RESULTS</b>The open field test showed that before drug intervention the SHR group had significantly higher numbers of line crossings and rearings than the WKY and SD groups (P<0.05); the WKY group had a significantly higher number of line crossings than the SD group (P<0.05); the SD group had a significantly higher number of groomings than the WKY group (P<0.05). After drug intervention, the GR agonist group had significantly lower numbers of line crossings and groomings than the SHR group (P<0.05). The Lat maze test indicated that before drug intervention the SHR group had significantly higher numbers of corner crossings and rearings than the WKY and SD groups (P<0.05); the WKY group had significantly higher numbers of rearings and leanings than the SD group (P<0.05). After drug intervention, the GR agonist group had significantly lower numbers of corner crossings and rearings than the SHR group (P<0.05); the GR inhibitor group had a significantly higher number of rearings than the SHR group (P<0.05); the WKY group had significantly higher numbers of rearings and leanings than the SD group (P<0.05).</p><p><b>CONCLUSIONS</b>SHR is an ideal animal model for mixed subtype ADHD, and further studies are needed to determine whether WKY rats can be used as an animal model for attention-deficit subtype ADHD. GR agonist can effectively improve spontaneous activity and non-selective attention in SHRs.</p>

Hepatitis B virus X protein up-regulates tumor necrosis factor-α expression in cultured mesangial cells via ERKs and NF-κB pathways

<p><b>OBJECTIVE</b>To investigate the effects of hepatitis B virus (HBV) X protein (HBx) on the expression of tumor necrosis factor-α (TNF-α) in glomerular mesangial cells (GMCs) and the underlying intracellular signal pathways.</p><p><b>METHODS</b>The plasmid pCI-neo-X that carries the X gene of hepatitis B virus was transfected into cultured GMCs. HBx expression in the transfected GMCs was assessed by Western-blot. TNF-α protein and mRNA were assessed by ELISA and semi-quantitative RT-PCR, respectively. Three kinase inhibitors-U0126, an inhibitor of extracellular signal-regulated kinases (ERKs); lactacystin, an inhibitor of nuclear factor-κB (NF-κB); and SB203580, a selective inhibitor of p38 MAP kinase (p38 MAPK) were used to determine which intracellular signal pathways may underlie the action of HBx on TNF-α expression in transfected GMCs.</p><p><b>RESULTS</b>A significant increase in HBx expression in pCI-neo-X transfected GMCs was detected at 36 h and 48 h, which was not affected by any of those kinase inhibitors mentioned above. A similar increase in the expression of both TNF-α protein and mRNA was also observed at 36 h and 48 h, which was significantly decreased in the presence of U0126 or lactacytin, but not SB203580.</p><p><b>CONCLUSIONS</b>HBx upregulates TNF-α expression in cultured GMCs, possibly through ERKs and NF-κB pathway, but not p38 MAPK pathway.</p>

Mutation of hepatitis B virus S gene in children with hepatitis B virus-associated glomerulonephritis / 中华儿科杂志

<p><b>OBJECTIVE</b>Hepatitis B virus-associated glomerulonephritis (HBV-GN) is an immune complex-mediated glomerulonephritis. The present study was conducted to identify HBV S gene mutation in children with HBV-GN.</p><p><b>METHODS</b>Serum HBV DNA was extracted in 53 children, including 30 with HBV-GN, 5 with HBV-carrying nephrosis (control group 1), and 18 HBV carriers (control group 2). HBV S gene sequence was amplified by polymerase chain reaction (PCR). The PCR products were sequenced directly and compared with AY167097.1, an epidemic HBV strain in China.</p><p><b>RESULTS</b>(1) The adw serotype of HBV was found in all the 30 cases with HBV-GN, 5 cases with HBV-carrying nephrosis and 17 HBV carriers except for 1, in whom adr serotype was identified. (2) HBV genotype B was found in 29 children with HBV-GN, 5 cases with HBV-carrying nephrosis and 17 HBV carriers, genotype E was found in a child with HBV-GN, and genotype C in an HBV carrier. (3) A total of 17 kinds of different single nucleotide change in HBV S gene were identified in 21 of 30 (70%) HBV-GN patients. Among them, 16 of 21 (76.2%) nucleotide mutations resulted in amino acid substitution. It was interesting that most (11/16, 68.8%) amino acid substitutions involved threonine, serine and tyrosine, the potential phosphorylation sites of mitogen-activated protein kinase (MAPK) and protein tyrosine kinase (PTK) in HBV protein. Single nucleotide changes which didn not result in amino acid substitution were found in 2 HBV-carrying nephrosis patients, 2 HBV carriers and 5 cases with HBV-GN.</p><p><b>CONCLUSION</b>Single nucleotide changes in HBV S gene were found in most children with HBV-GN. Most mutations in HBsAg resulted in amino acid substitutions involving threonine, serine and tyrosine, which may play a role in the pathogenesis of HBV-GN.</p>

Concentrations of serum iron and transferrin in children with nephrotic syndrome / 中国当代儿科杂志

<p><b>OBJECTIVE</b>Nephrotic syndrome (NS) is characterized by marked urinary excretion of albumin and other intermediated-size plasma proteins such as transferrin. The aim of this study was to determine the changes of serum iron and transferrin and the relationship between the serum and urinary transferrin.</p><p><b>METHODS</b>The indexes related to iron metabolism, including serum iron, ferritin, transferrin, total iron-binding capacity, transferrin saturation and hematological parameters (Hb, MCV, MCH), and urinary transferrin were measured in 37 children with NS before treatment and at the remission stage. Thirty-five age-matched healthy children served as controls.</p><p><b>RESULTS</b>Serum iron levels (18.8 +/- 3.8 micromol/L) in NS patients before treatment were significantly lower than in the healthy controls (22.2 +/-3.8 micromol/L) and those measured at the remission stage (21.0 +/- 3.5 micromol/L) (P < 0.01). Serum transferrin levels in NS patients before therapy (1.9 +/- 0.3 g/L) also decreased compared with those in the healthy controls (3.1 +/- 0.5 g/L) and those measured at the remission stage (2.9 +/- 0.6 g/L) (P < 0.01). In contrast, serum total iron-binding capacity and transferrin saturation were noticeably higher in NS patients before treatment than those in the healthy controls (total iron-binding capacity 56.4 +/- 9.2 micromol/L vs 50.7 +/- 6.8 micromol, P < 0.01; transferrin saturation 55.7 +/- 9.2 % vs 46.4 +/- 8.2%, P < 0.01) and were also higher than those measured at the remission stage (51.9 +/-7.7 micromol/L and 47.4 +/- 13.3%) (P < 0.01). Serum transferrin positively correlated to serum albumin (r = 0.609, P < 0.01) and negatively correlated to urinary transferrin (r = -0.550, P < 0.01) in NS patients before treatment.</p><p><b>CONCLUSIONS</b>Serum iron and transferrin levels markedly decreased in NS patients, which may be partially related to the urinary loss of transferrin.</p>

Study Progress of Biological Function of Hepatitis B Virus X Protein and Signal Transduction / 实用儿科临床杂志

Hepatitis B virus X protein(HBx) has a wide range of biological effects.It not only play important roles in the replication of the virus,but also in infects host cell proliferation and apoptosis,as well as the incidence of hepatocellular carcinoma.HBx trans-activation has a broad regulatory role in the virus itself and host genes.HBx,by interfering with multiple signaling pathways,affected a variety of biological characteristics of the host cell.

Hepatitis B Virus X Protein Upregulates Tumor Necrosis Factor-? Expression of Rat Mesangial Cell Line Via Extracellular Regulated Protein Kinases Pathway / 实用儿科临床杂志

Objective To investigate the extracellular regulated protein kinases (ERKs) pathway of hepatitis B virus(HBV) X protein(HBx) on glomerular mesangial cell(GMC) proliferation of rat and tumor necrosis factor(TNF)-? expression.Methods The HBV X gene was amplified by polymerase chain reaction(PCR),inserted into the eukaryotic expression vector PCI-neo and confirmed by restrict endonuclease digestion and sequence analysis.PCI-neo contained HBV X gene (PCI-neo-X) was transfected into cultured GMC via liposome.GMC proliferation,TNF-? and its mRNA expression were investigated in the condition of with or without U0126 in the culture media.HBx,ERK1/2 and phosphorynated-ERK1/2 (p-ERK1/2) expression in GMC were assessed by Western blot.TNF-? mRNA expression was assessed by semi-quantitative reverse transcriptase-PCR (RT-PCR).TNF-? level in supernatants was measured by enzymelinked immunosorbent assay(ELISA).GMC proliferation was assessed by methyl thiazolyl tetrazolium(MTT).Results HBx expression was found in transfected GMC,and became prominent at 36 and 48 hours after transfection whether with or without U0126 in culture media.TNF-? mRNA expression was significantly decreased in U0126 group compared with U0126-free group.TNF-? levels in supernatants in PCI-neo-X transfection without U0126 group were (189.0?18.1) ng/L at 36 hours and (172.3?24.3) ng/L at 48 hours after transfection,respectively.In contrast,TNF-? levels in supernatants with U0126 were (65.6?11.6) ng/L and (84.0?24.6) ng/L,respectively.The TNF-? le-vels in the latter groups were significantly lower than the formers (Pa

Significance of Changes of Interleukin-18 Expression Levels of Serum and Peripheral Blood Mononuclear Cells in Children with Steroid-Sensitive Nephrotic Syndrome / 实用儿科临床杂志

Objective To investigate the relationship between the steroid-sensitive nephrotic syndrome(SSNS) and interleukin-18(IL-18) and to approach the inhibitive role of dexamethasone(DEX) on expression of IL-18 of peripheral blood mononuclear cells(PBMC) in children with SSNS in vitro.Methods IL-18 levels of serum, urine and supernatants of PBMC cultured in vitro were measured by enzyme linked immunosorbent assay(ELISA) in 23 children with SSNS who were either before or after treatment. Fifteen age-matched healthy children served as normal control group, and another 18 children with respiratory infections as infectious control group.Results There were signi-ficant differences of IL-18 in serum and urine before and after treatment in children with SSNS (t=15.072,16.149 Pa