Adolescent ; Child ; Female ; Humans ; Leukemia, Myeloid, Acute ; diagnosis ; drug therapy ; pathology ; Male ; Prognosis

Child, Preschool ; Female ; Humans ; Infant ; Male ; Rotavirus Infections ; diagnosis ; therapy ; Vomiting ; etiology

OBJECTIVETo investigate the effects of ghrelin on the proliferation and differentiation of 3T3-L1 preadipocyte, and study the possible mechanisms.

METHODS3T3-L1 preadipocytes were cultured in vitro. The proliferation potentials of 3T3-L1 preadipocytes that were treated with different concentrations of ghrelin were evaluated by MTT methods. The levels of c-myc and thymidine kinase mRNA were detected using RT-PCR. 3T3-L1 preadipocytes were differentiated into the matured adipocytes with insulin (INS) or ghrelin. The morphological changes of 3T3-L1 adipocytes were observed and the differentiation rate was assayed by oil-red O staining. Total RNA was extracted from adipocytes at various times, and the levels of peroxisome proliferation activated receptor gamma (PPARgamma) and CAAT/enhancer binding protein(C/EBPalpha) mRNA expressions were detected using RT-PCR.

RESULTSGhrelin at concentrations of 10(-7) to 10(-15) mol/L significantly stimulated preadipocyte proliferation (p<0.05). The levels of c-myc and thymidine kinase mRNA significantly increased in 3T3-L1 preadipocytes with 10(-9) mol/L and 10(-11) mol/L ghrelin treatment (p<0.01). The 3T3-L1 preadipocytes treated with 10(-11) mol/L ghrelin had lots of lipid droplets in the cytoplasma, but the differentiation rate was lower than those treated with INS. Ghrelin of 10(-11) mol/L significantly increased the mRNA expression of PPARgamma and C/EBPalpha in the course of 3T3-L1 preadipocyte differentiation, compared with the normal control group (p<0.05). The PPARgamma and C/EBPalpha mRNA expression increased with the prolonged differentiation of preadipocytes induced by ghrelin or INS. There were significant differences in the levels of PPARgamma and C/EBPalpha mRNA expression between the 2nd and 8th days of differentiation(p<0.01).

CONCLUSIONSGhrelin promotes the proliferation and differentiation of 3T3-L1 preadipocytes. The proliferation of 3T3-L1 preadipocytes induced by ghrelin may be associated with increased c-myc levels. Ghrelin may promote differentiation of 3T3-L1 preadipocytes by increasing mRNA expression of PPARgamma and C/EBPalpha, thus enhances the sensitivity of adipocytes to INS.

3T3-L1 Cells ; Adipocytes ; cytology ; drug effects ; Animals ; CCAAT-Enhancer-Binding Protein-alpha ; genetics ; Cell Differentiation ; drug effects ; Cell Proliferation ; drug effects ; Genes, myc ; Ghrelin ; pharmacology ; Mice ; PPAR gamma ; genetics ; RNA, Messenger ; analysis ; Stem Cells ; cytology ; drug effects ; Thymidine Kinase ; genetics

OBJECTIVEImmunosuppressant tacrolimus (FK506) has shown neuroprotective effects on hypoxic-ischemic brain damage (HIBD) in the adult animal model. This study investigated whether FK506 has a protection against HIBD in neonatal rats by examining growthjassociated protein-43 (GAP-43) expression in the hippocampus.

METHODSNinety-six seven-day-old Sprague-Dawley rats were randomly divided into three groups: sham-operation, HIBD and FK506 intervention group. HIBD was induced in the later two groups. The FK506 intervention group was intraperitoneally injected with FK506 immediately after HIBD, at a dosage of 1 mg/kg daily, for three days. The HIBD group was injected with normal saline. Immunohistochemical technical was applied to examine GAP-43 expression in the hippocampus 24 and 72 hrs and 7 and 14 days after HIBD.

RESULTSCompared with the HIBD group, hematoxylin-eosin staining showed attenuated neuronal necrosis in the FK506 intervention group. In the HIBD group, the expression of GAP-43 increased significantly 72 hrs, and 7 and 14 days after HIBD compared with that in the sham-operation group. The GAP-43 expression in the FK506 intervention group was significantly higher than that in the HIBD group 72 hrs and 7 days after HIBD.

CONCLUSIONSFK506 might have neuroprotective effects against HIBD in neonatal rats.

Animals ; Animals, Newborn ; GAP-43 Protein ; analysis ; Hippocampus ; chemistry ; drug effects ; Hypoxia-Ischemia, Brain ; drug therapy ; metabolism ; pathology ; Immunosuppressive Agents ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Tacrolimus ; pharmacology

OBJECTIVETo study the effect of H2O2 on the proliferation and apoptosis of endothelial progenitor cells (EPCs) and the antogonistic effects of catechin on the cell apoptosis induced by H2O2 in rats.

METHODSImmuno-fluoreascence assay was applied to detect CD34, CD133 and VEGFR-2 expression. EPCs of generation 2 were divided into control cells, H2O2-treated cells and catechin-H2O2-treated cells (H2O2: 100 mg/L; catechin: 10 mg/L). Genomic DNA was extracted by the conventional method after intervention for the analysis of apoptosis ladder pattern. The MTT assay was applied to detect proliferation rate of EPCs.

RESULTSThe cultured cells at day 10 expressed CD34, CD133 and VEGFR-2. DNA apoptosis ladder pattern appeared in H2O2-treated cells 2 days after intervention. After 3 days of intervention DNA apoptosis ladder pattern appeared in both H2O2-treated cells and H2O2-catechinjtreated cells, with more ladders and grayer scale in H2O2 -treated cells. Compared with the controls, H2O2-treated cells and H2O2-catechin-treated cells showed significantly decreased proliferation rate (p<0.01), with the lowest proliferation rate at the 2nd day (p<0.05). The H2O2-catechin-treated cells showed increased proliferation rate than H2O2-treated cells at the 1st, 2nd and 3rd days.

CONCLUSIONSH2O2 may impair EPCs proliferation and induce EPCs apoptosis. Catechin may increase the capacity of EPCs for the resistance to apoptosis induced by H2O2.

AC133 Antigen ; Animals ; Antigens, CD ; analysis ; Antigens, CD34 ; analysis ; Apoptosis ; drug effects ; Catechin ; pharmacology ; Cell Proliferation ; drug effects ; Endothelial Cells ; cytology ; drug effects ; Female ; Glycoproteins ; analysis ; Hydrogen Peroxide ; toxicity ; Peptides ; analysis ; Rats ; Rats, Sprague-Dawley ; Stem Cells ; cytology ; drug effects ; Vascular Endothelial Growth Factor Receptor-2 ; analysis

OBJECTIVEIt has been proposed that nephrotic syndrome is a consequence of an imbalance between oxidant and anti-oxidant activity. Nephrin plays an important role in maintaining glomerular filtration barrier. This study aimed to explore the relationship between the expression of glomerular nephrin and oxidative stress reaction in rats with adriamycin (ADR)-induced nephrosis, and the protection of prednisone and vitamin E against renal injuries.

METHODSNephrosis was induced by single intravenous injection of ADR (5 mg/kg). The prednisone intervention group was administered with prednisone (10 mg/kg daily) between 1 and 4 weeks after ADR injection. The vitamin E intervention group received vitamin E of 20 mg/kg daily from 1 week before ADR injection till to 4 weeks after ADR injection. Control rats were intravenously injected with normal saline. After 7, 14, 21 and 28 days of ADR injection, the indexes of oxidative stress reaction of the renal cortex, malondialdehyde (MDA), superoxide dismutase (SOD) and total antioxidative capacity (T-AOC), were measured using the chemical chromatometry. The protein expression of glomerular nephrin was measured by immunohistochemistry.

RESULTSPrednisone or vitamin E treatment reduced urinary protein from 14 days to 28 days after ADR injection. MDA levels of renal cortex increased, while renal activities of SOD and T-AOC as well as nephrin protein contents decreased in untreated nephrosis group from 7 days after ADR injection compared with those in the control rats. Compared with the untreated nephrosis group, prednisone treatment resulted in an increase in nephrin protein contents 28 days after ADR injection; Vitamin E treatment decreased renal MDA levels and increased renal activities of SOD and T-AOC and nephrin protein contents 28 days after ADR injection. Nephrin staining showed a sable linear-like pattern along the capillary loops of glomerulus in the control rats. Nephrin staining presented a light tan discontinuous short linear-like or punctiform pattern along the capillary loops of glomerulus in the untreated ADR group. Prednisone or vitamin E treatment ameliorated abnormal expression of nephrin induced by nephrosis. Glomerular nephrin expression level was negatively correlated with renal MDA level and positively correlated with renal activities of SOD and T-AOC.

CONCLUSIONSA reduction of glomerular nephrin expression is closely related to oxidative stress reaction. Prednisone and vitamin E have protective effects against renal injuries induced by ADR in rats.

Animals ; Doxorubicin ; toxicity ; Kidney Glomerulus ; metabolism ; Male ; Malondialdehyde ; analysis ; Membrane Proteins ; analysis ; Nephrosis ; chemically induced ; metabolism ; prevention & control ; Oxidative Stress ; Prednisone ; pharmacology ; Rats ; Rats, Wistar ; Superoxide Dismutase ; metabolism ; Vitamin E ; pharmacology

OBJECTIVEAlveolar epithelium impairment is one of pathological changes associated with chronic lung disease (CLD). Hoxb5 is one of the few homeobox genes strongly expressed in the developing lung. This study investigated the expression of HoxB5, SPC and AQP5 in rats with CLD in order to explore the role of Hoxb-5 in impairment and reparation of alveolar epithelium.

METHODSEighty neonatal rats were randomly exposed to hyperoxia (model group) or to room air (control group) (n=40 each). The CLD model was induced by hyperoxia exposure. The expression of HoxB5, SPC and AQP5 protein and mRNA in the lung tissue was detected by immunohistochemistry and RT-PCR 1, 3, 7, 14 and 21 days after exposure.

RESULTSIn the model group HoxB5 expression significantly decreased 7, 14 and 21 days after hyperoxia exposure. SPC expression decreased 3 days after hyperoxia exposure but increased significantly 7, 14 and 21 days after hyperoxia exposure as compared to the control group. AQP5 expression was progressively reduced with prolonged hyperoxia exposure.

CONCLUSIONSHyperoxia exposure may lead to alveolar epithelial cell (AEC) damage in neonatal rats. The increased SPC expression and decreased AQP5 expression suggested that the ability of differentiation and transformation of AECII into AECI decreased in neonatal rats with CLD. The decreased HoxB5 expression following hyperoxia exposure might contribute to a decreased ability of differentiation of AECII.

Animals ; Animals, Newborn ; Aquaporin 5 ; analysis ; genetics ; Chronic Disease ; Female ; Homeodomain Proteins ; analysis ; genetics ; Hyperoxia ; complications ; Immunohistochemistry ; Lung ; pathology ; Lung Diseases ; etiology ; metabolism ; Male ; Pulmonary Surfactant-Associated Protein C ; analysis ; genetics ; RNA, Messenger ; analysis ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction

OBJECTIVETo examine plasma adiponectin (ADPN) and tumor necrosis factor-alpha (TNF-alpha) levels and their correlation in children with obesity in order to investigate the roles of both in the development of childhood obesity.

METHODSOne hundred and forty-seven children with obesity and 118 normal children who were randomly sampled from five primary schools from the Kaifu District in Changsha were enrolled. Physical shape indexes, including height, weight, waist circumference, hip circumference, and waist to hip ratio (WHR) were measured. Body mass index (BMI) was calculated. Blood pressure was measured. Percentage of body fat (%BF) was measured with dual energy X-ray absorptiometry. Plasmal levels of ADPN and TNF-alpha were detected using ABC-ELISA. Blood concentrations of triglycerides (TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL-C) and low density lipoprotein-cholesterol (LDL-C) were measured by automatic biochemistry analyzer. Fasting blood glucose level was measured by glucose oxidase method. Fasting blood insulin level was assayed by radioimmunity. Homeostasis model assessment for insulin resistance (HOMA-IR) was performed.

RESULTSPlasma ADPN levels in obese children significantly decreased compared with those in normal children (8.12+/-2.54 mg/L vs 12.22+/-4.68 mg/L; p<0.05), and had a negative correlation with plasma TNF-alpha levels, BMI, WHR and HOMA-IR (p<0.01), and with %BF, fasting insulin, systolic blood pressure and TG (p<0.05). Plasma TNF-alpha levels in obese children significantly increased compared to normal children (171.38+/-34.33 ng/L vs 91.07+/-21.60 ng/L; p<0.01) and positively correlated with BMI, WHR, %BF, fasting insulin, HOMA-IR, TG and systolic blood pressure (p<0.01), and negatively with HDL (p<0.05). Multiple stepwise regression analysis showed that ADPN, BMI and TNF-alpha were main influential factors for %BF (R2=0.926, p<0.01). There was a significant interaction between ADPN and TNF-alpha (p<0.05).

CONCLUSIONSPlasma ADPN levels decreased and plasma TNF-alpha levels increased in children with obesity and both were main influential factors for %BF in children. There was an interaction between ADPN and TNF-alpha, suggesting that they both participate in the development of childhood obesity.

Adiponectin ; blood ; Adolescent ; Blood Pressure ; Body Mass Index ; Child ; Cholesterol, HDL ; blood ; Female ; Humans ; Insulin Resistance ; Male ; Obesity ; blood ; etiology ; Regression Analysis ; Tumor Necrosis Factor-alpha ; blood

OBJECTIVETo study the changes and significance of NF-kappa B activation in peripheral blood mononuclear cells (PBMC) of children with epilepsy.

METHODSNF-kappa B activation in PBMC was assayed by the flow cytometry in 32 healthy children and 64 children with epilepsy before and after treatment. The 64 epileptic children were subdivided into three groups: systemic seizure, partial seizure and unknown classification.

RESULTSNF-kappa B activation in PBMC in three epilepsy subgroups were significantly higher than that in healthy controls. The systemic seizure group showed significantly increased NF-kappa B activation in PBMC compared with the partial seizure group (p<0.01) and the unknown classification group (p<0.05). After treatment NF-kappa B activation in PBMC in three epilepsy subgroups was significantly reduced (p<0.01).

CONCLUSIONSNF-kappa B activation in PBMC increased in children with epilepsy, and it was positively correlated with the severity of seizures.

Adolescent ; Child ; Child, Preschool ; Epilepsy ; blood ; drug therapy ; Female ; Flow Cytometry ; Humans ; Infant ; Leukocytes, Mononuclear ; metabolism ; Male ; NF-kappa B ; metabolism

OBJECTIVEMultilocular brain abscess in children is a serious neurosurgical emergency and remains a serious, life-threatening disease. This study evaluated the role of neuroendoscopy in treating multilocular brain abscess in children.

METHODSBetween January 2002 and June 2007, 16 children with multilocular brain abscess underwent an operation using a pure endoscopic procedure.

RESULTSIncreased intracranial pressure was relieved after operation in the 16 patients. CT/MRI after operation showed the abscess cavities disappeared and only the residual abscess walls existed in the 16 patients. Fourteen patients were followed up for 6 months to 5 years after surgery. Abscess walls disappeared in 13 patients and abscess recurred only in 1 patient.

CONCLUSIONSNeuroendoscopy for treatment of multilocular brain abscess is safe and effective in children.

Adolescent ; Anti-Bacterial Agents ; therapeutic use ; Brain Abscess ; surgery ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Male ; Neuroendoscopy ; methods