OBJECTIVE: To explore a feasibility of engraftment of systemically transplanted bone marrow stromal cells (BMSCs) and differentiation into lung epithelial cells in lipopolysaccharides (LPS)-injured lungs. METHODS: BMSCs were isolated from bone marrow of transgenic green fluorescent protein (GFP) C57BL/6J mice and systemically administered to bone marrow-suppressed wild-type C57BL/6J mice. A mouse model of lung injury was prepared by intratracheal instillation of LPS. Recipients were assigned to four groups: intratracheal PBS + BMSCs transplantation (CM), intratracheal LPS + BMSCs transplantation (LM), intratracheal PBS + irradiation + BMSCs transplantation (CIM) and intratracheal LPS+ irradiation + BMSCs transplantation (LIM). BMSCs engraftment in recipient lungs was determined by immunofluorescent staining 14 days after BMSCs administration. Alveolar epithelial type II cells were isolated from recipient lungs and the rate of GFP positive cells was measured by flow cytometry. Expression of surfactant protein (SP)-A, SP-C and aquaporin (AQP)-5 mRNA in the lungs was evaluated by real-time PCR. RESULTS: GFP and cytokeratin positive cells were observed in lung parenchyma of the CIM and the LIM groups, but not in the CM and the LM groups. The LIM group had more positive cells than the CIM group. The rates of GFP positive cells were higher in the CIM (11.10±3.19%) and the LIM groups (14.40±2.40%) than those in the CM and the LM groups (2.82±1.03% and 3.81±0.93%, respectively; P<0.05). The LIM group had higher mRNA expression of SP-C than the CM group (2.09±0.18 vs 1.38±0.30; P<0.05). CONCLUSIONS: Donor derived BMSCs can engraft in LPS-injured lungs and differentiate into lung epithelial cells, suggesting BMSCs transplantation might contribute to lung repair.［Chin J Contemp Pediatr, 2009, 11 (5):321-327］

Two clinical phenotypes for citrin deficiency (CD) have been reported. One is adult-onset citrullinemia type II (CTLN2) and another is neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD). A child with CD and who had failure to thrive (FTT) and dyslipidemia as main clinical manifestations is reported here. Both the weight-and length-for-age at 18 months dropped below the 3rd percentile in the corresponding WHO anthropometry percentile charts, while blood biochemical analysis revealed dramatically increased triglyceride and total cholesterol, together with reduced HDL-cholesterol. Inquiries revealed his aversion to rice and fondness for fish since the age of one year, a peculiar habit which could not be corrected. Since the age of two years, the peculiar diet became more obvious, and slightly increased citrulline and threonine levels were detected on blood amino acid analysis. At the age of two years and five months he was suspected to have CD. Since then, he has been fed in accordance with his own food preferences, and FTT improved gradually, with weight-for-age, in particular, recovering beyond the 3rd percentile at three years of age, and dyslipidemia was also ameliorated gradually. SLC25A13 gene analysis revealed a homozygote of 851del4, and CD was thus confirmed. Diet survey at four years and seven months revealed a fondness for high-protein and low-carbohydrate foods, such as seafood, meat, eggs and milk. This child presented with FTT and dyslipidemia as main clinical manifestations and this was a novel CD phenotype different from NICCD and CTLN2.［Chin J Contemp Pediatr, 2009, 11 (5):328-332］

Leigh syndrome is a genetically heterogeneous disease caused by defects in enzymes involved in aerobic energy metabolism and the Krebs' cycle. Mitonchondrial complex I deficiency is a main cause of Leigh syndrome. In this study, a Chinese child with Leigh syndrome caused by 13513G>A mutation was reported. The proband was the first child of his parents. The previously healthy boy presented with generalized epilepsy at 12 years of age. When he visited Peking University First Hospital at 13 years of age, he had subacute loss of vision in two eyes and temporal defect of visual field in the left eye. He walked with a spastic gait. His blood lactate and pyruvate levels were elevated. Muscle biopsy showed mild lipid accumulation in muscle fiber. An electrocardiogram showed incomplete right bundle branch block. Brain magnetic resonance imaging showed bilateral, symmetrical lesions in the basal ganglia, supporting the diagnosis of Leigh syndrome. 13513G>A mutation was identified by gene analysis in the patient, which led to mitochondrial respiratory chain complex I deficiency. Multivitamins and L-carnitine were administered. At present, the patient is 16 years old and has progressive deterioration with significant muscle weakness and body weight loss. He is absent from school. He has no obvious retardation in intelligence. 13513G>A mutation was first identified by gene analysis in Chinese population with Leigh syndrome. This may be helpful in genetic counseling.［Chin J Contemp Pediatr, 2009, 11 (5):333-336］

OBJECTIVE: To examine serum concentration of interleukin-18 (IL-18) and IL-18 mRNA expression in peripheral blood mononuclear cells (PBMCs) in children with primary nephrotic syndrome (PNS) and explore the possible role of IL-18 in steroid-resistant nephrotic syndrome (SRNS). METHODS: Sixty-six children with newly diagnosed PNS, including 39 cases of steroid sensitive nephrotic syndrome (SSNS) and 27 cases of SRNS, were enrolled. Forty healthy children were used as a normal control group. Blood samples were collected before and 8 weeks after glucocorticoid treatment. Serum concentration of IL-18 was measured using ELISA. IL-18 mRNA expression in PBMCs was detected by the RT-PCR method. The amount of 24-hr urine protein was measured by the biuret method. Serum contents of total cholesterol (T-Ch), triglyceride (TG), low density lipoprotein (LDL), total protein (TP), and albumin (Alb) were measured by the automatic biochemistry analyzer. RESULTS: Serum concentration of IL-18 and IL-18 mRNA expression in PBMCs in the SSNS and the SRNS groups were significantly higher than those in the normal control group before treatment (P<0.05). The SRNS group had increased serum protein concentration of IL-18 and IL-18 mRNA expression in PBMCs compared with the SSNS group before treatment (P<0.05). Serum LDL content in the SRNS group was also significantly higher than that in the SSNS group before treatment (P<0.05). After treatment, serum concentration of IL-18 and IL-18 mRNA expression in PBMCs in the SRNS group were significantly higher than those in the SSNS and the normal control groups (P<0.05). Serum concentration of IL-18 and IL-18 mRNA expression in PBMCs in the SSNS group were significantly reduced after treatment, but the alterations of IL-18 were not observed in the SRNS group after treatment. CONCLUSIONS: SRNS was associated with increased serum IL-18 concentration and IL-18 mRNA expression in PBMCs. Over-production of IL-18 may play a role in the development of SRNS.［Chin J Contemp Pediatr, 2009, 11 (5):337-340］

OBJECTIVE: To study and identify the protein markers in the urine of children with steroid-sensitive (SSNS) and steroid-resistant nephrotic syndrome(SRNS). METHODS: Total urinary proteins were extracted from children with SSNS before and after steroid therapy, SRNS, and healthy children (n=5 in each group). Urinary proteins were separated by immobilized pH gradient based on two-dimensional gel electrophoresis (2-DE). The silver-stained 2-DE gels were scanned with digital Image Scanner and analyzed with Image Master 2-DE Elite 3.01 software. Peptide mass fingerprint (PMF) of differential protein spots was obtained with MALDI-TOF-MS. Proteins were identified by Mascot software based on NCBI protein database. RESULTS: There were 66 spots with different expression of protein between SRNS children and SSNS children before steroid therapy, and 24 spots and 27 spots only occurred in SRNS children and SSNS children before steroid therapy, respectively. There were 75 spots with different expression of protein between SSNS children after steroid therapy and healthy controls, and 11 spots only occurred in SSNS children after steroid therapy. Eighteen protein spots with different expression (6 spots in each nephrotic group) were chose and analyzed by MALDI-TOF-MS, and 9 types of proteins were identified. CONCLUSIONS: Nine types of urinary proteins with different expression (6 spots in each nephrotic group) were identified between SRNS and SSNS children, and they might be the biomarkers for SRNS or SSNS.［Chin J Contemp Pediatr, 2009, 11 (5):341-345］

OBJECTIVE: To investigate the clinical significance of serum Cyst-C and urinary microalbumin in early renal impairment in children with Henoch-Schonlein purpura (HSP). METHODS: Forty-eight children with HSP and who had normal serum creatinine level and 31 healthy children were enrolled. Contents of serum Cyst-C and urinary microalbumin were measured using ELISA and immunoturbidimetry, respectively. Urinary routine examination was performed in children with HSP. The contents of serum Cyst-C and urinary microalbumin were re-examined one month after treatment (recovery phase). RESULTS: The contents of serum Cyst-C (2.24±0.81 mg/L) and urinary microalbumin (20.04±10.32 mg/L) in the HSP group at the acute phase were significantly higher than those in the control (0.85±0.20 and 2.30±1.38 mg/L respectively; P<0.01). Serum Cyst-C (1.70±0.30 mg/L) and urinary microalbumin contents (13.20±8.16 mg/L) were significantly reduced at the recovery phase compared with those at the acute phase in the HSP group (P<0.01). The proportion of urinary routine abnormality (33.3%) was significantly lower than that of urinary microalbumin (68.8%) and serum Cyst-C abnormalities (72.9%) in the HSP group (P<0.01). CONCLUSIONS: Serum Cyst-C and urinary microalbumin may serve as indexes in the assessment of early renal impairment in children with HSP.［Chin J Contemp Pediatr, 2009, 11 (5):346-348］

OBJECTIVE: To study the roles of CD4+CD25+ regulatory T cells and Foxp3 mRNA in peripheral blood as well as serum total immunoglobulin E (IgE) in the pathogenesis of bronchiolitis caused by respiratory syncytial virus (RSV). METHODS: The proportion of CD4+CD25+ regulatory T cells and expression of Foxp3 mRNA in peripheral blood, and total serum IgE level were tested by flow cytometry, RT-PCR and ELISA respectively in 57 children with RSV bronchiolitis (26 atopic patients and 31 nonatopic patients). Twenty five healthy children were used as the control group. RESULTS: The proportion of CD4+CD25+ regulatory T cells in peripheral blood in children with bronchiolitis, either in the atopic (7.7±1.6%)or the nonatopic group (8.8±2.1%), was significantly lower than that in the control group (10.5±1.6%) (P<0.01). Foxp3 mRNA expression in peripheral blood was significantly lower in both atopic and nonatopic children with bronchiolitis than that in the control group (P<0.01). Significantly increased total serum IgE level was noted in both atopic (241.2±102.5 IU/mL) and nonatopic children (125.5±63.2 IU/mL) with bronchiolitis compared with that in the control group (27.2±10.5 IU/ml) (P<0.01). There were significant differences in the proportion of CD4+CD25+ regulatory T cells and Foxp3 mRNA expression in peripheral blood (P<0.05) as well as total serum IgE level (P<0.01) between the atopic and the nonatopic group. The proportion of CD4+CD25+ regulatory T cells (r=-0.70, P<0.01) and Foxp3 mRNA expression in peripheral blood (r=-0.79, P<0.01) were closely negatively correlated to total serum IgE level. CONCLUSIONS: Both the proportion of CD4+CD25+ regulatory T cells and Foxp3 mRNA expression in peripheral blood were reduced, in contrast, the total serum IgE level increased in children with RSV bronchiolitis. This suggested that CD4+CD25+ regulatory T cells and Foxp3 mRNA together with IgE participated in the pathogenesis of RSV bronchiolitis.［Chin J Contemp Pediatr, 2009, 11 (5):349-353］

OBJECTIVE: The pathogenesis of bronchiolitis has not been fully identified. Immune function abnormality following virus infection may be associated with the pathogenesis. CD40 and CD40 ligand (CD40L) is a pair of co-stimulatory molecules in immunoreaction. They might play an important role in the development of bronchiolitis. This study aimed to investigate the expression of CD40 and CD40L in peripheral blood mononuclear cells (PBMCs) in children with bronchiolitis and explore their possible roles in the disease. METHODS: Thirty children with bronchiolitis, 26 children with bronchopneumonia and 30 healthy children (control) were enrolled. Flow cytometry was used to detect CD40 and CD40L expression in PBMCs. Total serum IgE level was measured using ELISA. RESULTS: Compared with the control group, CD40L expression significantly increased in the bronchiolitis and bronchopneumonia groups (P<0.05). The CD40L expression in the bronchiolitis group was significantly higher than that in the bronchopneumonia group (P<0.05). A significantly increased CD40 expression was also found in the bronchiolitis group when compared with the bronchopneumonia and the control group (P<0.01). Total serum IgE level in the bronchiolitis group was significantly higher than the bronchopneumonia and the control groups (P<0.01). CD40 and CD40L expression was positively correlated with serum IgE level in the bronchiolitis group (r=0.607, r=0.819, respectively; P<0.01). CONCLUSIONS: CD40 and CD40L expression in PBMCs and serum IgE level increased and there is a positive correlation between CD40 and CD40L expression and serum IgE level in children with bronchiolitis. Over-expression of CD40 and CD40L may play an important role in the development of bronchiolitis.［Chin J Contemp Pediatr, 2009, 11 (5):354-356］

OBJECTIVE: Insulin-like grouth factor-1 (IGF-1) is polypetide hormone that has demonstrated effects on neural cells. Up to now, there is few reports about the relation between serum IGF-1 and brain damage in neonates with hyperbilirubinemia. This study explored the potential role of serum IGF-1 in neonatal hyperbilirubinemia. METHODS: Serum levels of IGF-1 were measured using ECLIA in 57 term neonates with hyperbilirubinemia and 25 normal term neonates. Meanwhile, total serum bilirubin (TSB), unconjugated bilirubin (USB) and serum albumin (ALB) contents were measured by the automatic biochemistry analyzer and the ratio of USB/ALB (B/A) was calculated. The hyperbilirubinemia group was classified into three subgroups based on serum TSB levels: mild (221-256 μmol/L), moderate (257-342 μmol/L) and severe (>342 μmol/L). Serum TSB levels in the 25 normal neonates were less than 85 μmol/L (control group). NBNA was performed on the day of serum sample collection. RESULTS: Serum IGF-1 levels in the mild, moderate and severe hyperbilirubinemia groups (39.38±8.42, 30.77±4.65 and 26.34±2.05 ng/L, respectively) were obviously lower than those in the control group (50.16±15.73 ng/L) (P<0.01). There were significant differences among the three hyperbilirubinemia subgroups in serum IGF-1 levels (P<0.01). Mean NBNA scores in the mild, moderate and severe hyperbilirubinemia groups (35.01±2.26, 32.45±2.74 and 26.77±5.02, respectively) were significantly lower than those in the control group (38.24±0.78) (P<0.01). Significant differences in the NBNA scores were noted among the three hyperbilirubinemia subgroups (P<0.01). Serum IGF-1 levels were positively correlated to NBNA scores (r=0.603, P<0.01) and negatively correlated to the ratio of B/A (r=-0.483, P<0.01). CONCLUSIONS: Serum IGF-1 levels decreased obviously in neonates with hyperbilirubinemia and correlated to the severity of disease. IGF-1 might be associated with bilirubin-induced brain damage.［Chin J Contemp Pediatr, 2009, 11 (5):357-360］

OBJECTIVE: The patients with recurrent or refractory neuroblastoma have a very poor prognosis and high mortality. 10-hydroxycamptothecin (HCPT) is a new agent extracted from comptotheca acuminate, a native plant. It has been shown to be very effective in some solid tumors such as gastric and colon cancers, lung cancers and ovary cancers. However, its efficacy in neuroblastoma has not been determined. This study aimed to investigate the therapeutic effects of HCPT in the treatment of recurrent or refractory neuroblastoma in children. METHODS: Ten children with recurrent neuroblastoma and two children with refractory neuroblastoma were treated with HCPT. Of them, 5 children with recurrent neuroblastoma were treated with HCPT alone, and the other 7 patients received combination chemotherapy of HCPT plus other agents. The HCPT alone treatment group was injected with HCPT (7.5 mg/m2 daily) for 14 consecutive days. The combination chemotherapy group was alternately treated with the modified new protocol A1 (cyclophosomide 1 200 mg/m2 on day 1, etoposide 100 mg/m2 on days 1-5, HCPT 5 mg/m2 on days 1-3, cisplatin 90 mg/m2 on day 4) and the modified protocol B (ifosfomide 1.5 g/m2 on days 1-5, HCPT 5 mg/m2 on days 1-3, carboplatin 450 mg/m2 on day 2). RESULTS: Four patients (33.3%) achieved partial remission and 8 patients (66.7%) had stable disease. The median remission duration was 3.5 months (2-5 months). HCPT treatment as a single agent resulted in mild side effects. Myelosuppression and digestive disorders were found as the main adverse events in the combined chemotherapy group. No chemotherapy related deaths were found. CONCLUSIONS: HCPT is safe and effective in the treatment of recurrent or refractory neuroblastoma. The toxicities of HCPT are tolerable. The long-term efficacy of HCPT warrants further research.［Chin J Contemp Pediatr, 2009, 11 (5):361-363］

OBJECTIVE: To study clinical and imaging features of hypothalamic hamartoma in children. METHODS: Imaging findings and clinical manifestations of 38 children with hypothalamic hamartomas were retrospectively reviewed. The patients included 25 boys and 13 girls, ranging in age of onset from 1 month to 15 years. All the 38 patients were examined with pre-contrast and post-contrast T1 weighted MR imaging and with non-contrast T2 weighted MR imaging. Meanwhile, 10 patients received CT scan. Hypothalamic hamartomas were confimed by pathologic examinations in the 38 patients. RESULTS: Gelastic epilepsy, precocious puberty, other types of epilepsy and disturbance of intelligence were main manifestations in the 38 patients. Gelastic epilepsy was found as an initial clinical symptom in 17 cases, precocious puberty in 13 cases and other types of epilepsy in 8 cases. All masses were located in the suprasellar and interpeduncular cistern. They showed iso-density on CT scan, and homogeneous signal iso-intense to gray matter on T1 and T2 weighted MR images. With contrast MR images, there was no enhancement in the mass. The size or pedunculation of the mass was not correlated with clinical features. CONCLUSIONS: Hypothalamic hamartoma may be characterized by precocious puberty and/or gelastic epilepsy and specific imaging findings mentioned above.［Chin J Contemp Pediatr, 2009, 11 (5):364-366］

OBJECTIVE: PPAR-γ is associated with the differentiation, apoptosis, proliferation and cytokine secretion of immunologic cells. This study investigated peripheral blood lymphoblastic PPAR-γ mRNA expression and its correlation with plasma IL-13 contents in children with acute idiopathic thrombocytopenic purpura (ITP). METHODS: Fifty-three children with acute ITP who were in line with the standard test between September 2007 and July 2008 were enrolled. Fifty healthy children during the same period were used as the control group. PPAR-γ mRNA expression in peripheral blood lymphocytes were detected by RT-PCR. Plasma IL-13 contents were detected using ELISA. RESULTS: PPAR-γ mRNA expression in peripheral blood lymphocytes from acute ITP children were significantly higher than that in the control group (0.78 ± 0.03 vs 0.52 ± 0.05; P<0.05). Plasma IL-13 contents in children with acute ITP were also significantly higher than those in the control group (160.21 ± 34.26 pg / mL vs 121.42 ± 12.69 pg / mL; P<0.05). There was a positive correlation between plasma IL-13 level and lymphoblastic PPAR-γmRNA expression in children with ITP (r=0.89, P<0.05). CONCLUSIONS: PPAR-γ mRNA expression in peripheral blood lymphocytes increased and were positively correlated with plasma IL-13 contents in children with acute ITP, suggesting that PPAR-γ and IL-13 might participate in the pathogenesis of acute ITP.［Chin J Contemp Pediatr, 2009, 11 (5):367-370］

OBJECTIVE: To investigate the correlation between ABO blood type gene and attention-deficit hyperactivity disorder (ADHD) in children. METHODS: ABO blood types were determined using glass sheet method in 96 children with ADHD and their parents. O gene was identified using polymerase chain reaction and restriction fragment length polymorphism in patients with A or B blood type. Haplotype-based haplotype relative risk (HHRR), transmission-disequilibrium test (TDT) and Chi-square test were used to examine the association between ABO gene and ADHD. RESULTS: TDT results showed significant differences in the allele of ABO between the 96 children with ADHD and within-family controls(χ2=6.017, df=2, P<0.05). Chi-square test results showed differences in the allele of A and B (χ2=3.289, df=1, P=0.07) as well as O and B (χ2=3.629, df=1, P=0.057 ) between ADHD children and within-family controls. The frequencies of O and A genes were higher than that of B gene in ADHD children. CONCLUSIONS: There was correlation between ABO blood type gene and ADHD in children. The risk of ADHD is increased in the presence of alleles O and A, but the risk is reduced in the presence of allele B.［Chin J Contemp Pediatr, 2009, 11 (5):371-373］

OBJECTIVE: To study the effects of treatment with gonadotropin-releasing hormone analogs (GnRHa) on final height, weight and pubertal development in girls with central precocious puberty. METHODS: Twenty-six girls with central precocious puberty were treated with GnRHa for an average of 19.2±8.4 months. Pretreatment and posttreatment predicted adult heights (PAH) were evaluated based on the Bayley-Pineau table. The patients' heights and weights were measured monthly. Bone age (BA) was evaluated using Greulich-Plyle. Height standard deviation score for BA ［HtSDS (BA)］ was measured. After discontinuation of treatment, the patients were followed-up for the observation of height, weight, BA and menstruation. RESULTS: Final height averaged 158.0±4.0 cm in the 26 girls, which was greater than their target height (155.3±4.4 cm; P<0.01) and consistent with their posttreatment PAH (158.4±5.2 cm). The final height was positively corrrelated with initial height, PAH and HtSDS(BA). There was a positive correlation in the body mass index before and after treatment (r=0.724, P<0.01). Menarche occurred 13.2±6.1 months after discontinuation of treatment, with a mean menarche age of 12.2±0.7 years. CONCLUSIONS: GnRHa may increase final height in girls with central precocious puberty. Their final heights may be correlated with their initial heights and PAH. The pubertal development after GnRHa treatment in girls with central precocious puberty may be matched with normal children.［Chin J Contemp Pediatr, 2009, 11 (5):374-376］

OBJECTIVE: To study the value of Xstrain technology in the evaluation of cardiac function in children with tonsil adenoidal hypertrophy (TAH). METHODS: Thirty-five children with TAH (TAH group) and 20 normal age-matched children (control group) were enrolled. The left ventricular wall movement in the vertical, radial and circumferential directions and the right ventricular tricuspid annulus movement were detected using Xstrain technology. RESULTS: The systolic and early diastolic velocities of tricuspid annulus in the TAH group were higher than those in the control group. The systolic and diastolic circumferential velocities of the middle lateral wall and back wall of left ventricular in the TAH group were lower than those in the control group. The systolic and early diastolic vertical velocities of the basement of left ventricular wall in the TAH group were higher than those in the control group. There was no significant difference in the radial velocity between the two groups. CONCLUSIONS: Early changes in the cardiac function can be found by Xstrain technology in children with TAH. Xstrain technology can provide a reliable basis for cardiovascular evaluation in children with TAH.［Chin J Contemp Pediatr, 2009, 11 (5):377-379］

OBJECTIVE: The application and the efficacy of hyperbaric oxygen (HBO) in hypoxic-ischemic brain damage (HIBD) remain controversial. This study aimed to explore the effects of HBO on brain functional outcome and possible repair mechanisms in neonatal rats with intrauterine HIBD in aspects of the number of survived neurons and the central nervous electrophysiological conduction velocity. METHODS: A rat model of intrauterine HIBD was prepared. Subjects were divided into four groups at random: HIBD, HBO-treated HIBD group, normal control and HBO-treated normal control. After 24 hrs of the operation, the two HBO-treated groups received HBO treatment (0.02 MPa, 1 hr/d) for 14 days. When the rats were 4 weeks old, the electrophysiological changes in the central nervous system (CNS) were observed by brainstem auditory evoked potential (BAEP) for assessing brain function. Hematoxylin and eosin (HE) staining and Nissl's stainting were employed to observe the pathological change and the number of neurons in the hippocampus. RESULTS: The peak latency of waves II and IV and the interpeak latency of waves I-IV in the HBO-treated HIBD group were shortened compared with those in the untreated HIBD group (P<0.05). HE staining displayed that the pathological injuries in the hippocampus were alleviated in the HBO-treated HIBD group when compared with the untreated HIBD group. Nissl's staining showed that survived neurons in the HBO-treated HIBD group were more than the untreated HIBD group (P<0.05). The HBO-treated control group showed increased survived neurons compared with the untreated control group (P<0.05). CONCLUSIONS: Early HBO treatment might improve brain functional outcome through increasing synaptic transmission efficiency, improving central nervous electrophysiological conduction velocity and reducing neuron death in neonatal rats with intrauterine HIBD.［Chin J Contemp Pediatr, 2009, 11 (5):380-384］

OBJECTIVE: To study the anti-arrhythmic efficacy of ginsenoside Re (GSRe) and its protective effects against myocardial injuries in rabbits with isoproterenol-induced triggered ventricular arrhythmia (TVA). METHODS: TVA model was prepared by intravenous injections of isoproterenol at a constant speed of 5 mg/kg/min. When TVA appeared, rabbits were randomly injected with GSRe (5, 10 or 20 mg/kg), verapamil (0.4 mg/kg) or placebo. The duration of maintaining sinus rhythm was observed. Meanwhile, isoproterenol was continued to be injected at a constant speed of 5 mg/kg/min. After 1 hr of isoproterenol injection, the rabbits were sacrificed. Cardiac muscles in the cuspidate position of the left ventricle were sampled for optical microscopy and electron microscopy. RESULTS: GSRe and verapamil treatment restored sinus rhythm. The duration of sinus rhythm was 177.00±5.66 s within 3 minutes in the verapamil treatment group and was 177.83±5.31, 21.00±2.83 and 4.50±1.64 s, respectively, in the 20, 10 and 5 mg/kg GSRe treatment groups. Histopathologic examination demonstrated that GSRe treatment (20 and 10 mg/kg) alleviated myocardial injuries induced by TVA. CONCLUSIONS: GSRe has anti-arrhythmic efficacies and protective effects against myocardial injuries in rabbits with TVA. It may therefore be a possible therapy for TVA.［Chin J Contemp Pediatr, 2009, 11 (5):384-388］

OBJECTIVE: Some research has shown that p38 mitogen-activated protein kinase (p38MAPK) plays important roles in lung injuries induced by various factors. Its expression and role in hyperoxia-induced lung injury remains unknown. This study investigated the expression and role of p38MAPK in hyperoxia-induced lung injury juvenile rat model. METHODS: Hyperoxia-induced lung injury rat model was prepared by 90% O2 exposure. The location and expression of p38MAPK in lung tissues were detected by immunohistochemistry and Western blot respectively. Apoptosis index of lung was evaluated by TUNEL technique. The effect of SB203580, a p38MAPK inhibitor, on the apoptosis index of lung was observed. RESULTS: The expression of phosphor-p38MAPK increased obviously after hyperoxia. Positive phosphor-p38MAPK cells were mainly distributed in the alveolar, airway epithelial cells, pulmonary vascular endothelium cells and infiltrative inflammatory cells. The apoptosis index of lung also significantly elevated. SB203580 inhibited the activation of p38MAPK, and reduced the apoptosis index of lung. CONCLUSIONS: The phosphor-p38MAPK increased and was expressed in many kinds of lung cells in lung injury rat model. It may play a role in the induction of apoptosis in hyperoxia-induced lung injury.［Chin J Contemp Pediatr, 2009, 11 (5):389-392］

OBJECTIVE: To study the expression of basic fibroblast growth factor (b-FGF) and nuclear factor-κB (NF-κB) in the airway and the effect of budesonide on their expression in rats with asthma. METHODS: Forty-five Sprague-Dawley male rats were randomly divided into three group: placebo control, untreated asthma, and budesonide-treated asthma. Asthma was induced by intraperitoneal injection of 10% ovalbumin (OVA) on days 1 and 8 and then challenged by inhalation of 1% OVA aerosol. The budesonide-treated asthma group received an inhalation of budesonide (1 mg) 30 minutes after OVA challenge. The pathological changes of the airway were assessed, and the expression of b-FGF and NF-κB in the airway was assayed by hematoxylin and eosin staining and immunohistochemistry. RESULTS: Budesonide treatment alleviated airway injuries. Compared with the control group, b-FGF and NF-κB expression in the airway in the untreated asthma group increased significantly (P<0.05). The budesonide-treated asthma group demonstrated significantly decreased b-FGF (111.61±5.52 vs 126.21±6.46; P<0.05) and NF-κB expression (110.65±8.71 vs 134.15±9.42; P<0.05) in the airway as compared with the untreated asthma group. B-FGF expression was positively correlated to NF-κB expression in the budesonide-treated group. CONCLUSIONS: b-FGF and NF-κB may be associated with airway remodeling in rats with asthma. Budesonide can improve airway remodeling, possibly by decreasing the expression of b-FGF and NF-κB.［Chin J Contemp Pediatr, 2009, 11 (5):393-396］

OBJECTIVE: To study the proliferation and differentiation of neural stem cells in the subventricular zone (SVZ) in neonatal rats after bilateral common arteries occlusion. METHODS: Ninety-six 3-day-old Sparuge-Dawley rats were randomly divided into two groups: ischemia and control. Rats in the ischemia group were subjected to bilateral common arteries occlusion and the rats in the control group were sham-operated. All rats were administrated with 5-bromodeoxyuridine (BrdU) (50 mg/kg) via intraperitoneal injection. Rats were sacrificed and their brains were removed 1, 4, 7, 10, 14 and 35 days after ischemia. Using brain paraffin sections and immunofluorescence assays, the number of newborn cells in the SVZ was counted. Newborn neural stem cells and oligodendrocytes in the SVZ were observed, and then double marked with BrdU and nestin or osmium tetroxide (O4). RESULTS: The number of BrdU+ cells (neural stem cells) in the SVZ in the ischemia group was greater than in the control group 4, 7, 10 and 14 days after ischemia, and reached a peak at 4 days after ischemia (253.1±49.3 vs 133.5±17.7; P<0.01). By 35 days after ischemia, the number of BrdU+/O4+ cells (oligodendrocytes) in the corpus callosum (56.0±7.2 vs 17.0±6.4; P<0.01), the septal nuclei (45.0±11.9 vs 20.5±5.0; P<0.01), the striatum (34.5±4.2 vs 14.5±5.8; P<0.01) and the olfactory bulb (46.5±6.6 vs 23.5±8.4; P<0.01) in the ischemia group increased significantly as compared to the control group (P<0.01). CONCLUSIONS: Brain ischemia can activate the proliferation of neural stem cells in the SVZ and promote neural stem cells differentiation into oligodendrocytes. The immature brain may have the capacity for self-repair after ischemic brain injury.［Chin J Contemp Pediatr, 2009, 11 (5):397-400］