OBJECTIVE: Hypoxic-ischemic brain damage (HIBD) occurs frequently in premature infants, resulting death or neurological sequela in some survivors. Up to now, however, there are no diagnostic criteria for this disease. The aim of this study was to explore the diagnostic criteria and the grading principle for HIBD of premature infants. METHODS: The clinical data of 453 premature infants who were diagnosed with HIBD based on the diagnostic criteria for HIBD of term infants, including medical history, clinical manifestations, laboratory results and imaging findings, were studied retrospectively. RESULTS: A preliminary diagnostic criteria for HIBD of premature infants was propounded based on clinical and pathologic features of brain damage of premature infants. Of the 453 premature infants, 346(76%) matched the diagnostic criteria. Of the 346 cases, PaO2 (42.21±8.33 mmHg) and /or SaO2 (68.49±5.19%) decreased in 208 patients and the BE value (-10.86±3.41 mmol/L) decreased in 138 patients. The sensitivity and specificity of cranial computer tomography for the diagnosis of HIBD in premature infants was 100% and 17.8%, respectively. Cranial ultrasound displayed a sensitivity of 87.9% and specificity of 100% for the diagnosis of HIBD in premature infants. CONCLUSIONS: The diagnostic criteria used for HIBD for term infants is not suitable for premature infants. This study puts forward the reference diagnostic criteria of premature HIBD as following: ① evidence of hypoxia; ② neurological symptoms and signs; ③imaging findings: severe brain edema, germinal matrix intraventricular hemorrhage (GMH-IVH), periventricular leukomalacia (PVL), or brain infarction, and/or the resistance index (RI) >0.75 or <0.55 showed by cranial ultrasound; ④Brain damage caused by infection, electrolyte disturbance and congenital metabolic disease was excluded. The grading principle of premature HIBD is proposed as follows: MILD HIBD when cranial ultrasound shows grade I-II of GMH-IVH or PVL, and SEVERE HIBD when cranial ultrasound shows grade III-IV of GMH-IVH or PVL.［Chin J Contemp Pediatr, 2007, 9 (4):293-296］

OBJECTIVE: To study the risk factors for intracranial hemorrhage in very low birth weight infants. METHODS: Data from 169 very low birth weight (VLBW) infants (birth weight 1000-1500 g; gestational age 23-36 weeks) were studied retrospectively. Twenty-nine perinatal and postnatal factors were analyzed by Crosstabs Test with SPSS 12.0. A logistic regression analysis was used to identify the risk factors associated with the development of intracranial hemorrhage. RESULTS: Multivariate logistic analysis revealed that rupture of membranes (OR=0.146, 95%CI=0.22-0.964, P<0.05), 1-minute Apgar score ≤ 7 (OR=0.112, 95%CI=0.21-0.591, P<0.01), pulmonary surfactant therapy (OR=0.110, 95%CI=0.24-0.504, P<0.01), mechanical ventilation therapy (OR =0.076, 95%CI=0.009-0.668, P<0.05), mechanical ventilation duration > 72 hrs(OR=0.053, 95%CI=0.007-0.410, P<0.01), prothrombin time > 20 seconds (OR=4.186, 95%CI=1.606-10.923, P<0.01), pH value on day 1 of life <7.25 (OR=0.421, 95%CI=0.179-0.995, P<0.05)and hyponatremia on day 1 (OR= 0.27, 95%CI=0.077-0.940, P<0.05) or 2 (OR=2.480, 95%CI=1.053-5.838, P<0.05) of life were risk factors for intracranial hemorrhage. CONCLUSIONS: 1-minute Apgar score ≤7 and mechanical ventilation treatment were leading risk factors for intracranial hemorrhage, followed by abnormal coagulation and electrolytes related to perinatal asphyxia in VLBW infants. These findings can be used to improve the surveillance and prophylaxis measures in VLBW infants at high risk.［Chin J Contemp Pediatr, 2007, 9 (4):297-300］

OBJECTIVE: Nogo-A antibody IN-1 can neutralize Nogo-A, a neurite growth inhibitory protein, promoting axonal regeneration following lesions of the central nervous system (CNS) in adult rats. This study aimed to examine the effect of ventricle injection of Nogo-A antibody on neuronal regeneration in neonatal rats following hypoxic-ischemic brain damage (HIBD). METHODS: A model of neonatal HIBD was prepared by the ligation of the left common carotid artery, followed by 8% hypoxia exposure. Forty HIBD rats were randomly given a ventricle injection of 10 μL Nogo-A antibody IN-1 (IN-1 group) or 10 μL artificial cerebrospinal fluid (artificial CSF group) (n=20 each). Another 20 neonatal rats were sham-operated, without hypoxia-ischemia, and were used as the controls. The levels of Nogo-A and GAP-43 protein in the brain were measured by immunohistochemistry. RESULTS: The number of immunohistory positive cells of Nogo-A in the brain in the IN-1 group (28.61±1.70) was obviously less than that in the artificial CSF (39.52±1.40) and the sham-operated groups (32.78±1.87) (both P<0.01). There were significant differences in the Nogo-A protein expression between the artificial CSF and the sham-operated groups (P<0.01). The GAP-43 protein expression in the IN-1 group (31.14±1.88) was noticeably higher than that in the artificial CSF group (27.73±1.43 ) (P<0.01). Both the IN-1 and the artificial CSF groups showed lower GAP-43 protein levels than the sham-operated groups (33.64±1.24) (both P<0.01). CONCLUSIONS: Nogo-A antibody can reduce the expression of Nogo-A protein in the brain and thus promote neuronal regeneration in neonatal rats following HIBD. An increased GAP-43 protein expression in the brain after Nogo-A antibody administration shows an enhanced neuronal regeneration in the neonatal rats following HIBD.［Chin J Contemp Pediatr, 2007, 9 (4):301-304］

OBJECTIVE: To study the effect of cerebral mild hypothermia on cerebral mitochondrial ATPase activities in neonatal rats with hypoxic-ischemic brain damage(HIBD), METHODS: Eighty-four seven-day-old Wistar rats were randomly assigned into four groups: sham-operated normothermic, sham-operated mild hypothermic, HIBD normothermic and HIBD mild hypothemic, HIBD was induced by left common carotid artery ligation, followed by 8% hypoxia exposure. At each time interval of 2, 6, and 12 hrs post-hypoxia-ischemia (HI), 7 rats were sacrificed and the brain tissues were sampled for detecting the activities of mitochondrial Na+K+ATPase and Ca2+ATPase. RESULTS: The activities of mitochondrial Ca2+ATPase decreased significantly in the two HIBD groups compared with those of the two sham-operated groups at 2, 6, and 12 hrs post-HI. The HIBD mild hypothemic group had higher mitochondrial Ca2+ATPase activities compared with the HIBD normothermic group at 2, 6, and 12 hrs post-HI (5.25±0.61 μmol/mgPr. h vs 3.17±0.81 μmol/mgPr, h, 4.59±0.81 μmol/mgPr. h vs 2.26±0.53 μmol/mgPr. h, 4.61±0.62 μmol/mgPr. h vs 1.31±0.78 μmol/mgPr. H, respectively) (P<0.01). The activities of mitochondrial Na+K+ATPase decreased significantly in the two HIBD groups compared with those of the two sham-operated groups at 6 and 12 hrs post-HI. A significant difference was observed in the mitochondrial Na+K+ATPase activities between the HIBD mild hypothemic and HIBD normothermic groups at 6 and 12 hrs post-HI（5.25±0.66 μmol/mg Pr. h vs 3.76±0.78 μmol/mgPr. h, 4.74±0.80 μmol/mgPr. h vs 3.12±0.53 μmol/mgPr, h; P<0.01）. CONCLUSIONS: Mild hypothermia following HIBD inhibits the decline in cerebral mitochondrial Ca2+ and Na+K+ ATPase activities in neonatal rats, thus providing protective effects against HIBD.［Chin J Contemp Pediatr, 2007, 9 (4):305-307］

OBJECTIVE: A recent study has suggested that hyperbaric oxygen (HBO) therapy administered within 3 hrs following hypoxic-ischemic brain damage (HIBD) may alleviate brain white matter damage (WMD) in neonatal rats. However it is unclear whether a delayed HBO therapy (more than 3 hrs following HIBD) has neuroprotective effects in neonatal rats. This study aimed to explore the effect of HBO therapy administered at different time points following HIBD on WMD in neonatal rats. METHODS: The HIBD model was prepared according to the Rice-Vannucci procedure in 7-day-old Sprague-Dawley rats. HBO therapy was administered at 3, 6, 12, 24 or 72 hrs after HIBD, once daily for consecutive 7 days. T-maze test, the foot-fault test and the radial arm maze test were performed after 14 days of HIBD. Myelin basic protein (MBP) in the callositas and corpora striata was examined by immunohistochemical method 28 days after HIBD. RESULTS: The rats receiving HBO therapy at 3, 6 and 12 hrs after HIBD performed significantly better in the T-maze test, the radial arm maze test and the foot-fault test than the untreated HIBD rats. There were no significant differences in the behavioral test results between the HBO-treated groups administered HBO at 24 and 72 hrs after HIBD and the untreated HIBD group. The MBP expression in the HBO-treated groups treated within 12 hrs after HIBD was significantly higher than that in the untreated HIBD group (P< 0.05). When the HBO therapeutic window was delayed to 24 hrs after HIBD, there were no significant differences in the MBP expression between the HBO-treated and the untreated HIBD groups. CONCLUSIONS: HBO therapy administered within 12 hrs following HIBD can alleviate brain WMD in neonatal rats, but the efficacy of HBO therapy administered 24 hrs after HIBD does not appear to be satisfactory.［Chin J Contemp Pediatr, 2007, 9 (4):308-312］

OBJECTIVE: To study the expression of the AMPA receptor subunit glutamate receptor 2 (GluR2) and the cellular free calcium concentration in the white matter of neonatal rats with periventricular leukomalacia (PVL) and their roles in the pathogenesis of PVL. METHODS: A PVL model was prepared by unilateral carotid artery ligation (UCL) followed by exposure to 6% oxygen for 4 hrs in 2-day-old rats. The neonatal rats performed a sham operation, without hypoxia-ischemia (HI), were used as the control group. At 12, 24, 48 and 72 hrs of HI, the expressions of GluR2 mRNA and protein in the white matter were detected using real time quantitative PCR and Western blot respectively. Spectrophotofluorimetry and Fura 2/AM were used to detect the cellular free calcium concentration. RESULTS: The expressions of GluR2 mRNA and protein in the white matter were significantly reduced in the PVL group at 24 hrs of HI, and remained at lower expressions until 72 hrs of HI compared with the control group (P<0.05). The cellular free calcium concentrations increased significantly in the PVL group at 12 hrs of HI, and remained at higher levels until 72 hrs of HI compared with the control group (P<0.05). CONCLUSIONS: The expressions of GluR2 mRNA and protein in the white matter decreased whereas the cellular free calcium concentration increased in neonatal rats with PVL. The decreased expression of GluR2 might lead to the overloading of cellular calcium in the white matter, which may cause neuronal damage and death.［Chin J Contemp Pediatr, 2007, 9 (4):313-316］

OBJECTIVE: Recent studies have indicated that the signal pathway of NgR-P75NTR- RhoA plays a key role in nerve injury and remodeling, but its exact mechanism and the role of the downstream molecule RhoA regulated by P75NTR remain unclear in hypoxia-ischemia (HI) neonatal animals. The present study was designed to assess the expression of P75NTR protein and RhoA mRNA in neonatal white matter and to investigate their relationship in newborn rats with white matter damage(WMD).METHODS: The rat WMD model was established by the ligation of right common carotid artery, followed by 6% hypoxia exposure for 4 hrs. The control group was sham-operated, without HI treatment. The histological changes of brain tissue were observed under light and electron microscopes. Expression of P75NTR protein and RhoA mRNA in the brain white matter after 12, 24, 48 and 72 hrs and 7 days of HI were detected by RT-PCR and immunohistochemistry, respectively. RESULTS: Periventricular white matter damage was observed by 48 hrs of HI. Expression of P75NTR protein increased in the striatum and callosum zones at 12 hrs, peaked at 48 hrs, and remained at a higher level than control until 72 hrs of HI in the WMD group (P<0.01). After 7 days of HI expression of P75NTR protein was no longer statistically different from controls. The RhoA mRNA was higher in the WMD group for the first 72 hrs and then declined to control values. CONCLUSIONS: Increased P75NTR protein might mediate apoptosis of nerve cells and inhibit the regeneration of neuron axons.The subsequent decline back to control value may be correlated with the aggregation of necrosis of nerve cells after HI. The patterns of RhoA mRNA expression were consistent with those of P75NTR protein, suggesting that the increased P75NTR level may promote RhoA mRNA expression. ［Chin J Contemp Pediatr, 2007, 9 (4):317-320］

OBJECTIVE: To study the changes of ephrin-B3 mRNA expression and cellular apoptosis in the brain of neonatal rats with periventricular leukomalacia (PVL) and to explore the possible role of ephrin-B3 in the pathogenesis of PVL. METHODS: Two-day-old SD rats were randomly assigned to two groups: PVL and control. PVL model was prepared by right common carotid artery ligation followed by 4-hr 6% oxygen exposure. The control group, without ligation of the artery and hypoxia treatment, was sham operated. The rats were then sacrificed and brain tissues were collected at 0, 8, 24, 48 and 72 hrs and at 7 days of hypoxic-ischemia (HI). Hematoxylin and eosin staining was used for pathologic studies. Real time RT-PCR was applied to detect brain ephrin-B3 mRNA expression. DAPI staining was applied to detect neuronal apoptosis. ResultsThe brain ephrin-B3 mRNA expression increased significantly in the PVL group at 8, 24, 48 and 72 hrs and at 7 days of HI compared with that of the control group (P< 0.05). The apoptotic cells in the brain of the PVL group were significantly more than that of the control group at 8, 24, 48 and 72 hrs of HI (P<0.05).CONCLUSIONS: ephrin-B3 mRNA expression and cellular apoptosis in the brain increased significantly in neonatal rats with PVL, which suggests that ephrin-B3 may participate in the pathogenesis of PVL in neonatal rats.

OBJECTIVE: To study the effects of calcium and calmodulin dependent kinase against hypoxic neuronal injury and its possible mechanisms. MethodsEmbryonic cortical neurons of 17-day pregnant embryo Sprague-Dawley rats were cultured in vitro and the cultured neurons were randomly allocated into different groups that exposed to hypoxia or hypoxia +calcium channel antagonist. Nimodipine and MK-801 were used to block the L-voltage sensitive calcium channel and NMDA receptor respectively before hypoxia. The methyl thiazolyl tetrazolium(MTT) method was used to determine the cell viability. Fluo-4AM, an intracellular calcium indictor, was used to detect the changes of intracellular calcium after hypoxia. The expressions of CaMKⅡ and CaMKⅣ were detected by Western blot. ResultsThe cell viability of the nimodipine or MK-801-treated groups was significantly higher than that of the untreated hypoxia group. The intracellular calcium level of the nimodipine-treated group decreased rapidly after hypoxia. Compared to nimodipine treatment, MK-801 treatment could inhibit hypoxia-induced calcium influx for a longer time. Nimodipine treatment decreased the CaMKⅡexpression while MK-801 treatment decreased the CaMKⅣ expression. CONCLUSIONS: Nimodipine and MK-801 protect neurons from hypoxic injury possibly by the inhibition of CaMKⅡ and CaMKⅣ expressions respectively.［Chin J Contemp Pediatr, 2007, 9 (4):324-326］

Laron syndrome is an autosomal recessive disorder caused by defects of growth hormone receptor (GHR)gene. It is characterized by severe postnatal growth retardation and characteristic facial features as well as high circulating levels of growth hormone (GH) and low levels of insulin-like growth factor I (IGF-I) and insulin-like growth factor binding protein-3 (IGFBP-3). This report described the clinical features and GHR gene mutations in 2 siblings with Laron syndrome in a Chinese family. Their heights and weights were in the normal range at birth, but the growth was retarded after birth. When they presented to the clinic, the heights of the boy (8 years old) and his sister (11 years old) were 80.0 cm (－8.2 SDS) and 96.6 cm (－6.8 SDS) respectively. They had typical appearance features of Laron syndrome such as short stature and obesity, with protruding forehead, saddle nose, large eyes, sparse and thin silky hair and high-pitched voice. They had higher basal serum GH levels and lower serum levels of IGF-I, IGFBP-3 and growth hormone binding protein (GHBP) than normal controls. The peak serum GH level after colonidine and insulin stimulations in the boy was over 350 ng/mL. After one-year rhGH treatment, the boy's height increased from 80.0 cm to 83.3 cm. The gene mutation analysis revealed that two patients had same homozygous mutation of S65H (TCA →CCA) in exon 4, which is a novel gene mutation. It was concluded that a definite diagnosis of Laron syndrome can be made based on characteristic appearance features and serum levels of GH, IGF-I, IGFBP-3 and GHBP. The S65H mutation might be the cause of Laron syndrome in the two patients.［Chin J Contemp Pediatr, 2007, 9 (4):335-338］

A case of juvenile psoriatic arthritis in a 12 year-old boy was reported. The patient had a history of one and half a year of bilateral heel pain, followed by pain in the right knee and ankle and right hip joint. He developed psoriatic lesions affecting his nails and skin. He had increased erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) contents. Human leukocyte antigen (HLA) B27 was detected but serum rheumatoid factor was not in the patient. A skin biopsy revealed psoriasis and ultrasonography demonstrated synovitis in right knee and ankle. Juvenile psoriatic arthritis was diagnosed based on his physical, laboratory and skin biopsy findings. A treatment with nonsteroidal anti-inflammatory drugs and sulfasalazine produced no effect. Leflunomide in conjunction with anti-TNF biologic agents (Etanercept) was administered, followed by symptomatic improvement 2 weeks later.［Chin J Contemp Pediatr, 2007, 9 (4):339-342］

OBJECTIVE: Hepatic veno-occlusive disease(HVOD) is one of the most serious complications after allogenic hematopoietic stem cell transplantation (allo-SCT). Endothelial injury, leading to deposition of coagulation factous in the terminal hepatic venules, is believed to the key event in the pathogenesis of HVOD. This study was designed to explore the efficacy of low-dose heparin and prostaglandin E1(PGE1) in the prevention of HVOD after allo-SCT in children with β-thalassemia major. METHODS: Forty-three children with β-thalassemia major received allo-SCT. For the prevention of HVOD, 23 of the 43 patients received low-dose heparin (100 IU/kg?d) and also received PGE1 (7.2 μg/kg?d) by continuous intravenous infusion (study group) from the beginning of conditioning treatment to the 30th day after allo-SCT. Patients who received continuous infusions of PGE1 (7.2 μg/kg?d) alone were used as the control group (n=20). RESULTS: HVOD occurred in 6 patients (26.1%) in the study group (3 mild, 3 moderate). Twelve patients in the control group had HVOD (60.0%) (3 mild, 3 moderate, 6 severe)(P<0.05). In the study group, 5 cases of HVOD were treated successfully and one died from other complications. Of the 12 cases of HVOD in the control group, 10 patients were treated successfully and two patients died from HVOD. There were no obvious drug adverse effects in the two groups. CONCLUSIONS: Low-dose heparin and PGE1 is more effective than PGE1 alone for the prevention of HVOD after allo-SCT.［Chin J Contemp Pediatr, 2007, 9 (4):343-346］

OBJECTIVE: To study the relationship between the changes of inflammation-associated factors, C-reactive protein (CRP), procalcitonin (PCT), erythrocyte sedimentation rate (ESR), white blood cell (WBC) and neutrophils, and the severity in children with Mycoplasma pneomoniae pneumonia (MPP). METHODS: Ninety-two children with acute MPP consisting of 52 cases with concomitant systemic inflammation response syndrome (SIRS) and 40 cases without SIRS were enrolled in this study. The 52 cases with concomitant SIRS were classified into two groups based on the severity of SIRS: mild SIRS (n= 25) and severe SIRS (n=27). CRP, PCT, ESR and WBC count and the percentage of neutrophils (NE%) were detected on admission and one week after anti-inflammation treatment. RESULTS: All of patients showed increased serum CRP contents at admission. The serum CRP contents were the highest in the severe SIRS group, followed by the mild SIRS and non-SIRS groups on admission (P< 0.05 or 0.01). The serum CRP contents were reduced in all of patients after 1-week treatment. The severe SIRS group still demonstrated higher serum CRP contents than the non-SIRS and the mild SIRS groups (P< 0.01). The severe SIRS group had increased serum PCT contents on admission, which were significantly higher than those of the mild SIRS and non-SIRS groups (P< 0.01). After 1-week treatment, the serum PCT contents were reduced in the severe SIRS group but remained higher than in the mild SIRS and non-SIRS groups (P<0.01). ESR increased significantly in the severe SIRS group than in the mild SIRS and non-SIRS groups on admission (P < 0.01). One-week treatment did not significantly decrease ESR in all three groups. The WBC count and NE% in the mild and severe SIRS groups were significantly higher than in the non-SIRS group and the severe SIRS group had higher WBC count and NE% than the mild SIRS group on admission (P<0.05). The WBC count and NE% decreased after 1-week treatment in the mild and severe SIRS groups (P<0.05). One inflammation-associated factor (only CRP) increase was predominant in the non-SIRS group (65%), 2 factors increase in the mild SIRS group (56%), and three or more factors increase in the severe SIRS group (70.4%). CONCLUSIONS: The detection of inflammation-associated factors, CRP, PCT, ESR, WBC and neutrophils, are valuable to the evaluation of severity in MPP.［Chin J Contemp Pediatr, 2007, 9 (4):347-350］

OBJECTIVE: To investigate the clinical features, treatment modalities and the prognosis of advanced neuroblastoma in children. METHODS: The medical records of 63 children with stage III or IV neuroblastoma from January 1996 to December 2005 were retrospectively reviewed. Sixty patients were treated by tumor resection and (or) chemotherapy and (or) radiation. Fourteen out of the 60 patients received another autologous peripheral blood stem cell transplantation. RESULTS: Of the 63 patients with advanced neuroblastoma, the male/female ratio was 2.7:1 and the median age at diagnosis was 4 years old. Most of the initial symptoms included pyrexia, abdominal pain, abdominal mass, and leg or articular pain. Primary tumor sites were adrenal (38%), retroperitoneal (35%), mediastinal (17%), pelvic (6%) and cervical (2%). The sites of metastasis at diagnosis included local (41%) and (or) distant (37%) lymph nodes, bone marrow (60%), bone (46%) and liver (16%). The median survival time of the 63 patients was 32.7 months. The 2-year survival rate was 44.3%. Statistical analysis demonstrated that unfavorable survival prognostic factors were the following: age >1 year at diagnosis (P<0.05); serum neuro-specific enolase > 100 mg/L (P<0.05); serum lactic dehydrogenase > 1500 U/L (P<0.01); serum ferritin >150 mg/L (P<0.05). The overall survival period of the patients was prolonged through total resection of the primary tumor (P<0.05). Intensive chemotherapy in combination with autologous peripheral blood stem cell transplantation could also result in a prolonged overall survival period (P<0.01). CONCLUSIONS: Neuroblastoma with advanced stages often presents with various clinical manifestations and has a poor prognosis. It is beneficial to improve the prognosis of neuroblastoma through an early diagnosis and a comprehensive therapy including total resection of the primary tumor, autologous peripheral blood stem cell transplantation and intensive chemotherapy. ［Chin J Contemp Pediatr, 2007, 9 (4):351-354］

OBJECTIVE: To investigate the influence of neonatal maturity on active oxygen metabolism in neutrophils and possible causes of a high susceptibility to bacterial infection in preterm infants. METHODS: Thirty-five preterm infants born at a gestation age of 26-32 weeks (≤32 weeks group, n=15) and at 33-36 weeks (> 32 weeks group, n=20) and 23 full-term infants (control group) were enrolled in this study. The samples of whole cord blood from the two preterm groups and the control group were stimulated in vitro with live bacteria,Staphylococcus aureus( S. aureus) and Escherichia coli (E. coli) and stained with hydroethedine, an indicator of superoxide. The percentage of neutrophils which produced superoxide and the mean fluorescence intensity for superoxide production were measured by flow cytometry. The incidence of bacterial infection during hospital stay was compared between the two preterm groups. RESULTS: Under S. aureus or E. coli stimulation, the percentage of neutrophils which produced superoxide in the ≤32 weeks group was significantly lower than that of the > 32 weeks group and the control group (P<0.01). The percentage of neutrophils which produced superoxide was closely related to gestational age in preterm infants ( y＝2.66 x, P＜0.01).There were no significant differences in the blood level of superoxide production in neutrophils among the three groups. The incidence of bacterial infection during hospital stay in the ≤32 weeks group (40%) was significantly higher than that the > 32 weeks group (10%) (P<0.05). CONCLUSIONS: The capability of active oxygen metabolism in neutrophils was significantly related to the gestational age in preterm infants. The decreased capability of active oxygen metabolism might be contributed to a higher susceptibility to bacterial infection in preterm infants.［Chin J Contemp Pediatr, 2007, 9 (4):355-357］

OBJECTIVE: To determine the molecular defects of β-thalassemia intermedia in Guangdong Province and to provide basis for gene diagnosis and gene therapy of this disorder. METHODS: DNA analysis of the α, β and γ globin genes was performed in 18 children with β-thalassemia intermedia from Guangdong Province using polymerase chain reaction (PCR ), microarray technique, Southern blot and direct sequencing. RESULTS: Of the 18 patients,one was identified as the homozygote of TATA box-28 (A→G) change, one as the homozygote of βE26 (G→A) mutation, ten as compound heterozygotes of TATA box- 28(A→G) mutation with other β-globin mutations, two as compound heterozygotes of βE26 (G→A ) mutation with other β globin mutations, and four as double heterozygotes for β globin and α globin mutations including -SEA and -α4.2. CONCLUSIONS: The molecular defects of β- thalassemia intermedia in Guangdong Province were highly heterogeneous and its spectrum was different from the reports from other provinces of China.［Chin J Contemp Pediatr, 2007, 9 (4):358-360］

OBJECTIVE: To study the effects of meconium-stained amniotic fluid on the cord blood IgE level in neonates. METHODS: A total of 404 neonates with meconium-stained amniotic fluid who were born by cesarean delivery between August 2003 and August 2005 (meconium-stained group) and 256 neonates with normal amniotic fluid delivered by cesarean (control group) were enrolled in this study. The meconium-stained group consisted of 80 cases of mild, 62 cases of moderate and 262 cases of severe meconium-stained amniotic fluid. The cord blood IgE level was measured using ELISA. RESULTS: The cord blood IgE level in the meconium-stained group was statistically higher than that in the control group(t = 4.03, P < 0.01). There were significant differences between the mild and severe meconium-stained subgroups and the control group for the cord blood IgE level (F = 4.28, P< 0.01）. The cord blood IgE level in neonates with premature rupture of the membrane between the meconium-stained and the control groups was statistically different. Sexes, gestational age, birth weight and birth order were not associated with the IgE level of cord blood. CONCLUSIONS: The cord blood IgE levels in neonates with meconium-stained amniotic fluid increase. Premature rupture of the membranes may be associated with an increase of cord blood IgE level. ［Chin J Contemp Pediatr, 2007, 9 (4):361-363］

OBJECTIVE: To investigate the electrogastrogram (EGG) characteristics of healthy neonates. Methods: Twenty healthy neonates born at 37-39 weeks of gestation (11 males and 9 females, Apagar's score 9.3±0.4) were enrolled in this study. EGG recordings were performed for half an hour pre- and postprandially at an interval of a week from birth until age 4 weeks. The EEG variables measured included the percentage of normal gastric rhythm, the percentage of tachygastria and bradygastria, the fed-to-fasting ratio of the EEG dominant power, as well as the EEG dominant frequency and its instability coefficient. The paired sample t test (95% CI) was used to compare the recordings. RESULTS: Between birth and age 28 days, the percentage of normal gastric rhythm ranged from 38.2±4.9% to 39.7±3.5% of recorded time, tachygastria was observed in the range of 23.7±5.4% to 23.5±4.3% of recorded time, and bradygastria was shown to be in the range of 38.1±5.5% to 36.8±3.9% of recorded time in the 20 neonates before meal. Statistically significant differences were not seen in neonates with different ages as well as during pre- and postprandial periods. The EEG dominant frequency of neonates before meal was 2.38±0.5, 2.43±0.2, 2.54±0.3, 2.57±0.2 and 2.59±0.1 cpm at birth and at postnatal age of 7, 14, 21 and 28 days respectively. There were no significant differences in the dominant frequency and the coefficient of instability of the dominant frequency during pre- and postprandial periods. The EEG dominant frequency at postnatal age of 14, 21 and 28 days during pre- and postprandial periods was significantly higher than that at birth and at postnatal age of 7 days (P<0.05). The coefficient of instability of the dominant frequency at postnatal age of 21 and 28 days was significantly lower than that at birth and at postnatal age of 7 and 14 days (P<0.05). There were no statistically significant differences in the fed-to-fasting ratio of EGG dominant power in neonates with different ages. CONCLUSIONS: The pattern of electrical activity in the normal neonatal stomach appears to be different from that demonstrated in adults and children. The percentage of normal gastric rhythm is lower, and tachygastria and bradygastria are more frequently seen. The EEG dominant frequency increases with postnatal age in neonates.［Chin J Contemp Pediatr, 2007, 9 (4):364-366］

OBJECTIVE: To study the relationship of Helicobacter pylori (H. pylori) infection with the development and relapse of Henoch-Schonlein purpura (HSP) with gastrointestinal involvement in children. METHODS: Thirty-six HSP children with gastrointestinal manifestations and 16 of 32 HSP children without gastrointestinal involvement underwent gastroscopy and rapid urease test for H. pylori detection. Thirty healthy children served as the control group. All of the patients received 14C urea breath test and serum H. pylori antibody detections. H. pylori infection was definited when two of detection approaches demonstrated positive. RESULTS: Twenty-one of 36 HSP patients with gastrointestinal manifestations were confirmed with H. pylori infection (58.3%). Of them, the relapsed patients had an H. pylori positive rate of 81.3% (13/16), which was significantly higher than that of the newly diagnosed patients （45.0%，9/20) (χ2=4.49, P<0.05). Nine of 32 HSP patients without gastrointestinal manifestations were confirmed with H. pylori infection (28.1%); 2 of 30 healthy children showed H. pylori positive （6.7%, 2/30). There was a significant difference in the H. pylori positive rate among the three groups (χ2=14.7, P<0.01). CONCLUSIONS: H.pylori infection may be associated with the development and relapse of HSP with gastrointestinal involvement in children.［Chin J Contemp Pediatr, 2007, 9 (4):367-369］

OBJECTIVE: To examine the expression of mRNA of vascular endothelial growth factor (VEGF) in a rat model of hyperoxia-induced retinopathy and to investigate the role of VEGF in the process of neovascularization in retinopathy. METHODS: One hundred fifty one-day-old neonatal Sprague-Dawley rats were randomly divided into hyperoxia-induced retinopathy and normal control groups. The rats in the retinopathy group were exposed to (80±2)% oxygen for 7 days and then replaced by room air. The rats in the control group were exposed to room air all the time of the experiment. The morphologic changes of retinal vessels were estimated by observing the vascular pattern in adenosine diphosphate ase (ADPase) stained retina flat mounts. The newborn vessels were quantified by haematoxylin and eosin staining. Reversal transcription-polymerase chain reaction (RT-PCR) was used to detect the VEGF mRNA expression. RESULTS: In the retinopathy group at 7 days of age, most of central radial vessels became constricted and blocked, and central perfusion decreased obviously. After switching to room air exposure for 7 days (14 days of age), noticeable retinal neovascularization appeared. The expression of VEGF mRNA in the retinopathy group at 7 days of hyperoxia exposure was noticeably lower than in the control group, and increased gradually after switching to room air exposure. At 9 and 14 days of age, the expression of VEGF mRNA in the retinopathy group was noticeably higher than in the control group. The expression of retinal VEGF mRNA in the retinopathy group increased before neovascularization occurred, and decreased with regression of new vessels. CONCLUSIONS: Hyperoxia exposure may decrease the transcription of VEGF mRNA and the growth of retinal blood vessels. The relative hypoxia after hyperxia withdrawal can up-regulate the transcription of VEGF mRNA, resulting in a significant retinal neovascularization. The abnormal expression of VEGF in the retina may play an important role in the development of neovascularization in retinopathy.［Chin J Contemp Pediatr, 2007, 9 (4):371-374］

OBJECTIVE: To investigate the effects of bifidobacteria on malondialdehyde (MDA) content and intercellular adhesion molecule-1 (ICAM-1) expression in serum and ileum tissues of young rats with endotoxin-induced intestinal damage, and possible protective mechanisms of bifidobacteria on intestines. METHODS: Eigteen-day-old Wistar rats were randomly administered with normal saline (NS), lipopolysaccharide (LPS, 5 mg/kg) or LPS + bifidobacteria. Bifidobacteria (0.5 mL, twice a day) was intragastrically administrated 7 days prior to LPS injection until the end of the experiment. MDA contents in serum and ileum were detected by the TBA method. Expression of ICAM-1 protein and mRNA were evaluated by immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) after 2, 6, 24 and 72 hrs of LPS injection. RESULTS: The serum and ileum MDA contents in the untreated LPS group increased significantly and reached a peak at 6 hrs of LPS injection when compared with the NS control group (ileum: 99.88±12.62 nmol/mg prot vs 84.25±12.96 nmol/mg prot, P<0.05; serum: 1.67±0.30 nmol/mL vs 1.13±0.20 nmol/mL, P<0.05). The MDA contents in ileum (92.75±9.28 nmol/mg prot) and serum (1.17±0.23 nmol/mL) in the bifidobacteria-treated group at 6 hrs of LPS injection were significantly lower than in the LPS group (P <0.05）.The expression of ICAM-1 protein in the untreated LPS group remarkably increased at 6, 12, 24 and 72 hrs of LPS injection when compared with the NS control group (P<0.01). The bifidobacteria-treated group displayed lower ICAM-1 protein levels than the untreated LPS group at 72 hrs of LPS injection (P<0.01). The ICAM-1 mRNA expression in the untreated LPS group significantly increased at 2hrs of LPS injection when compared with the NS control group (P<0.01). The ICAM-1 mRNA expression in the bifidobacteria-treated group began to decrease at 2 hrs of LPS injection and was reduced again at 24 hrs after experiencing increase at 6 and 12 hrs of LPS injection when compared with the untreated LPS group (P<0.01). CONCLUSIONS: The serum and ileum MDA contents and the expression of ICAM-1 protein and mRNA increased in young rats with endotoxin-induced intestinal damage. Bifidobacteria supplementation can decrease MDA contents and inhibit ICAM-1 expressions, thus providing protections for intestines.［Chin J Contemp Pediatr, 2007, 9 (4):375-378］