Abstract:

OBJECTIVE: It is not known whether endothelial factor-1 (ET-1) and nitric oxide (NO) are involved in glomerulosclerosis. This study aimed at studying the changes and roles of ET-1 and NO in the process of glomerulosclerosis and the effects of the angiotensin converting enzyme inhibitor (ACEI), benazepril, and the angiotension Ⅱ receptor type Ⅰ antagonist, losartan. METHODS: Glomerulosclerosis was induced in rats by resecting one side of the kidneys and injecting adriblastine. The rats were randomly assigned into a glomerulosclerosis group (D group), a benazepril-treated glomerulosclerosis group (DB group), and a losartan-treated glomerulosclerosis group (DL group), 10 per group. Ten rats were sham-operated (Control group) and were injected with normal saline into caudal veins. After 6 weeks of benazepril or losartan administration, the mRNA expressions of ET-1 and iNOS in renal cortex were measured by reverse transcription polymerase chain reaction (RT-PCR). The protein levels of ET-1 and iNOS in renal cortex were detected by Western blotting, and the renal tissue Collagen Ⅳ and fibronectin were measured by immunohistochemistry. RESULTS: By the 4th week of adriblastine administration, urinary protein, serum cholesterol and blood urea nitrogen increased, while serum albumin decreased in Group D compared with those of the Control group (all P< 0.05). RT-PCR and Western blotting demonstrated that the mRNA and protein expressions of ET-1 increased 3.58 and 2.83 times, and the mRNA and protein expressions of iNOS increased 4.28 and 3.15 times in the renal cortex of the Group D when compared with those of the Control group. The expressions of Collagen Ⅳ and fibronectin also significantly increased in Group D. After 6 weeks of benazepril or losartan treatment, the deposition of extracellular matrix in the Groups DB and DL was significantly reduced and mRNA and protein expressions of ET-1 and iNOS had decreased compared with those of the Group D. Meanwhile, the expressions of Collagen Ⅳ and fibronectin also decreased in the two treatment groups. CONCLUSIONS: ET-1 and NO may participate in the process of glomerulosclerosis. Inhibition of ET-1 and iNOS blocks accumulation of extracellular matrix, and may avert glomerulosclerosis.

Abstract:

OBJECTIVE: Most newborn infants with hyperbilirubinemia have gastrointestinal tract symptoms. The aim of this study is to investigate the effect of hyperbilirubinemia on gastrointestinal hormone levels in newborn infants. METHODS: Fasting plasma motilin and serum gastrin levels were measured using a radioimmunoassay in 50 term newborns with hyperbilirubinemia (Hyperbilirubinemia group). Fasting plasm motilin and serum gastrin levels from thirty normal term newborns were used as controls. RESULTS: The plasma motilin level in the Hyperbilirubinemia group (659±37 ng/L) was significantly higher than that of the controls (486±28 ng/L) (P< 0.01). The plasma motilin level was positively correlated with the serum bilirubin level. The serum gastrin level in the Hyperbilirubinema group was not different from that of the controls. CONCLUSIONS: The plasma motilin level is correlated with the level of bilirubin in the newborn. The abnormal increase in the level of motilin may be related to the development of gastrointestinal symptoms newborns with hyperbilirubinemia.

Abstract:

OBJECTIVE: Previous studies suggest that dexamethasome (DEX) pretreatment can reduce hypoxic-ischemic brain damage (HIBD), but the mechanism for this effect has not been identified. This study examined the effects of DXM pretreatment on NF-κB activation and neuronal apoptosis in the brain of neonatal rats with HIBD, in order to identify a possible mechanism for the protective effect of DEX pretreatment in HIBD. METHODS: Forty-two 6-day-old Sprague-Dawley (SD) rats were randomly assigned to 5 groups: Normal controls (n=8), Sham-operated (n=8), HIBD (n=8), DEX pretreated (P-DEX, n=9) and DEX treated (DEX, n=9).HIBD was induced by hypoxia exposure combined with ligation of the left common carotid artery. DEX (0.1 mg/kg) was administered to rats in the P-DEX group 24 hrs before HI and to rats in the DEX group immediately after HI. After 72 hrs of HI, the rats were sacrificed and then the brain tissues were removed. Apoptosis was examined by means of terminal-deoxynucleotidyl transferase mediated d-UTP nick end labeling (TUNEL). The expression of p65 protein in tissue sections was detected by immunohistochemistry. The expression of IκBα protein was measured by Western blotting. Co-localization of p65 protein expression and apoptosis was determined with double-label immunofluorescence. RESULTS: The number of p65 positive cells and apoptotic cells was greater and the expression of the IκBα protein was less in the HIBD and DEX groups (P< 0.01) when compared with the Normal control and Sham-operated groups (P< 0.01). There were fewer p65 positive cells and apoptotic cells, and the level of IκBα protein expression was greater in the P-DEX group (P< 0.01) compared with the HIBD group. There were no significant differences between the DEX and HIBD groups. In the HIBD group, the level of NF-κB activation and the extent of neuronal apoptosis were significantly correlated (r= 0.775, P< 0.01). CONCLUSIONS: The activation of NF-κB may play an important role in the development of neuronal apoptosis in neonatal rats with HIBD. The protective effects of DEX pretreatment may work through the inhibition of NF-κB activation which may then inhibit neuronal apoptosis.

Abstract:

OBJECTIVE: Abnormal connective tissue proliferation in muscle following muscle fibre degeneration-regeneration is a feature of muscular dystrophy. Tissue inhibitors of metalloproteinases (TIMPs) are multifunctional proteins that can modify cellular activities and modulate matrix turnover. Transforming growth factor-β1 (TGF-β1) can promote tissue fibrosis. This paper studied the role of TIMP-1 and TGF-β1 in the pathogenesis of various muscular dystrophies. METHODS: Plasma TIMP-1 and TGF-β1 levels were measured by ELISA in patients with various muscular dystrophies. Forty-one patients with non-muscle disorders were used as the Control group. RESULTS: The plasma TIMP-1 level was significantly elevated in patients with Duchenne muscular dystrophy (DMD, 122.52± 63.87 ng/ml) (P< 0.05) and congenital muscular dystrophy (CMD, 124.87± 63.14 ng/ml) (P< 0.05) when compared with that of the Control group ( 85.71± 29.13 ng/ml). Patients with Becker muscular dystrophy (BMD) had no significant elevation of the TIMP-1 level compared with the Control group. Compared with the Control group ( 6.24± 1.12 ng/ml), the plasma TGF-β1 level was significantly elevated in patients with DMD ( 26.26± 5.79 ng/ml) (P< 0.01) and CMD ( 31.35± 9.77 ng/ml) (P< 0.05), but not in patients with BMD ( 3.46± 1.38 ng/ml). There was a correlation between the concentrations of TIMP-1 and TGF-β1 (r= 0.6350,P< 0.01). CONCLUSIONS: The plasma TIMP-1 and TGF-β1 levels were elevated in patients with DMD or CMD. This elevation suggests that TIMP-1 and TGF-β1 are correlated with the clinical severity of muscular dystrophy and suggests that they may play a role in the genesis of muscular dystrophy.[WT5"H

Abstract:

OBJECTIVE: Febrile seizures (FS) occur more frequently in children between the ages of six months and five years, especially when they have a fever (38-42℃). The pathophysiological mechanism for FS is not clear at the moment. To explain the changes of cellular energy metabolism during FS, the expression of uncoupling protein-4 (UCP4) was studied after recurrent FS in the hippocampus using developing rats. METHODS: FS were induced in the rats by exposure to a hot water bath. Seventy-two developing rats were divided into a Control group (n=24), a FS group (n=24), and a Febrile without seizure group (Febrile group, n=24). The mRNA and protein expression of UCP4 in the rat hippocampus was studied after the hyperthermia stimulation using immunohistochemistry, in situ hybridization and Western blot analysis. RESULTS: The UCP4 content in the hippocampus was higher in the FS group than that in both of the Control and Febrile groups, while the UCP4 content in the Febrile group was the lowest among the three groups. The highest mean intergrated density value (IDV) /area was 22 150.63± 423.40 in the FS group, followed by the Control group ( 14 830.75± 641.91) and the Febrile group ( 10 511.63± 302.07) (both P< 0.05). CONCLUSIONS: Increased expression of UCP4 in the FS group suggested an increased uncoupling process in mitochondria. Consequently, recurrent FS could decrease ATP production and affect the mitochondrial reserve function.

Abstract:

OBJECTIVE: It is still unexplained whether hypoxia of renal tissues induced by asphyxia is closely related to acute renal tubular epithelial cells (RTEs) injury. This paper aims to study the effect of hypoxia on G 1/S transition in neonatal pig's RTEs in vitro so as to explore the relationship between hypoxia and acute RTEs injury. METHODS: A hypoxic cell model of G 1/S transition of RTEs in neonatal piglets was established by sodium cyanide exposure. Some of the hypoxic G 1/S cells received cantharidin and were used as the Intervention group. The non-hypoxic and non-interfered G 1/S cells were used as the Control group. Cell distribution rate and cell apoptosis rate of G 1 and S phases were determined by flow cytometry 0, 60, 120 and 180 minutes after cessation of hypoxia. The cell p21 expression was measured by immunocytochemistry. RESULTS: The cell cycle distribution rate of the S phase in the Hypoxic group 0 and 60 minutes after cessation of hypoxia ( 1.4%± 2.5% and 0.5%± 0.9%) were lower than those of the Intervention group ( 98.3%± 1.6% and 99.0%± 1.0%) (P< 0.01). The cell apoptosis rates in the Hypoxic group 120 and 180 minutes after cessation of hypoxia ( 33.6%± 0.8% and 37.5%± 1.2%) were higher than those of the Intervention group ( 20.9%± 1.7% and 22.5%± 1.1%) and the Control group ( 25.6%± 1.1% and 23.6%± 1.4%) (P< 0.01). The cell distribution rate of the G 1 phase had a positive liner correlation with cell p21 expression of the same term (r= 0.64, P< 0.01), but it was not related to the cell apoptosis rate. CONCLUSIONS: Acute RTEs injury in the perinatal period is closely related to hypoxia. The possible mechanism is that hypoxia may restrain the advance of G 1/S transition and increase cell apoptosis rate of the S phase.

Abstract:

OBJECTIVE: To study the mechanism of the kidney injury and the protective effect of dexamethasone (Dex) on kidneys in neonatal rats with endotoxemia. METHODS: One hundred and fifty 7-day-old newborn Wistar rats were randomly assigned into 3 groups: a LPS group, a Dex group and a Control group. The LPS group was injected intraperitoneally by a single bolus of lipopolysaccharide (LPS, 5 mg/kg). The Dex group received an injection with LPS 5 mg/kg plus Dex 5 mg/kg. The Control group received the same volume of 0.9% sodium chloride as the other two groups. The rats were sacrificed at 0, 2, 4, 6, 24 hrs of post-infection (10 rats each). The nitric oxide (NO) levels in kidneys were measured by colorimetric analysis. The nitric oxide synthase (NOS) concentrations of the kidney were measured by the biochemical method. The superstructure of the kidney was observed under the electron microscope. RESULTS: The NO levels of the kidneys in the LPS group were higher than those of the Control group at 2 hrs of post-injection ( 1.69± 0.44 nmol/mg vs 1.20± 0.36 nmol/mg; P< 0.05), increasing to be 2.3 times greater than the Control group at 24 hrs ( 3.12± 0.41 nmol/mg vs 1.35± 0.38 nmol/mg; P< 0.01). The NO levels of the Dex group ( 1.63± 0.27 nmol/mg) were also higher than those of the Control group at 2 hrs (P< 0.05), while they were lower than those of the LPS group at 24 hrs ( 2.10± 0.27 nmol/mg; P< 0.05). The NOS contents of the kidneys at 2 hrs of post-injection ( 0.47± 0.15 U/ml) and at 24 hrs ( 0.65± 0.27 U/ml)in the LPS group were both higher than those of the Control group ( 0.38± 0.12 U/ml and 0.38± 0.15 U/ml; both P< 0.05). The NOS content elevated at 6 hrs in the Dex group compared with that of the Control group, but it was lower than that of the LPS group at 24 hrs ( 0.51± 0.07 U/ml vs 0.65± 0.27 U/ml; P< 0.05). Under the electron microscope, the complete renal glomerulus GBM and clear epithelial cell foot processes were found, and the complete renal tubule epithelial cells and brush border were also found in the Control group. In the LPS group, renal glomerulus GBM was fractured, epithelial cell foot processes had obvious confluence, a great quantity of mesangial cells mitochondria presented vacuolation, and renal tubules epithelial cell mitochondria were expanded to bubbles at 24 hrs of post-injection. In the Dex group, renal glomerulus GBM almost recovered to normal, partial epithelial cell foot processes were slightly fused, and a small quantity of mitochondria vacuolation in mesangial cells and the brush border in renal tubules were found at 24 hrs of post-injection. CONCLUSIONS: LPS can stimulate the kidneys to produce more NOS which induces to synthesize excessive NO in neonatal rats. Dex can protect kidneys from NO damage by inhibiting the NOS production and yielding a decrease of the NO level.

Abstract:

OBJECTIVE: Previous studies have shown that the reduced glucocorticoid (GC) sensitivity is associated with the mutations of glucocorticoid receptor (GCR) in patients with acute lymphocytic leukemia or with lupus nephritis. It has not been confirmed whether GC-resistance is the result of abnormal function of GCR induced by the alteration of GCR gene in children with primary nephrotic syndrome (PNS). The purpose of this study is to investigate the correlation between GC-resistance and the polymorphisms of GCR in DNA-binding domain and hormone-binding domain in children with PNS. METHODS: DNA was isolated from peripheral blood leukocytes in 100 children with PNS (44 with GC-sensitive, 56 with GC-resistance) and 100 healthy controls and each exon of the DNA-binding domain and hormone binding domain of GCR was amplified by the polymerase chain reaction (PCR). Single-strand conformation polymerase (SSCP) analysis of the PCR products was carried out for screening polymorphisms. DNA fragments displaying an abnormal migration pattern during SSC analysis were subjected to direct sequencing. RESULTS: PCR-SSCP analysis in all of the PCR products from the GC-resistance and GC-sensentivity cases did not display an abnormal DNA fragment migration pattern. Polymorphism of GCR in neither the DNA-binding domain nor the hormone-binding domain was found. CONCLUSIONS: There is no correlation between GC-resistance and the polymorphisms of GCR in DNA-binding domain and hormone-binding in children with PNS.

Abstract:

OBJECTIVE: In view of the different opinions on the effects of non-nutritive sucking (NNS) on premature infants, this paper aims at evaluating the effects of NNS on nutrient and gastrointestinal hormones insulin (INS) and somatostatin (SS) levels in premature infants. METHODS: Thirty-eight healthy, appropriate for gestational age, premature infants who accepted intermittent nasogastric feeding (INGF) were randomly assigned into a NNS group and a non-NNS group according to INGF with and without NNS. They were fed with the same milk formula. Plasma INS and SS levels were detected by radioimmunoassay (RIA). RESULTS: The birth-weight regaining time in the NNS group was significantly shorter than that in the N-NNS group ( 8.8± 3.7 d vs 11.1± 3.0 d; P< 0.05). Within two weeks after feeding, there were no significant differences in the increase of body weight, length and head circumference between the two groups. The time of reaching 418.4 kJ/kg of caloric intake daily by enteral feeding in the NNS group was significantly shorter than that in the N-NNS group ( 12.3± 5.1 d vs 15.7± 5.2 d; P< 0.05); while the feeding time through the nasogastric tube was the same for both groups. There was a lower incidence of gastric residue in the NNS group ( 16.7%) compared with that in the N-NNS group (50%) (P< 0.05). After a week of initial feeding, the plasma INS level in the NNS group was significantly higher than that in the N-NNS group ( 37.1± 11.3 μU/ml vs 29.6± 8.8 μU/ml; P< 0.05). By the end of the second week the plasma INS level in the NNS group was also higher than that in the N-NNS group ( 50.3± 18.4 μU/ml vs 40.0± 9.9 μU/ml; P< 0.05). The plasma SS level in the NNS group was significantly lower than that in the N-NNS group by the end of both the first and second weeks ( 454.6± 136.4 pg/ml vs 595.3± 260.1 pg/ml and 595.6± 172.1 pg/ml vs 727.2± 220.8 pg/ml; both P< 0.05). CONCLUSIONS: NNS can promote INS secretion and suppress SS secretion, which is of benefit to gastrointestinal development and growth, and to improving the tolerance of enteral feeding.

Abstract:

OBJECTIVE: To explore the relationship among maternal choriamnionitis, cord interleukin-6 (IL-6) concentration, brain damage and neurological deficits in the first 3 years of life, and to study the significance of cord IL-6 in the evaluation of the prognosis of preterm neonatal brain damage. METHODS: Twenty-six preterm neonates born between May, 1998 and February, 1999 were enrolled in this study. The cord IL-6 concentration was detected by ELISA. Maternal choriamnionitis was confirmed by histological examination of the placenta. All infants had either ultrasonography or CT in the first three days of their lives and a subsequent follow-up visit within three years of their lives. RESULTS: The incidence of neurological deficits was higher in preterm infants with brain damage than that in those without. The incidence of neurological deficits was also higher in those whose mothers had choriamnionitis. The cord IL-6 concentration in preterm infants with neurological deficits was higher than that in those without. CONCLUSIONS: Maternal chorioamnionitis may result in an increased incidence of brain damage and subsequent development of neurological deficits in preterm infants. It is therefore very important to prevent and treat maternal intrauterine infections early with the view to decreasing the risk of subsequent neurologic deficits. Cord IL-6 may be elevated in maternal chorioamnionitis and may predict the subsequent development of neurological deficits.

Abstract:

OBJECTIVE: To explore the relationship between Helicobacter pylori (Hp) infection and the gastric mucosa and serum interleukin-8 (IL-8) levels in children so as to study the role of IL-8 in Hp-related gastrointestinal diseases. METHODS: Fifty-three children with recurrent upper abdominal pain or other related complaints were given endoscopy inspection. The gastric mucosa was collected for Hp qualitative detection by both rapid urea enzyme test and histopathologic examination. The gastric and serum IL-8 levels were detected using ELISA. RESULTS: Hp infection was confirmed in 29 children. The gastric IL-8 level in children with Hp infection ( 32.86± 3.92 pg/mg) was significantly higher than that of children without Hp infection ( 13.75± 2.19 pg/mg) (P< 0.01). There was no difference in serum IL-8 level between them. After the treatment of Hp infection, the gastric IL-8 level in children with Hp infection decreased significantly ( 15.91± 3.15 pg/mg) (P< 0.01), while serum IL-8 level of children with Hp infection was not different before and after treatment. CONCLUSIONS: Hp infection can induce the inflammatory cells of the gastric mucosa to secrete IL-8. IL-8 may play an important role in the pathogenesis of Hp-related gastrointestinal diseases.

Abstract:

OBJECTIVE: To measure the levels of blood gastrin (GAS), motilin (MTL) and somatostation (SS) in children with chronic gastritis and to explore the relationship between blood GAS, MTL and SS levels and the pathogenesis of chronic gastritis in children. METHODS: Fasting blood GAS, MTL and SS levels were measured by radioimmunoassay in 50 children with chronic gastritis [Gastritis group, 21 Helicobacter pylori (Hp) positive, 29 Hp negative] and compared to those in 30 age-matched normal children (Control group). Gastroscopy was performed for the children in the Gastritis group and then mucosal speciments obtained from antrum of stomach and duodenal ampulla were sent for RUT and histopathologic Giemas staining. RESULTS: (1) The serum GAS level in the Gastritis group ( 141.5± 28.0 ng/L) was significantly higher than that in the Control group ( 68.7± 17.9 ng/L) (P< 0.01). In the Gastritis group, the serum GAS level in children who were Hp-positive ( 173.0± 46.0 ng/L) was significantly higher than that in those who were Hp-negative ( 110.0± 20.0 ng/L) (P< 0.01). (2) The serum MTL level in the Gastritis group was significantly lower than that in the Control group ( 199.5± 61.0 ng/L vs 281.0± 76.0 ng/L) (P< 0.01). There was no statistically significant difference in MTT between the Hp-positive and Hp-negative children. (3) The serum SS level in the Gastritis group was also lower than that in the Control group ( 166.4± 18.0 ng/L vs 229.0± 45.0 ng/L) (P< 0.05). In the Gastritis group, the serum SS level in Hp-positive children was significantly lower than those who were Hp-negative ( 144.5± 11.0 ng/L vs 187.4± 26.0 ng/L) (P< 0.01). CONCLUSIONS: Blood GAS, MTL and SS levels are different in children with chronic gastritis, which might be part of the pathogenesis of chronic gastritis. Determinations of blood GAS and SS levels may be useful in the diagnosis of Hp infection in chronic gastritis.

Abstract:

OBJECTIVE: To study the correlation of plasma acylation-stimulating protein (ASP) with body mass index (BMI) and blood lipid in children with obesity. METHODS: Thirty children with simple obesity and 30 healthy children were involved in this study. Plasma ASP levels were determined using ELISA. Blood lipid levels were detected with fully automatic biochemical analyser by turbidimetry. RESULTS: The levels of plasma ASP ( 73.87± 24.04 g/L vs 39.47± 13.68 g/L), cholesterol ( 5.71± 0.61 mmol/L vs 4.29± 0.49 mmol/L), triglyceride ( 1.77± 0.30 mmol/L vs 1.02± 0.25 mmol/L) and apoprotein B ( 0.98± 0.20 mmol/L vs 0.85± 0.11 mmol/L) increased significantly in obese children compared to those in the healthy children (P< 0.01 or P< 0.05). ASP was positively correlated to BMI, triglyceride and cholesterol levels (r= 0.43, P< 0.05; r= 0.48, P< 0.05; r= 0.68, P< 0.01, respectively). The ASP levels were significantly higher in the obese children with family history of obesity than those in the obese children without ( 103.4± 10.57 g/L vs 71.15± 24.9 g/L, P< 0.01). CONCLUSIONS: Plasma ASP may be used as a marker for evaluating fat metabolism in children with obesity. It might be valuable in predicting the possibility of developing cardiovascular diseases in their later lives.

Abstract:

OBJECTIVE: Extracellular signal-regulated kinase (ERK) is closely related to cellular growth, differentiation and proliferation. This paper aims at (1) detecting ERK1/2 levels in the myocardial cell of viral myocarditis; (2) assessing the effect of ERK specific inhibitor PD98059 on cell viabilities and (3) studying the role of ERK in early viral myocarditis. METHODS: Myocardial cells from neonatal SD rats were incubated in vitro and were randomly assigned into four groups: a Coxsackievirus B3 (CVB3) group, a 20 μmol/L and a 50 μmol/L PD98059 groups and a Control group. CVB3 group was inoculated with CVB3 solutions. The PD98059 groups were initially inoculated with PD98059 for 30 min and then was inoculated with CVB3 solutions. The Control group was treated with DMEM plus 10% FBS. Western Blot was used to detect the ERK 1/2 levels and ERK activation product (P-ERK1/2) levels. Cell viabilities were measured with MTT assay. Cell cytopathic effect (CPE) was used to evaluate myocardial cell lesions. RESULTS: The ERK1/2 levels were not significantly different among the four groups. P-ERK1/2 levels in the CVB3 group were higher than those of the Control group ( 135.57± 0.71 vs 119.41± 1.97; P< 0.01) and also higher than those of the 20 μmol/L and 50 μmol/L PD98059 groups ( 113.75± 1.03 and 42.56± 2.17 respectively; both P< 0.01). P-ERK1/2 levels in the 20 μmol/L PD98059 group were significantly higher those in the 50 μmol/L PD98059 group (P< 0.01). Myocardial cell viabilities of the PD98059 groups ( 0.53± 0.13 and 0.41± 0.04) were higher than the CVB3 group ( 0.17± 0.04) (P< 0.01). There were no differences in myocardial cell viabilities between the two PD98059 groups. Compared with the CVB3 group, myocardial cell lesions in the PD98059 groups occurred later and were less. CONCLUSIONS: CVB3 infection seems to trigger ERK signal transduction pathway. PD98059 may protect myocardial cells from injuries.

Abstract:

OBJECTIVE: This study aims to investigate the immune state of children with Mycoplasma pneumoniae pneumonia (MPP) so as to provide evidence for determining the treatment regime of MPP. METHODS: Enzyme linked immunoassay was used to measure serum interleukin-6 (IL-6) and soluble interleukin-6 receptor (sIL-6R) levels in children with either MPP (MPP group, n=41) or bronchopneumonia with negative MP-IgM (non-MPP group, n=20). Twenty healthy children served as the Normal control group. RESULTS: Serum levels of IL-6 and sIL-6R in the MPP group were significantly higher than those of the Normal control group in both the acute and recovery stages (P< 0.01). Serum IL-6 levels of the non-MPP group in the acute and recovery stages were significantly higher than those of the Normal control group (P< 0.01, P< 0.05, respectively), while serum sIL-6R level was not different between them. In the recovery stage,serum IL-6 levels in both the MPP and non-MPP groups reduced significantly compared with those of the acute stage (P <0.01), while serum sIL-6R levels remained at a high level. The children in the MPP group had higher levels of serum IL-6 and sIL-6R in the acute stage than those of the non-MPP group (P< 0.05). In the recovery stage, the serum sIL-6R levels of the MPP group were still significantly higher than those of the non-MPP group (P< 0.01), while the difference of serum IL-6 between the two groups was not significant. CONCLUSIONS: There may be more remarkable immune function disorders in children with MPP compared to children with non-MPP. Immune regulation therapy seems to be necessary for children with MPP.

Abstract:

目的：评价新生儿尿液常规检查结果以及与胎龄、日龄、窒息程度的关系，反映不同新生儿肾功能状态及其不同特点，以便结合其他检查为早期发现肾功能异常提供帮助。方法：对216例新生儿尿液常规检查结果进行分析。结果：①尿糖阳性率为 9.4%，多为微量，极少达+，与胎龄、日龄及窒息程度均无明显相关性。②尿蛋白阳性率 26.2%，为微量～+，与日龄呈负相关，与窒息程度呈正相关性(均P<0.05)。其中胎龄28～34周组尿蛋白阳性率明显高于34周～和36～42周组，有窒息患儿尿蛋白阳性率明显高于无窒息者。③尿比重无窒息组(1.007)和重度窒息组(1.011)有明显差异，窒息程度与尿比重呈明显正相关(P<0.05)。④尿pH值与胎龄、窒息程度呈负相关(均P<0.05)，其中出生1 d组和>1 d组差异有显著性。结论：不同胎龄和日龄新生儿如注意输糖浓度和速度可控制尿糖出现；早产儿尿蛋白阳性率较高，随胎龄增加有所下降，应注意窒息的影响，结合其他肾功能指标，及时做出肾功能异常的判断，避免肾功能衰竭的发生；窒息新生儿尿比重增高，应注意液体量的适量供给，避免出现水肿；日龄越小的新生儿肾脏酸处理能力越差，窒息影响这一功能的成熟，对于有窒息史的早产儿应注意喂养情况及热量供给，避免酸碱紊乱发生。［中国当代儿科杂志，2004, 6(4): 303-306］

Abstract:

目的：肾病综合征(NS)治疗中的复发、激素耐药或依赖等仍是目前临床上的难题。该研究探讨卡介苗多糖核酸(BCG-PSN)辅治小儿肾病综合征(NS)的临床效果。方法：观察组中29例初治单纯性肾病综合征患儿在常规激素长疗程疗法的基础上加用BCG-PSN肌肉注射，每次 0.5 ～1 mg，每2日1次，疗程12周。同期选择26例初治单纯性NS患儿单独用激素长疗程疗法治疗作对照。另9例肾炎性NS患儿和11例复治NS患儿则以上法加用BCG-PSN治疗后，仅作治疗前后对照或描述性观察。结果：观察组患儿首次尿蛋白转阴需 14.29 ± 3.45 d ，明显少于对照组 22.10 ± 8.85 d；年均复发次数 1.34 ± 1.25 次，也少于对照组 4.13 ± 2.54 次，差异有显著性( P < 0.01 )；非频繁复发率低于对照组( 24.1% vs 53.9% )，无复发率高于对照组( 65.5% vs 23.1% )；年均呼吸道感染人次 2.60 ± 1.72 次也低于对照组 4.12 ± 5.31 次，差异有显著性( P < 0.01 )。其余20例非初治单纯性NS患儿辅用BCG-PSN治疗也取得较满意疗效。结论：BCG-PSN辅治小儿NS可以缩短尿蛋白转阴所需时间，降低年均复发例数，减少年均呼吸道感染人次，提高无复发率。

Abstract:

目的：近年来婴幼儿哮喘发病率逐渐增加，与环境因素(过敏原)有密切关系。该文探讨过敏原检测系统(CAP系统)中吸入性过敏原过筛Phadiatop试验和食物过敏原过筛Fx5E试验在婴幼儿哮喘的病因诊断中的价值。方法：对68例婴幼儿哮喘应用荧光酶联免疫，行Phadiatop试验和Fx5E试验并与传统的过敏原诊断方法皮肤试验相比较。 结果：①过敏因素是婴幼儿哮喘的一个重要因素，有48.5% 患儿血清Fx5E阳性，有 38.2% 患儿血清Phadiatop阳性；②Phadiatop的阳性率为 60.4% ，皮肤点刺试验阳性率 37.2% ，经χ 2检验，两种方法的阳性率差异有显著性(χ 2 = 4.65 ，P < 0.05 )；③婴幼儿哮喘患儿中食物IgE的阳性率比吸入IgE的阳性率更高。 结论：过敏因素是婴幼儿哮喘的一个重要因素；婴幼儿哮喘患儿中食物过敏情况比吸入物过敏更重要；Phadiatop试验和Fx5E试验是一项简便、可靠的过敏原过筛试验。

Abstract:目的:儿童十二指肠溃疡临床表现常不典型，常因并发出血就诊，为探讨儿童十二指肠溃疡并出血的有效治疗方法，该文采用立止血联合洛赛克治疗并观察其疗效。方法:38例患儿随机分为治疗组和对照组，治疗组应用立止血+洛赛克，对照组应用止血敏+西咪替丁，比较两组平均住院日、显效率、有效率。 结果:两组平均住院日比较，治疗组 8.4 ± 1.0 d ，对照组 12.3 ±1.5 d ，两组比较差异有显著性( t = 9.019 ， P < 0.01 )。两组疗效比较，显效率治疗组 87.5% 、对照组 50.0% ，两组比较差异有显著性(χ 2= 4.241 ，P < 0.05 )；有效率治疗组100%、对照组 90.9% ，两组比较差异无显著性(χ 2= 0.253 ， P > 0.05 )。 结论:立止血联合洛赛克治疗能明显缩短活动性出血病程、平均住院日。

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目的：小儿过敏性紫癜并发急腹症前后，其影像学表现无论是腹部X线、CT或B超，以前均有报道，但综合在一起讨论其特点的报道较少。该文回顾性分析36例小儿过敏性紫癜并发急腹症患儿的临床资料，探讨其影像学特点及临床意义。方法：回顾性分析36例小儿过敏性紫癜并发急腹症患儿的临床资料。结果：出现并发症前，B超、CT检查均显示多发节段性受累肠壁水肿增厚，肠管狭窄，受累区域肠系膜模糊不清；出现并发症后，B超在检查并发肠套叠时具有价廉、准确的特点；在检查并发肠坏死穿孔时，腹部X线正立、侧卧位像及CT有较高的敏感性；在检查肠梗阻及监测其变化时，腹部X线正立、侧卧位像有重要的意义。结论：在出现并发症前，小儿过敏性紫癜的影像学表现重要性在于可以与需要手术的其他急腹症相鉴别，典型的影像学表现可以提示诊断；在出现并发症后，可以及时发现并发症和指导临床治疗。

Abstract:目的：探讨X线钡剂检查对小儿消化道疾病诊断和治疗的作用。方法：采用回顾性分析方法对160例有消化道症状且经X线钡剂检查确诊之患儿的临床表现、检查结果及部分患儿转归进行总结。结果 160例经X线钡剂检查发现阳性征象75例。其中慢性胃炎21例；胃、十二指肠溃疡16例；食管炎9例；先天性肥大性幽门狭窄8例；贲门失弛缓症8例；食道静脉曲张5例；食管烧伤和瘢痕狭窄3例；先天性巨结肠3例；结肠息肉2例。32例腹痛、呕吐患儿钡剂检查无异常发现，未做任何治疗仅经钡剂检查后症状全部消失。随访1～2年无复发。 结论 小儿消化道疾病X线钡剂检查阳性率 47%；钡剂检查对部分无器质性病变但有消化道症状的患儿有治疗作用，其机制有待探讨。［中国当代儿科杂志，2004, 6(4): 315-316］

Abstract:

目的：评价手法分离术治疗学龄前期女孩轻到中等度小阴唇粘连的效果。方法：对10例诊断为小阴唇粘连的学龄前期女孩采用局麻下手法分离术治疗。结果：局麻下手法分离术成功地分离了10例患儿的小阴唇粘连，追踪观察 6个月无复发。结论：手法分离术是一个快速而安全的治疗小阴唇粘连的方法，且能有效地预防其复发。

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目的：促皮质素(ACTH)作为治疗婴儿痉挛的一线药物尚无统一的剂量和治疗效果，该研究旨在观察持续静脉滴注ACTH治疗婴儿痉挛的疗效。方法：31例年龄2个月至3岁的婴儿痉挛患儿，用小剂量ACTH 20～25 U，每日持续静脉滴注8 h以上，疗程2周，然后口服泼尼松每日 1.5 ～2 mg/kg，共4周，再逐步减量直至停药。观察治疗后发作控制情况、EEG改变、血象、肝肾功能、血电解质及不良反应。结果：22例(71.0%)在静脉滴注ACTH 2周内发作得到完全控制及之后连续30 d无发作。治疗后EEG有改善，血象、肝肾功能及血电解质无异常改变。11例患儿出现短暂的兴奋症状，1例出现高血压，1例出现骨质疏松表现，无1例出现严重的不良反应。结论：持续静脉滴注ACTH治疗婴儿痉挛近期疗效肯定。 ［中国当代儿科杂志，2004, 6(4): 319-320］

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目的：听觉事件相关电位是测定人脑认知加工功能或心理活动的客观指标，应用听觉事件相关电位检测，以探讨抽动-秽语综合征(TS)患儿的认知功能。方法：对30例TS患儿进行听觉事件相关电位P300测定，并与30例健康对照组儿童比较。结果：TS患儿听觉事件相关电位P300潜伏期明显延长、波幅明显降低，与健康对照组相比差异有显著性意义(P＜0.01＝。结论：听觉事件相关电位作为电生理检查，可客观反映TS患儿认知功能障碍，亦可作为治疗效果的评价指标。 ［中国当代儿科杂志，2004, 6(4): 321-322］

Abstract:目的：为了探讨超氧化物歧化酶在小儿急性白血病(AL)发生、发展中的作用，该文探讨急性白血病(AL)患儿化疗前后血清总超氧化物歧化酶(T-SOD)、锰-超氧化物歧化酶(Mn-SOD)、铜-锌超氧化物酶(Cu-Zn-SOD)活力变化及临床意义。方法：应用放免法对21例AL患儿化疗前后血清T-SOD，Mn-SOD，Cu-Zn-SOD活力进行检测，并与21例健康儿童作对照。结果：AL患儿化疗前血清T-SOD，Mn-SOD活力低于正常对照组，差异有显著性( P < 0.05 )，而Cu-Zn-SOD活力与正常对照组比较差异无显著性意义(P > 0.05 )。经化疗达完全缓解后T-SOD，Mn-SOD活力较化疗前升高，差异有显著性( P < 0.05 )，接近正常水平。结论：总SOD，Mn-SOD活力变化可能与小儿急性白血病的发生发展密切相关，二者的动态检测有利于观察病情变化。

Abstract:目的：探讨小儿扩张型心肌病(DCM)病因、DCM与病毒性心肌炎(VMC)关系以及两者之间的鉴别，提高对小儿DCM临床认识。方法：该研究以DCM、VMC患儿各33例为研究对象，以33例健康儿为对照，应用酶联免疫吸附试验检测血清中柯萨奇病毒(CoxB)IgM抗体浓度和心肌酶浓度，彩色多普勒超声心动图观测心脏形态改变及心功能状况。结果：①DCM组，CoxB IgM抗体阳性率33.3%；②与正常健康组比较，DCM抗CoxB IgM阴性组心肌酶谱各项指标差异无显著性(P>0.05)；DCM抗CoxB IgM阳性组和VMC组心肌酶谱各项指标均显著升高，差异有显著性(P<0.01)；③超声心动图示心脏房室腔扩大、心脏收缩与舒张功能降低，肺动脉平均压升高，DCM组均重于VMC组，差异有显著性(P<0.01)。结论：①CoxB病毒感染与小儿VMC、DCM发病存在密切关系；②超声心动图对DCM诊断具有颇高的价值；③DCM与VMC的鉴别诊断须综合多项指标方能作出正确判断。 ［中国当代儿科杂志，2004, 6(4): 325-327］

Abstract:目的：新生儿缺氧缺血性脑病(HIE)患儿的酸碱紊乱及阴离子间隙(AG)状态研究报道较多，但窒息新生儿AG值与HIE发生的关系尚未见报道。该文探讨窒息新生儿AG值与HIE发生率之间的关系，以帮助早期诊治。方法：采用瑞士产AVL-945型血气分析仪作血气分析，同时测定电解质，计算出AG值。结果：105例窒息新生儿均存在程度不等的酸中毒，正常AG组与高AG组之间pH值和BE值差别无显著意义( P > 0.05 )，两组之间HIE发生率差异有显著性意义( P < 0.05 )。结论：窒息新生儿AG值可作为预测HIE发生的重要指标，并对临床治疗有一定的指导意义。

Abstract:目的：左室射血分数是反映心脏收缩功能的指标，通过测定左室射血分数探讨窒息缺氧对新生儿心功能的影响。方法：采用彩色超声心动图对40例窒息新生儿生后2～3 d进行左室射血分数测定，经治疗7～10 d后复查，并以40例年龄、体重相近的正常新生儿作为对照组。结果：窒息新生儿左室射血分数56.6±5.7 明显低于正常新生儿 70.6±6.0，差异有显著性意义(P<0.05)；窒息组经治疗后7～10 d，再与对照组相比，左室射血分数差异无显著性意义(P>0.05)。结论：窒息缺氧可引起心肌损伤，心脏功能下降，左室射血分数明显降低，经治疗可以逆转。 ［中国当代儿科杂志，2004, 6(4): 329-330］

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