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.

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.

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.

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.

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

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

No abstvact available