OBJECTIVE: Some research has shown that androgen has a neuroprotection against hypoxia-ischemia brain damage (HIBD). However, the relevant mechanism has not been fully elucidated. This study aimed to explore the neuroprotection of androgen against HIBD in neonatal rats and the possible mechanism. METHODS: Sixty-four seven-day-old Sprague-Dawley (SD) rats were randomly assigned into three groups: Sham-operation, HIBD and Androgen. The HIBD model was induced by ligation of the left carotid common artery along with hypoxia exposure in neonatal rats from the latter two groups. The Sham-operation group was not subjected to hypoxia-ischemia (HI). The Androgen intervention group received an injection of testosterone propionate (25 mg/kg) immediately after HIBD. Bcl-2 and Bax protein expressions in the cortex and hippocampal CA region were detected by immunohistochemical method at 6, 24 and 72 hrs and at 7 days after HI. The contents of SOD and MDA in the brain tissue homogenate were measured by the thiobarbituric acid (TBA) method and the xanthine oxidase luminescence method respectively at 6, 24 and 48 hrs after HI. RESULTS: There were few Bcl-2 and Bax immune positive cells in the cortex or hippocampus in the left hemisphere in the Sham-operation group at 6 hrs after operation. This was significantly different from the HIBD control and Androgen intervention groups(P< 0.01). The expression of Bcl-2 protein in the cortex and hippocampus of the Androgen intervention group was significantly higher than that of the HIBD control group at 6, 24 and 72 hrs after HI (P<0.05 or 0.01). The expression of Bax protein in the cortex and hippocampus of the Androgen intervention group was significantly lower than that of the HIBD control group at 24 hrs after HI (P﹤0.05).The SOD content in the brain tissue homogenate of the HIBD control group was significantly reduced, in contrast, the MDA content in the brain tissue homogenate of the HIBD control group increased significantly at 6 hrs after HI compared with the Sham-operation group (P<0.05). The SOD content was reduced to a nadir and the MDA content increased to a peak at 24 hrs after HI in the HIBD control group. Androgen intervention increased significantly the SOD activity at 6,24 and 48 hrs after HI and decreased significantly the MDA content at 6 and 24 hrs after HI as compared with the HIBD control group(P<0.05 or 0.01). CONCLUSIONS: The neuroprotection of androgen against neonatal HIBD is produced possibly through an increase of Bcl-2 protein expression and a reduction in Bax protein expression, thus decreasing neuronal apoptosis after HI.There may also be a reduction in the consumption of antioxidant and an inhibition of the formation of oxidant free radicals to alleviate neuronal damage following HI.
OBJECTIVE: Cerebral electrical admittance plethysmography is a novel noninvasive technique for evaluating cerebral hemodynamics. This study aimed to measure the reference values of cerebral electrical admittance plethysmogram in healthy newborns. METHODS: Bilateral cerebral electrical admittance plethysmography was performed in 40 healthy newborns. RESULTS: The values of various indexes of cerebral electrical admittance plethysmogram in 40 newborns were obtained by this technique. The index of Admittance Differential Loop (ADL) I+II at the third and fourth days after birth was significantly higher than that at the first day of life (P<0.05). There were significant differences in the index of ADL I+II and the ratio of Hs to b-S (Hs/ b-S) among different birth weight groups (P<0.05). No significant differences were found in all the indexes of cerebral electrical admittance plethysmogram between the left and right brain of newborns. Gender and parturition mode had also no effects on these indexes. CONCLUSIONS: The research reported the reference values of cerebral electrical admittance plethysmogram in healthy newborns. The postnatal age and birth weight are influencing factors for the cerebral electrical admittance plethysmogram.
OBJECTIVE: To investigate the levels and roles of serum growth hormone (GH) and prolactin (PRL) in neonatal hypoxic-ischemic encephalopathy (HIE). METHODS: Serum GH and PRL levels were measured by radioimmunoassay in 54 neonates with HIE (20 mild, 19 moderate and 15 severe HIE) at the acute and convalescence stages. Twenty normal neonates were used as controls. RESULTS: Serum GH levels were significantly lower, but PRL levels were significantly higher in moderate and severe HIE neonates at the acute stage compared with those of controls and mild HIE neonates (P<0.01). There were noticeable differences in serum levels of GH and PRL between the moderate and severe HIE cases (P<0.01). During the convalescence stage, serum GH levels increased and PRL levels decreased in moderate and severe HIE neonates compared with those at the acute stage (P<0.01); serum GH and PRL levels in each sub-group of HIE restored to the levels of controls. There was a closely negative correlation between GH and PRL levels at the acute stage of HIE (r=-0.8759, P<0.01). CONCLUSIONS: GH and PRL might be involved in the pathophysiological process of HIE. The levels of GH and PRL closely relate to the severity of HIE at the acute stage.
OBJECTIVE: To investigate the association of the polymorphism of I181L, V183L and E237G in the high affinity immunoglobulin E receptor β-chain (FcεR1β) with the susceptibility of childhood asthma and the serum total immunoglobulin E(IgE) level. METHODS: The coding variants of I181L, V183L and E237G and the serum total IgE level were detected using amplification refractory mutation system-polymerase chain reaction (ARMS-PCR) and double antibody sandwich ELISA respectively in 50 asthmatic children and 40 normal controls from Sichuan Province. The association of gene mutation with the susceptibility of asthma and the serum total IgE level was analyzed. RESULTS: There were 5 cases of I181L mutation, 2 of V183L mutation, and 7 of E237G mutation in the Asthmatic group. There was no mutation in the Normal control group. The frequency of I181L and E237G mutation in the Asthmatic group were statistically higher than in the Normal control group (P<0.01). The serum total IgE level in the Asthmatic subgroup with I181L mutation (2.837±0.407) or E237G mutation (3.044±0.419) was significantly higher than in the Asthmatic subgroup without gene mutation (2.156±0.638) and the Normal control group (1.348±1.291) (P<0.05 or 0.01). CONCLUSIONS: The polymorphism of FcεR1βI181L and E237G is a susceptible gene of childhood asthma and closely associates with the increased serum total IgE level.
OBJECTIVE: To study the atopy spectrum and the influence of clinical characteristics upon it in asthmatic children under 4 years of age. METHODS: Clinical data of 62 asthmatic children under 4 years of age, including age, sex, the age of first wheezing attack, the total times of wheezing attack, the duration of history of wheezing, and the allergic history of both children and parents, were collected. The screening tests on allergens (fx5E,mx2 and Phadiatop)were conducted by fluoroenzyme-immunometric assay using the UniCAP100 system. The total serum IgE level was also measured. Logistic regression was used to analyze the effect of clininal characteristics on allergic sensitization. RESULTS: The positive rates of fx5E, mx2 and Phadiatop were 40.3%, 14.5% and 14.5% respectively, and the total allergic sensitization screening test rate was 46.8%. The sensitization rate to inhalant allergens was 24.2%. The allergic history of parent )s), the sensitization to food allergens, the age of first wheezing attack and total serum IgE level were main factors influencing the sensitization to inhalant allergens. CONCLUSIONS: About a quarter of asthmatic children under 4 years of age showed sensitization to inhalant allergens. The asthmatic history of parent (s), the sensitization to food allergens, the age of first wheezing attack greater than 2 years and the significantly higher total serum IgE level may increase the possibility of sensitization to inhalant allergens in asthmatic children under 4 years of age.
OBJECTIVE: To study the changes of intracellular interleukin-6 (IL-6) and interferon-γ (IFN-γ) expressions in children with acute lymphoblastic leukemia (ALL) at different stages, and to examine the correlation between IL-6 and IFN-γ in ALL children. METHODS: The levels of intracellular IL-6 and IFN-γ in venous blood lymphocytes were detected by flow cytometry in 42 children with ALL at diagnosis and at remission stage. Twenty healthy children were used as the controls. RESULTS: The intracellular IL-6 level in ALL children at diagnosis was 81.74±9.31, which was much higher than that in the Control group (5.67±0.96 ) (P<0.01). The intracellular IFN-γ level in ALL children (1.31±0.32) was significantly lower than that in the Control group (1.46±0.49) (P<0.01). However, the intracellular IL-6 level (27.52±3.40) decreased remarkably in ALL patients at remission stage (P<0.01), but was still higher than that in the Control group (P<0.01). In contrast, the intracellular IFN-γ level (1.97±0.72) increased noticeably in ALL patients at remission stage, which was higher than that at diagnosis and the Control group (P<0.01). A negative correlation was found between the intracellular IL-6 and the IFN-γ levels in ALL patients (r=-0.476, P< 0.05). CONCLUSIONS: Intracellular IL-6 and IFN-γ levels may be used as the markers for monitoring the response to treatment in ALL patients. There is a negative correlation between intracellular IL-6 and IFN-γ levels in ALL children.
OBJECTIVE: To assess the role of probiotics in the prevention of neonatal necrotizing enterocolitis (NEC) and to investigate the risk factors for NEC. METHODS: A total of 2 528 hospitalized neonates between January 2002 and May 2005 were assigned into either receiving prophylactic use of probiotics bifoco (Prevention group, n=1 182) or without probiotics supplementation (Control group, n=1 346). The incidence of NEC was compared between the two groups. The risk factors for NEC were investigated by conditional logistic regression multifactorial analysis. RESULTS: There were 19 cases of NEC in the Control group (1.41%), but only 6 cases in the Prevention group (0.51%) (P<0.05). Gestational age (OR=5.521), hypoxic-ischemic encephalopathy (OR=3.887), specticemia (OR=4.854) and critical illness scores (OR=5.989) were the risk factors for NEC, while the prophylactic use of probiotics was an independent protective factor for NEC (OR=0.255). CONCLUSIONS: The prophylactic use of probiotics may reduce the incidence of NEC in neonates.
OBJECTIVE: Nephrotic syndrome (NS) is characterized by marked urinary excretion of albumin and other intermediated-size plasma proteins such as transferrin. The aim of this study was to determine the changes of serum iron and transferrin and the relationship between the serum and urinary transferrin. METHODS: The indexes related to iron metabolism, including serum iron, ferritin, transferrin, total iron-binding capacity, transferrin saturation and hematological parameters (Hb, MCV, MCH), and urinary transferrin were measured in 37 children with NS before treatment and at the remission stage. Thirty-five age-matched healthy children served as controls. RESULTS: Serum iron levels (18.8±3.8 μmol/L) in NS patients before treatment were significantly lower than in the healthy controls (22.2±3.8 μmol/L) and those measured at the remission stage (21.0±3.5 μmol/L) (P<0.01). Serum transferrin levels in NS patients before therapy (1.9±0.3 g/L) also decreased compared with those in the healthy controls (3.1±0.5 g/L) and those measured at the remission stage (2.9±0.6 g/L) (P<0.01). In contrast, serum total iron-binding capacity and transferrin saturation were noticeably higher in NS patients before treatment than those in the healthy controls (total iron-binding capacity 56.4±9.2 μmol/L vs 50.7±6.8 μmol, P<0.01; transferrin saturation 55.7±9.2 %vs 46.4±8.2%, P<0.01) and were also higher than those measured at the remission stage (51.9±7.7 μmol/L and 47.4±13.3%) (P<0.01). Serum transferrin positively correlated to serum albumin (r=0.609, P<0.01)and negatively correlated to urinary transferrin (r=-0.550, P<0.01) in NS patients before treatment. CONCLUSIONS: Serum iron and transferrin levels markedly decreased in NS patients, which may be partially related to the urinary loss of transferrin.
OBJECTIVE: The present study investigated the behavioral patterns of autistic children during infancy to provide clues for early identification of childhood autism. METHODS: The abnormal behaviors of 30 children with autism and 26 children with other developmental disorders in infancy were investigated. RESULTS: The children with autism presented a series of abnormal behaviors, including no social smile, no eye contact and no respond to own name, and joint attention deficiency, which were distinguished from the children with other developmental disorders. The imitation and attachment behaviors were significantly different between the two groups. Repetitive motor actions and interest peculiarity were only seen in children with autism. CONCLUSIONS: The children with autism may present a series of abnormal behaviors as early as in infancy. The abnormal behaviors facilitate early diagnosis of autism.
OBJECTIVE: To study the relationship between pathogenic bacteria in the nasal middle meatus and acute bacterial respiratory infection in children. METHODS: Three hundred and twenty eight children with respiratory infection (mean age 8 years) were included into the prospective cohort study. The mucosal fluid specimens from the nasal middle meatus were collected under an endoscope for bacterial culture. The patients with bacterial culture positive were defined as the Exposed group and those with bacterial culture negative as the Non-exposed group. The grouping of the patients was blinded to the patients, patients' parents and physicians. Both groups received anti-virus and symptomatic treatments, without antibiotic administration. Five days later, the patients were evaluated as to whether they had bacterial infection based on the leucocyte count and CRP results. RESULTS: Of the 328 patients, 168 had a positive nasal bacterial culture. The incidence of bacterial respiratory infection in the Exposed group [51.2% (86/168)] was significantly higher than in the Non-exposed group [ 13.1% (21/160)] (P<0.01). The relative risk of bacterial respiratory infection occurrence in patients with nasal bacterial culture positive was 3.9002. CONCLUSIONS: The children with respiratory infection who had potential pathogenic bacteria in the nasal middle meatus were more prone to develop bacterial respiratory infection.
OBJECTIVE: This study was designed to investigate the value of serologic examination in the diagnosis of childhood herpes simplexvirus (HSV) infection. METHODS: Serum samples were collected from 2 436 outpatients and inpatients. The samples were divided into two groups. Group 1 consisted of 321 samples which were assayed for HSV-1 IgG, HSV-1 IgM, HSV-2 IgG or HSV-2 IgM antibody using herpes simplex virus antibody kits between January 2003 and November 2005. Group 2 consisted of 2 115 samples which were assayed for HSV-2 IgG and IgM antibodies by TORCH testing between October 2004 and November 2005. RESULTS: In Group 1, the total seroprevalence of HSV infection was 44.6%, with 38.9% being HSV-1 positive and 15.9% HSV-2 positive; HSV-IgM positivity was found in 41.1% and 25.5% were HSV-IgG positive; HSV-1 seroprevalence significantly increased with age (P <0.05). In Group 2 the seroprevalence of HSV-2 infection was 1.9%; all of the samples were HSV-2 IgG positive. CONCLUSIONS: HSV serologic examination is useful in the diagnosis of HSV infection in children.
OBJECTIVE: Immunsuppressive therapy is a major therapy for severe aplastic anemia, and antithymocyte /antilymphocyte globulin (ATG/ALG) is usually used. This study investigated the therapeutic effect of ATG/ALG on severe aplastic anemia and explored the management of therapy-related complications. METHODS: Clinical data of 28 children with severe aplastic anemia who received ATG/ALG treatment from December, 1994 through to September, 2005 were analyzed retrospectively. RESULTS: Of the 28 patients, 2 were nearly cured (7.1%), 4 were relieved (14.3%) and 12 were improved (42.9%) based on a hemoglobin/white blood cell/platelet count. These results represented an overall effective rate of 64.3%. Clinical evidence of serum sickness developed in 19 patients, manifesting as fever (n=9), cutaneous eruptions (n=12), arthralgias (n=7), myalgia (n=7) and arthrocele (n=3). Serum sickness occurred 5-17 days after ATG/ALG administration and lasted for 1-15 days (mean 4.4 days). Three children with mild serum sickness symptoms recovered without any treatment. The symptoms of the other 16 patients disappeared after 3-5 days of methylprednisolone treatment (10 mg/kg daily). However, 3 patients had relapses at 2-4 days after termination of methylprednisolone therapy. Another course of methylprednisolone therapy was administered to the 3 patients until the symptoms disappeared. The patients with no serum sickness or with mild serum sickness had a better response to ATG/ALG therapy than those who had severe serum sickness (100% vs 60%; P<0.05). CONCLUSIONS: ATG/ALG therapy for severe aplastic anemia is effective. Serum sickness is a common complication in children with severe aplastic anemia following ATG/ALG therapy, but can be improved by methylprednisolone application.
OBJECTIVE: To study the effect of valsatan (angiotensin II receptor antagonist, AT1) on hepatocyte growth factor (HGF) in the airways and airway remodeling in asthmatic rats. METHODS: Thirty-two rats were randomly assigned into A-D four groups. Group A was normal control without treatment. Groups B-D were challenged by ovalbumin (OVA) for 2 weeks, 4 weeks and 4 weeks respectively to induce asthma. Group D received intragastric administration of valsatan (30 μg/kg daily for 4 weeks) after OVA challenge. The expressions of HGF, angiotonin II (AngII) and transforming growth factor (TGF-β_1) in the airways were detected by immunihistochemical staining. The pathological changes of airways were observed by Haematoxylin & Eosin staining. RESULTS: The HGF expression of Group B was significantly higher than that of Group A (10.69±0.96% vs 5.49±1.34%; P<0.05). Group C also showed an increased HGF level (11.85±0.87%) compared with Group A (P<0.05). The HGF level in Group D (15.58±1.06%) was significantly higer than that of both Group B and Group C (P<0.05). The expressions of TGF-β_1 and AngII increased with the challenged time, while valsatan treatment decreased significantly the levels of both. Valsatan treatment attenuated airway injuries of asthmatic rats induced by OVA sensitization/challenge. CONCLUSIONS: HGF has protective effects on airways and anti-fibrotic effects. Valsatan can improve airway remodeling possibly by increasing HGF levels in asthmatic rats.
OBJECTIVE: To investigate the effect of inhaled nitric oxide (NO) on surfactant protein A (SP-A) and mannose binding ability (MBA) in neonatal rats with hyperoxia-induced lung injury. METHODS: Sixty-four neonatal rats were randomly exposed to room air (Control group), >95% oxygen for 6 days (Hyperoxia group), 10 ppm NO for 24 hrs (NO group), and >95% oxygen for 6 days along with 10 ppm NO for 24 hrs (Hyperoxia + NO group). After 2 and 6 days of exposure, the lung pathologic changes, gene and protein expressions of SP-A and MBA were measured. RESULTS: The rats from the Hyperoxia group presented with obvious lung injuries. The SP-A expressions of mRNA (0.81 ± 0.04 vs 1.53±0.25) and protein (59.45 ± 18.37 vs 89.77±16.41) in the Hyperoxia group decreased significantly 2 days after exposure but increased significantly 6 days after exposure (SP-A mRNA 0.81±0.02 vs 0.63 ± 0.03; SP-A protein 93.57±13.71 vs 47.73±21.69) compared with those of the Control group (P<0.05). NO treatment alleviated the hyperoxia-induced pathologic injuries 2 days after exposure. The SP-A mRNA expression (0.55±0.91) in the Hyperoxia + NO group was significantly reduced as compared to both the Control and Hyperoxia groups (P<0.05), and the SP-A protein expression (55.12±17.53) in the Hyperoxia + NO group was noticeably lower than that of the Control group ( P<0.01) 2 days after exposure. The SP-A protein expression in the Hyperoxia + NO group (67.33±18.59) was significantly lower than that of the Hyperoxia group 6 days after exposure (P<0.05). Two days after exposure, the NO group had significantly higher MBA than the Control group (0.821 ± 0.133 vs 0.58 ± 0.158); the Hyperoxia + NO group had significantly higher MBA than the Hyperoxia group (0.43 ± 0.175 vs 0.738 ± 0.141) (P<0.05). CONCLUSIONS: Inhaled low dose NO may decrease SP-A protein expression and increase MBA of the lung tissue. This lessens the pathologic lung injury in neonatal rats with hyperoxia.
OBJECTIVE: To investigate the effect of vascular endothelial growth factor (VEGF) on the apoptosis of human acute leukemia HL-60 cell line and to analyze the role of the related apoptosis genes, such as Bcl-2 and Mcl-1, in the process of apoptosis of human acute leukemia cells. METHODS: HL-60 cells were treated with different concentrations of VEGF (2 μg/L, 20 μg/L or 100 μg/L ) or 20 mg/L of etoposide (VP16, an apoptosis inducter) alone or VEGF plus VP16. After 18 hrs of treatment, the apoptosis rate of HL-60 cells was detected by single-cell gel electrophoresis and flow cytometry. The expressions of Bcl-2 and Mcl-1 of HL-60 cells were detected by RT-PCR. The Control group did not receive any treatment. Immunocytochemistry was used to detect the VEGF and Mcl-1 protein in bone marrow cells from 8 patients with newly diagnosed or relapsed leukemia, 14 leukemia patients in complete remission, and from 5 normal children. RESULTS: Different concentrations of VEGF markedly inhibited the apoptosis of HL-60 cells and decreased the apoptosis induced by VP16 exposure. The Bcl-2 and Mcl-1 mRNA and protein in HL-60 cells treated with VEGF were significantly higher than those in the Control group. The expressions of VEGF and Mcl-1 protein in bone marrow cells of the newly diagnosed and relapsed patients were significantly higher than in patients in complete remission. CONCLUSIONS: VEGF can inhibit the apoptosis of HL-60 cells possibly through increasing the expressions of Bcl-2 and Mcl-1 mRNA and protein, which may represent one of the mechanisms responsible for human acute leukemia. The expressions of VEGF, Bcl-2 and Mcl-1 might be used as the markers for the prognostic evaluation of leukemia.
OBJECTIVE: To study the effect of glutamine on intestinal epithelial apoptosis by examining changes regarding Bcl-2 and Bax mRNA expressions in the small intestine of young rats with endotoxemia and to explore the protective mechanism that glutamine may have. METHODS: A total of 120 18-day-old rats were randomly assigned into Endotoxemia, Glutamine-treated and Control groups (n=40 each). The endotoxemia model was established by intraperitoneal injection of endotoxin (4 mg/kg of O55B5 Escherichia coli lipopolysaccharide). Rats in the Glutamine-treated group were intraperitoneally injected with N(2)-L-alanyl-L-glutamine (2 g/kg) along with endotoxin. Rats in the Control group were intraperitoneally injected with an equal volume of normal saline. The entire ileum was collected at 2, 4, 6, 24, and 72 hrs after injection. Bcl-2 and Bax mRNA expressions were detected by semi-quantities reverse transcriptase chain reaction. RESULTS: Bcl-2 mRNA was not expressed in the Control and the Endotoxemia groups but increased in the Glutamine-treated group at each time point.Bax mRNA expression was weak in the Control group, and significantly increased in the Endotoxemia group at each time point.The Glutamine-treated group showed noticeably reduced Bax mRNA expression at 2 hrs post-injection while other time points were similar to the Control group. The ratio of Bax and Bcl-2 mRNA expression at each time point in the Endotoxemia group was significantly higher than that in the Control group while the Glutamine-treated group demonstrated significantly lower ratio of Bax and Bcl-2 mRNA expression than both. CONCLUSIONS: Glutamine treatment increased Bcl-2 mRNA expression and decreased Bax mRNA expression, as a result, the ratio of Bax and Bcl-2 mRNA expression decreased. The effects of glutamine resulted in a suppression of intestinal epithelial apoptosis and maintained the integrity of the gut barrier structure.
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