Nutritional assessment and clinical application of nutritional risk screening tools in critically ill children / 中国当代儿科杂志

OBJECTIVE@#To investigate the nutritional status of critically ill hospitalized children and to explore the value of nutritional risk screening tools in the nutritional risk assessment.@*METHODS@#The clinical data of 211 critically ill children who were admitted to the pediatric intensive care unit from November 2017 to April 2018 were collected to evaluate their nutritional status on admission and at discharge. Two nutritional risk screening tools, STRONGkids and PYMS, were used for nutritional risk screening in the 211 children.@*RESULTS@#Among the 211 patients, 68 (32.2%) were found to have malnutrition on admission, with 34 cases each of moderate and severe malnutrition. Moderate or high nutritional risk was found in 154 cases (73.0%) with STRONGkids and 165 cases (78.2%) with PYMS. Using weight-for-age Z-score as the gold standard to evaluate the efficacy of the two nutritional risk screening tools, the areas under the receiver operating characteristic curves of STRONGkids and PYMS were 0.822 and 0.759 respectively. Both tools had a significant clinical value in screening for malnutrition (P0.05). With the optimal cut-off value of 3 points, the sensitivities of STRONGkids and PYMS for screening of malnutrition were 92.1% and 76.2% respectively. The children with moderate or high nutritional risk on admission had a significantly poorer prognosis than those with low nutritional risk (P=0.014 and 0.001 respectively). The children with severe malnutrition had a significantly poorer prognosis than those with normal nutrition (P=0.0009).@*CONCLUSIONS@#The detection rates of malnutrition and nutritional risk are high in critically ill children. Malnutrition/high nutritional risk is related to a poor prognosis. Both STRONGkids and PYMS have a clinical value for nutritional risk screening in critically ill children, and they have similar clinical efficacy; however, STRONGkids is more sensitive.

HMGB1/TLR4/NF-κB signaling pathway and role of vitamin D in asthmatic mice / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the changes in the mRNA and protein expression of high-mobility group box 1 (HMGB1), Toll-like receptor 4 (TLR4), and nuclear factor-kappa B (NF-κB) in lung tissues of asthmatic mice and the interventional effect of vitamin D.</p><p><b>METHODS</b>A total of 48 BALB/c mice were randomly divided into control group, asthma group, and 1,25-(OH)Dintervention group, with 16 mice in each group. An animal model of asthma was established, and lung tissue samples were taken in each group at weeks 1 and 2 of ovalbumin challenging. Conventional hematoxylin-eosin staining was used to measure airway wall thickness. Immunohistochemical staining was used to observe the expression of HMGB1, TLR4, and NF-κB in lung tissues. Quantitative real-time PCR and Western blot were used to investigate the changes in the mRNA and protein expression of HMGB1, TLR4, and NF-κB.</p><p><b>RESULTS</b>At weeks 1 and 2 of ovalbumin challenging, compared with the control group, the asthma group had a significant increase in airway wall thickness and the intervention group had a significant reduction compared with the asthma group (P<0.05). The asthma group had significantly higher mRNA expression of HMGB1, TLR4, and NF-κB in lung tissues than the control group, and the intervention group had significantly lower mRNA expression of TLR4 and NF-κB than the asthma group (P<0.05). At week 1 of ovalbumin challenging, there was no significant difference in the mRNA expression of HMGB1 between the intervention group and the asthma group (P>0.05). At week 2, the intervention group had a significant reduction in the mRNA expression of HMGB1 compared with the asthma group (P<0.05). At weeks 1 and 2 of ovalbumin challenging, the asthma group had significantly higher protein expression of HMGB1, TLR4, and NF-κB in lung tissues than the control group, and the intervention group had significantly lower expression than the asthma group (P<0.05). Airway wall thickness was positively correlated with the mRNA expression of HMGB1, TLR4, and NF-κB in lung tissues (r=0.804, 0.895, and 0.834; P<0.05).</p><p><b>CONCLUSIONS</b>The HMGB1/TLR4/NF-κB signaling pathway plays an important role in the pathogenesis of asthma, and an appropriate amount of 1,25-(OH)Dhas a regulatory effect on this pathway and may prevent the progression of asthma. Therefore, 1,25-(OH)Dis expected to become a new choice for the treatment of asthma.</p>

Relationship of HMGB1 and TLR4 with airway inflammation in asthma and the role of vitamin D / 西安交通大学学报(医学版)

Objective To evaluate the relationship of high mobility group box 1 (HMGB1) and TLR4 with airway inflammation and the role of vitamin D.Methods Totally 24 BALB/c mice were randomly divided into control group,asthma group,and 1,25-(OH)2D3 group,each having 8 mice.The pathological changes in lung tissue of the mice were observed by hematoxylin-eosin (HE) staining,bronchial wall thickness was measured with computer pathological image analysis system software.The expressions of HMGB1 and TLR4 in lung tissue were detected by immunohistochemical method.Bronchoalveolar lavage fluid (BALF) was collected for cytological examination;the contents of HMGB1,TLR4,IL-4 and IFN-γ in BALF and the peripheral blood were detected by enzyme-linked immunosorbent assay (ELISA).Results The expressions of HMGB1 and TLR4 in lung tissue were stronger in asthma group,but weaker in intervention group.The total number of leukocytes as well as the percentages of eosinophils,neutrophils and lymphocytes increased significantly in BALF in asthma group,but significantly decreased in intervention group (all P ＜ 0.05).The ratio of monocyte/macrophage significantly decreased in asthma group,but increased significantly in intervention group (P＜0.05).The contents of HMGB1,TLR4 and IL-4 in BALF and the peripheral blood were significantly higher in asthma group than in control and intervention groups,whereas IFN-γ level was significantly lower than that in control and intervention groups (all P＜0.05).HMGB1 and TLR4 contents had a positive correlation with the total number of cells and IL-4 concentration in BALF,respectively (r1=0.796,0.730;r2=0.695,0.648;all P＜0.05).Conclusion HMGB1 and TLR4 were associated with airway inflammation and immune disorders.An appropriate amount of 1,25-(OH)2D3 can relieve airway inflammation,which may be associated with regulating Th1/Th2 cells balance.

The tidal breathing lung function changes and clinical significance of severe pneumonia in infants and young children during convalescent period / 中华实用儿科临床杂志

Objective To investigate the changes in tidal breathing lung function of severe pneumonia in re-covery phase and correlation with the condition and prognosis in infants and the young children.Methods Tidal breathing lung function of 44 cases of severe pneumonia infants and 50 cases of mild pneumonia infants in their recovery phase were measured by infantile spirometer made in Germany.According to ratio of exhaled volume at peak tidal expi-ratory flow to total expiratory volume(VPTEF /VE),severe pneumonia infants were divided into normal,mild,moderate and severe groups.All these children were followed up for the frequency of rehospitalization because of lower respiratory tract infections and the frequency of wheezing within 1 year after discharge.Statistical were analyzed by using t test andχ2 test.Results Compared with the mild pneumonia infants,the respiratory rate(RR)of the severe pneumonia infants was significantly increased [(36.31 ±0.78)times/min vs (30.83 ±0.74)times/min](P 0.05).Thirteen cases of se-vere pneumonia infants were followed up for 1 year.Of all these 1 3 cases,pulmonary function in 1 case restored to nor-mal within 3 months;that of 6 cases restored to normal within 6 months;the conditions of 3 cases restored to normal within 1 year;while the pulmonary function of other 3 cases was still abnormal 1 year after discharge.Conclusions Lung function damage of severe pneumonia infants is more serious than the mild pneumonia in infants in their recovery phase.For severe pneumonia infants,the more serious of lung function damages,the more likely to be re -hospitaliza-tion because of lower respiratory tract infections and wheezing in short time.

Effects of different doses of 1,25-(OH)2D3 on expression of HMGB1 and IL-17 in the lungs of asthmatic mice / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the effects of 1,25-(OH)(2)D(3) on airway remodeling and expression of high mobility group box 1 (HMGB1) and IL-17 in asthmatic mice.</p><p><b>METHODS</b>Fifty female mice were randomly divided into 5 groups: control, asthma, low-dose, middle-dose, and high-dose intervention groups (n=10 each). Asthma was induced by intraperitoneal injections of ovalbumin (OVA) and aerosol inhalation of OVA solution. The low-dose, middle-dose, and high-dose intervention groups were administered with 1,25-(OH)(2)D(3) solution at the dosage of 1, 4 and 10 μg/kg respectively by intraperitoneal injections before asthma challenge. The airway structural changes were assessed by hematoxylin and eosin staining. mRNA expression levels of HMGB1 and IL-17 in the lung tissues were evaluated by RT-PCR. The protein levels of HMGB1 and IL-17 in the lung tissues were observed by immunohistochemistry.</p><p><b>RESULTS</b>The airway wall thickness, protein and mRNA expression levels of HMGB1 and IL-17 were higher in the untreated asthma group than in the control group (P<0.05). The airway wall thickness, protein and mRNA expression levels of HMGB1 and IL-17 were lower in the middle-dose and low-dose intervention groups than in the untreated asthma group, and the middle-dose intervention group demonstrated lower airway wall thickness, protein and mRNA expression levels of HMGB1 and IL-17 than in the low-dose intervention group (P<0.05). However, the airway wall thickness, protein and mRNA expression levels of HMGB1 and IL-17 in the high-dose intervention group were higher than in the untreated asthma group (P<0.05).</p><p><b>CONCLUSIONS</b>HMGB1 and IL-17 may be involved in the airway remodeling process in asthmatic mice. A moderate amount of HMGB1 and IL-17 may be involved in the airway remodeling process in asthmatic mice. A moderate amount of 1,25-(OH)(2)D(3) can improve the airway remodeling, but a higher dose of 1,25-(OH)(2)D(3) may affect adversely the airway remodeling process.</p>

Study of genetic susceptibility in 135 children with allergic asthma / 国际儿科学杂志

Objective To discuss the frequency distribution of single nucleotide polymorphisms (SNP) of four asthma-related gene loci in asthmatic children of Henan,and to investigate its association with genetic susceptibility to childhood asthma and some clinical phenotypes of asthma Methods Fluorogenic quantitative PCR and sequencing technique were employed to detect the frequency distributions of the SNP of the four asthma-related gene loci in 135 asthmatic children and 98 healthy controls.Results The genotype DD of angiotensin-converting enzyme (ACE)had a significantly higher frequency in the asthmatic children than in the healthy controls (x2 =26.475,P ＜ 0.01),and the frequency of D allele was also significantly higher in the asthmatic children than in the healthy controls (x2 =24.242,P ＜0.01).The genotype AG of Adrenaline receptor beta 2 subtypes (ADRB2) had a significantly higher frequency in the asthmatic children than in the healthy controls (x2 =22.505,P ＜0.01),and the frequency of allele was also significantly higher in the asthmatic children than in the healthy controls (x2 =6.759,P ＜ 0.01).Conclusions Genotype DD of ACE and genotype AG of ADRB2 are related to genetic susceptibility to childhood asthma and may be the risk factor for childhood asthma of Henan.Another two asthma genes involved in this study are not be able to repeat.

Effect of 1,25-(OH)2D3 on expression of HMGB1 and TLR4 in the lungs of asthmatic mice / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the effects of 1,25-(OH)(2)D(3) on the airway remodeling and expression of high-mobility group box 1 (HMGB1) and Toll-like receptor 4 (TLR4) in the lungs among asthmatic mice.</p><p><b>METHODS</b>Thirty female mice (BALB/c strain) were randomly divided into control, asthma and 1,25-(OH)(2)D(3) intervention groups. An asthmatic mouse model was established by intraperitoneal injection and aerosol inhalation of ovalbumin. The intervention group was given 1,25-(OH)(2)D(3) by intraperitoneal injection 0.5 hour before each aerosol inhalation, while the control group used normal saline instead. The hematoxylin-eosin staining was used to observe the mouse airway structural changes. The mRNA and protein expression of HMGB1 and TLR4 was measured by RT-PCR and immunohistochemistry, respectively. Pearson correlation analysis was performed.</p><p><b>RESULTS</b>The asthma group had a significantly increased airway wall thickness compared with the control group (P<0.05); the intervention group had a significantly lower increase in airway wall thickness than the asthma group (P<0.05). The mRNA and protein expression of HMGB1 and TLR4 was significantly higher in the asthma group than in the control group (P<0.05); the mRNA and protein expression of HMGB1 and TLR4 in the intervention group was significantly lower than that in the asthma group, but still higher than that in the control group (P<0.05). A positive correlation was found between the protein expression of HMGB1 and TLR4 (P<0.01), and so was their mRNA expression (P<0.01).</p><p><b>CONCLUSIONS</b>HMGB1 and TLR4 may be involved in asthmatic airway remodeling. 1,25-(OH)(2)D(3) can reduce the airway remodeling in asthmatic mice, which may be related to the downregulation of HMGB1 and TLR4 expression in the lungs of asthmatic mice.</p>

Effect of 1,25-(OH)2D3 on expression of TIM-4 in the lungs of asthmatic mice / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To establish a mouse model of asthmatic airway remodeling and investigate the effects of 1,25-(OH)2D3 on airway structure and T cell immunoglobulin mucin protein-4 (TIM-4) expression in asthmatic mice.</p><p><b>METHODS</b>Thirty female mice (BALB/c strain) were randomly divided into control, asthma and 1,25-(OH)2D3 intervention groups. An asthmatic mouse model was induced using ovalbumin. Lung tissue of the mice was collected, mRNA expression of TIM-4 was evaluated by RT-PCR and airway remodeling and protein expression of TIM-4 were observed by hematoxylineosin staining and immunohistochemistry.</p><p><b>RESULTS</b>Typical airway remodeling was found in the asthma group, and TIM-4 expression in this group was significantly higher than in the control group (105±9 vs 42±5; P<0.05). Compared with the asthma group, the 1,25-(OH)2D3 intervention group showed improvement in airway remodeling and a decrease in TIM-4 expression (78±6) (P<0.05).</p><p><b>CONCLUSIONS</b>TIM-4 may be involved in the airway remodeling of mice. As a new type of immunoregulator, 1,25-(OH)2D3 can downregulate expression of TIM-4 in the lungs and improve airway remodeling in asthmatic mice.</p>

Effects of bacterial lipopolysaccharide on serum IL-4, serum IL-8 and pulmonary VEGF expression in mice with asthma / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the regulatory role of bacterial lipopolysaccharide (LPS ) in the development of bronchial asthma by examining the effects of LPS on serum IL-4, serum IL-8 and pulmonary vascular endothelial growth factor (VEGF) expression in mice with asthma.</p><p><b>METHODS</b>Twenty-seven BALB/c mice were randomly assigned into control, asthma and LPS-treated asthma groups (n=9 each). Serum IL-4 and IL-8 concentrations were measured using ELISA. VEGF expression in lung tissues was examined using the immunohistochemical method.</p><p><b>RESULTS</b>Serum IL-4 and IL-8 concentrations in the asthma group were significantly higher than in the control group (P<0.05). LPS treatment significantly decreased serum IL-4 and IL-8 concentrations compared with the asthma group (P<0.05), although levels were significantly higher than in the control group (P<0.05). Airway VEGF expression in the asthma group was significantly higher than in the control group (P<0.05). LPS treatment significantly decreased airway VEGF expression compared with the asthma group (P<0.05), although concentrations remained higher than in the control group (P<0.05).</p><p><b>CONCLUSIONS</b>LPS can decrease serum IL-4, serum IL-8 and pulmonary VEGF expression in mice with asthma, and thus can possibly reduce both airway inflammation and airway vascular remodeling.</p>

Roles of FIZZ1 and NOTCH1 in asthma / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the roles of FIZZ1 and NOTCH1 in the pathogenesis of asthma and the effect of rosiglitazone on airway remodeling.</p><p><b>METHODS</b>Forty-five healthy 6 to 8-week-old Sprague-Dawley rats were randomly divided into a control group and asthma groups with and without rosiglitazone treatment. The paraffin slices of lung tissues were made to assess the histological changes. a-SMA protein, a specific marker of airway remodeling, in lung tissues was measured by immunohistochemistry. FIZZl-mRNA and NOTCH1-mRNA expression in lung tissues was measured by RT-PCR.</p><p><b>RESULTS</b>The characteristic changes of airway remodeling were observed in the untreated asthma group. The histological changes in the airway were less severe in the rosiglitazone treated asthma group. Positive a-SMA staining, FIZZl-mRNA and NOTCH1-mRNA were highly expressed in peribronchial lung sections isolated from the untreated asthma group. Rosiglitazone treatment decreased significantly the expression of a-SMA protein, FIZZl-mRNA and NOTCH1-mRNA compared with the untreated asthma group, but the expression of a-SMA protein, FIZZl-mRNA and NOTCH1-mRNA in the rosiglitazone treated asthma group remained higher than the control group. a-SMA expression was positively correlated with FIZZl-mRNA (r=0.826, P<0.01) and NOTCH1-mRNA expression (r=0.9, P<0.01). FIZZl-mRNA expression was positively correlated with NOTCH1-mRNA expression (r=0.76, P<0.01).</p><p><b>CONCLUSIONS</b>FIZZl and NOTCH1 may induce an increase in a-SMA expression. FIZZl and NOTCH1 play a critical role in the process of airway remodeling. Rosiglitazone treatment may inhibit airway remodeling in asthmatic rats.</p>

Effects of electric stimulation at the cerebellar fastigial nucleus on astrocytes in the hippocampus of neonatal rats with hypoxic-ischemic brain damage / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the effects of electric stimulation at the cerebellar fastigial nucleus on astrocytes in the hippocampus of neonatal rats with hypoxic-ischemic brain damage (HIBD) and the possible mechanism.</p><p><b>METHODS</b>One hundred and eighty 7-day-old neonatal Sprague-Dawley rats were randomly divided into three groups: sham-operation (control group) and HIBD with and without electric stimulation (n=60 each). The HIBD model of neonatal rats was prepared by the Rice-Vennucci method. Electric stimulation at the cerebellar fastigial nucleus was given 24 hrs after the operation in the electric stimulation group once daily and lasted for 30 minutes each time. The other two groups were not subjected to electric stimulation but captured to fix in corresponding periods. Rats were sacrificed 3, 7, 14 and 21 days after stimulations to observe the glial fibrillary acidic protein (GFAP) expression by immunohistochemisty and the ultrastructural changes of astrocytes in the hippocampus under an electron microscope.</p><p><b>RESULTS</b>Immunohistochemical analysis showed the expression of GFAP in the HIBD groups with and without electric stimulation increased significantly compared with the control group on day 3, reached the peak on day 7, and the increased expression remained till to day 21. The GFAP expression in the electric stimulation group was significantly lower than that in the untreated HIBD group at all time points. Under the electron microscope, the astrocytes in the untreated HIBD group were swollen and the amount of organelles was reduced, while the swelling of astrocytes was alleviated and the organelles remained in integrity in the electric stimulation group.</p><p><b>CONCLUSIONS</b>The electric stimulation at the cerebellar fastigial nucleus can inhibit the excessive proliferation of astrocytes and relieve the structural damage of astrocytes in neonatal rats following HIBD.</p>

Expression of Galectin-9 and Tim-3 in lungs of mice with asthma / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the expression of Galectin-9 and Tim-3 in lungs of mice with asthma and the effect of rosiglitazone (PPAR-γ agonist) on their expression.</p><p><b>METHODS</b>Fortyfive BALB/c SPF female mice were randomized into control group and asthma groups with and without rosiglitazone intervention. After ovalbumin stimulation and rosiglitazone intervention the pathological changes of the lung tissues were observed. Galectin-9 and Tim-3 mRNA levels in lung tissues were determined using RT-PCR. The levels of IL-4 and IFN-γ in peripheral blood were measured using ELISA.</p><p><b>RESULTS</b>The expression of Galectin-9 and Tim-3 mRNA of lung tissues in the untreated asthma group increased significantly compared with the control and the rosiglitazone treated groups (P<0.05). A significantly increased blood expression of IL-4 and a significantly decreased blood expression of IFN-γ were found in the untreated asthma group compared with the control and the rosiglitazone-treated groups (P<0.05). The expression of Galectin-9 and Tim-3 mRNA was positively correlated with blood IL-4 level (r=0.792, r=0.794 respectively; P<0.05), but negatively correlated with blood IFN-γ level (r=-0.692, r=-0.757 respectively; P<0.05).</p><p><b>CONCLUSIONS</b>Galectin-9 and Tim-3 mRNA levels in lungs increase in mice with asthma and significantly correlate with the levels of blood Th1/Th2 cytokines. This suggests that Galectin-9 and Tim-3 are closely related to inflammatory process in asthma. Rosiglitazone treatment may decrease the expression of Galectin-9 and Tim-3.</p>

Effects of levetiracetam on the expression of NCAM and GAP-43 mRNA in the hippocampus of rats with epilepsy / 中国当代儿科杂志

<p><b>OBJECTIVE</b>This study explored the effects of levetiracetam (LEV) on the expression of nerve cell adhesion molecule (NCAM) and growth-associated protein 43 (GAP-43) mRNA in the hippocampus of rats with epilepsy induced by lithium-pilocarpine (Li-PILO) in order to provide a basis for investigating the antiepileptic mechanism of LEV and its doseresponse.</p><p><b>METHODS</b>Forty-eight Wistar rats were randomly divided into a normal control, a Li-PILO model and two LEV treatment groups (LEV: 150 and 300 mg/kg) (n=12 each). The LEV treatment groups received LEV by intragastric administration 6 hrs after status epilepticus (once daily for 2 two weeks). The expressions of NCAM and GAP-43 mRNA in the hippocampus was determined by real-time PCR.</p><p><b>RESULTS</b>The expression of NCAM and GAP-43 mRNA in the Li-PILO model group was significantly higher than in the normal control group (P<0.05). LEV treatment of 150 and 300 mg/kg significantly decreased the expression of NCAM and GAP-43 mRNA compared with the Li-PILO model group (P<0.05). The LEV treatment group at the dose of 300 mg/kg showed significantly lower expression of NCAM and GAP-43 mRNA than the 150 mg/kg LEV treatment group (P<0.05).</p><p><b>CONCLUSIONS</b>Li-PILO can up-regulate the expressions of NCAM and GAP-43 mRNA in the hippocampus of rats with epilepsy. LEV can inhibit the expression of NCAM and GAP-43 mRNA and the effect is associated with the dose of LEV.</p>

The presence of Ureaplasma urealyticum and Mycoplasma honinis in umbilical cord and the association with the outcome of premature infant / 中华微生物学和免疫学杂志

Objective To evaluate the frequency of the infections with Ureaplasma urealyticum and/or Mycoplasma honinis in preterm 23 to 32 week births and the association with the outcomes of new born. Methods One hundred and eighty-seven mother/premature infant dyads with deliveries between 23 and 32 weeks gestational age. Ueaplasma urealyticum, Mycoplasma honinis and IL-6 were determined by PCR and radioimmunity. Medical information and outcome of newborns were recorded. Results Compared with control group, the incidence of Ureaplasma urealyticum and/or Mycoplasma honinis, IL-6 and preterm premature rupture of the fetalmembranes ( PPROM ) were higher in spontaneous group. The PPROM were more common among infants with a positive Ureaplasma urealyticum and/or Mycoplasma honinis. Infants with positive cord blood Ureaplasma urealyticum and/or Mycoplasma honinis were likely to have neonatal systemic inflammatory response syndrome (SIRS) and bronchopulmonary dysplasia (BPD), but not significantly different for respiratory distress syndrome (RDS). Conclusion Infection with Ureaplasma urealyticum and/or Mycoplasma honinis may play an important role in the causal pathway for spontaneous preterm labor, and impact the outcome of premature infants.

Effect of epidermal growth factor receptor on airway remodeling in asthmatic mice and its mechanism / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To explore the relationship of airway remodeling with epidermal growth factor receptor (EGFR) and heparin-binding epidermal growth factor-like growth factor (HB-EGF) levels in asthmatic mice and the effect of EGFR tyrosine kinase inhibitor (AG1478) on airway remodeling.</p><p><b>METHODS</b>Twenty-four male BALB/c mice were randomly divided into three groups: normal control, asthma, AG1478-treated. Mice were sensitized and challenged with ovalbumin (OVA) and a mouse mode1 of asthma was prepared. Collagen deposition was determined in Masson-stained lung sections. Periodic acid Schiff (PAS) staining was used to observe the proliferation of goblet cells. Immunohistochemistry was used to determine the protein expression of HB-EGF. RT-PCR was used to determine the mRNA expression of HB-EGF and EGFR.</p><p><b>RESULTS</b>The characteristic changes of airway remodeling occurred in the asthma group. The expression of HB-EGF and EGFR in the epithelial cells of bronchi in the asthma group was significantly higher than that in the normal control group. Compared with the asthma group, the AG1478-treated group had decreased inflammation reactions, decreased collagen deposition and proliferation of goblet cells and lower expression of EGFR and HB-EGF.</p><p><b>CONCLUSIONS</b>EGFR tyrosine kinase inhibitor (AG1478) ameliorates the progression of airway remodeling in mice with asthma by inhibitions of EGFR and HB-EGF expression and EGFR signal pathway.</p>

Expression of stromal cell derived factor-1 and CXC chemokine receptor 4 and the effects of budesonide on their expression in mice with asthma / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the expression of stromal cell derived factor-1(SDF-1) and CXC chemokine receptor 4 (CXCR4) in the airway and the effect of budesonide on their expression in mice with asthma.</p><p><b>METHODS</b>Thirty BALB/c male mices were randomly divided into three groups: placebo control, untreated asthma, and budesonide-treated asthma. The asthma group were induced by intraperitoneal injection of 10% ovalbumin (OVA ) on days 1, 8 and 15, and then from days 22 to 34, challenged by inhalation of 2% OVA aerosol every other day. The budesonide-treated asthma group received an inhalation of budesonide (1 mg ) before OVA challenge. The pathological changes of the airway were assessed by hematoxylin and eosin staining. The immunohistochemistry was used to estimate the expression of SDF-1 in the lung. RT-PCR was used to evaluate the expression of CXCR4 in the lung.</p><p><b>RESULTS</b>Compared with the control group, SDF-1 and CXCR4 expression in the lung in the untreated asthma group increased significantly (p<0.05). The budesonide-treated asthma group demonstrated significantly decreased SDF-1 (0.426+/-0.052 vs 0.361+/-0.065; p<0.05) and CXCR4 (0.829+/-0.027 vs 0.723+/-0.094; p<0.05) expression in the lung as compared with the untreated asthma group. Both SDF-1 (r=0.744, p<0.01) and CXCR4 (r=0.553, p<0.01)were positively correlated with the thickness of the airway wall.</p><p><b>CONCLUSIONS</b>SDF-1 and CXCR4 may be associated with airway remodeling in mice with asthma. Budesonide can improve airway remodeling, possibly by decreasing the expression of SDF-1 and CXCR4.</p>

Expression of regulatory T cells and Foxp3 gene in peripheral blood of children with aplastic anemia / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To investigate the levels of CD4+CD25+CD127(low) regulatory T cells (Tregs) and the expression of Foxp3 gene in peripheral blood of children with aplastic anemia (AA) and to study their roles in the pathogenesis of AA.</p><p><b>METHODS</b>Twenty-one children with chronic AA, 9 with acute AA and 15 healthy children were enrolled. The proportion of CD4+CD25+ CD127low Tregs in CD4+ T cells was evaluated by flow cytometric analysis. The level of Foxp3 mRNA was ascertained by RT-PCR.</p><p><b>RESULTS</b>The percentage of peripheral blood CD4+T cells and CD4+CD25+ and CD4+CD25+CD127(low) Tregs in CD4+T cells in both the acute and chronic AA groups was significantly lower than that in the normal control group (P<0.05).The acute AA group had more decreased CD4+ T cells and CD4+CD25+ and CD4+CD25+CD127(low) Tregs percentage compared with the CAA group (P<0.05). The expression of Foxp3 mRNA in peripheral blood decreased obviously in the acute AA group (0.47 + or - 0.08%) compared with that in the normal control (0.71 + or - 0.12%) and the CAA groups (0.68 + or - 0.14%) (P<0.05).</p><p><b>CONCLUSIONS</b>The low expression of Tregs and Foxp3 mRNA in peripheral blood may be involved in pathogenesis of AA.The more decreased Tregs and Foxp3 mRNA expression in acute AA than chronic AA suggests their possible roles in the assessment of the severity of AA.</p>

Expression of basic fibroblast growth factor and nuclear factor-kappaB and the effect of budesonide on their expression in rats with asthma / 中国当代儿科杂志

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

Study of pathogen aetiology and drugs resistance in neonatal septicemia / 中国综合临床

Objective To study pathogen aetiology and distribution of drug resistance in neonatal septice-mia. Methods A retrospective study of positive organisms of blood cultures and the results of antimicrobial suscep-tibility testing was conducted from January 2000 to December 2006 in 1293 cases of neonatal septicemia;The results were divided into three groups:the earlier group,the middle group and the later group. The strains were identified by VITEK-AMS and antibiotics susceptibility was tested by K-B method, results were interpreted according to NCCLS. inant in three groups(76.3% ,74.1% and 65.7% ) (P <0.05). Among Gram-pesitive coccus,the most prevalent strains was staphylococcus, Gram-negative bacilli increased gradually,accounting for 21.3% ,21.3% and 28.4% in cpidermids to erythromycin and sulfamethoxazole/trimethoprim were rather higher:93.3% ,73.7% vs 87.8% vs 100.0%, respectively, the resistance -rates to penicillin were less,but to susceptible to vancomyein,piperacill/tazo-batam,amikacinand ciprofloxacin;gram-negative bacilli were only sensitible to imipenem, cefepime, and cefopera zone/sulbactam;multiresistances of drug strains was commonly seen. Condusions It is important for using antibi-otics rationally according to drug sensitivity test, because multiresistant strains and opportunistic pathogen are com-monly seen.

Expression of angiopoietin-1 and its tyrosine kinase receptor Tie-2 in the airway of asthmatic rats / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To study the effect of dexamethasone on airway morphology and on the expression of angiopoietin-1 (Ang-1) and its tyrosine kinase receptor Tie-2 in the airway of asthmatic rats.</p><p><b>METHODS</b>Forty-five Sprague-Dawley rats were randomly divided into control, asthmatic, and dexamethasone-treated asthmatic groups. Asthma was induced by repeated sensitization and challenge with ovalbumin in the latter two groups. The dexamethasone intervention group received an intraperitonea injection of dexamethasone (2 mg/kg) before asthma challenge. Immunohistochemistry was used to measure the expression of Ang-1 and Tie-2 in the airway. Airway thickness was estimated by a computerized digital image analyzer.</p><p><b>RESULTS</b>Airway thickness in the asthmatic group (33.9333+/-8.3791 micro m2/micro m) increased significantly compared with that in the control group (21.1333+/-2.7740 micro m2/micro m) (P<0.01). The dexamethasone intervention group also showed increased thickness of the airway (27.4000 +/- 4.6105 micro m2/micro m) compared with the control group (P<0.01), but the airway thickness in the dexamethasone intervention group was significantly reduced compared with that in the untreated asthmatic group (P<0.01). The expression of Ang-1 (103.9487+/-8.2914 vs 76.0320+/-3.7728; P<0.01) and Tie-2 (99.2307+/-8.1913 vs 75.3153+/-3.7321; P<0.01) in the airway increased significantly in the asthmatic group compared to controls. The expression of Ang-1 and Tie-2 in the airway of the dexamethasone intervention group (90.6180+/-5.2339 and 86.6633+/-3.7321, respectively) was statistically higher than that in the control group (P<0.01) but statistically lower than that in the untreated asthmatic group (P<0.01). Ang-1 and Tie-2 expression in the airway was positively correlated with the thickness of airway (r(Ang)-1=0.719r(Tie)-2=0.746P<0.01). There was also a positive correlation between Ang-1 and Tie-2 expression (r=0.742P<0.01).</p><p><b>CONCLUSIONS</b>The expression of Ang-1 and Tie-2 in the airway increased in asthmatic rats and was positively correlated with the thickness of the airway. Ang-1 and Tie-2 may participate in the process of airway remodeling in asthma. Dexamethasone can decrease the expression of Ang-1 and Tie-2 in the airway and relieve the changes of airway morphology.</p>