No abstract available
The guideline provides evidence-based recommendations for parenteral and enteral nutrition to neonates in a critical state. It is developed by the interdisciplinary expert group in accordance with officially accepted standards based on various relevant literatures. The guideline is organized into the following sections: enteral nutrition (EN) support, parenteral nutrition (PN) support and a combination of PN & EN support. The EN or PN therapy provides appropriate energy and nutrients to babies that cannot be fed by oral route. For the premature and the very low birth weight infants with delayed gastric emptying and intestinal peristalsis, neurological immaturity and respiratory compromise, the PN therapy is the only choice. The formula to calculate the calorie supplement by PN is offered in the guideline when a combination of PN & EN support is administered.
OBJECTIVE: To study a possible association between the three functional polymorphisms in the promoter region of dopamine D4 receptor (DRD4) gene and chronic tic disorder. METHODS: Genomic DNA was isolated from the venous blood leukocytes of 84 unrelated patients with chronic tic disorder (Study group) and 100 healthy unrelated individuals (Control group). Polymorphisms of DRD4, -1240L/S, -616C/G and -521C/T, were genotyped by the allele-specific primer (ASP) PCR. Genotype, allele and haplotype frequencies were analysed by SHEsis online. RESULTS: There were significant differences in both allele and genotype frequencies (χ~2 =8.419, P<0.01;χ~2=7.860, P<0.05 respectively) of DRD4-616C/G between the Study and the Control groups. Haplotypic frequencies of LCT (-1240L/S, -616C/G, -521C/T) in the Study group were noticeably higher than in the Control group (χ~2 =6.371, P<0.05). CONCLUSIONS: There is an association between the DRD4-616C/G polymorphism and chronic tic disorder. The individuals with haplotype LCT (-1240L/S, -616C/G, -521C/T) are susceptible to this disorder.
OBJECTIVE: To compare the differences in cerebral oxygenation responses between the infants born preterm and full-term infants and to evaluate the early cognitive ability of infants born preterm. METHODS: Cerebral oxygenation after light stimulation was detected by near infrared spectroscopy (NIRS) in preterm infants at 3 or 6 months corrected gestational age (GA). The results were compared with those of age-matched infants born at term. RESULTS: The start and peak response time of cerebral oxygenation occurring after light stimulation in preterm infants at 3 months corrected GA was 17.2±5.2 and 38.4±9.6 seconds respectively, which were significantly longer than in age-matched term infants (13.1± 2.7 and 28.9±5.0 seconds respectively) (P<0.05). The maximum response value of hemoglobin, oxyhemoglobin and regional oxygen saturation of the preterm infants at 3 months corrected GA was (1.2±0.5)%, (1.5±0.6)%, and (1.3±0.4) % respectively , which were significantly lower than that of the term infants [(2.3±0.3)%, (2.8±0.3)%and (2.4±0.5)% respectively] (P<0.05). Cerebral oxygenation responses to light stimulation in preterm infants examined at 6 months corrected GA were not significantly different from age-matched term infants. CONCLUSIONS: Cerebral oxygenation responses to light stimulation in infants born preterm at 3 months corrected GA are not as good as age-matched term infants, but were close to the level of age-matched term infants at 6 months corrected GA. This suggests that the early cognitive ability of preterm infants before 3 months corrected GA might fall behind age-matched term infants.
OBJECTIVE: To study the pathogenic bacteria of lower respiratory tract infection (LRTI), and age and gender distribution and drug resistance of the pathogenic bacteria in children. METHODS: Sputum specimens for bacterial cultures were collected in sterile tubes from all of the children with LRTI who had been admitted to the Children's Hospital of Zhejiang University between August 2001 and July 2002. Antibiotic susceptibility tests were performed using the Vitek system , the Kirby-Bauer diffuse method and the Etest method after bacteria were identified. RESULTS: Among the 4 238 patients with LRTI during the study period, 1 181 patients were bacteria-positive, with a positive rate of 27.9%. Streptococcus pneumoniae (S. pneumoniae) was the most common (222 strains), followed by Haemophilus influenzae (H. influenzae) (216 strains), Klebsiella pneumoniae (K. pneumoniae) (216 strains), Escherichia coil (E. coli) (169 strains) and Staphylococcus aureus (S. aureus) (89 strains). The isolation rate of S. pneumoniae in females was significantly higher than in males (6.2% vs 4.7%; P<0.05). However, the isolation rates of K. pneumoniae and S. aureus in males were higher than in females (5.1% vs 4.1% and 2.5% vs 1.5%, respectively; P<0.05). A higher incidence of LRTI due to S. pneumoniae and H. influenzae was found in the 1-3 years group, while the incidence of LRTI due to K. pneumoniae, E. coli, S. aureus and E. cloacae was higher in patients under 1 year of age. Antibiotic susceptibility tests showed that rates of penicillin-non-susceptible S. pneumoniae, ampicillin resistant H. influenzae, oxacillin-resistant S. aureus and ESBL-positive K. pneumoniae and E. coli were 55.0%, 16.5%, 41.2%, 42.6% and 4.5%, respectively. CONCLUSIONS: S. pneumoniae, H. influenzae, K. pneumoniae, E. coli and S. aureus were common pathogens of LRTI in children. The infection rate varied with age and gender. Antibiotics for treating LRTI should be selected based on the drug susceptibility test.
OBJECTIVE: The etiology of acute lower respiratory tract infection (LRTI) in children in Wenzhou City remains poorly defined. This study investigated the etiological agents responsible for acute LRTI and patterns of the antibiotic resistant bacterial pathogens in children with acute LRTI from Wenzhou City. METHODS: Lower respiratory tract secretions were obtained from 454 children with acute LRTI (aged 1 month to 10 years, median age 6 months) within 24 hrs after admission for bacterial culture. Meanwhile respiratory viruses were detected by the Direct immunofluorescence (DIF) assay. The K-B method was applied for the drug susceptibility test. RESULTS: Etiological agents were identified in 297 cases out of 454 patients (65.4%). Viral pathogens were identified in 229 cases (50.4%), bacteria in 135 cases (29.7%) and mixed viral-bacterial infections in 67 cases (14.8%). The isolating rate of Respiratory syncytial virus (RSV) was the highest (180 cases, 39.6%) in all of the samples. The isolating rates of other viral pathogens were as follows: Parainfluenza virus 3 type (PIV3) (6.6%), Adenovirus (2.2%), Influenza A (0.9%) and Influenza B (0.7%) . Of the 135 strains of bacterial pathogens, 19 kinds of bacterial pathogens were isolated. The predominant isolate was Klebsiella pneumoniae (K. pneumoniae) (9.9%), followed by Escherichia coli (E.coli) (4.4%), Streptococcus pneumoniae (S. pneumoniae) (4.2%) and Staphylococcus aureus (S. aureus) (4.2%). The isolating rates of K. pneumoniae and E.coli with extended-spectrum beta-lactamases strains (ESBLs) positive were 42.2% and 65.0%, respectively. The pathogens isolated of the first 5 places in children with acute LRTI under six months were RSV, K. pneumoniae , PIV-3, E.coli and S. aureus in turn. RSV, PIV3, S. pneumoniae, K. pneumoniae and E.coli were found to be the pathogens of the first 5 places in children with acute LRTI between six months and three years. The resistant rates of K. pneumoniae and E.coli to ampicillin were 97.8% and 75.0%, respectively. K. pneumoniae and E.coli with positive ESBLs were resistant to cephalosporin. The resistant rates of S. pneumoniae to erythromycin and penicilin were 100% and 68.4% , respectively. The resistant rates of S. aureus to erythromycin and penicillin were 94.7% and 89.5%, respectively. CONCLUSIONS: RSV is the most common pathogen responsible for acute LRTI in children in Wenzhou City, followed by K. pneumoniae and PIV3. The rate of antibiotic resistance of common bacteria and the isolating rate of Gram-negative bacillus with ESBLs positive are high.
OBJECTIVE: Interferon-gamma (IFN-γ) and interleukin-4 (IL-4)are typical cytokines produced by CD4~+T cells under antigenic stimulations, and the changes of serum levels of the two cytokines can indirectly reflect the immune state and the progress of inflammation. The aim of this study was to investigate the changes of IFN-γ and IL-4 in peripheral blood of children with Mycoplasmal pneumonia. METHODS: The peripheral blood concentrations of IFN-γ and IL-4 were measured using ELISA in 40 children with Mycoplasmal pneumonia at the acute stage. The samples from 40 healthy children were used as the Control group. RESULTS: The serum concentrations of IFN-γ and IL-4 in the Mycoplasmal pneumonia group were 99.43±13.18 and 44.61±17.46 pg/mL, respectively, which were higher than those in the Control group (86.23±6.31 and 25.97±9.40 pg/mL respectively; P<0.05). CONCLUSIONS: There was an imbalance in cytokine secretion in children with Mycoplasmal pneumonia at the acute phase, suggesting that adjuvant immunological therapy is needed for Mycoplasmal pneumonia.
OBJECTIVE: To observe the TH cell subset function in children with recurrent tonsillitis (RT) at the remission stage and to study the effects of astragalus membranacus (AM) on TH cell subset function. METHODS: The peripheral blood mononuclear cells (PBMC) from 27 children with RT at the remission stage were stimulated with either phytohemagalutinin (PHA) (RT-PHA group) or PHA together with AM (RT-AM group) and were then cultured in vitro for 48 hrs. The samples from 21 healthy children stimulated with PHA were used as the Control group. The levels of interferon-γ(IFN-γ) and interleukin-4 (IL-4) in the supernatants of PBMC were detected using ELISA. RESULTS: The IFN-γ level and the ratio of IFN-γ/ IL-4 in the RT-PHA group were statistically lower than those in the Control group (P<0.01). The level of IFN-γ and the ratio of IFN-γ/IL-4 in the RT-AM group were markedly higher than those in the RT-PHA group (P< 0.01), but were significantly lower than those in the Control group (P<0.05). There were no differences in the IL-4 level among the three groups. CONCLUSIONS: TH1 cell subset dysfunction may exit in RT children at the remission stage, suggesting that TH1 cell subset dysfunction plays an important role in the pathogenesis of RT. AM can improve TH1 cell subset function and therefore shows an important significance in treating RT.
OBJECTIVE: To study the polarization and immune regulation of TH cells in patients with bronchial asthma. METHODS: Thirty-eight hospitalized children with bronchial asthma (ranging from 4-12 years old) and 29 age-matched healthy children (Control group) were enrolled in this study. Serum IL-2 and IFN-γ levels were detected using ELISA. The percentage of TH1 and TH2 cells was detected by intracellular staining. RESULTS: The serum levels of IL-2 (15.94± 3.07 μg/L) and IFN-γ (487.2±43.6 pg/mL ) in asthmatic patients were significantly lower than those in the Control group (24.73±4.37 μg/L and 654.07±14.64 pg/mL respectively; P<0.01). The percentage of TH1 in asthmatic patients decreased significantly compared with that in the Control group [(11.24±2.43)% vs (16.67±2.73)%; P<0.01 ]; in contrast, the percentage of TH2 increased compared with that in the Control group [(19.85 ± 4.46)% vs (16.08±6.17)% ; P< 0.05 ]. CONCLUSIONS: The serum levels of IL-2 and IFN-γ, and the number of TH1 cells decreased in asthmatic patients. The decreased number of TH1 cells and the ratio of TH1/TH2 suggest an abnormal polarization of TH1 and TH2 cells. The changes may be associated with the inhibition of cellular immune function in asthmatic patients.
OBJECTIVE: To study the roles of IL-4, IL-5 and IgE in childhood cough variant asthma (CVA). METHODS: The IL-4 and IL-5 levels in peripheral blood mononuclear cell (PBMC) and the serum IgE levels were determined using ELISA in children with CVA in the acute stage (n=21) and in the convalesce stage (n=9). The samples from 30 children with acute bronchial asthma and from 30 healthy children were used as controls. RESULTS: The levels of PBMC IL-4 (91.57±12.19 ng/L)and IL-5 (13.28±0.31 ng/mL) in children with CVA in the acute stage were significantly higher than those in the convalesce stage (74.68±11.54 ng/L, 6.53±0.28 ng/mL) and also higher than those in the healthy controls (70.32±18.16 ng/L, 5.29±0.36 ng/mL) (P< 0.01 ). The levels of serum IgE in children with CVA in the acute stage (279.6±41.3 KU /L) were strikingly higher than those in the convalesce stage (153.8±37.5 KU/L) (P<0.01). The levels of serum IgE in children with CVA either in the acute stage or in the convalesce stage were significantly higher than those in healthy controls (90.6±44.8 KU /L ) (P<0.01). There were no significant differences in the levels of IL-4, IL-5 and IgE between children with acute CVA and acute asthma. CONCLUSIONS: A combined determination of PBMC IL-4 and IL-5 and serum IgE may be valuable for the diagnosis and the outcome evaluation of CVA. IL-4 and IL-5 may play a role in the pathogenesis of CVA. It is speculated that CVA may have similar pathogenesis to bronchial asthma since acute CVA patients have similar IL-4, IL-5 and IgE levels to children with acute bronchial asthma.
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OBJECTIVE: To detect the level of glucose-6-phosphate dehydrogenase (G-6-PD) mRNA expression in children with G-6-PD deficiency and their lineal family members in order to explore possible mechanisms of the disease at the transcriptional level. METHODS: RNA was extracted from peripheral blood of 41 children with G-6-PD deficiency and of their lineal family members (29 father lineages and 40 mother lineages). cDNA was then harvested using the reverse transcription method. G-6-PD mRNA expression was detected by quantitative real-time PCR (QRT-PCR). The detection results of G-6-PD mRNA expression in three groups (Patient, Father lineage and Mother lineage) were compared using Statistical Software SPSS 10.0 system. RESULTS: The mean G-6-PD mRNA value in the Patient, Father lineage and Mother lineage groups were 0.57±0.19, 0.74 ±0.21 and 0.67±0.21 respectively. The G-6-PD mRNA value in the Patient group was significantly lower than both Father lineage (t=-3.18, P<0.01) and Mother lineage groups (t=-2.54, P<0.05 ). CONCLUSIONS: The expression of G-6-PD mRNA decreased in children with G-6-PD deficiency, suggesting that the pathogenesis of this disorder relates to the varying levels of gene transcription.
OBJECTIVE: To explore the cardiac function of left and right ventricles in children with bronchial asthma at the acute stage and its association with the disease severity. METHODS: The cardiac function was evaluated by using the American Acuson 128XP/10 Doppler echocardiography in 24 children with acute severe bronchial asthma and 40 children with acute mild bronchial asthma. Thirty-four healthy children were used as normal controls. RESULTS: The injury of right ventricle diastolic function was predominant in children with mild asthma, and the right ventricle systolic function was also decreased. The systolic and diastolic function of left ventricle remained normal. In children with severe bronchial asthma, the injury of left ventricle systolic function was commonly seen, and the left ventricle diastolic function and the right ventricle systolic and diastolic function were also damaged. CONCLUSIONS: The cardiac function damage occurs in children with acute bronchial asthma and may be correlated with the disease severity.
This paper reported a case of congenital hyperinsulinism and reviewed the relevant literatures regarding to the etiology, pathogenesis, clinical and pathological features, diagnosis and treatment of this disorder. The baby (male), with gestational age of 36 weeks and birth weight 4 200 g, was delivered by caesarean section. It presented with hypoglycemia immediately after birth (0.8 mmol/L). Through the course of the disease, the baby's blood sugar manifested with 1.2-2.8 mmol/L although glucocorticoid was administered. 10% glucose solutions were intravenously infused at a speed of 10-17 mg/(kg·min)for this patient to retain a stable blood sugar level. The plasma insulin level was 24.13 U/L and blood sugar level was 1.5 mmol/L on day 30 of his life. The ratio of plasma insulin (U/L)and plasma glucose (mg/dL) was 0.89. These results suggest an inappropriate insulin secretion resulting in persistent hypoglycemia in this baby and so it was definitely diagnosed with congenital hyperinsulinism.
OBJECTIVE: Concerns of the effect of glucose on perinatal hypoxic-ischemic brain damage are increasing. It was previously considered that the glucose transporter (GLUT)genes and their productions played an important role in the regulation of cerebral energy metabolism. The present study aimed to explore the effect of different blood glucose levels on the expression of cerebral GLUT3 mRNA in neonatal rats with hypoxia-ischemia (HI), and to evaluate the neuroprotective effect of glucose against HI insults. METHODS: A total of 250 7-day-old neonatal SD rats were randomly divided into 10 groups (n=25 each): Normal control, Sham-operated, HI, Hypoglycemia, Hypoglycemia pre- and post-HI, Mild hyperglycemia pre- and post-HI, Severe hyperglycemia pre- and post-HI. Blood glucose levels of normal, hypoglycemia, mild hyperglycemia and severe hyperglycemia were defined as 5- 7 mmol/L, 3- 4 mmol/L, 10-15 mmol/L and 16-25 mmol/L, respectively. The expression of GLUT3 mRNA was detected with RT-PCT technique at 2, 24, 48 and 72 hrs and at 7 days after HI. RESULTS: There was a correlation between increases in GLUT3 mRNA expression and postnatal age in the Normal control group. HI significantly enhanced the expression of GLUT3 mRNA from 2 hrs, peaking at 24 hrs after HI, and then significantly decreased at 72 hrs and 7 days after HI when compared with the Normal Control group (P< 0.01 ). GLUT3 mRNA expression in the Hypoglycemia pre-HI group was the lowest among all groups with HI at each time point after HI, and a statistically significant difference was found at 72 hrs after HI when compared with the HI group (P<0.05). The expressional levels of GLUT3 mRNA in the Severe hyperglycemia pre-HI group were striklingly higher than those in any other groups with HI (P<0.05 or 0.01). The GLUT3 mRNA expression patterns in the Mild and Severe hyperglycemia post-HI and the Hypoglycemia post-HI groups were similar to the Hypoglycemia pre-HI group. CONCLUSIONS: GLUT3 mRNA expression and the synthesis of GLUT3 can be down-regulated by hypoglycemia pre-HI, coupled with aggravation of cerebral pathology, but up-regulated by higher hyperglycemia pre-HI, coupled with improvement of cerebral pathology. This suggested that adepuate glucose supplement before HI can improve the cerebral function against HI insults in neonatal rats.
OBJECTIVE: This study investigated the effects of flurothyl-induced neonatal recurrent seizures on γ-aminobutyric acid B1 receptor (GABAB1R) expression in neonatal and adult rat brain, and explored the possible relationship between the alterations of GABAB1R in mature brain and the changes of spatial memory and seizure susceptibility in adult rats. METHODS: Forty-eight postnatal day (P) 7 Sprague-Dawley rats were randomly assigned into two groups: Control and Seizure group (n=24 each). Seizures were induced by inhalant flurothyl daily for six consecuive days in rat pups from the Seizure group. Twelve rats selected randomly in each group were sacrificed on the 7th day after the last seizure for detecting the expressions of GABAB1R mRNA and protein in cerebral cortex and hippocampus by reverse transcription-polymerase chain reaction (RT-PCR) and immuno-histochemistry method. The spatial memory was tested by using the Morris water maze task during P61 to P64 and the seizure threshold was measured at P75 following intraperitoneal injection of pentylenetetrazol ( PTZ ) in the remaining rats. The rats were then sacrificed for detecting the expressions of GABAB1R mRNA and protein in cerebral cortex and hippocampus. RESULTS: The expressions of GABAB1R mRNA and protein in the cerebral cortex on the 7th day after the last seizure and at P75 decreased significantly in the Seizure group when compared with the Control group (P<0.05). The GABAB1R protein expression in the dentate gyrus on the 7th day after the last seizure in the Seizure group was significantly lower than that in the Control group (P<0.05), but the GABAB1R mRNA expression in the hippocampus was not different from that in the Control group. There were no significant differences in the expressions of GABAB1R mRNA and protein in the hippocampus between the two groups at P75. The escape latencies in water maze of the rats in the Seizure group at P64 were significantly longer than those in the Control group (98 533.8± 27 205.4 ms vs 46 723.3±40 666.5 ms; P<0.05). There were no differences in the seizure threshold between the two groups. CONCLUSIONS: The expressions of GABAB1R mRNA and protein in the cerebral cortex and hippocampus of neonatal rats with recurrent seizures decreased significantly, suggesting the changes of GABAB1R may be related to acute brain injury following neonatal recurrent seizures and the memory deficit in adult rats caused by neonatal recurrent seizures.
OBJECTIVE: This study investigated the hypothesis that 5-aminolevulinic acid-mediated photodynamic therapy (ALA-PDT) might alleviate acute graft-versus-host disease (GVHD) following allogenic bone marrow transplantation (allo-BMT) in mice. METHODS: Acute GVHD model following allo-BMT was established in 40 recipient BALB/C mice. Fifty C57BL/6J mice were used as donors and another 10 BALB/C mice as blank control without any intervention. Recipients received a lethal dose of 8.5 Gy ~ 60 Co radiation for 10 minutes before transplantation and then were randomly divided into four groups of 10 mice (A-D). Group A was injected with normal saline injection and served as controls. Group B received pure donor bone marrow and spleen cell infusion. Group C received donor bone marrow and mixed donor-recipient spleen cell infusion. Group D was administered with an infusion of donor bone marrow cells and mixed donor-recipient spleen cells treated with ALA-PDT. The 28th day survival rate, incidence of acute GVHD and hematological and pathological changes after transplantation were examined. RESULTS: All the mice from the Blank control group survived. The survival rates for Groups A-D on the 28th day were 0, 0, 10% and 60% respectively. Group D showed a significantly higher survival rate than the other three groups (P<0.01). Most of the mice in Groups B and C developed GVHD but only two developed in Group D. Moreover Group D had less severe hematological and pathological changes when compared with Groups B and C. CONCLUSIONS: ALA-PDT significantly alleviated GVHD and increased the 28th day survival rate for allo-BMT mice. ALA-PDT may be a promising therapy for GVHD following allo-BMT. Future studies should focus on the underlying mechanism of its therapeutic effect.
OBJECTIVE: Previous studies have shown that bacillus calmette-guerin (BCG) can deviate TH2 response toward TH1 response, resulting in a suppressive effect on the development of asthma/atopy. This study examined the effect of BCG treatment on regulatory T cells in asthmatic mice to investigate the possible mechanism. METHODS: Kunming mice were sensitized and challenged with ovalbumin (OVA) to establish asthmatic models. Asthmatic mice were injected intradermally with BCG five days before and after sensitization. After 24 hrs of last challenge, bronchoaveolar lavage fluid (BALF) and peripheral blood were collected .The total cells and eosinophils were counted in the BALF. The percentage of CD_4~+CD_ 25 ~+ in peripheral blood was detected with flow cytometry. Single spleen cell suspension was prepared and cultured in 1640 medium for 48 hrs and then the cytokine IL-10 level in the supernatant was determined using ELISA. The mice which were challenged with normal saline were used as the Normal control group. RESULTS: The number of total cells and eosinophils in BALF in asthmatic mice [(27.27±5.36)×10~7/L and (6.59±1.32)×10~7/L respectively] were more than in the Normal control group [(1.52±0.36)×10~7/L and zero respectively] (P<0.01). The number of total cells and eosinophils in BALF in asthmatic mice were reduced after BCG treatment [(13.71±3.17)×10~7/L and (1.43± 0.37 )× 10~7/L respectively] (P<0.01). The percentage of CD_4~+CD_ 25 ~+ in peripheral blood of asthmatic mice [( 11.59± 1.33)%] was noticeably lower than that of the Control group [(13.66±1.68)%] (P<0.01), but increased significantly in asthmatic mice after BCG treatment [(14.40±2.70)%] (P<0.05). The IL-10 level in spleen cell supernatant in the BCG-treated group (7.79±1.34 pg/mL) also increased compared with that in the untreated asthmatic mice (5.54±0.66 pg/mL) (P<0.01). CONCLUSIONS: BCG can markedly inhibit the airway inflammation in asthmatic mice possibly by promoting the production of regulatory T cells.
OBJECTIVE: Lung fibrosis is the ultimate outcome of hyperoxia-induced chronic lung diseases (CLD) and connective tissue growth factor (CTGF) is correlated with fibrosis. This study investigated the role of CTGF in hyperoxia-induced CLD. METHODS: Fifty premature rats were randomly exposed to hyperoxia (Model group) and to room air (Control group) (n=25 each). CLD was induced by hyperoxia exposure. The expression of CTGF was detected by immunohistochemical method at 1, 3, 7, 14 and 21 days after exposure. The severity of pulmonary fibrosis was evaluated. RESULTS: In the Control group there was a slight expression of CTGF in the bronchial epithelial cells and vascular endothelial cells. The intensity and range of CTGF expression in the Model group were similar to the Control group on days 1, 3 and 7 of exposure. On the 14th day, CTGF was expressed in some alveolar epithelial cells, fibroblasts and interstitial cells, and the intensity of CTGF expression increased significantly compared with the Control group, with the IODT of CTGF of 10.53±4.24 vs 5.58±1.18 (P<0.01). On day 21, the expression intensity and range of CTGF in the Model group (IODT: 16.61±5.39) increased compared with that of Control group (P<0.01). The expression of CTGF was correlated with the degree of fibrosis in the Model group on days 14 and 21(r=0.903, r=0.926 respectively, P<0.01). CONCLUSIONS: The CTGF expression increased with the time of hyperoxia exposure and the development of fibrosis. CTGF is closely related to the development of hyperoxia-induced pulmonary fibrosis.
OBJECTIVE: This study aimed to determine whether pentylenetetrazol-induced status epileticus (SE) can induce dentate granule cell neurogenesis in the developing rat and the effect of MK-801, a noncompetitive antagonism of N-methy-D-aspartate receptor (NMDAR), on neurogenesis. METHODS: Two hundred and sixteen postnatal days 7, 14, 21 or 28 Sprague Dawley (SD) rats were involved in this study. Each age group consisted of 54 rats which were randomly assigned into a SE group, a SE+MK-801 group and a Normal control group (n=18 each). SE was induced by intraperitoneal injection of PTZ (80 mg/kg). The SE+MK-801 group was injected intraperitoneally with MK-801 ( 1 mg/kg ) at 1 hr after SE episode. All rats were given 5-bromodeoxyuridene (BrdU) intraperitonealy to label newborn cells at 6, 13 and 27 days after seizures and then were sacrificed 24 hrs after BrdU injection. The immunohischemistry method was used to measure the expression of BrdU, TuJl (βIII tubulin), and glial fibrillary acidic protein (GFAP) in the dentate gyrus of hippocampus of rats. RESULTS: The number of the BrdU positive cells in the SE group was significantly higher than in the age-matched normal controls at 7 and 14 days after SE episode (P<0.05 or 0.01). Approximately 82.5% and 80.3% of BrdU-labeled cells in the SE and the Control groups were co-expressed TuJ1 respectively. MK-801 treatment decreased the BrdU positive cells compared with the SE group at 7 and 14 days after SE seizures (P< 0.01 ). On the 28th day after SE episode there were no differences among the three groups for the BrdU positive cells. CONCLUSIONS: PTZ -induced SE can increase the dentate granule cell neurogenesis in the developing rat. NMDAR plays an important role in neurogenesis following seizures.
OBJECTIVE: This study aimed to investigate the protective effects of recombinant intestinal trefoil factor (rITF) against intestinal injuries and the possible mechanism by examining the changes of diamine oxidase (DAO) and TNF-α and the intestinal ultrastructural changes in lipopolyseccharide (LPS) induced intestinal injuries. METHODS: Ninety-six ten-day-old Wistar rats were randomly injected with either normal saline (1 mL/kg, Control group), LPS (1 mL/kg) or LPS (1 mL/kg) + rITF (0.1 mL) intraperioneally. At 2, 6, 24 and 72 hrs after administration plasma DAO activity was determined using absorption spectrometry; and the intestinal protein and mRNA expression of TNF-α were measured using immunohistochemistry and RT-PCR methods. The intestinal ultrastructural changes were observed by electron microscopy. RESULTS: The plasma DAO activity in the LPS group began to increase at 2 hrs, peaked at 6 hrs and remained at significantly higher levels until 72 hrs after administration compared with the Control group (P <0.01). The plasma DAO activity in the LPS + rITF group decreased noticeably compared with the LPS group at all time points(P < 0.01 or 0.05). A significant difference in the plasma DAO activity was only observed at 6 hrs after administration between the LPS + rITF and the Control group. The expression of TNF-α protein in the LPS group significantly increased at each time point, peaking at 6 hrs after LPS administration, with the IODT of TNF-α of 37 247.64±3387.59 vs 6 191.02±482.32 (P <0.01) compared with the Control group. rITF treatment decreased the expression of TNF-α protein although it remained significantly higher than in the Control group (P<0.01). The TNF-α mRNA was weakly expressed in the Control group but strikingly increased after LPS injection (P<0.01). Compared with the LPS group, the TNF-α mRNA expression in the LPS + rITF group decreased at all time points(P < 0.01 or 0.05). Vacuole changes of mitochodrium, cell nucleus condense, break and depletion of part of microvilli, and widen and disrupted tight junction were observed in the LPS group. The ultrastructural changes of intestinal tissues were improved in the LPS + rITF group. CONCLUSIONS: rITF can decrease the plasma DAO activity and inhibit the expression of TNF-α, resulting in a protective effect against intestinal injuries induced by LPS in young rats.
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