Objective To discuss pathogens findings in children with severe pneumonia.Methods Bacteria was detected by using sputum culture and blood culture in sterile culture media.Viruses and atypical pathogenic antibodies were detected by using indirect immunofluorescence.Influenza A (H1N1) virus RNA were tested using RT-PCR.According to the results of bacterial culture and drug sensitive test,we can guide the use of antibiotics,and individualize treatment was carried out,including anti-inflammatory,organ function support.Results Bacteria was found in 69 children by using sputum culture.Gram negative bacteria accounted for 57.47％.Gram positive bacteria accounted for 42.53％.Escherichia coli(14.94％),Haemophilus influenzae (20.96％) and klebsiella pneumoniae(13.79％) were the main strains of Gram negative bacteria,Staphylococcus aureus (21.84％)and Streptococcus pneumonia(16.1％)were the main strains of Gram positive bacteria.Bacteria was found in 7 (8.00％) children by using blood culture.Virus were identified in 11 out of 123 patients,including 2 cases of respiratory syncytial virus antibody positive,2 cases of adenovirus antibodies positive,4 cases of influenza B virus antibody positive,2 cases of parainfluenza virus antibody positive and influenza A(H1N1) virus from only one case,Mycoplasma pneumonia agents were identified in 8 patients.Eighty-nine children (72.36％) complicated with sepsis,85 children (69.11％) with respiratory failure,48 children (39.02％) with gastrointestinal dysfunction,32 children (26.02％) with heart failure,18 children(14.63％) with septic shock,13 cases (10.57％) with toxic encephalopathy,5 children (4.07％) with disseminated intravascular coagulation.Among them,17 children (13.82％) complicated with multiple organ dysfunction syndrome.In the 123 children with severe pneumonia,46 cases (37.4％) were cured,73 cases (59.35％) improved,and 4 cases died (3.25％) with critical multiple organ dysfunction syndrome.Conclusion The detection rate of pathogen is high in this study.We should pay more attention to individualize therapy for complication,so that the cure rate could be increased.

Objective:To monitor the blood pressure in pediatric patients with coarctation of the aorta (CoA) before and 8 years after surgery, and explore the mechanism of elevated blood pressure in pediatric patients with repaired CoA.Methods:A cohort of 23 pediatric patients who underwent CoA repair between January 2010 and October 2010 in Guangzhou Women and Children's Medical Center was studied. And 20 age-, sex-match patients with isolated ventricular septal defect (VSD) who underwent surgery at the same time, 20 age-, sex-match health patients with normal echocardiographic findings were included in the study. Systolic blood pressure (SBP), diastolic blood pressure (DBP), arm-leg SBP gradient, right carotid intima-media thickness (CIMT), serum transforming growth factor-β1 (TGF-β1) were monitored at baseline(1 day before surgery) and 8-year follow-up (8 years after surgery).Results:There were no differences in SBP and DBP among patients with CoA, patients with VSD and health children at baseline ( P>0.05). But at 8-year follow-up, 2 patients with CoA exhibited hypertension. Not only that, patients with CoA had higher SBP than patients with VSD and health children at 8-year follow-up ( P<0.05). Patients with CoA had higher arm-leg SBP gradient than patients with VSD and health children at baseline ( P<0.01). But there were no differences in arm-leg SBP among patients with CoA, patients with VSD and health children at 8-year follow-up ( P>0.05). Patients with CoA had increased CIMT and higher serum levels of TGF-β1 at baseline and 8-year follow-up ( P<0.05). The preoperative levels of CIMT and serum TGF-β1 in the patients with CoA were highly positively correlated with their levels at 8-year follow-up, respectively ( P<0.01). There was a strong correlation between the levels of CIMT and serum TGF-β1 in patients with CoA, both preoperatively and postoperatively ( P<0.01). The preoperative and postoperative levels of CIMT and serum TGF-β1 in the patients with CoA were highly positively correlated with SBP at 8-year follow-up, respectively( P<0.05). Conclusion:Although surgery can successfully cure the anatomical " stenosis" , patients with CoA have elevated systolic blood pressure than normal people and patients with simple congenital heart disease (such as VSD). And some of the patients with CoA suffer from hypertension at long-term follow-up, even they are normotensive preoperatively. It may be related to vascular remodeling, in which TGF-β signaling pathway may be involved. Monitoring CIMT and TGF-β1 in patients with CoA preoperatively may be significative for prediction for the levels of SBP postoperatively.

OBJECTIVE: To investigate a revision of the Trauma and Injury Severity Score (TRISS) weight coefficients in order to overcome the inference from foreign coefficients on Chinese trauma scoring. METHODS: The data of 1 297 Chinese trauma patients were studied for trauma scoring with the Revised Trauma Score-Injury Severity Score-TRISS (RTS-ISS-TRISS) system to get a serial of new weight coefficients through analyzing a multivariation logical regression between the outcome and the injury severity. RESULTS: ISS was higher but the Age Score and probability of survival (Ps) of the death group were lower than those of the survival group. New values of RTS-ISS-Age coefficients differed from the Major Trauma Outcome Study (MTOS) ones, through which the constant b(0) decreased its negative value, and ISS weight b(2) increased its negative value, but RTS weight b(1) and age weight b(3) changed with the trauma types. MTOS's values and new values of weight coefficients were used on 1297 patients for prognosis by calculating Ps. The accuracy of new values (90.13%) was a little higher than that of MTOS's (89.5%), with a promotion in specialization but a loss in sensitivity. CONCLUSIONS: A revision of TRISS's weight coefficients is either necessary or feasible. To achieve this purpose, a Chinese trauma database with large capacity is recommended.

Objective: To establish an animal model of hypoxia-induced bronchopulmonary dysplasia asso-ciated with pulmonary hypertension (BPD-PH). Methods: C57BL/6 male and female specific pathogen free mice mated and female mice with their offspring mice were randomly divided into normoxic group and hypoxia group by way of numerical method.Normoxic group was placed in the indoor environment directly.Hypoxia group was placed in 120 mL/L oxygen concentration environment within 12 hours after birth.Body weight gain and mortality of the neonatal mice were recorded.The mice lungs and hearts were harvested on day 14 for immunofluorescence staining and HE staining, and Western blot was used to observe the morphological changes and vascular endothelial growth factor (VEGF) protein level. Results: The mortality rates of normoxic group and hypoxic group were 11.8% and 47.3%, respectively.Compared with the normoxic group, body weight of hypoxia group increased slowly, as the final body weight of 2 groups were (12.40±2.33) g and (5.50±0.32) g, respectively, and the difference was significant (χ²=13.38, t=20.50, all P<0.01). Hypoxia group showed higher right ventricular hypertrophy index [(96.00±0.15)% vs.(40.40±4.00)%, t=41.67, P<0.01], fusion of alveolar, diminished microvasculature, thickening alveolar septal, decreased alveolar radiation coefficient (RAC)(19.73±2.33 vs.10.90±1.85) and increased mean linear intercept(MLI) (33.2±4.33 vs.58.70±7.27) with statistical significance, respectively (t=16.27, 9.53, all P<0.01). In the lung HE staining, pulmonary arterial thickening, pulmonary smooth muscle cell proliferation and intimal roughness in immunofluorescence, significantly decreased expression of VEGF protein level by Western blot were observed in hypoxic group (0.41±0.04 vs.1.19±0.08, t=15.10, P<0.01). Conclusions Hypoxia-induced mouse BPD-PH model was consistent with the pathophysiological process of pulmonary vascular remodeling of pulmonary hypertension, which increase pulmonary vascular resistance eventually leading to right ventricular hypertrophy.