Objective To investigate the clinical effect,safety,and value of bronchofibroscopeguided bronchoalveolar lavage and topical antibiotics in the treatment of pediatric patients with severe pneumonia.Methods A total of 60 patients with severe pneumonia was randomly divided into two groups with 30 cases in each group.Patients in the control group were treated with conventional anti-infection therapy,while patients in the treatment group were treated with bronchofibroscope-guided bronchoalveolar lavage and topical antibiotics on the basis of conventional therapy.The sputum positive rate,clinical effect,hospital stays,treatment costs,and adverse reactions were compared to analyze its value.Results The total effective rate of treatment group was 93.3％,which was significantly higher than that (60.0％) in the control group (P ＜0.01).The sputum positive rate of treatment group was 80.0％,which was significantly higher than that (43.3％) in the control group (P ＜0.01).The hospital stays and the treatment costs of the treatment group were both significantly less than those in control group (P ＜0.01 orP ＜0.05).No serious complications were found in patients of the treatment group.Conclusions Bronchofibroscope-guided bronchoalveolar lavage and topical antibiotics in the treatment of pediatric patients with severe pneumonia show exactly clinical effects and significant improvement in dyspnea,which shortens the hospital stays,reduces the treatment costs,and has no seriously adverse reactions.Therefore,it is worthy of clinical promotion and application.

AIM To explore possible action mechanism of antidepressants. METHODS Using flow cytometry, the cell proliferation was detected. The proliferation of hippocampal progenitor cells and level of brain derived neurotrophic factor (BDNF) were measured by immunohistochemistry. RESULTS Treatment with N methyl D aspartate (NMDA) 600 ?mol?L -1 for 3 d significantly decreased the percentage of S phase in PC12 cells, while in the presence of classical antidepressants, desipramine (DIM) or fluoxetine (FLU) 1, 5 ?mol?L -1 , the percentage of S phase increased. Furthermore, the proliferation of hippocampal progenitor cells, as well as the BDNF level in dentate gyrus (subgranular zone) significantly decreased in chronically stressed mice for 24 d, while chronic administration with DIM or FLU 10 mg?kg -1 (ip) normalized it. Meanwhile, the BDNF level in dentate gyrus also elevated after DIM or FLU treatments. CONCLUSION Up regulation of the hippocampal neurogenesis is the common action mechanism for antidepressants, which may be closely related to the elevation of BDNF level at the same time.

Objective To investigate the psychological characteristics of neurosis and strategy for nursing care.MethodsThe effects of psychological nursing on neurosis were analysed retrospectively.ResultsPsychological nursing could decrease the time in hospital in patient with neurosis except somatoform disorders other than hypochondriasis.ConclusionPsychological nursing is important to neurosis.

Objective:To investigate the role and mechanism of Nod-like receptor protein 3 (NLRP3) in chronic kidney disease (CKD)-related neointimal hyperplasia (NH) of vessels.Methods:Wild type C57BL/6J male mice were randomly divided into normal control group ( n=6) and experimental group ( n=18), by removal of 5/6 kidney and ligation of left common carotid artery to establish a NH model. After established successfully, the mice in NH experimental group were randomly divided into NH model group, NLRP3 inhibitor group, and drug control group ( n=6/group). C57BL/6J male mice with NLRP3 gene knockout group did not do any treatment after the establishment of NH model. After 3 weeks of feeding, the blood and vascular tissue samples of mice were collected. The pathological changes of vascular tissue samples in mice were observed by hematoxylin-eosin staining. The expressions and localization of NLRP3-related protein were observed by immunofluorescence staining. The expression of NLRP3 mRNA in vascular tissue was detected by quantitative real-time PCR. The activity of caspase-1 in vascular tissue was measured by colorimetric method. Human aortic smooth muscle cells (HASMCs) were treated with 10% uremic serum to simulate the body's internal environment during the uremic phase. NLRP3 small interfering RNA (siRNA) was transfected or NLRP3 inhibitor glibenclamide was added to the cell cultures. The expression of NLRP3 mRNA in HASMCs was detected by quantitative real-time PCR. The activity of caspase-1 in HASMCs was detected by colorimetric method. Results:Compared with the control group, the levels of serum creatinine and blood urea nitrogen were significantly increased in the NH model group (both P<0.01). The vascular histopathology showed that vascular intima thickened, vascular smooth muscle cells proliferated and hypertrophied, nuclei were deeply stained, and cells arranged disorderly and migrated to vascular intima in the experimental group. Quantitative analysis showed that the ratio of neointima to lumen increased significantly in the NH model group than that in control group ( P<0.01). Compared with the control group, the immunofluorescence staining of vascular tissue showed that the expressions of NLRP3, caspase-1, IL-18, IL-1β and proliferating cell nuclear antigen (PCNA) protein in the NH model group increased (all P<0.01), while the expression of α-SMA decreased ( P<0.01). NLRP3 was mainly located in vascular smooth muscle cells (VSMCs). VSMCs showed a synthetic phenotype. Compared with the NH model group, the expression of NLRP3, caspase-1, IL-18, IL-1β and PCNA protein in the NLRP3 inhibitor group and NLRP3 gene knockout group decreased (all P<0.01), the expression of α-SMA increased ( P<0.01), and the pathological changes of blood vessels alleviated. Compared with healthy serum group, the expression of NLRP3, IL-18, and IL-1β and bromodeoxyuridine (BrdU) uptake in uremic serum-stimulated group were increased (all P<0.01). After transfection of NLRP3 siRNA and addition of glibenclamide, the expression of NLRP3, IL-18, and IL-1β in VSMCs in uremic serum-stimulated group decreased, and BrdU intake decreased (all P<0.01). Conclusions:NLRP3 inflammatory bodies play an important role in promoting CKD-related neointimal hyperplasia of vessels, and glibenclamide can effectively reduce neointimal hyperplasia.

Objective Even after successful surgical repair,patients with coarctation of the aorta (CoA) are at high risk of long-term morbidity and mortality due to cardiovascular events,which is probably related to persistent arterial disfunction during long-terr follow-up after operation,The aim of the study was to explore the alterations of vascular structure and function in children with successfully repaired CoA in the short-and mid-term follow-up.Methods A cohort of 20 children who underwent CoA repair between January 2010 and October 2010 in Guangzhou women and children's Medical Center was studied.There were 14 males and 6 females in CoA group,which comprised 6 patients with isolated CoA,14 patients with CoA associated with intracardia anomalies,whose median age of operation was 4 months (rang from lmonth to 10.0 years).And 20 patients with isolated ventricular septal defect (VSD) were included as VSD group during the same time,with 12 males and 8 females,whose median age of operation was 5 months (rang from 1 month to 12.0 years).Resting blood pressure,flow-mediated dilation (FMD) of the brachial artery,carotid intima-media thickness (IMT) were compared in CoA group and VSD group,including preoperative media data and follow-up of 1 month,6 months and 1 year.In addition,as comparison to the operation group,20 health children with normal echocardiographic findings,whose median age was 5 months (rang from 3 month to 10.0 years),were selected as health group for the 1-year following up.None of them had obesity,hyperlipidemia,diabetes mellitus,metabolic diseases or systemic inflammatory disease.Results As a result of the datas before operation and those I month,6 months and 1 year after operation,all children were normotensive at rest.In the same period,Carotid IMT in CoA group[(0.47 ± 0.10)mm,(0.49 ±0.10) mm,(0.57 ±0.07)mm,(0.61 ± 0.07) mm]was significantly thicker than that in VSD group[(0.41 ±0.11) mm,(0.43 ±0.11)mm,(0.51 ±0.08) mm,(0.55 ±0.08) mm](P＜0.05) and health group[(0.40 ±0.09) mm,(0.42 ±0.11)mm,(0.50 ±0.08) mm,(0.57 ±0.08) mm](P ＜0.05),Brachial artery FMI in children with CoA[(5.4,6 ±1.51)％,(5.71 ±1.88)％,(5.42±1.69)％,(5.27±1.02)％]was significantly lower than that in the VSD control group[(6.69±1.45) ％,(6.66±1.21)％,(6.81 ±1.03)％,(6.43±1.34)％](P＜0.05) and health group[(6.59 ±1.84)％,(6.84±1.41)％,(6.91 ±1.31)％,(6.56±1.62)％](P＜0.05).Significant difference could not be found in neither the IMT nor the FMI between the VSI control group and health group in 4 period respectively,P ＞ 0.05.Conclusion Children after successful coarctation repair have abnomal structural and functional properties of the aorta above the place of coarctation even their blood pressure at rest is normal.These results confirm that the alterations in mechanical properties of carotid arteries as well as the generalized endothelial dysfunction in children with coarctation of the aorta are persistent,which can not be prevented or reversed by surgical repair,and which may partly explain the high incidence of cardiovascular disease observed in their adulthood and reduced life expectancy,furtherly supporting the claim that coartation of the aorta is a systemic vascular disorder which needs long-term follow-up of vascular function.

Objective:To study the effects of arsenic exposure on necroptosis pathway and inflammatory response of mouse myocardial cells.Methods:Sixty male C57BL/6J mice were randomly divided into control group (group C) and low, medium, and high dose arsenic exposure groups (groups L, M, H) based on body weight using a random number table method. Each group had 15 mice, and they drank 0.00, 0.15, 1.50, and 15.00 mg/L arsenic trioxide (As 2O 3) solution prepared with deionized water. The exposure period was 12 weeks. Hematoxylin-eosin (HE) staining and Masson trichrome staining of paraffin-embedded heart tissues were used to observe the histopathology changes of the heart. Transmission electron microscopy (TEM) was used to evaluate the ultrastructural changes of myocardial cells. The quantitative real-time PCR (qRT-PCR) was used to detect the mRNA expression of inflammatory genes [tumor necrosis factor (TNF)-α and interleukin(IL)-6] and the genes involved in necroptosis pathway [receptor-interacting protein (RIP) 1, RIP3 and mixed-lineage kinase domain-like protein (MLKL)]. Protein expressions of RIP1 and RIP3 in the heart were assessed by western blotting. Results:Histopathological examination results showed there were myocardial necrosis, inflammatory cells infiltration and fibroblasts hyperplasia and other changes in groups M and H. TEM analysis revealed marked ultrastructural changes in groups M and H, including fractured myofibril, fractured Z lines of sarcomere, and swollen mitochondria with fractured cristae. Compared with group C (1.00 ± 0.00), the mRNA expression of RIP1 in group H was significantly up-regulated (1.41 ± 0.06, P < 0.05); the mRNA expressions of RIP3 (1.29 ± 0.14, 1.56 ± 0.08), MLKL (1.23 ± 0.05, 1.36 ± 0.07), TNF-α (2.20 ± 0.10, 2.23 ± 0.18) and IL-6 (1.87 ± 0.16, 1.63 ± 0.15) were significantly up-regulated in groups M and H ( P < 0.05). The protein expressions of RIP1 (0.43 ± 0.04, 0.50 ± 0.04) and RIP3 (0.68 ± 0.02, 0.84 ± 0.05) in groups M and H were higher than those in group C (0.25 ± 0.01, 0.45 ± 0.04, P < 0.05). Conclusion:Subchronic arsenic exposure induces histopathological changes such as myocardial necrosis and fibrosis in mice, inducing necroptosis and inflammatory reactions in myocardial cells.

OBJECTIVE: To study the mechanism of tumor necrosis factor( TNF)-α and its receptor( TNFR) signal transduction pathways in regulating cell apoptosis of alveolar macrophage( AM) in coal workers' pneumoconiosis( CWP).METHODS: Twenty-four coal workers with pneumoconiosis at stage Ⅰ were selected as CWP group and four observation subjects exposed to coal were chosen as observation group by using simple random sampling method. The bronchoalveolar lavage fluids of whole-lung lavage of two groups were collected. AMs were separated and purified. Then they were divided into 6 groups: a control group,a superoxide dismutase( SOD) group,a TNF/TNFR group,an anti-TNF-α antibody group,a Caspase-8 suppression group and a nuclear factor-κB( NF-κB) suppression group. The AMs of 6 groups with corresponding treatment were cultivated. After 24 hours,the cells were harvested and proteins extracted. The relative expression of TNF-α,TNFR1,TNFR2,Caspase-8,Caspase-3,NF-κB P50 and NF-κB P65 protein was detected by Western blotting. RESULTS: The protein relative expression of TNF-α,TNFR2,Caspase-8,Caspase-3,NF-κB P50 and NF-κB P65 in CWP group was significantly higher than those in the observation group( P < 0. 05). The protein relative expression of TNF-α,TNFR1,Caspase-8,Caspase-3 and NF-κB P50 in the TNF/TNFR group and the anti-TNF-αantibody group was lower than that of the control group( P < 0. 05). The above indexes in the anti-TNF-α antibody group were lower than that of the NF-κB suppression group( P < 0. 05). The protein relative expression of TNFR1,Caspase-8and Caspase-3 in the TNF/TNFR group was higher than that of the SOD group and the Caspase-8 suppression group( P <0. 05). The protein relative expression of TNFR1,Caspase-8 and NF-κB P50 in the TNF/TNFR group was lower than that of the NF-κB suppression group( P < 0. 05). Among the CWP patients,the relative expression of TNFR2 and NF-κB P65 in the TNF/TNFR group was lower than that of the control group( P < 0. 05),and higher than that of the SOD group( P <0. 05). CONCLUSION: AM apoptosis mediated by TNF-α/TNFR/NF-κB signal transduction pathway plays an important role in the occurrence and development of CWP. The TNF-α/TNFR/NF-κB signal transduction pathways inhibited or blocked at different stages can affect the expression of proteins related to AM apoptosis.