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1.
Medicine (Baltimore) ; 98(44): e17806, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31689863

RESUMO

Hypoalbuminemia and anemia are frequent among in patients with traumatic brain injury (TBI). We assess whether serum albumin and hemoglobin at admission can predict outcome in children with moderate to severe TBI.This retrospective study was conducted in a tertiary pediatric hospital between May 2012 and Jun 2018 included children with an admission Glasgow Coma Scale of ≤13.A total of 213 patients were included of whom 45 died in hospital. Multivariate logistic regression showed that hypoalbuminemia (serum albumin <30 g/L) was independently associated with mortality (adjusted odds ratio [OR] = 3.059; 95% confidence interval [CI]: 1.118-8.371; P = .030) in children with moderate to severe TBI, while anemia (hemoglobin <90 g/L) was not independently associated with mortality (adjusted OR = 1.742; 95% CI: 0.617-4.916; P = .295). Serum albumin was significantly superior to hemoglobin (area under the curve [AUC] 0.738 vs AUC 0.689, P < .05) under receiver operating characteristic curve analysis. Hypoalbuminemia was also associated with reduced 14-day ventilation-free days, 14-day intensive care unit (ICU)-free days, and 28-day hospital-free days.Serum albumin at admission was superior to hemoglobin in predicting the mortality in children with moderate to severe TBI and also associated with reduced ventilator-free, ICU-free, and hospital-free days.


Assuntos
Lesões Encefálicas Traumáticas/sangue , Lesões Encefálicas Traumáticas/mortalidade , Hemoglobina A Glicada/metabolismo , Mortalidade Hospitalar , Albumina Sérica/metabolismo , Anemia/complicações , Anemia/diagnóstico , Biomarcadores/sangue , Lesões Encefálicas Traumáticas/complicações , Lesões Encefálicas Traumáticas/terapia , Estudos de Casos e Controles , Criança , Pré-Escolar , Cuidados Críticos , Feminino , Escala de Coma de Glasgow , Humanos , Hipoalbuminemia/complicações , Hipoalbuminemia/diagnóstico , Masculino , Valor Preditivo dos Testes , Respiração Artificial , Estudos Retrospectivos
2.
PLoS One ; 14(9): e0222591, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31536567

RESUMO

BACKGROUND: Lactate is used to evaluate the prognosis of adult patients with trauma. However, the prognostic significance of admission serum lactate in the setting of pediatric traumatic brain injury (TBI) is still unclear. We aim to investigate the impact of admission lactate on the outcome in children with moderate to severe TBI. METHODS: This retrospective study was conducted in a tertiary pediatric hospital between May 2012 and Jun 2018 included children with an admission Glasgow Coma Scale (GCS) of ≤13. Two hundred and thirteen patients were included in the analysis and 45 patients died in hospital. RESULTS: Admission lactate and glucose were significantly higher in non-survivors than those in survivors (P < 0.05). Admission lactate was positively correlated with admission glucose and negatively correlated with GCS in all patients (n = 213), subgroup of isolated TBI (n = 112) and subgroup of GCS ≤ 8 (n = 133), respectively. AUCs of lactate could significantly predict the mortality and were higher than those of glucose in all patients, subgroup of isolated TBI and subgroup of GCS ≤ 8, respectively. Multivariate logistic regression showed that admission lactate (Adjusted OR = 1.189; 95% CI: 1.002-1.410; P = 0.047) was independently associated with mortality, while admission glucose (Adjusted OR = 1.077; 95% CI: 0.978-1.186; P = 0.133) wasn't an independent risk factor of death. Elevated admission lactate (> 2 mmol/L) was associated with death, reduced 14-day ventilation-free days, 14-day ICU-free days and 28-day hospital-free days. CONCLUSIONS: Admission serum lactate can effectively predict the mortality of children with moderate to severe TBI. Elevated admission lactate is associated with death, reduced ventilator-free, ICU-free, and hospital-free days. Admission serum lactate could be used as a prognostic biomarker of mortality in children with moderate to severe TBI.

3.
Brain Inj ; 31(3): 396-400, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28296528

RESUMO

OBJECTIVE: Hyperglycaemia is common amongst children with traumatic brain injury (TBI). We aim to investigate the association between early hyperglycaemia and poor clinical outcomes in children with moderate to severe TBI. METHODS: We performed a retrospective study in a tertiary paediatric hospital between May 2012 and October 2014 of all patients with TBI who were aged <16 years with a Glasgow Coma Scale (GCS) of ≤13. The primary outcome was death. Secondary outcomes were 14 ventilation-free, 14 paediatric intensive care unit (PICU)-free and 28 hospital-free days. We defined hyperglycaemia as glucose >11.1 mmol/L (200 mg/dL). RESULTS: There were 109 patients with a median age of 54 months [inter-quartile range (IQR): 17-82]. Median glucose on arrival was 6.1 mmol/L (IQR: 5.2-9.8). Median GCS in our cohort was 8 (IQR: 6-12). Multivariate logistic regression demonstrated that initial hyperglycaemia [odds ratio (OR): 15.23; 95% confidence interval (CI): 3.74-62.00; P < 0.001], and GCS <8 (OR: 13.02; 95% CI: 2.31-73.33; P = 0.004) were risk factors for mortality. Multivariate linear regression showed that initial hyperglycaemia was a risk factor for reduced ventilation-free, PICU-free and hospital-free days. CONCLUSIONS: Early hyperglycaemia predicts for in-hospital mortality, reduced ventilation-free, PICU-free and hospital-free days in children with moderate to severe TBI.


Assuntos
Lesões Encefálicas Traumáticas/complicações , Mortalidade Hospitalar , Hiperglicemia/etiologia , Hiperglicemia/mortalidade , Glicemia/metabolismo , Lesões Encefálicas Traumáticas/mortalidade , Criança , Pré-Escolar , Estudos de Coortes , Feminino , Escala de Coma de Glasgow , Humanos , Lactente , Unidades de Terapia Intensiva Pediátrica , Tempo de Internação , Modelos Lineares , Masculino , Fatores de Risco , Resultado do Tratamento
4.
Zhongguo Dang Dai Er Ke Za Zhi ; 17(11): 1204-9, 2015 Nov.
Artigo em Chinês | MEDLINE | ID: mdl-26575879

RESUMO

OBJECTIVE: To investigate the distribution and drug sensitivity of pathogens and risk factors for ventilator-associated pneumonia (VAP) in children with congenial heart disease (CAD) after surgery. METHODS: According to the occurrence of VAP, 312 children with CAD who received mechanical ventilation after surgery for 48 hours or longer between January 2012 and December 2014 were classified into VAP (n=53) and non-VAP groups (n=259). Sputum samples were collected and cultured for pathogens in children with VAP. The drug sensitivity of pathogens was analyzed. The risk factors for postoperative VAP were identified by multiple logistic regression analysis. RESULTS: The sputum cultures were positive in 51 out of 53 children with VAP, and a total of 63 positive strains were cultured, including 49 strains of Gram-negative bacteria (78%), 9 strains of Gram-positive bacteria (14%) and 5 strains of funqi (8%). The drug sensitivity test showed that Gram-negative bacteria were resistant to amoxicillin, piperacillin, cefotaxime and ceftazidime, with a resistance rate of above 74%, and demonstrated a sensitivity to amikacin, polymyxin and meropenem (resistance rate of 19%-32%). Single factor analysis showed albumin levels, preoperative use of antibiotics, duration of mechanical ventilation, times of tracheal intubation, duration of anesthesia agent use, duration of acrdiopulmonary bypass, duration of aortic occlusion and use of histamin2-receptor blockade were significantly different between the VAP and non-VAP groups (P<0.05). The multiple logistic regression showed albumin levels (<35 g/L), duration of mechanical ventilation (≥ 7 d), times of tracheal intubation (≥ 3), duration of acrdiopulmonary bypass (≥ 100 minutes) and duation of aortic occlusion (≥ 60 minutes) were independent risk factors for VAP in children with CAD after surgery. CONCLUSIONS: Gram-nagative bacteria are main pathogens for VAP in children with CAD after surgery. The antibiotics should be used based on the distribution of pathogens and drug sensitivity test results of pathogens. The effective measures for prevention of VAP should be taken according to the related risk factors for VAP to reduce the morbidity of VAP in children with CAD after surgery.


Assuntos
Cardiopatias Congênitas/cirurgia , Pneumonia Associada à Ventilação Mecânica/etiologia , Antibacterianos/farmacologia , Bactérias Gram-Negativas/isolamento & purificação , Humanos , Modelos Logísticos , Testes de Sensibilidade Microbiana , Pneumonia Associada à Ventilação Mecânica/prevenção & controle , Fatores de Risco , Escarro/microbiologia
6.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue ; 24(10): 616-9, 2012 Oct.
Artigo em Chinês | MEDLINE | ID: mdl-23040780

RESUMO

OBJECTIVE: To explore the expression of α-smooth muscle actin (α-SMA) during the lung injury induced by hyperoxia in infantile rats. METHODS: Sixty-four male Sprague-Dawley (SD) rats about 3 weeks were randomly assigned into normal control group which exposured to room air [fraction of inspired oxygen (FiO(2)) was 0.21] and hyperoxia exposure group (95%O(2)) according to random digits table. Eight rats in each group were randomly sacrificed at day 1, 7, 14 and 21.Pulmonary tissue remodeling was observed by hematoxylin-eosin (HE) staining. Immunohistochemistry method was performed to evaluate the expression of α-SMA in pulmonary tissue, further Western blotting was also made to determine the expression of α-SMA. RESULTS: The early histopathologic changes after HE were inflammation and edema in pulmonary tissue, while the later changes were interstitial hyperplasia and fibroblast proliferation. The expression of α-SMA was very slight in bronchial epithelium, alveolar epithelium and alveolar interstitium in normal control group, but increased with the time of hyperoxia exposure prolonged and peaked at 21st day. Western blotting detected that the expression of α-SMA after hyperoxia exposure for 1 day and 7 days in hyperoxia exposure group presented no difference compared with normal control group (1.02±0.12 vs. 1.00±0.13, 1.05±0.14 vs. 0.99±0.12, both P>0.05), but the expression of α-SMA after hyperoxia exposure for 14 days and 21 days was increased compared with normal control group (1.27±0.21 vs. 1.05±0.15, 2.26±0.28 vs. 1.05±0.14, P<0.05 and P<0.01). CONCLUSIONS: Pulmonary fibrosis remodeling was caused by hyperoxia exposure. The expression of α-SMA in pulmonary tissue in hyperoxia exposure groups obviously increased, and could play an important role in pulmonary fibrosis remodeling.


Assuntos
Actinas/metabolismo , Hiperóxia/metabolismo , Lesão Pulmonar/metabolismo , Animais , Hiperóxia/complicações , Pulmão/metabolismo , Lesão Pulmonar/etiologia , Masculino , Ratos , Ratos Sprague-Dawley
7.
Exp Lung Res ; 36(6): 352-61, 2010 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-20653470

RESUMO

The production of reactive oxygen species (ROS) during hyperoxia contribute to alveolar epithelial apoptosis. In the present study, the molecular mechanisms of oxidative stress-induced alveolar epithelial cell apoptosis were investigated. The cytoprotective effects of N-acetylcysteine (NAC) were evaluated. Treatments using 500 muM H(2)O(2) can induce primary alveolar type II epithelial cell apoptosis. During this procedure, c-Jun N-terminal kinase (JNK) was activated. SP600125, a specific inhibitor of JNK, can partially block H(2)O(2)-induced alveolar type II epithelial cells (ATII cells). SP600125 also attenuated Bax protein content and p53 nuclear accumulation induced by H(2)O(2). NAC (5 mM) pretreatment decreased H(2)O(2)-induced ATII cell apoptosis. The high level of intracellular reactive oxygen species (ROS) induced by H(2)O(2) was also attenuated by NAC pretreatment. Taken together, H(2)O(2) can induce primary ATII cells apoptosis and increase JNK phosphorylation. NAC, a precursor of glutathione (GSH) synthesis, can protect ATII cells from H(2)O(2)-induced apoptosis through scavenging ROS.


Assuntos
Acetilcisteína/farmacologia , Células Epiteliais Alveolares/efeitos dos fármacos , Apoptose/efeitos dos fármacos , Depuradores de Radicais Livres/farmacologia , Peróxido de Hidrogênio/toxicidade , Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo , Oxidantes/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Espécies Reativas de Oxigênio/metabolismo , Células Epiteliais Alveolares/enzimologia , Células Epiteliais Alveolares/patologia , Animais , Antracenos/farmacologia , Células Cultivadas , Citoproteção , Relação Dose-Resposta a Droga , Regulação para Baixo , Glutationa/metabolismo , Proteínas Quinases JNK Ativadas por Mitógeno/antagonistas & inibidores , Masculino , Fosforilação , Inibidores de Proteínas Quinases/farmacologia , Ratos , Ratos Sprague-Dawley , Fatores de Tempo , Proteína Supressora de Tumor p53/metabolismo , Proteína X Associada a bcl-2/metabolismo
8.
Zhongguo Dang Dai Er Ke Za Zhi ; 11(5): 389-92, 2009 May.
Artigo em Chinês | MEDLINE | ID: mdl-19470265

RESUMO

OBJECTIVE: Some research has shown that p38 mitogen-activated protein kinase (p38MAPK) plays important roles in lung injuries induced by various factors. Its expression and role in hyperoxia-induced lung injury remains unknown. This study investigated the expression and role of p38MAPK in hyperoxia-induced lung injury juvenile rat model. METHODS: Hyperoxia-induced lung injury rat model was prepared by 90% O(2) exposure. The location and expression of p38MAPK in lung tissues were detected by immunohistochemistry and Western blot respectively. Apoptosis index of lung was evaluated by TUNEL technique. The effect of SB203580, a p38MAPK inhibitor, on the apoptosis index of lung was observed. RESULTS: The expression of phosphor-p38MAPK increased obviously after hyperoxia. Positive phosphor-p38MAPK cells were mainly distributed in the alveolar, airway epithelial cells, pulmonary vascular endothelium cells and infiltrative inflammatory cells. The apoptosis index of lung also significantly elevated. SB203580 inhibited the activation of p38MAPK, and reduced the apoptosis index of lung. CONCLUSIONS: The phosphor-p38MAPK increased and was expressed in many kinds of lung cells in lung injury rat model. It may play a role in the induction of apoptosis in hyperoxia-induced lung injury.


Assuntos
Hiperóxia/complicações , Proteínas Quinases p38 Ativadas por Mitógeno/fisiologia , Animais , Apoptose , Modelos Animais de Doenças , Feminino , Imidazóis/uso terapêutico , Immunoblotting , Lesão Pulmonar/tratamento farmacológico , Lesão Pulmonar/enzimologia , Lesão Pulmonar/etiologia , Sistema de Sinalização das MAP Quinases , Masculino , Fosforilação , Piridinas/uso terapêutico , Ratos , Ratos Wistar , Proteínas Quinases p38 Ativadas por Mitógeno/análise
9.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue ; 20(10): 578-81, 2008 Oct.
Artigo em Chinês | MEDLINE | ID: mdl-18926064

RESUMO

OBJECTIVE: To study in vitro the influence of 60% oxygen and the protective effect of calcitonin gene-related peptide (CGRP) on type II alveolar epithelial cells (AEC II) isolated from the lung of premature rat. METHODS: AEC II were isolated from the lung of 19-day rat fetus, and they were then cultured in six-well plates. The cells were randomly divided into four groups: air group, hyperoxia group, hyperoxia plus CGRP group, hyperoxia plus CGRP and CGRP8-37 (CGRP receptor antagonist) group. Cells of air group and hyperoxia group were exposed to 21% air or 60% oxygen, respectively, while in hyperoxia plus CGRP group CGRP was added, and in hyperoxia plus CGRP and CGRP8-37 group CGRP and CGRP8-37 were added before exposure to 60% oxygen. Cells in four groups were cultured for 24 hours, and then ground into homogenates for detection of malondialdehyde (MDA), total antioxidant capacity (TAOC) and superoxide dismutase (SOD) with ultraviolet spectrophotometer. Reactive oxygen species (ROS) and apoptosis rate of AEC II were analyzed by flow cytometry and the mRNA level of surfactant associated protein C (SPC) was measured by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The levels of ROS, MDA and apoptosis rate were increased whereas TAOC, SOD and SPC mRNA expression declined in hyperoxia group compared with those in air group (all P<0.01). In contrast, MDA, ROS and apoptosis rate were significantly lower and levels of TAOC, SOD and SPC mRNA expression were significantly higher in hyperoxia plus CGRP group than those in hyperoxia group (all P<0.01). The differences in 6 parameters above between hyperoxia group and hyperoxia plus CGRP and CGRP8-37 group were not statistically significant. CONCLUSION: Exposure of AEC II from immature rat to 60% oxygen for 24 hours may produce oxidative injury, inducing apoptosis and decrease in SPC mRNA level of AEC II of premature rat in vitro, while CGRP may play a protective role against hyperoxic lung injury by its antioxidant property, and also inhibition of AEC II apoptosis and promotion of the SPC mRNA expression.


Assuntos
Células Epiteliais Alveolares/efeitos dos fármacos , Peptídeo Relacionado com Gene de Calcitonina/farmacologia , Oxigênio/toxicidade , Células Epiteliais Alveolares/metabolismo , Células Epiteliais Alveolares/patologia , Animais , Animais Recém-Nascidos , Apoptose/efeitos dos fármacos , Hipóxia Celular , Células Cultivadas , Feminino , Masculino , Malondialdeído/metabolismo , Ratos , Ratos Sprague-Dawley , Superóxido Dismutase/metabolismo
10.
Artigo em Chinês | MEDLINE | ID: mdl-18279588

RESUMO

OBJECTIVE: To investigate the effects of oxidative stress on the survival and apoptosis of alveolar epithelial type II (ATII) cells, as well as the mechanisms of apoptosis. METHODS: 500 mumol/L H(2)O(2) was added into primary ATII cells at different times and cell viability, apoptotic ratio and the expression of Bax and p53 were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry (FCM) and Western blotting analysis, respectively. The change in mitochondrial membrane potential (MMP) was detected by fluorescence microscopy and FCM. RESULTS: The cell viability and MMP were decreased by H(2)O(2) compared with the controls (F(1)=85.211, F(2)=72.453, respectively, both P<0.05). The cell apoptotic ratios were increased with the time of the stimulation prolonged compared with the controls (F=54.002, P<0.05). H(2)O(2) increased Bax and p53 protein levels (F(1)=28.118, F(2)=43.456, both P<0.05). CONCLUSION: High level of oxidative stress can inhibit ATII cells proliferation, and induce cells apoptosis and decrease the MMP. Up-regulation of the expression of Bax and p53 may contribute to its apoptosis effects.


Assuntos
Células Epiteliais Alveolares/patologia , Apoptose , Estresse Oxidativo , Proteína Supressora de Tumor p53/metabolismo , Proteína X Associada a bcl-2/metabolismo , Células Epiteliais Alveolares/metabolismo , Animais , Sobrevivência Celular , Células Cultivadas , Masculino , Potencial da Membrana Mitocondrial , Ratos , Ratos Sprague-Dawley
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