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1.
Chinese Journal of Clinical Nutrition ; (6): 78-83, 2017.
Article in Chinese | WPRIM | ID: wpr-512460

ABSTRACT

Objective To determine postoperative resting energy expenditure ( REE) in children with congenital heart disease ( CHD) requiring open heart surgery , to compare measured resting energy expenditure (MREE) with current predictive equations (PEE), and to investigate the possible influencing factors on the metabolic status of the postoperative CHD children .Methods From February 2015 to June 2015 , 150 ventila-ted children admitted to the cardiac intensive care unit after surgery for congenital heart disease in Shanghai Children's Medical Center were enrolled consecutively .Indirect calorimetry ( IC) measurements were performed using metabolic cart 4 hours after surgery .General clinical data were recorded .Results Totally 104 male and 46 female patients were enrolled, with a median age of 14 months (8.3-36.0 months).The non-protein re-spiratory quotient of patient was 0.79 ±0.20, MREE was (264.76 ±61.74) kJ/(kg· d), and PEE using Schofield equations was (278.51 ±93.42) kJ/(kg· d).Although there was no significant differences (P=0.096 ) between MREE and PEE , the agreement was poor between them ( R2 =0.119 ) .Multivariate stepwise regression analysis showed that MREE had significant positive correlation with risk adjustment in congenital heart surgery (RACHS-1) score (P=0.012) and negative correlation with age (P=0.010).Up to 97.33%of children (146/150) had lower energy intake compared with MREE on the 1st postoperative day .Conclu-sions MREE does not increase after surgery in CHD children;however , the substrate utilization is influenced . Factors influencing the postoperative REE include RACHS-1 score and age.The energy intake at 1st day after surgery is generally lower than REE in these children .

2.
International Journal of Pediatrics ; (6): 744-748, 2017.
Article in Chinese | WPRIM | ID: wpr-663877

ABSTRACT

Congenital heart disease(CHD)is the most common congenital developmental defects in chil-dren,with an incidence ranging from 0.3% to 1% in China.Activity energy expenditure and food specific dy-namic effects caused by chronic continuous hypoxia can increase energy expenditure in children with congenital heart disease.Human body component changes and heart failure could also result in energy consumption in-crease,together with feeding deficiency due to oral sensory disorders and disrupted swallowing function,which lead to the increased incidence of malnutrition in children(up to 50%).Surgical trauma and related treatments will make significant metabolism change to the perioperative CHD children,and there has been a high prevalence of deteriorating nutritional status among them.Too much or too little perioperative energy intake are both unfa-vorable to children's clinical outcomes.Therefore,this study intends to review the influence factors of perinatal energy metabolism in children with CHD,to provide evidences of perioperative clinical nutritional support of children with CHD.

3.
Chinese Journal of Radiation Oncology ; (6): 471-474, 2010.
Article in Chinese | WPRIM | ID: wpr-387481

ABSTRACT

Objective To investigate whether gemcitabine (GEM) could enhance radiosensitivity of human non-small cell lung cancer cells and its related mechanism.Methods Clonogenic assay was used to analyze radiosensitivity enhancement by GEM on p53 mutant human lung adenocarcinoma cell line 973.Alterations of cell cycle distribution and apoptosis were measured by flow cytometry.Results Mild radiosesitizing effect was observed when 10 nmol/L GEM was administrated before or after irradiation.Marked radiosesitizing effect was demonstrated when 100 nmol/L GEM was administrated before or after irradiation, with much stronger effect of pre-irradiation GEM treatment.Mutation of p53 gene affected cell cycle redistribution and cell apoptosis, but had no relationship with radiosensitivity enhancement of GEM.Conclusions 100 nmol/L GEM could significantly enhance radiosensitivity of human lung cancer cells.However, this effect may not be associated with p53 gene mutation, cell cycle redistribution or cell apoptosis.

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