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1.
Journal of Experimental Hematology ; (6): 767-774, 2020.
Article in Chinese | WPRIM | ID: wpr-829045

ABSTRACT

OBJECTIVE@#To study the risk factors and infection characteristics of nosocomial infection in children with acute lymphoblastic leukemia (ALL) and analyze the relationship between different nutritional status and nosocomial infection, early treatment response.@*METHOD@#The clinical data of 133 children with ALL treated with CCCG-ALL-2015 from June 2016 to June 2019 (chemotherapy stage, risk level, MRD), infection during hospitalization (course of infection, laboratory indicators, sites of infection, outcome) and nutritional status (sex, age, height/ length, weight) were enrolled. The Chi 2 test and Logistic regression analysis were used for statistical analysis.@*RESULTS@#The rate of nosocomial infection was 19.9% in 133 children with ALL, in which 3 were infection-related death. Sex, immunophenotype and risk showed no significantly affect on the occurrence of nosocomial infection (P>0.05), but neutrophil count, hemoglobin level, platelet count, chemotherapy stage, length of stay in hospital and nutritional status showed affect on the occurrence of nosocomial infection (P<0.05). Logistic multivariate regression analysis showed that chemotherapy stage, length of hospital stay, neutrophils and nutritional status were the independent risk factors, in which the respiratory tract infection was the most common. Gram-positive bacteria, Gram-negative bacteria and fungi accounted for 44.1%, 52.9% and 2.9% respectively. The negative rate of MRD in day 19 and day 46 between different nutritional status groups showed statistically significant (P<0.05).@*CONCLUSION@#Neutrophil count, chemotherapy stage, length of stay in hospital and nutritional status are independent risk factors for nosocomial infection. Among of them, nutritional status negatively correlated with nosocomial infection, and the poorer nutritional status, the higher risk of nosocomial infection. Malnutrition, overweight and obesity can affect the early treatment response of ALL children. The level of nutrition at first diagnosis can be used as a bad factor to evaluate the early treatment response of ALL children.


Subject(s)
Child , Humans , Cross Infection , Gram-Negative Bacteria , Nutritional Status , Precursor Cell Lymphoblastic Leukemia-Lymphoma , Retrospective Studies
2.
Biomolecules & Therapeutics ; : 121-129, 2018.
Article in English | WPRIM | ID: wpr-713584

ABSTRACT

Oxidized low-density lipoprotein (ox-LDL)-induced macrophage foam cell formation and apoptosis play critical roles in the pathogenesis of atherosclerosis. Thioredoxin-1 (Trx) is an antioxidant that potently protects various cells from oxidative stress-induced cell death. However, the protective effect of Trx on ox-LDL-induced macrophage foam cell formation and apoptosis has not been studied. This study aims to investigate the effect of recombinant human Trx (rhTrx) on ox-LDL-stimulated RAW264.7 macrophages and elucidate the possible mechanisms. RhTrx significantly inhibited ox-LDL-induced cholesterol accumulation and apoptosis in RAW264.7 macrophages. RhTrx also suppressed the ox-LDL-induced overproduction of lectin-like oxidized LDL receptor (LOX-1), Bax and activated caspase-3, but it increased the expression of Bcl-2. In addition, rhTrx markedly inhibited the ox-LDL-induced production of intracellular reactive oxygen species (ROS) and phosphorylation of p38 mitogen-activated protein kinases (MAPK). Furthermore, anisomycin (a p38 MAPK activator) abolished the protective effect of rhTrx on ox-LDL-stimulated RAW264.7 cells, and SB203580 (a p38 MAPK inhibitor) exerted a similar effect as rhTrx. Collectively, these findings indicate that rhTrx suppresses ox-LDL-stimulated foam cell formation and macrophage apoptosis by inhibiting ROS generation, p38 MAPK activation and LOX-1 expression. Therefore, we propose that rhTrx has therapeutic potential in the prevention and treatment of atherosclerosis.


Subject(s)
Humans , Anisomycin , Apoptosis , Atherosclerosis , Caspase 3 , Cell Death , Cholesterol , Foam Cells , Lipoproteins , Macrophages , p38 Mitogen-Activated Protein Kinases , Phosphorylation , Reactive Oxygen Species , Receptors, Oxidized LDL , Thioredoxins
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