Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 3 de 3
Filter
1.
Biomedical and Environmental Sciences ; (12): 602-613, 2019.
Article in English | WPRIM | ID: wpr-773366

ABSTRACT

OBJECTIVE@#To comparatively study the toxicity of four metal-containing nanoparticles (MNPs) and their chemical counterparts to the air-blood barrier (ABB) permeability using an in vitro model.@*METHODS@#ABB model, which was developed via the co-culturing of A549 and pulmonary capillary endothelium, was exposed to spherical CuO-NPs (divided into CuO-40, CuO-80, and CuO-100 based on particle size), nano-Al2O3 (sheet and short-rod-shaped), nano-ZnO, nano-PbS, CuSO4, Al2(SO4)3, Zn(CH3COO)2, and Pb(NO3)2 for 60 min. Every 10 min following exposure, the cumulative cleared volume (ΔTCL) of Lucifer yellow by the model was calculated. A clearance curve was established using linear regression analysis of ΔTCL versus time. Permeability coefficient (P) was calculated based on the slope of the curve to represent the degree of change in the ABB permeability.@*RESULTS@#The results found the increased P values of CuO-40, CuO-80, sheet, and short-rod-shaped nano-Al2O3, Al2(SO4)3, and Pb(NO3)2. Among them, small CuO-40 and CuO-80 were stronger than CuO-100 and CuSO4; no difference was observed between Al2(SO4)3 and sheet and short-rod-shaped nano-Al2O3; and nano-PbS was slightly weaker than Pb(NO3)2. So clearly the MNPs possess diverse toxicity.@*CONCLUSION@#ABB permeability abnormality means pulmonary toxicity potential. More studies are warranted to understand MNPs toxicity and ultimately control the health hazards.


Subject(s)
Humans , A549 Cells , Blood-Air Barrier , Metabolism , Epithelium , Metabolism , Metal Nanoparticles , Toxicity , Particle Size , Permeability
2.
Biomedical and Environmental Sciences ; (12): 670-677, 2011.
Article in English | WPRIM | ID: wpr-235583

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the association of polymorphisms of STAT6 gene and air pollutants of PM(10), NO(2), and SO(2), with asthma in Chinese children.</p><p><b>METHODS</b>418 subjects aged 14 years and under were recruited in a case-control study. The association between STAT6 polymorphisms and childhood asthma were tested by allele frequency, genotype analysis, and MDR analysis. Exposure to outdoor air pollutants was estimated by a 5-day moving average level. Statistical analyses were performed with SAS 9.1 software.</p><p><b>RESULTS</b>Only 3 alleles of GT repeats at exon 1 of STAT6 were found in Chinese children. C258T and T710C were 2 new SNPs of STAT6 at 3'-UTR. Children who carried T allele of C258T were more common in asthma children than in control subjects (P<0.05). The MDR analysis showed that GT repeats, C258T and T710C of STAT6 polymorphisms interacted together in leading to susceptibility to childhood asthma among Chinese people. After confounding factors were controlled, such as SNP C258T, family history of asthma, frequency of influenza within a year, the 5-day average of SO(2) was tested to be a key risk factor of asthma in Chinese children (P<0.05).</p><p><b>CONCLUSION</b>Chinese children differed in polymorphisms of STAT6 and in its relation with childhood asthma.</p>


Subject(s)
Adolescent , Child , Child, Preschool , Female , Humans , Male , Air Pollutants , Toxicity , Asian People , Genetics , Asthma , Epidemiology , Genetics , Case-Control Studies , China , Epidemiology , Dinucleotide Repeats , Genetic Predisposition to Disease , Polymorphism, Single Nucleotide , STAT6 Transcription Factor , Genetics , Sulfur Dioxide , Toxicity
3.
Chinese Journal of Hematology ; (12): 383-385, 2006.
Article in Chinese | WPRIM | ID: wpr-243942

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the significance of mutation and single nucleotide polymorphism (SNP) of class III receptor tyrosine kinases such as PDGFRbeta and SHIP in acute myeloid leukemia (AML) patients.</p><p><b>METHODS</b>Screening of the mutation and SNP of PDGFRbeta and SHIP by genomic PCR, RT-PCR, directly sequencing and Mass-ARRAY system was carried out in 273 AML patients.</p><p><b>RESULTS</b>The mutations of PDGFRbeta R685C and SHIP Q1153L were detected for the first time in AML patients. The positivity ratio was 0.73% and 0.36% respectively.</p><p><b>CONCLUSION</b>The mutations of PDGFRbeta R685C and SHIP Q1153L may contribute to leukemogenesis of AML.</p>


Subject(s)
Humans , Inositol Phosphates , Genetics , Leukemia, Myeloid, Acute , Genetics , Mass Spectrometry , Mutation , Polymerase Chain Reaction , Polymorphism, Single Nucleotide , Receptor, Platelet-Derived Growth Factor beta , Genetics , Reverse Transcriptase Polymerase Chain Reaction
SELECTION OF CITATIONS
SEARCH DETAIL