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1.
Pietras T Szemraj J Panek M Witusik A Banasiak M Antczak A Górski P 《Molecular biology reports》2012,39(3):2163-2167
Cyclooxygenase two (COX-2) is an important enzyme metabolizing arachidonic acid. In contrast to constitutive cyclooxygenase
one (COX-1), COX-2 is induced by proinflammatory factors. Polymorphism −765G/C in COX-2-encoding gene promoter is associated
with development of Alzheimer’s disease, depression, carcinoma of the pancreas in smokers, breast cancer and rheumatoid arthritis.
It is interesting whether the −765G/C polymorphism in COX-2-encoding gene promoter can be associated with COPD, a disease
which is inflammatory in character. It is highly probable as the breast and pancreas cancers, whose associations with the
analyzed polymorphism have been studied, are smoking-dependent tumors. Additionally, tobacco smoke has been demonstrated to
induce COX-2 in the lungs. The study group consisted of 122 COPD patients (48 females, 74 males). The control group consisted
of 149 healthy nonsmoking subjects (83 females, 66 males). Polymerase chain reaction/restriction fragment length polymorphism
was used for genotyping. A statistically significant difference in genotype distribution was observed as a result of the comparison
between healthy subjects and patients with COPD. The distribution of alleles in both groups conformed with Hardy–Weinberg
equilibrium. In the group of COPD patients, GG allele was found in 79 subjects, GC in 36, and CC in 7 subjects (F = 0.094,
P = 0.296927); in the control group, 73 subjects had GG allele, 68—GC and 8—CC (F = 0.12728, P = 0.120265). The allele frequency revealed differences between those groups, attaining the level of statistical significance
(χ2 = 29.043, df = 2, P = 0.0000. The carriers of −765G allele are at 1.53-fold higher risk of developing COPD. The presence of GG genotype does
not increase significantly the risk of the disease. It is also noteworthy that the carriers of CC or GC genotypes are at significantly
lower risk of developing COPD than the group of subjects with GG genotype. 相似文献
2.
Kamio K Yoshida T Gao C Ishii T Ota F Motegi T Kobayashi S Fujinawa R Ohtsubo K Kitazume S Angata T Azuma A Gemma A Nishimura M Betsuyaku T Kida K Taniguchi N 《Biochemical and biophysical research communications》2012,424(1):112-117
Fut8 (α1,6-Fucosyltransferase) heterozygous knock-out (Fut8(+/-)) mice had an increased influx of inflammatory cells into the lungs, and this was associated with an up-regulation of matrix metalloproteinases, MMP-2 and MMP-9, after treatment with porcine pancreatic elastase (PPE), exhibiting an emphysema-prone phenotype as compared with wild type mice (Fut8(+/+)). The present data as well as our previous data on cigarette-smoke-induced emphysema [8] led us to hypothesize that reduced Fut8 levels leads to COPD with increased inflammatory response in humans and is associated with disease progression. To test this hypothesis, symptomatic current or ex-smokers with stable COPD or at risk outpatients were recruited. We investigated the association between serum Fut8 activity and disease severity, including the extent of emphysema (percentage of low-attenuation area; LAA%), airflow limitation, and the annual rate of decline in forced expiratory volume in 1 s (FEV(1)). Association with the exacerbation of COPD was also evaluated over a 3-year period. Serum Fut8 and MMP-9 activity were measured. Fut8 activity significantly increased with age among the at risk patients. In the case of COPD patients, however, the association was not clearly observed. A faster annual decline of FEV(1) was significantly associated with lower Fut8 activity. Patients with lower Fut8 activity experienced exacerbations more frequently. These data suggest that reduced Fut8 activity is associated with the progression of COPD and serum Fut8 activity is a non-invasive predictive biomarker candidate for progression and exacerbation of COPD. 相似文献
3.
Timothy Tilert Charles Dillon Ryne Paulose-Ram Eva Hnizdo Brent Doney 《Respiratory research》2013,14(1):103