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Background  

Ankylosing spondylitis is a chronic inflammatory rheumatic disorder which usually begins in early adulthood. The diagnosis is often delayed by many years. MR imaging has become the preferred imaging method for detection of early inflammation of the axial skeleton in ankylosing spondylitis.  相似文献   
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Breast cancer tissue is able to maintain the tissue estradiol level in spite of the massive decrease in plasma estradiol associated with menopause, whereas fatty tissue from breasts with malignancies more closely reflects the changes in plasma. In the present study estrone and estradiol levels in fatty tissues from different origins were compared to evaluate the capacity of distant fatty tissues to act as estrogen reservoirs. Abdominal fat was obtained from 25 premenopausal and 20 postmenopausal women who underwent surgery for non-oncological reasons. Estrone and estradiol levels in these tissues were compared to those in breast fatty tissue from breast cancer patients. Plasma estrogen levels were not different in the two groups. In both groups, median plasma estradiol levels dropped sharply with menopause (from 363 to 40 pmol/l in breast cancer patients; from 280 to 45 pmol/l in the non-oncological patients; p less than 0.002), whereas a significant decrease in plasma estrone was observed only in the breast cancer patients (from 238 to 140 pmol/l; p less than 0.02). In premenopausal women, median estrone and estradiol levels in breast fatty tissue (1135 and 375 fmol/g, respectively) and abdominal tissue (1390 and 470 fmol/g, respectively) were not different. In postmenopausal women, however, significantly higher estrone levels (663 vs. 508 fmol/g; p less than 0.01) and estradiol levels (245 vs. 187 fmol/g; p less than 0.02) were found in abdominal fatty tissue. In view of the absolute estrogen levels in breast and abdominal fatty tissue and in plasma, we conclude, however, that it is unlikely that remote fat contributes substantially to the maintenance of estrogen levels in breast cancer tissue.  相似文献   
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Objectives

The aim of the study was to characterize the differences in the frequencies of NS3 and NS5A resistance-associated variants (RAVs) among Polish therapy-naive genotype 1 (G1) hepatitis C virus (HCV)-monoinfected and human immunodeficiency virus (HIV)/HCV-coinfected patients including clustering patterns and association of RAV frequency with liver fibrosis.

Methods

NS3/NS5A RAVs were identified by population sequencing in 387 directly acting antiviral treatment-naive G1-infected individuals (54 with genotype 1a (G1a) and 333 with genotype 1b (G1b)). Liver fibrosis was assessed based on histopathology or ultrasound elastography. Phylogenetic clusters were identified using maximum likelihood models. For statistics, chi-squared or two-sided Fisher's exact tests and multivariate logistic regression models were used, as appropriate.

Results

NS3 RAVs were found in 33.33% (18/54) for G1a and 2.62% (8/297) for G1b whereas NS5A variants were present in 5.55% (3/54) G1a and 9.31% (31/333) G1b sequences. Variations in NS5A 31 and 93 codon positions were found only in G1b (4.2% (14/333) for L31I/F/M and 5.39% (17/333) for Y93H). NS5A RAVs were more frequent among patients with advanced liver fibrosis (17.17% (17/99) for F3–F4 versus 6.94% (17/245) for F0–F2; p 0.004) or liver cirrhosis (20.34% (12/59) for F4 versus 7.72% (22/285) for F0–F3; p 0.003). Liver cirrhosis (F4) was associated with higher odds ratio of the NS5A RAVs among HCV-infected patients (odds ratio 2.34, 95% CI 1.004–5.291; p 0.049). NS5A RAVs were less frequent among sequences forming clusters and pairs (5.16% (8/155) versus 11.21% (26/232); p 0.039).

Conclusions

Presence of NS5A RAVs correlated with progression of liver fibrosis and represents de novo selection of variants rather than transmission of drug resistance. Hence, the presence of NS5A RAVs may be a predictor for a long-lasting HCV infection.  相似文献   
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目的:研究低氧时小鼠肺组织中低氧诱导因子-1α(HIF-k)表达的变化。方法:实验用雄性小鼠,低氧仓浓度分别为10%、7%、5%。用免疫荧光组织化学技术及共聚焦显微术,检测小鼠在低氧条件下肺组织中HIF-1α表达的变化。结果:正常组小鼠肺组织HIF-1α无表达,低氧组HIF-1α表达增加,且随低氧时间的延长及低氧强度的增加而增强。结论:低氧可诱导小鼠肺组织中HIF-1α的表达增强,(HIF-k)可能参与肺组织细胞凋亡的发生。  相似文献   
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