| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-99 |
Sentence |
denotes |
Glucocorticoid-mediated repression of cytokine gene transcription in human arteritis-SCID chimeras. |
| T1 |
0-99 |
Sentence |
denotes |
Glucocorticoid-mediated repression of cytokine gene transcription in human arteritis-SCID chimeras. |
| T2 |
100-212 |
Sentence |
denotes |
Giant cell arteritis (GCA) is a vasculitic syndrome that preferentially affects medium and large-sized arteries. |
| T2 |
100-212 |
Sentence |
denotes |
Giant cell arteritis (GCA) is a vasculitic syndrome that preferentially affects medium and large-sized arteries. |
| T3 |
213-364 |
Sentence |
denotes |
Glucocorticoid therapy resolves clinical symptoms within hours to days, but therapy has to be continued over several years to prevent disease relapses. |
| T3 |
213-364 |
Sentence |
denotes |
Glucocorticoid therapy resolves clinical symptoms within hours to days, but therapy has to be continued over several years to prevent disease relapses. |
| T4 |
365-532 |
Sentence |
denotes |
It is not known whether and how glucocorticoids affect the function of the inflammatory infiltrate or why the disease persists subclinically despite chronic treatment. |
| T4 |
365-532 |
Sentence |
denotes |
It is not known whether and how glucocorticoids affect the function of the inflammatory infiltrate or why the disease persists subclinically despite chronic treatment. |
| T5 |
533-720 |
Sentence |
denotes |
GCA is self-sustained in temporal arteries engrafted into SCID mice, providing a model in which the mechanisms of action and limitations of glucocorticoid therapy can be examined in vivo. |
| T5 |
533-720 |
Sentence |
denotes |
GCA is self-sustained in temporal arteries engrafted into SCID mice, providing a model in which the mechanisms of action and limitations of glucocorticoid therapy can be examined in vivo. |
| T6 |
721-1001 |
Sentence |
denotes |
Administration of dexamethasone to temporal artery-SCID chimeras for 1 wk induced a partial suppression of T cell and macrophage function as indicated by the reduced tissue concentrations of IL-2, IL-1beta, and IL-6 mRNA, and by the diminished expression of inducible NO synthase. |
| T6 |
721-1001 |
Sentence |
denotes |
Administration of dexamethasone to temporal artery-SCID chimeras for 1 wk induced a partial suppression of T cell and macrophage function as indicated by the reduced tissue concentrations of IL-2, IL-1beta, and IL-6 mRNA, and by the diminished expression of inducible NO synthase. |
| T7 |
1002-1115 |
Sentence |
denotes |
In contrast, synthesis of IFN-gamma mRNA was only slightly decreased, and expression of TGF-beta1 was unaffected. |
| T7 |
1002-1115 |
Sentence |
denotes |
In contrast, synthesis of IFN-gamma mRNA was only slightly decreased, and expression of TGF-beta1 was unaffected. |
| T8 |
1116-1268 |
Sentence |
denotes |
These findings correlated with activation of the IkappaBalpha gene and blockade of the nuclear translocation of NFkappaB in the xenotransplanted tissue. |
| T8 |
1116-1268 |
Sentence |
denotes |
These findings correlated with activation of the IkappaBalpha gene and blockade of the nuclear translocation of NFkappaB in the xenotransplanted tissue. |
| T9 |
1269-1455 |
Sentence |
denotes |
Dose-response experiments suggested that steroid doses currently used in clinical medicine are suboptimal in repressing NFkappaB-mediated cytokine production in the inflammatory lesions. |
| T9 |
1269-1455 |
Sentence |
denotes |
Dose-response experiments suggested that steroid doses currently used in clinical medicine are suboptimal in repressing NFkappaB-mediated cytokine production in the inflammatory lesions. |
| T10 |
1456-1626 |
Sentence |
denotes |
Chronic steroid therapy was able to deplete the T cell products IL-2 and IFN-gamma, whereas the activation of tissue-infiltrating macrophages was only partially affected. |
| T10 |
1456-1626 |
Sentence |
denotes |
Chronic steroid therapy was able to deplete the T cell products IL-2 and IFN-gamma, whereas the activation of tissue-infiltrating macrophages was only partially affected. |
| T11 |
1627-1725 |
Sentence |
denotes |
IL-1beta transcription was abrogated; in contrast, TGF-beta1 mRNA synthesis was steroid resistant. |
| T11 |
1627-1725 |
Sentence |
denotes |
IL-1beta transcription was abrogated; in contrast, TGF-beta1 mRNA synthesis was steroid resistant. |
| T12 |
1726-1959 |
Sentence |
denotes |
The persistence of TGF-beta1-transcribing macrophages, despite paralysis of T cell function, may provide an explanation for the chronicity of the disease, and may identify a novel therapeutic target in this inflammatory vasculopathy. |
| T12 |
1726-1959 |
Sentence |
denotes |
The persistence of TGF-beta1-transcribing macrophages, despite paralysis of T cell function, may provide an explanation for the chronicity of the disease, and may identify a novel therapeutic target in this inflammatory vasculopathy. |