INT77677

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Context Info
Confidence 0.49
First Reported 1998
Last Reported 2009
Negated 0
Speculated 1
Reported most in Body
Documents 30
Total Number 31
Disease Relevance 33.19
Pain Relevance 11.18

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

Anatomy Link Frequency
macrophages 2
plasma 2
monocytes 2
liver 1
body 1
Saa (Mus musculus)
Pain Link Frequency Relevance Heat
spinal inflammation 701 99.90 Very High Very High Very High
Inflammation 791 99.68 Very High Very High Very High
Inflammatory stimuli 18 99.20 Very High Very High Very High
Inflammatory response 98 98.40 Very High Very High Very High
spondylitis 51 98.00 Very High Very High Very High
cytokine 142 97.92 Very High Very High Very High
corticosteroid 19 93.24 High High
rheumatoid arthritis 69 92.12 High High
Crohn's disease 75 91.00 High High
cINOD 68 90.52 High High
Disease Link Frequency Relevance Heat
Alzheimer's Dementia 188 99.92 Very High Very High Very High
Low Back Pain 752 99.90 Very High Very High Very High
Stress 444 99.68 Very High Very High Very High
Atherosclerosis 149 99.48 Very High Very High Very High
INFLAMMATION 626 99.20 Very High Very High Very High
Colitis 207 98.90 Very High Very High Very High
Disease 741 98.88 Very High Very High Very High
Coronary Artery Disease 2 98.68 Very High Very High Very High
Amyloidosis 132 98.64 Very High Very High Very High
Targeted Disruption 76 97.96 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This supposition would also be in accord with the rapidity of the effect: in a time-resolved analysis of plasma SAA during atherogenesis, we report here a strong elevation of plasma SAA within two weeks of cholesterol-feeding in female E3L mice.
Positive_regulation (elevation) of SAA in plasma associated with targeted disruption and atherosclerosis
1) Confidence 0.49 Published 2007 Journal Genome Biol Section Body Doc Link PMC2375038 Disease Relevance 1.78 Pain Relevance 0.34
SAA was significantly elevated in the HC group, pointing to a hepatic inflammatory response to cholesterol feeding (Table 1) that is associated with early atherosclerotic lesion formation.


Positive_regulation (elevated) of SAA associated with inflammatory response, inflammation and atherosclerosis
2) Confidence 0.49 Published 2007 Journal Genome Biol Section Body Doc Link PMC2375038 Disease Relevance 1.13 Pain Relevance 0.25
Patients with AS had increased SAA levels, with a mean value of 9.52 ± 7.49 mg/L.
Positive_regulation (increased) of SAA associated with spinal inflammation
3) Confidence 0.45 Published 2007 Journal Yonsei Medical Journal Section Body Doc Link PMC2628111 Disease Relevance 1.61 Pain Relevance 1.25
For example, liver-derived inflammation markers such as C-reactive protein (CRP) and serum amyloid A (SAA) increase rapidly (within days) after consumption of an excess amount of dietary lipids [8,10], and thus by far precede the onset of early aortic lesion formation [8].
Positive_regulation (increase) of SAA in liver associated with inflammation and alzheimer's dementia
4) Confidence 0.41 Published 2007 Journal Genome Biol Section Body Doc Link PMC2375038 Disease Relevance 1.25 Pain Relevance 0.33
To investigate whether serum amyloid A (SAA) levels are increased in patients with ankylosing spondylitis (AS) and whether its levels correlate well with AS disease activity.


Spec (whether) Positive_regulation (increased) of SAA associated with spinal inflammation, alzheimer's dementia and disease
5) Confidence 0.35 Published 2007 Journal Yonsei Medical Journal Section Abstract Doc Link PMC2628111 Disease Relevance 1.08 Pain Relevance 0.52
A time course study with 1% w/w cholesterol (HC diet) showed that plasma SAA levels started to increase after 2 weeks and that plasma SAA levels continued to increase over time (Figure 4c).
Positive_regulation (increase) of SAA in plasma associated with inflammation
6) Confidence 0.33 Published 2007 Journal Genome Biol Section Body Doc Link PMC2375038 Disease Relevance 1.42 Pain Relevance 0.50
, and its level is more sensitive than CRP.6,21-23 Other reports on PMR suggested that serum SAA is more predominant than ESR or CRP with regard to sensitivity and specificity, respectively, and its level can reflect the disease activity effectively.8,24,25 But, in AS, SAA has not been studied as extensively as in RA or PMR, and we could find only a few studies investigating the association between SAA and disease activity of AS.21,26,27 One of these studies reported that SAA levels in patients with AS correlated well with BASDAI scores, and that ESR and CRP levels seem to be a good indicator of disease activity.21 Our results were also similar to those previously reported, but we tried to identify the superiority of SAA to ESR or CRP in determining the extent of AS disease activity.
Positive_regulation (superiority) of SAA associated with spinal inflammation, polymyalgia rheumatica, rheumatoid arthritis and disease
7) Confidence 0.33 Published 2007 Journal Yonsei Medical Journal Section Body Doc Link PMC2628111 Disease Relevance 1.44 Pain Relevance 0.70
In conclusion, we found a significant elevation of SAA levels in patients with AS as compared to controls, and a strong positive correlation between SAA level and AS disease activity.
Positive_regulation (elevation) of SAA associated with spinal inflammation and disease
8) Confidence 0.33 Published 2007 Journal Yonsei Medical Journal Section Body Doc Link PMC2628111 Disease Relevance 1.05 Pain Relevance 0.60
, which are important inducers of SAA production35,36 Our patient with amyloidosis was on glucocorticoids, and thus, there is a possibility that the suppression of inflammatory cytokines with glucocorticoids might also suppress the synthesis of SAA.
Positive_regulation (inducers) of SAA associated with amyloidosis, inflammation and cytokine
9) Confidence 0.33 Published 2007 Journal Yonsei Medical Journal Section Body Doc Link PMC2628111 Disease Relevance 1.38 Pain Relevance 0.61
These findings may suggest that SAA can be used as a more sensitive laboratory marker than ESR or CRP for monitoring disease activity of AS.
Positive_regulation (used) of SAA associated with spinal inflammation and disease
10) Confidence 0.33 Published 2007 Journal Yonsei Medical Journal Section Body Doc Link PMC2628111 Disease Relevance 1.06 Pain Relevance 0.61
These findings indicate a usefulness of SAA measurement for monitoring disease activity.
Positive_regulation (usefulness) of SAA associated with disease
11) Confidence 0.33 Published 2007 Journal Yonsei Medical Journal Section Body Doc Link PMC2628111 Disease Relevance 1.03 Pain Relevance 0.54
In those with normal ESR or CRP levels, SAA levels and BASDAI scores were elevated (p < 0.05) and showed a trend of positive correlation with one another.


Positive_regulation (elevated) of SAA
12) Confidence 0.30 Published 2007 Journal Yonsei Medical Journal Section Abstract Doc Link PMC2628111 Disease Relevance 1.01 Pain Relevance 0.49
Particularly, of the 20 patients with increased SAA levels, 16 (80%) patients had a normal ESR, and nine (45%) had normal CRP levels.
Positive_regulation (increased) of SAA
13) Confidence 0.30 Published 2007 Journal Yonsei Medical Journal Section Body Doc Link PMC2628111 Disease Relevance 0.71 Pain Relevance 0.41
Patients with AS had a significantly higher mean SAA level than controls (9.52 ± 7.49 mg/L versus 2.73 ± 1.57 mg/L, p < 0.05), and the mean BASDAI score of patients with elevated SAA levels was significantly higher than that of patients with normal SAA levels (5.6 ± 1.3 versus 4.4 ± 1.5, p < 0.05).
Positive_regulation (elevated) of SAA associated with spinal inflammation
14) Confidence 0.30 Published 2007 Journal Yonsei Medical Journal Section Abstract Doc Link PMC2628111 Disease Relevance 1.14 Pain Relevance 0.60
Our data showed that SAA levels were increased in patients with AS and correlated well with disease activity.
Positive_regulation (increased) of SAA associated with spinal inflammation and disease
15) Confidence 0.30 Published 2007 Journal Yonsei Medical Journal Section Abstract Doc Link PMC2628111 Disease Relevance 0.73 Pain Relevance 0.32
The mean BASDAI score of patients with increased SAA levels was significantly higher than that of patients with normal SAA levels (p < 0.05).
Positive_regulation (increased) of SAA
16) Confidence 0.30 Published 2007 Journal Yonsei Medical Journal Section Body Doc Link PMC2628111 Disease Relevance 0.68 Pain Relevance 0.48
Serum amyloid A (SAA), a kind of apolipoprotein, is one of the acute phase proteins and is primarily synthesized in the liver by activated monocytes and macrophages.1 Previous studies have shown that in vivo concentrations of SAA can be dramatically increased (up to 1000-fold) in plasma during acute inflammatory conditions, and its increase is as greatly amplified as CRP level.2,3 This dramatic induction of SAA in response to pro-inflammatory stimuli is due largely to the synergistic effects of cytokine signaling pathways, primarily those of the interleukin (IL)-1, IL-6 and tumor necrosis factor (TNF)-?.
Positive_regulation (increased) of SAA in macrophages associated with necrosis, inflammation, cancer, alzheimer's dementia, disorder of lipid metabolism, cytokine and inflammatory stimuli
17) Confidence 0.30 Published 2007 Journal Yonsei Medical Journal Section Body Doc Link PMC2628111 Disease Relevance 1.81 Pain Relevance 0.34
In particular, significant elevations of both SAA levels and BASDAI scores were noted in those with normal ESR and CRP levels, and SAA levels and BASDAI scores showed a trend of positive correlation with one another in these patients.
Positive_regulation (elevations) of SAA
18) Confidence 0.30 Published 2007 Journal Yonsei Medical Journal Section Body Doc Link PMC2628111 Disease Relevance 1.12 Pain Relevance 0.61
Serum amyloid A (SAA), a kind of apolipoprotein, is one of the acute phase proteins and is primarily synthesized in the liver by activated monocytes and macrophages.1 Previous studies have shown that in vivo concentrations of SAA can be dramatically increased (up to 1000-fold) in plasma during acute inflammatory conditions, and its increase is as greatly amplified as CRP level.2,3 This dramatic induction of SAA in response to pro-inflammatory stimuli is due largely to the synergistic effects of cytokine signaling pathways, primarily those of the interleukin (IL)-1, IL-6 and tumor necrosis factor (TNF)-?.
Positive_regulation (induction) of SAA in macrophages associated with necrosis, inflammation, cancer, alzheimer's dementia, disorder of lipid metabolism, cytokine and inflammatory stimuli
19) Confidence 0.30 Published 2007 Journal Yonsei Medical Journal Section Body Doc Link PMC2628111 Disease Relevance 2.06 Pain Relevance 0.46
Of the patients studied, 75% increased their SAA level 24 h after angioplasty.
Positive_regulation (increased) of SAA
20) Confidence 0.28 Published 1998 Journal Clin Cardiol Section Body Doc Link 9755382 Disease Relevance 0.06 Pain Relevance 0

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