INT15007

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Context Info
Confidence 0.49
First Reported 1991
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 31
Total Number 33
Disease Relevance 17.82
Pain Relevance 6.99

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
macrophage 2
vasculature 2
limb 2
neutrophils 2
myeloid cells 1
Pbrgcsf1 (Mus musculus)
Pain Link Frequency Relevance Heat
cytokine 374 100.00 Very High Very High Very High
Inflammation 200 100.00 Very High Very High Very High
chemokine 66 99.52 Very High Very High Very High
ischemia 188 99.24 Very High Very High Very High
Nerve growth factor 3 98.72 Very High Very High Very High
Inflammatory response 32 98.28 Very High Very High Very High
Pain 15 97.94 Very High Very High Very High
peripheral neuropathy 6 97.72 Very High Very High Very High
rheumatoid arthritis 1 97.40 Very High Very High Very High
substance P 1 96.48 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 238 100.00 Very High Very High Very High
Malignant Fibrous Histiocytoma 5 99.96 Very High Very High Very High
Leukocytosis 2 99.96 Very High Very High Very High
Toxicity 70 99.56 Very High Very High Very High
Hematological Disease 28 99.54 Very High Very High Very High
Appetite Loss 1 99.30 Very High Very High Very High
Cv Unclassified Under Development 92 99.24 Very High Very High Very High
Injury 11 99.06 Very High Very High Very High
Cv General 4 Under Development 88 99.04 Very High Very High Very High
Infection 205 99.00 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The mobilization growth factor G-CSF was used for in a total dose of 16 micrograms/kg/day s.c. administered in two daily doses.
Gene_expression (used) of G-CSF
1) Confidence 0.49 Published 2001 Journal Vnitr Lek Section Abstract Doc Link 11693058 Disease Relevance 0.23 Pain Relevance 0.09
G-CSF expression is often induced during infection and is thought to play an important role in the regulation of the systemic and local neutrophil response to the infection [34], a process known as stress or emergency granulopoiesis.
Gene_expression (expression) of G-CSF in neutrophil associated with stress, emergencies and infection
2) Confidence 0.36 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2904706 Disease Relevance 1.07 Pain Relevance 0
However, the depressed levels of G-CSF in the COX inhibitor treated groups appear not to have significantly affected BAL fluid neutrophil levels; in fact, neutrophils were slightly elevated on day 4 in the celecoxib treated group.
Gene_expression (levels) of G-CSF in neutrophils
3) Confidence 0.36 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2904706 Disease Relevance 0.94 Pain Relevance 0
Significantly impaired levels of G-CSF and GM-CSF and of other cytokines such as TNF?
Gene_expression (levels) of G-CSF associated with cytokine
4) Confidence 0.33 Published 2010 Journal J. Biol. Chem. Section Abstract Doc Link 20736176 Disease Relevance 0.61 Pain Relevance 0.44
We showed here that G-CSF and EPO synergized to produce better functional recovery from stroke and limb ischemia than either factor alone, which might be due to much enhanced angiogenesis and significant relevant neuroprotection.
Gene_expression (produce) of G-CSF in limb associated with stroke and ischemia
5) Confidence 0.30 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2852409 Disease Relevance 0.64 Pain Relevance 0.27
Similar to BAL fluid, levels of G-CSF in serum on day 4 were significantly lower in the celecoxib treated group versus control; there was a trend for reduced levels in the SC-560 treated group versus control on day 5.
Gene_expression (levels) of G-CSF
6) Confidence 0.28 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2904706 Disease Relevance 0.20 Pain Relevance 0.35
Because NA-BMCs are not a homogenous cell population, remaining MSCs are also able to support host hematopoiesis, e.g. by induction of G-CSF production.
Gene_expression (production) of G-CSF associated with hematological disease
7) Confidence 0.27 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701999 Disease Relevance 0.23 Pain Relevance 0
Among the members of this family, IL-17A is the most studied, and it is secreted by activated T cells and acts on stromal cells to produce pro-inflammatory cytokines, such as GM-CSF, G-CSF, CXCL1, and CXCL8 (IL-8) [44].
Gene_expression (produce) of G-CSF in stromal cells associated with inflammation and cytokine
8) Confidence 0.26 Published 2007 Journal BMC Immunol Section Body Doc Link PMC1891101 Disease Relevance 0.43 Pain Relevance 0.56
Without G-CSF treatment, HIF-1?
Gene_expression (treatment) of G-CSF
9) Confidence 0.26 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2852409 Disease Relevance 0.06 Pain Relevance 0.03
In contrast, G-CSF or EPO+G-CSF injection did not stimulate the additive upregulation of serum EPO in the Tg-HIF-1?
Gene_expression (injection) of G-CSF
10) Confidence 0.26 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2852409 Disease Relevance 0.40 Pain Relevance 0.16
At one week after cerebral ischemia, CBF was significantly greater in the ischemic cortex of the EPO+G-CSF-treated rats than that in EPO, G-CSF or control (each group n?
Gene_expression (cortex) of G-CSF in cortex associated with cv general 4 under development and ischemia
11) Confidence 0.26 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2852409 Disease Relevance 0.47 Pain Relevance 0.34
The anti-apoptotic protein Bcl-2 was significantly upregulated in EPO+G-CSF, EPO, and G-CSF groups, compared with control group (Fig. 4J), and the EPO+G-CSF combination induced significantly greater expression of Bcl-2 than EPO or G-CSF alone 24 hr after ischemia (Fig. 4J).
Gene_expression (expression) of G-CSF associated with ischemia and apoptosis
12) Confidence 0.26 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2852409 Disease Relevance 0.49 Pain Relevance 0.21
In contrast, G-CSF or EPO+G-CSF injection did not stimulate the additive upregulation of serum EPO in the Tg-HIF-1?
Gene_expression (injection) of G-CSF
13) Confidence 0.26 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2852409 Disease Relevance 0.40 Pain Relevance 0.15
Although either EPO or G-CSF has been shown to express neuroprotective and angiogenic effects in stroke animal models [1], [6], [19] and limb ischemia [22], no report has yet focused on the enhanced ability of these two cytokines in combination to induce neuroplasticity and angiogenesis.
Gene_expression (express) of G-CSF in limb associated with stroke, ischemia and cytokine
14) Confidence 0.23 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2852409 Disease Relevance 0.54 Pain Relevance 0.20
The mechanism associated with EPO expression regulation and G-CSF in the present study may be similar to a previously described molecular mechanism involved in VEGF expression regulation and macrophage colony-stimulating factor (M-CSF) in cell monocytes and macrophages [29].
Gene_expression (expression) of G-CSF in macrophage
15) Confidence 0.23 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2852409 Disease Relevance 0.30 Pain Relevance 0.06
It has very recently been shown that the implantation of tumour cells in mice upregulates Bv8 in serum, bone marrow and spleen myeloid cells, and that G-CSF is a positive major regulator of Bv8 expression [5].
Gene_expression (expression) of G-CSF in myeloid cells associated with cancer
16) Confidence 0.21 Published 2008 Journal BMC Immunol Section Body Doc Link PMC2584092 Disease Relevance 0.44 Pain Relevance 0.33
No patients received G-CSF with both primary or secondary prophylactic aim.
Neg (No) Gene_expression (received) of G-CSF
17) Confidence 0.20 Published 2006 Journal BMC Cancer Section Body Doc Link PMC1475875 Disease Relevance 1.60 Pain Relevance 0.05
Circulating levels of IL-6 and KC, as well as MIP-2, sTNFR-I and G-CSF, in dying septic mice (“+ CLP, moribund”, Fig. 6B, middle panel) were markedly higher than those in healthy mice (“-CLP”, Fig. 6B, left Panel), but dramatically lower than those in non-dying septic mice (“+ CLP, non-moribund”, Fig. 6B, right panel).
Gene_expression (levels) of G-CSF
18) Confidence 0.19 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2048740 Disease Relevance 0.51 Pain Relevance 0.11
Sixty normal subjects were given injections of G-CSF or GM-CSF alone; GM-CSF and G-CSF concurrently for 4, 5, or 6 days; or a sequential regimen of GM-CSF for 3 or 4 days followed by G-CSF for 2 or 3 days.
Gene_expression (injections) of G-CSF
19) Confidence 0.18 Published 1999 Journal Transfusion Section Body Doc Link 9920165 Disease Relevance 0 Pain Relevance 0
Sixty normal subjects were given injections of G-CSF or GM-CSF alone; GM-CSF and G-CSF concurrently for 4, 5, or 6 days; or a sequential regimen of GM-CSF for 3 or 4 days followed by G-CSF for 2 or 3 days.
Gene_expression (injections) of G-CSF
20) Confidence 0.18 Published 1999 Journal Transfusion Section Body Doc Link 9920165 Disease Relevance 0 Pain Relevance 0

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