INT1120

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Context Info
Confidence 0.67
First Reported 1978
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 33
Total Number 33
Disease Relevance 22.86
Pain Relevance 7.56

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

lipid binding (C3) extracellular space (C3) extracellular region (C3)
Anatomy Link Frequency
spinal cord 3
synovial fluids 1
liver 1
CSF 1
brain 1
C3 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
intrathecal 4 100.00 Very High Very High Very High
cytokine 252 99.52 Very High Very High Very High
Spinal cord 928 99.10 Very High Very High Very High
Sciatic nerve 5 97.44 Very High Very High Very High
ischemia 16 96.76 Very High Very High Very High
Thermal hyperalgesia 3 95.96 Very High Very High Very High
antagonist 17 95.88 Very High Very High Very High
Eae 2 95.72 Very High Very High Very High
allodynia 4 94.52 High High
chemokine 2 92.16 High High
Disease Link Frequency Relevance Heat
Pressure And Volume Under Development 203 99.92 Very High Very High Very High
Congenital Anomalies 4 99.64 Very High Very High Very High
Cirrhosis 291 99.20 Very High Very High Very High
Viral Meningitis 6 99.18 Very High Very High Very High
Spinal Cord Injury 1120 98.60 Very High Very High Very High
Drug Induced Neurotoxicity 48 98.40 Very High Very High Very High
Disease 67 98.28 Very High Very High Very High
Injury 927 98.06 Very High Very High Very High
Neurodegenerative Disease 66 97.60 Very High Very High Very High
Nervous System Injury 11 97.58 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Complement inhibition using systemic injections of soluble complement receptor 1 (AVANT Immunotherapeutics, Inc., Needham, USA) into rats markedly suppressed C3 deposition and T-cell and macrophage recruitment to the injured nerve, and produced significant alleviation of thermal hyperalgesia and mechanical allodynia.
Gene_expression (deposition) of C3 in nerve associated with allodynia and thermal hyperalgesia
1) Confidence 0.67 Published 2007 Journal Eur. J. Neurosci. Section Abstract Doc Link 18052971 Disease Relevance 1.18 Pain Relevance 1.20
Inverse correlation between C4 level and C3 breakdown products were found in synovial fluids of different groups.
Gene_expression (products) of C3 in synovial fluids
2) Confidence 0.58 Published 1978 Journal Allerg Immunol (Leipz) Section Abstract Doc Link 152571 Disease Relevance 0.42 Pain Relevance 0.08
The panel of examined inbred rat strains included DA(RT1AV1), PVG.1AV1, LEW.1AV1, LEW.1N, BN(RT1N) and E3(RT1U), and the following parameters were determined: (1) MHC class II expression on glia; (2) expression of glial fibrillary acidic protein, C3 complement, and microglial response factor-1 mRNAs in glia; (3) levels of the tumor necrosis factor-alpha and interleukin-1beta cytokine mRNAs; (4) degree of motoneuron loss.
Gene_expression (expression) of C3 in motoneuron associated with necrosis, cancer, sprains and strains and cytokine
3) Confidence 0.56 Published 2001 Journal J. Comp. Neurol. Section Abstract Doc Link 11169991 Disease Relevance 0.88 Pain Relevance 0.13
Moreover, the levels of C1 as well as those of C2 and C3 were markedly increased in the peripheral serum of day-21 rats within 15 min of LH administration.
Gene_expression (levels) of C3
4) Confidence 0.55 Published 1984 Journal Endocrinology Section Abstract Doc Link 6697963 Disease Relevance 0.08 Pain Relevance 0.08
In the C1-2 and C3-4 subgroups, labeled neurons were present from C1 to C8 DRGs, while in C5-6 subgroups they were from C3 to C8.
Gene_expression (present) of C3 in neurons
5) Confidence 0.54 Published 2006 Journal Chin. J. Traumatol. Section Body Doc Link 17096935 Disease Relevance 0.05 Pain Relevance 0
Many of the commonly regulated transcripts are immune related and include the complement components C1q, C3, and C4, which we find are expressed only by microglia.
Gene_expression (expressed) of C3 in microglia
6) Confidence 0.53 Published 2007 Journal J. Neurosci. Section Abstract Doc Link 17687047 Disease Relevance 0.83 Pain Relevance 0.78
During follow-up after sciatic nerve injury, all animals in the operated groups showed recovery of components C1 and C2 and of the reflex H wave, whereas component C3 was detected in a significantly lower proportion of animals in groups with tube repair.
Gene_expression (detected) of C3 in sciatic nerve associated with nervous system injury and sciatic nerve
7) Confidence 0.53 Published 2002 Journal J. Neurophysiol. Section Abstract Doc Link 11929897 Disease Relevance 0.44 Pain Relevance 0.25
Our data confirm C3 expression by PMNs in culture, and demonstrate the expression of C1q and C4 by PMNs, providing a more complete characterization of PMN expression of the early complement proteins in culture.
Gene_expression (expression) of C3
8) Confidence 0.47 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2443364 Disease Relevance 0.31 Pain Relevance 0.16
As shown in Figure 3 by rt-PCR, both unstimulated PMNs and stimulated PMNs expressed mRNAs encoding for C1q, C3, and C4, but not C6, C7, and C9 in culture.
Gene_expression (expressed) of C3
9) Confidence 0.47 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2443364 Disease Relevance 0.05 Pain Relevance 0.19
As discussed above for hydrogen peroxide production, different activation mechanisms by PMA and cytokines may also account for the difference in C3 expression observed in this experiment, because in contrast to TNF-?
Gene_expression (expression) of C3 associated with cytokine
10) Confidence 0.47 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2443364 Disease Relevance 0.05 Pain Relevance 0.21
Unlike the controversial expression/production of terminal proteins by PMNs, expression/production of C3 by PMNs has been clearly demonstrated in culture [16,17].
Gene_expression (expression) of C3
11) Confidence 0.41 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2443364 Disease Relevance 0.36 Pain Relevance 0.19
As demonstrated in previous studies that showed PMNs synthesis and release of C3 in culture [16,17], and in the present study that showed PMNs express high levels of C3 mRNAs and proteins in vitro and in the injured spinal cord, it is likely that PMNs may contribute to the elevated level of complement involved in post-injury neurogenesis.
Gene_expression (synthesis) of C3 in spinal cord associated with spinal cord injury, injury, neurodegenerative disease and spinal cord
12) Confidence 0.41 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2443364 Disease Relevance 1.77 Pain Relevance 0.41
Additionally, of all the PMNs that infiltrating the spinal cord epicenter region, most (over 70%) were also positive for C1q or C3 (Figure 8C &8D).
Gene_expression (positive) of C3 in spinal cord associated with spinal cord
13) Confidence 0.41 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2443364 Disease Relevance 0.50 Pain Relevance 0.26
Although previous studies have shown that cultured PMNs express mRNAs encoding for C3 and Factor B, it is not clear from these studies whether PMNs express other early complement proteins or terminal proteins necessary for C5b-9/MAC formation.
Gene_expression (express) of C3
14) Confidence 0.41 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2443364 Disease Relevance 0.06 Pain Relevance 0.08
As demonstrated in previous studies that showed PMNs synthesis and release of C3 in culture [16,17], and in the present study that showed PMNs express high levels of C3 mRNAs and proteins in vitro and in the injured spinal cord, it is likely that PMNs may contribute to the elevated level of complement involved in post-injury neurogenesis.
Gene_expression (express) of C3 in spinal cord associated with spinal cord injury, injury, neurodegenerative disease and spinal cord
15) Confidence 0.41 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2443364 Disease Relevance 1.74 Pain Relevance 0.40
Expression of C1q, C3, C4, C5, C6, C7, C9, CD59, Crry, and GADPH mRNAs in cultured PMNs was assayed by rt-PCR.
Gene_expression (Expression) of C3
16) Confidence 0.41 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2443364 Disease Relevance 0 Pain Relevance 0
However, microglia, the resident immune cells of the brain, produce large amounts of the receptors for C1q and C3 and thus are likely to be responsible for the removal of unwanted synapses (Eroglu and Barres, 2010).
Gene_expression (produce) of C3 in brain
17) Confidence 0.38 Published 2011 Journal Frontiers in Neurology Section Body Doc Link PMC3018771 Disease Relevance 0.50 Pain Relevance 0.23
Stimulated or unstimulated PMNs expressed mRNAs encoding for C1q, C3, and C4, but not C5, C6, C7 or C9 in culture.
Gene_expression (expressed) of C3 in PMNs
18) Confidence 0.36 Published 2008 Journal J Neuroinflammation Section Abstract Doc Link PMC2443364 Disease Relevance 1.32 Pain Relevance 0.34
Complement protein C1q or C3 was also detected in less than 30% of cultured PMNs.
Gene_expression (detected) of C3
19) Confidence 0.36 Published 2008 Journal J Neuroinflammation Section Abstract Doc Link PMC2443364 Disease Relevance 1.24 Pain Relevance 0.37
We have shown that cultured PMNs expressed mRNAs encoding for the early proteins C1q, C3, and C4, but not the terminal proteins C5, C6, C7, and C9 in vitro.
Gene_expression (expressed) of C3
20) Confidence 0.36 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2443364 Disease Relevance 0.59 Pain Relevance 0.12

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