INT49197

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Context Info
Confidence 0.41
First Reported 1995
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 10
Disease Relevance 7.95
Pain Relevance 0.74

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

extracellular space (SELE) cell adhesion (SELE) plasma membrane (SELE)
Anatomy Link Frequency
neutrophils 2
leukocyte 1
mononuclear cells 1
SELE (Homo sapiens)
Pain Link Frequency Relevance Heat
ischemia 5 97.60 Very High Very High Very High
Inflammatory response 7 88.68 High High
Inflammation 105 88.04 High High
anesthesia 1 85.60 High High
cva 11 79.20 Quite High
alcohol 1 69.12 Quite High
cytokine 57 68.44 Quite High
tolerance 20 62.44 Quite High
Potency 2 30.96 Quite Low
Inflammatory mediators 6 24.00 Low Low
Disease Link Frequency Relevance Heat
Diabetes Mellitus 414 100.00 Very High Very High Very High
Hypertension 44 97.84 Very High Very High Very High
Brain Injury 144 97.80 Very High Very High Very High
Cv Unclassified Under Development 5 97.60 Very High Very High Very High
Coronary Artery Disease 156 96.56 Very High Very High Very High
Nicotine Addiction 17 96.24 Very High Very High Very High
Adhesions 125 95.46 Very High Very High Very High
Peripheral Arterial Disease 104 94.64 High High
Sepsis 4 91.40 High High
Injury 92 91.00 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In assessing the interaction of E-selectin genotypes with diabetes (environment), we followed the approach of Yang and Khoury (1997).
E-selectin Binding (interaction) of associated with diabetes mellitus
1) Confidence 0.41 Published 2007 Journal BMC Med Genet Section Body Doc Link PMC1933415 Disease Relevance 0.49 Pain Relevance 0
Ultrastructural investigation showed that reactivity for E-selectin matched neutrophil accumulation of the skeletal muscle tissue.
E-selectin Binding (reactivity) of in neutrophil
2) Confidence 0.36 Published 1995 Journal Ultrastruct Pathol Section Abstract Doc Link 7543227 Disease Relevance 0.42 Pain Relevance 0.21
Thus, in addition to the variable representing the interaction between diabetes and E-selectin, we included cholesterol, triglyceride, gender, age, hypertension, family history of CAD and smoking (Table 3).
E-selectin Binding (interaction) of associated with nicotine addiction, coronary artery disease, diabetes mellitus and hypertension
3) Confidence 0.30 Published 2007 Journal BMC Med Genet Section Body Doc Link PMC1933415 Disease Relevance 1.63 Pain Relevance 0
Correspondingly, we found the highest levels of sE-selectin, sICAM and sVCAM in association with poor neurological outcome (i.e., GOS 1-3) in NS resuscitated patients.
sE-selectin Binding (association) of
4) Confidence 0.28 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819256 Disease Relevance 0.97 Pain Relevance 0.07
Initial tethering and rolling of marginated cells along the vessel wall is mediated by L- (leukocyte; CD62L) and E- (endothelial; CD62E) selectins binding to sialyl-LewisX carbohydrate counter-receptors.
CD62E Binding (binding) of in leukocyte
5) Confidence 0.27 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819256 Disease Relevance 0.87 Pain Relevance 0.19
However, we did find the concurrent association of the AC genotype in the E-selectin gene and EE genotype of ICAM-1 gene in 24 TPG patients.
selectin Binding (association) of
6) Confidence 0.25 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2828103 Disease Relevance 0.52 Pain Relevance 0.04
Genotyping of E-selectin
selectin Binding (Genotyping) of
7) Confidence 0.25 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2828103 Disease Relevance 0.14 Pain Relevance 0
The S128R polymorphism of the E-selectin gene is of interest for two reasons: first, it is overrepresented in certain patient groups affected by disease that is characterized by an increased adhesiveness of leukocytes to the endothelium; such as atherosclerosis and myocardial infarction and secondly, it is a functional polymorphism since it modifies ligand affinity.5,6 This mutation confers an alteration in selectin ligand-binding specificity which leads to a gain of function under flow conditions, possibly amplifying the number of leukocytes that roll and subsequently adhere to the endothelium.7 Furthermore, S128R transduced endothelial cells support significantly more rolling and adhesion of neutrophils and mononuclear cells compared to epithelial cells (EC)s transduced with wild-type E-selectin.8 Substitution of the E-selectin epidermal growth factor domain residue Ser128 with an arginine residue results in E-selectin proteins that have lost the requirement for alpha1–3-linked fucose and are thus able to bind to sialyllactosamine.
selectin Binding (bind) of in mononuclear cells associated with atherosclerosis, disease, adhesions and myocardial infarction
8) Confidence 0.24 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2828103 Disease Relevance 0.77 Pain Relevance 0.08
Elevated levels of sICAM-1 were also associated with an increased risk of type 2 diabetes; however, the association was not independent of other diabetes risk factors including E-selectin, while vWF was not associated with risk of type 2 diabetes (Thorand et al 2006).
E-selectin Binding (association) of associated with diabetes mellitus
9) Confidence 0.10 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2350146 Disease Relevance 1.36 Pain Relevance 0.07
The S128R polymorphism of the E-selectin gene is of interest for two reasons: first, it is overrepresented in certain patient groups affected by disease that is characterized by an increased adhesiveness of leukocytes to the endothelium; such as atherosclerosis and myocardial infarction and secondly, it is a functional polymorphism since it modifies ligand affinity.5,6 This mutation confers an alteration in selectin ligand-binding specificity which leads to a gain of function under flow conditions, possibly amplifying the number of leukocytes that roll and subsequently adhere to the endothelium.7 Furthermore, S128R transduced endothelial cells support significantly more rolling and adhesion of neutrophils and mononuclear cells compared to epithelial cells (EC)s transduced with wild-type E-selectin.8 Substitution of the E-selectin epidermal growth factor domain residue Ser128 with an arginine residue results in E-selectin proteins that have lost the requirement for alpha1–3-linked fucose and are thus able to bind to sialyllactosamine.
selectin Binding (bind) of in neutrophils associated with atherosclerosis, disease, adhesions and myocardial infarction
10) Confidence 0.08 Published 2010 Journal Vascular Health and Risk Management Section Body Doc Link PMC2828103 Disease Relevance 0.77 Pain Relevance 0.08

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