INT175392

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Context Info
Confidence 0.08
First Reported 2003
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 13
Total Number 15
Disease Relevance 10.16
Pain Relevance 0.89

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

transferase activity, transferring glycosyl groups (Ugcg) Golgi apparatus (Ugcg) lipid metabolic process (Ugcg)
Anatomy Link Frequency
IB4 3
lung 2
immune cells 1
skeletal system 1
skin 1
Ugcg (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammatory response 135 99.54 Very High Very High Very High
Inflammation 212 99.52 Very High Very High Very High
Central nervous system 153 96.48 Very High Very High Very High
dexamethasone 75 78.88 Quite High
corticosteroid 10 50.00 Quite Low
headache 10 48.88 Quite Low
Multiple sclerosis 3 20.20 Low Low
cytokine 22 5.00 Very Low Very Low Very Low
cINOD 11 5.00 Very Low Very Low Very Low
ketamine 9 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Stress 56 100.00 Very High Very High Very High
INFLAMMATION 365 99.52 Very High Very High Very High
Infection 457 99.08 Very High Very High Very High
Breast Cancer 7 98.24 Very High Very High Very High
Chronic Obstructive Pulmonary Disease 324 97.52 Very High Very High Very High
Neurocysticercosis 270 97.48 Very High Very High Very High
Nicotine Addiction 30 96.76 Very High Very High Very High
Skin Cancer 2 96.36 Very High Very High Very High
Lymphatic System Cancer 2 95.72 Very High Very High Very High
Solid Tumor 5 94.96 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Furthermore, there are other clinical examinations which clearly show a negative impact of GCs, e.g. an increased metastatic potential in breast cancer patients and an enhanced risk of skin cancer and lymphomas among users of systemic GCs [11-13].
GCs Neg (negative) Binding (impact) of in skin associated with lymphatic system cancer, breast cancer and skin cancer
1) Confidence 0.08 Published 2006 Journal BMC Cancer Section Body Doc Link PMC1434760 Disease Relevance 1.38 Pain Relevance 0
The rapid release of tegument material upon host penetration correlated with the loss of IB4 bound GCs and associates with the reduced number of discoidal bodies and mitochondria.
GCs Binding (bound) of in IB4
2) Confidence 0.08 Published 2008 Journal PLoS Neglected Tropical Diseases Section Body Doc Link PMC2274955 Disease Relevance 0.06 Pain Relevance 0.08
In contrast to the early disappearance of IB4 bound GCs, WGA bound GCs present in the tegument before infection were detected during several previously characterized stages of murine, porcine and human NCC.
GCs Binding (bound) of in IB4 associated with neurocysticercosis and infection
3) Confidence 0.08 Published 2008 Journal PLoS Neglected Tropical Diseases Section Body Doc Link PMC2274955 Disease Relevance 0.70 Pain Relevance 0
Peanut lectin-binding GCs, in contrast, remained on the parasite and were not detected in host cells.
GCs Binding (binding) of
4) Confidence 0.07 Published 2008 Journal PLoS Neglected Tropical Diseases Section Abstract Doc Link PMC2274955 Disease Relevance 0.86 Pain Relevance 0.07
The parasitic origin of the lectin-binding GCs found in host cells was confirmed using antibodies against T. solium and M. corti.
GCs Binding (binding) of
5) Confidence 0.07 Published 2008 Journal PLoS Neglected Tropical Diseases Section Abstract Doc Link PMC2274955 Disease Relevance 0.79 Pain Relevance 0.07
IB4 and GCs bound to hydrazide-Alexa 488 appear to play an important role in the evasion of the early stages of host response, but NCC and many other parasitic diseases are long-lasting, chronic infections in which the microorganisms persist over long periods [2],[35].
GCs Binding (bound) of in IB4 associated with parasitic infection, infection and neurocysticercosis
6) Confidence 0.06 Published 2008 Journal PLoS Neglected Tropical Diseases Section Body Doc Link PMC2274955 Disease Relevance 0.47 Pain Relevance 0.06
Samples infected with T. solium also showed continuous release of ConA bound GCs at various times post infection.
GCs Binding (bound) of associated with infection
7) Confidence 0.06 Published 2008 Journal PLoS Neglected Tropical Diseases Section Body Doc Link PMC2274955 Disease Relevance 0.70 Pain Relevance 0
Interestingly, the GCs bound by this lectin disappear from areas of parasite-host contact and are essentially undetected on the parasite's tegument after 1 wk and throughout later post-infection times.
GCs Binding (bound) of associated with infection
8) Confidence 0.06 Published 2008 Journal PLoS Neglected Tropical Diseases Section Body Doc Link PMC2274955 Disease Relevance 0.26 Pain Relevance 0.10
The GCs labeled with hydrazide-alexa 488 and recognized by IB4 appear to be involved in the first response generated by these organisms in the CNS microenviroment as they are phagocytosed by immune cells.
GCs Binding (recognized) of in immune cells associated with central nervous system
9) Confidence 0.06 Published 2008 Journal PLoS Neglected Tropical Diseases Section Body Doc Link PMC2274955 Disease Relevance 0.23 Pain Relevance 0.11
It has been shown that the glycosidic portion of glycoproteins and other glycoconjugates (GCs) expressed by T. solium metacestodes are highly antigenic, being recognized by serum from infected patients and mainly studied as potential targets in serological diagnosis [14],[16],[19].
GCs Binding (recognized) of
10) Confidence 0.05 Published 2008 Journal PLoS Neglected Tropical Diseases Section Body Doc Link PMC2274955 Disease Relevance 0.57 Pain Relevance 0.07
Predicted values for modified GCS and SSR derived from the training group, and observed values for weaning outcome in the prospective group were closely correlated.
GCS Binding (modified) of
11) Confidence 0.05 Published 2003 Journal BMC Pulm Med Section Body Doc Link PMC305355 Disease Relevance 0.15 Pain Relevance 0
As the innate or helper T cell type 1 (TH1) inflammatory response is well documented as responding well to GCs, the enhanced and relatively GC-insensitive inflammatory cell present in the lungs of patients with COPD is likely to incorporate an underlying factor.
GCs Binding (responding) of in lungs associated with inflammatory response, inflammation and chronic obstructive pulmonary disease
12) Confidence 0.04 Published 2010 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2939685 Disease Relevance 1.54 Pain Relevance 0.14
in a manner that results in a reduction of its ligand-binding ability.91 A negative feedback mechanisms used by GCs to regulate the inhibitory effect of p38 MAPK on GR?
GCs Binding (binding) of
13) Confidence 0.04 Published 2010 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2939685 Disease Relevance 0.98 Pain Relevance 0.11
/Akt pathway restores the ability of GCs to repress inflammatory mediator expression in patients with COPD comparable to smokers with normal lung function.96 However, although the mechanism by which inhibition on PI3K?
GCs Binding (ability) of in lung associated with nicotine addiction, inflammation and chronic obstructive pulmonary disease
14) Confidence 0.04 Published 2010 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2939685 Disease Relevance 0.74 Pain Relevance 0.05
Glucocorticoids (GCs) are steroidal stress hormones which have many different Biological functions.1,2 Through binding to GC receptors, they exert most of their effects, such as regulating tissue differentiation during development, controlling intermediary metabolism and coordinating the adjustment of physiological processes in response to stress.3–5 Because of these effects, synthetic GCs have been developed which are widely used in the treatment of allergic, inflammatory, lymphoproliferative disorders, and autoimmune diseases.6–10 However, such a treatment is not without shortcomings: GCs exert a negative impact on the skeletal system as they result in a rapid, early phase of bone loss which is followed by a more chronic and progressive phase due to excessive bone resorption, in which finally the bone mass declines because of impaired bone formation.11 The administration of GCs is the most frequent secondary cause of osteoporosis and it has been demonstrated that more than one third of individuals treated with GCs for 5 to 10 years will have an osteoporotic fracture.12,13
GCs Binding (binding) of in skeletal system associated with stress, autoimmune disease, hypersensitivity, osteoporotic fractures, osteoporosis, hypercalcemia, lymphoproliferative disease and inflammation
15) Confidence 0.03 Published 2010 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2878955 Disease Relevance 0.74 Pain Relevance 0.04

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