INT149669

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Context Info
Confidence 0.46
First Reported 2005
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 12
Total Number 13
Disease Relevance 14.17
Pain Relevance 2.07

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

cytosol (MEFV) cytoskeleton (MEFV) nucleus (MEFV)
intracellular (MEFV) cytoplasm (MEFV)
Anatomy Link Frequency
filaments 3
plasma 1
blood 1
viscera 1
lymph 1
MEFV (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 520 99.72 Very High Very High Very High
Pain 56 98.42 Very High Very High Very High
abdominal pain 18 95.52 Very High Very High Very High
Fibrositis 97 88.24 High High
Arthritis 13 80.80 Quite High
Crohn's disease 7 64.96 Quite High
psoriasis 2 56.00 Quite High
shoulder pain 1 55.88 Quite High
spinal inflammation 2 55.12 Quite High
anesthesia 23 50.00 Quite Low
Disease Link Frequency Relevance Heat
Fever 738 100.00 Very High Very High Very High
Familial Mediterranean Fever 36 100.00 Very High Very High Very High
Disease 297 99.76 Very High Very High Very High
INFLAMMATION 523 99.72 Very High Very High Very High
Tumor Necrosis Factor Receptor-associated Periodic Syndrome 12 99.40 Very High Very High Very High
Pain 51 98.42 Very High Very High Very High
Syndrome 73 98.24 Very High Very High Very High
Increased Venous Pressure Under Development 20 97.08 Very High Very High Very High
Hemorrhage 16 97.04 Very High Very High Very High
Suppuration 44 96.82 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In the unloaded condition and at the beginning of the loaded condition, a parallel network including M1-S1, posterior SII-insular, and posterior cingulate cortices accounted for the MEF activities.
Positive_regulation (accounted) of MEF in posterior
1) Confidence 0.46 Published 2009 Journal Hum Brain Mapp Section Abstract Doc Link 18266218 Disease Relevance 0.53 Pain Relevance 0.07
In contrast, the W232A mutation in PSTPIP1 abolished pyrin binding; consequently, PSTPIP1 filaments were primarily straight, not extensively branched (Figure 4I–K), confirming that the reticularization of PSTPIP1 filaments is a direct consequence of pyrin binding.
Positive_regulation (consequence) of pyrin in filaments
2) Confidence 0.46 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2702820 Disease Relevance 0 Pain Relevance 0
Domains of pyrin and PSTPIP1 required for pyrin recruitment and pyrin-mediated filament redistribution
Positive_regulation (required) of pyrin in filament
3) Confidence 0.46 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2702820 Disease Relevance 0 Pain Relevance 0
Based on the fact that multiple rare MEFV variants were capable of causing FMF if present on both chromosomes, we decided to test the transmission of rare variants from parents to offspring collectively.
Positive_regulation (causing) of FMF associated with familial mediterranean fever
4) Confidence 0.44 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2794536 Disease Relevance 0.42 Pain Relevance 0.08
Because of the increasing number of immigrants FMF should be considered in the initial differential diagnosis of patients of Mediterranean origin presenting with abdominal pain.
Positive_regulation (increasing) of FMF associated with abdominal pain
5) Confidence 0.41 Published 2008 Journal Dtsch. Med. Wochenschr. Section Abstract Doc Link 18651363 Disease Relevance 1.17 Pain Relevance 0.28
First, our studies show clearly that the SH3 domain of PSTPIP1 is not required for pyrin binding nor is it necessary for pyrin-mediated reticularization of PSTPIP1 filaments.
Neg (not) Positive_regulation (required) of pyrin in filaments
6) Confidence 0.40 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2702820 Disease Relevance 0.05 Pain Relevance 0.03
The genes responsible for all these autoinflammatory HPFS have been identified, and include MEFV (encoding pyrin) responsible for FMF, TNFRSF1A for TRAPS, mevalonate kinase for HIDS, CIAS1/NLRP3 for CAPS, and the PSTPIP1 gene responsible for PAPA syndrome.
Positive_regulation (include) of MEFV associated with syndrome, tumor necrosis factor receptor-associated periodic syndrome, acne, familial mediterranean fever and fever
7) Confidence 0.39 Published 2010 Journal F1000 Med Rep Section Body Doc Link PMC2948378 Disease Relevance 3.42 Pain Relevance 0.20
The genes responsible for all these autoinflammatory HPFS have been identified, and include MEFV (encoding pyrin) responsible for FMF, TNFRSF1A for TRAPS, mevalonate kinase for HIDS, CIAS1/NLRP3 for CAPS, and the PSTPIP1 gene responsible for PAPA syndrome.
Positive_regulation (include) of FMF associated with syndrome, tumor necrosis factor receptor-associated periodic syndrome, acne, familial mediterranean fever and fever
8) Confidence 0.19 Published 2010 Journal F1000 Med Rep Section Body Doc Link PMC2948378 Disease Relevance 3.50 Pain Relevance 0.23
As the propofol plasma concentration was dropped during the second 20 minute interval the MEF was noted to increase to 3.5 Hz, and it continued to trend towards baseline during the third 20 minute interval.
Positive_regulation (increase) of MEF in plasma
9) Confidence 0.12 Published 2009 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2801588 Disease Relevance 0 Pain Relevance 0
Citing extensive evidence from his own cases and dissections, he pointed to a number of symptoms and signs which, he argued, must be seen as indications of inflammation, namely “rigors, quick, firm corded pulse, acute fixed pain, tumefaction and increased heat”,144 and a number of findings on dissection—increased vascularity, excitement, suppuration and gangrene, with the effusion of serum and coagulable lymph—which were also highly indicative of inflammation.145 He added, furthermore, that those who had treated puerperal fever as an inflammatory affection, and had used methods of depletion, such as bleeding and purging, had had better success rates than others.146
Positive_regulation (treated) of puerperal fever in lymph associated with pain, suppuration, inflammation, hemorrhage, fever and increased venous pressure under development
10) Confidence 0.06 Published 2005 Journal Medical History Section Body Doc Link PMC1088248 Disease Relevance 1.51 Pain Relevance 0.38
In 1773, Denman had commented on a “peculiarity” in puerperal fever which he believed had never been noticed before—namely “an erysipelatous appearance of a dusky red colour on the knuckles, wrists, elbows, knees, or ankles, about the size of a shilling and sometimes larger”.89 Fifteen years later, in his account of the epidemic lasting from 1787 to 1788, John Clarke also mentioned the relevance of “erysipelas” to this disease.90 Philip Pitt Walsh, whilst arguing that puerperal fever was a manifestation of the category “synochus”, also stated that the inflammation involved was of an erysipelatous kind.91

The Influence of Morbid Anatomy on Theories of Puerperal Fever

Positive_regulation (noticed) of puerperal fever in knees associated with skin infection, inflammation, disease and fever
11) Confidence 0.06 Published 2005 Journal Medical History Section Body Doc Link PMC1088248 Disease Relevance 1.52 Pain Relevance 0.10
“The vessels become completely filled with blood, and are ripe for inflammation”.79 This theory was refuted by Thomas Kirkland, who argued that, if this were the cause of puerperal fever, the disease would be much more prevalent and much more uniformly distributed across the population than in fact it was.80 Physicians used evidence from morbid anatomy to support their arguments.
Positive_regulation (cause) of puerperal fever in blood associated with inflammation, disease and fever
12) Confidence 0.06 Published 2005 Journal Medical History Section Body Doc Link PMC1088248 Disease Relevance 1.09 Pain Relevance 0.35
This theory, which was most firmly espoused by Leake and Hulme in their treatises of 1772, fitted well with the idea that inflammation resulted directly from pressure on the abdominal viscera which, when suddenly released, gave rise to a lentor of the blood.77 Hulme even suggested that the spasmodic contraction of uterine vessels might be a secondary consequence of the pain attendant on the primary site of inflammation—the omentum.78 He asserted that puerperal fever was directly caused by interruption of blood flow consequent upon pressure from the gravid uterus.
Positive_regulation (caused) of puerperal fever in viscera associated with pain, inflammation and fever
13) Confidence 0.06 Published 2005 Journal Medical History Section Body Doc Link PMC1088248 Disease Relevance 0.96 Pain Relevance 0.37

General Comments

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