INT69417

Context Info Confidence 0.29 First Reported 1997 Last Reported 2010 Negated 0 Speculated 0 Reported most in Body Documents 4 Total Number 5 Disease Relevance 3.92 Pain Relevance 0.49

cell differentiation (RASGRP1) Golgi apparatus (RASGRP1) endoplasmic reticulum (RASGRP1) cytoplasm (RASGRP1) cytosol (RASGRP1) lipid binding (RASGRP1)

Anatomy Link Frequency HeLa 2 spinal cord 2 RASGRP1 (Homo sapiens)

Pain Link Frequency Relevance Heat Spinal cord 3 99.28 cINOD 2 97.04 Inflammation 5 96.56 ischemia 24 89.84 Catecholamine 6 50.28 Pain 1 25.00 Dopamine 4 5.00 opiate 2 5.00 Inflammatory response 2 5.00 imagery 2 5.00

Disease Link Frequency Relevance Heat Cancer 126 100.00 Familial Adenomatous Polyposis 3 100.00 Sepsis 88 99.68 Increased Venous Pressure Under Development 4 99.08 Pressure Volume 2 Under Development 8 97.78 INFLAMMATION 7 96.56 Cv Unclassified Under Development 22 89.84 Coronary Heart Disease 2 87.44 Diabetes Mellitus 2 86.56 Hypertension 2 86.16

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Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

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Disease term

Although we did identify a relationship between arterial hypotension and circulating Ang II after the first day of severe sepsis, the modest statistical significance and lack of a similar relationship between hypotension and PRA (a biologic precursor to Ang II) temper our enthusiasm to declare arterial pressure a dominant factor leading to persistent RAS activation during sepsis.

Positive_regulation (leading) of Positive_regulation (activation) of RAS associated with pressure volume 2 under development and sepsis

1) Confidence 0.29 Published 2010 Journal Crit Care Section Body Doc Link PMC2875539 Disease Relevance 1.27 Pain Relevance 0.08

We note that the levels of PRA and Ang II measured in our septic subjects are elevated nearly two-fold compared to outpatients with risk factors for vascular disease [33,34], arguing that the acute septic state contributes to RAS activation.

Positive_regulation (contributes) of Positive_regulation (activation) of RAS associated with increased venous pressure under development

2) Confidence 0.27 Published 2010 Journal Crit Care Section Body Doc Link PMC2875539 Disease Relevance 1.24 Pain Relevance 0.06

We report here using Northern blot analysis with these cDNA probes that noxious stimulation causes a marked and coincident increase in rap 1A, rap 1B and H-ras mRNAs in the rat spinal cord.

Positive_regulation (causes) of Positive_regulation (increase) of ras in spinal cord associated with spinal cord

3) Confidence 0.15 Published 1997 Journal Brain Res. Mol. Brain Res. Section Abstract Doc Link 9149109 Disease Relevance 0 Pain Relevance 0.13

Inactivation of the APC tumour-suppressor gene, and the activation of K-ras, have a combined effect on increasing tissue polyamine contents due to increased synthesis and decreased catabolism of the polyamines.

Positive_regulation (Inactivation) of Positive_regulation (activation) of ras associated with cancer and familial adenomatous polyposis

4) Confidence 0.06 Published 2003 Journal Biochem. Soc. Trans. Section Abstract Doc Link 12653645 Disease Relevance 0.73 Pain Relevance 0.22

In contrast, transfection of HeLa cells with anti-sense let-7 molecules reduced the expression of let-7 and in turn, allowed for an approximately 70% increase in RAS levels [66].

Positive_regulation (allowed) of Positive_regulation (increase) of RAS in HeLa

5) Confidence 0.05 Published 2008 Journal Current Genomics Section Body Doc Link PMC2674802 Disease Relevance 0.69 Pain Relevance 0

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