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Context Info
Confidence 0.38
First Reported 2005
Last Reported 2006
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 2
Disease Relevance 3.67
Pain Relevance 0.08

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

cytosol (SLC12A3) transport (SLC12A3) plasma membrane (SLC12A3)
transmembrane transport (SLC12A3)
SLC12A3 (Homo sapiens)
Pain Link Frequency Relevance Heat
Pain 1 81.96 Quite High
cINOD 1 45.20 Quite Low
COX-2 inhibitor 1 24.48 Low Low
depression 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Bartter Syndrome 15 99.96 Very High Very High Very High
Syndrome 19 98.84 Very High Very High Very High
Hypomagnesemia 16 98.72 Very High Very High Very High
Chondrocalcinosis 5 98.24 Very High Very High Very High
Apoptosis 2 97.48 Very High Very High Very High
Pressure Volume 2 Under Development 1 96.64 Very High Very High Very High
Osteoporosis 1 96.24 Very High Very High Very High
Acid Base Imbalance 2 86.52 High High
Fatigue 5 83.28 Quite High
Myalgia 1 81.96 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Additionally, the association between GS (NCCT inactivation) and high bone mineral density provides a new insight into the possible role of thiazides in osteoporosis management.
Negative_regulation (inactivation) of NCCT associated with osteoporosis and bartter syndrome
1) Confidence 0.38 Published 2005 Journal J. Rheumatol. Section Abstract Doc Link 16142886 Disease Relevance 1.91 Pain Relevance 0.08
Hypomagnesemia in GS is possibly explained by the observation that a complete block of NCCT by chronic thiazide treatment results in an increased rate of apoptosis in DCT cells in rats [2].
Negative_regulation (block) of NCCT associated with hypomagnesemia, syndrome and apoptosis
2) Confidence 0.36 Published 2006 Journal BMC Nephrol Section Body Doc Link PMC1481527 Disease Relevance 1.77 Pain Relevance 0

General Comments

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