INT195085

Context Info Confidence 0.56 First Reported 2006 Last Reported 2010 Negated 0 Speculated 1 Reported most in Body Documents 12 Total Number 13 Disease Relevance 12.26 Pain Relevance 2.33

extracellular space (S100b) extracellular region (S100b) nucleus (S100b) cytoplasm (S100b)

Anatomy Link Frequency brain 4 astrocytes 1 molar 1 microglia 1 S100b (Mus musculus)

Pain Link Frequency Relevance Heat Glutamate 92 100.00 fluoxetine 18 99.84 ischemia 12 97.88 Neuritis 3 94.76 cva 12 93.16 endometriosis 4 82.04 Pain 5 80.96 cytokine 107 78.12 diabetic neuropathy 4 76.72 sSRI 96 75.60

Disease Link Frequency Relevance Heat Injury 290 99.74 Brain Injury 134 99.64 Stab Wounds 60 99.60 Apoptosis 193 99.20 Syndrome 13 98.28 Disease 221 98.04 Cerebral Malaria 26 98.04 Cv Unclassified Under Development 9 97.88 Infarction 4 97.52 Alzheimer's Dementia 40 96.68

Sentences Mentioned In

Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

S100B is expressed primarily in the astrocytes of the human cortex and melanocytes as well as myeloid dendritic cells [42].

Gene_expression (expressed) of S100B in astrocytes

1) Confidence 0.56 Published 2009 Journal J Transl Med Section Body Doc Link PMC2666642 Disease Relevance 0.77 Pain Relevance 0.08

Elevated levels of S100B have been found in patients following brain trauma, ischemia/infarction, Alzheimer's disease, and Down's syndrome [42].

Gene_expression (levels) of S100B in brain associated with syndrome, ischemia, disease, infarction and brain injury

2) Confidence 0.49 Published 2009 Journal J Transl Med Section Body Doc Link PMC2666642 Disease Relevance 0.93 Pain Relevance 0.08

1, S100B, and NF-L mRNA expressions at 8 wpi (Figs. 5A, 6A)?

Gene_expression (expressions) of S100B

3) Confidence 0.46 Published 2008 Journal BMC Infect Dis Section Body Doc Link PMC2442079 Disease Relevance 0.74 Pain Relevance 0.03

Similarly, it was suggested that elevated S100B levels are involved in the development of Down's syndrome and AD [61]; its expression was also correlated with the density of dystrophic neuritis with overexpressed A?

Gene_expression (levels) of S100B associated with syndrome, disease and neuritis

4) Confidence 0.46 Published 2008 Journal BMC Infect Dis Section Body Doc Link PMC2442079 Disease Relevance 1.76 Pain Relevance 0.09

expression in microglia by S100B requires the concurrent activation of NF-?

Gene_expression (expression) of S100B in microglia

5) Confidence 0.43 Published 2009 Journal J Transl Med Section Body Doc Link PMC2666642 Disease Relevance 0.69 Pain Relevance 0

While the interaction of RAGE with S100B can produce anti-apoptotic signals, micro-molar concentrations of S100B will produce oxyradicals, inducing apoptosis.

Gene_expression (produce) of S100B in molar associated with apoptosis

6) Confidence 0.43 Published 2009 Journal J Transl Med Section Body Doc Link PMC2666642 Disease Relevance 0.98 Pain Relevance 0.21

1, S100B, and NF-L mRNA expressions at 8 wpi (Figs. 5A, 6A)?

Gene_expression (expressions) of S100B

7) Confidence 0.40 Published 2008 Journal BMC Infect Dis Section Body Doc Link PMC2442079 Disease Relevance 0.74 Pain Relevance 0.03

The older mice had higher levels of S100B.

Gene_expression (levels) of S100B

8) Confidence 0.27 Published 2007 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2656299 Disease Relevance 1.11 Pain Relevance 0.92

Our results show that in both WT and receptor-null mice, stab wound injury increased GLAST, GLT-1, GS and S-100B protein expression at 3 day post injury by 8, 6, 4 and 12 fold, respectively (Fig. 7).

Gene_expression (expression) of S-100B protein associated with injury and stab wounds

9) Confidence 0.12 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.44 Pain Relevance 0.28

Thus, a neocortical stab wound injury induces the expression of GLT-1, GLAST, the GS, and S-100B, but our data indicate that this induction is independent of IL-1R1.

Gene_expression (expression) of S-100B associated with injury and stab wounds

10) Confidence 0.12 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.81 Pain Relevance 0.15

To assess the functional state of astrocytes after traumatic brain injury, we analyzed the expression of two glutamate transporters, glutamate aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1/EAAT2), the glutamate transaminase, glutamine synthetase (GS) and the calcium regulatory protein S-100B.

Spec (analyzed) Gene_expression (expression) of protein S-100B in brain associated with glutamate and brain injury

11) Confidence 0.10 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.67 Pain Relevance 0.25

As astrocytes also buffer levels of brain calcium and as the calcium binding protein S-100B also has neurotrophic properties [38-40], we measured the levels of S-100B after injury.

Gene_expression (levels) of S-100B in brain associated with injury

12) Confidence 0.08 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.82 Pain Relevance 0.16

Axons are the most susceptible to ischemic or toxic damage in different brain areas, and axonal injury detected by elevated CSF levels of tau protein and S-100B (markers of axonal damage) were observed during cerebral malaria in Kenyan children [25].

Gene_expression (levels) of S-100B in brain associated with injury and cerebral malaria

13) Confidence 0.01 Published 2010 Journal Parasit Vectors Section Body Doc Link PMC2995786 Disease Relevance 1.82 Pain Relevance 0.05

General Comments

This test has worked.