INT105921

Context Info Confidence 0.23 First Reported 2002 Last Reported 2010 Negated 0 Speculated 0 Reported most in Body Documents 13 Total Number 13 Disease Relevance 3.92 Pain Relevance 1.39

transferase activity, transferring glycosyl groups (FUT1) Golgi apparatus (FUT1) carbohydrate metabolic process (FUT1)

Anatomy Link Frequency kidney 3 blood 1 parenchymal cells 1 tubules 1 Kupffer cells 1 FUT1 (Homo sapiens)

Pain Link Frequency Relevance Heat cINOD 13 99.28 imagery 12 92.64 Inflammation 20 84.88 diclofenac 1 68.20 Paracetamol 2 66.52 fibrosis 32 40.44 Versed 12 36.24 Analgesic 6 23.36 ischemia 25 5.00 chemokine 13 5.00

Disease Link Frequency Relevance Heat Cirrhosis 342 100.00 Injury 174 98.88 Liver Disease 16 97.24 Adverse Drug Reaction 1 95.04 Liver Failure 4 86.72 INFLAMMATION 22 84.88 Severe Combined Immunodeficiency 5 81.20 Obesity 5 80.40 Paralysis 1 80.00 Diabetes Mellitus 5 79.92

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Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

We also determined the intrahepatic localization of both HSC-targeted forms of 15dPGJ2. 15dPGJ2-M6PHSA predominantly accumulated in the HSC (64%) and Kupffer cells (39%).

Localization (localization) of HSC in Kupffer cells associated with cirrhosis

1) Confidence 0.23 Published 2007 Journal Pharm Res Section Body Doc Link PMC1915609 Disease Relevance 0.62 Pain Relevance 0

The other construct 15dPGJ2-pPBHSA predominantly co-localizes with HSC and parenchymal cells.

Localization (localizes) of HSC in parenchymal cells associated with cirrhosis

2) Confidence 0.22 Published 2007 Journal Pharm Res Section Body Doc Link PMC1915609 Disease Relevance 0.56 Pain Relevance 0

In contrast, binding of 15dPGJ2-pPBHSA to cultured HSC was not affected by polyinosinic acid, suggesting that scavenger receptors are not involved in the binding of pPBHSA to HSC.

Localization (cultured) of HSC associated with cirrhosis

3) Confidence 0.22 Published 2007 Journal Pharm Res Section Body Doc Link PMC1915609 Disease Relevance 0.78 Pain Relevance 0

Here, we demonstrate that HSC migrate to the injured kidney and are even able to migrate into damaged tubules.

Localization (migrate) of HSC in tubules

4) Confidence 0.15 Published 2009 Journal Nephrology Dialysis Transplantation Section Body Doc Link PMC2698094 Disease Relevance 0.40 Pain Relevance 0.03

Unexpectedly, neutralization of endogenous SDF-1 or HSC-associated CXCR4 did not result in a significantly decreased migration of exogenous HSC to the ischemic injured or contralateral kidney (Figure 1C).

Localization (neutralization) of HSC in kidney

5) Confidence 0.15 Published 2009 Journal Nephrology Dialysis Transplantation Section Body Doc Link PMC2698094 Disease Relevance 0.06 Pain Relevance 0

The neutralizing capacity of anti-CXCR4 was determined by adding HSC pre-incubated with CXCR4 (20 ?

Localization (pre) of HSC

6) Confidence 0.15 Published 2009 Journal Nephrology Dialysis Transplantation Section Body Doc Link PMC2698094 Disease Relevance 0.05 Pain Relevance 0

Moreover, gating strategies to separate the CD34+ HSC from irrelevant cell populations, as well as inclusion of CD34dim and CD34bright populations were established.

Localization (separate) of HSC

7) Confidence 0.15 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2972200 Disease Relevance 0 Pain Relevance 0

To localize the exogenous HSC in the injured kidney, we visualized the presence of these cells in renal tissue.

Localization (localize) of HSC in kidney

8) Confidence 0.14 Published 2009 Journal Nephrology Dialysis Transplantation Section Body Doc Link PMC2698094 Disease Relevance 0.23 Pain Relevance 0.09

However, we could not observe an increased migration of the HSC towards the ischemic or contralateral kidneys locally injected with recSDF-1 compared to the control group.

Localization (migration) of HSC

9) Confidence 0.14 Published 2009 Journal Nephrology Dialysis Transplantation Section Body Doc Link PMC2698094 Disease Relevance 0.08 Pain Relevance 0

Twenty-four hours later, there was a significant (P = 0.03) increase in HSC migrating to the ischemic injured kidney compared to the contralateral kidney as assessed by flow cytometric analysis (Figure 1).

Localization (migrating) of HSC in kidney

10) Confidence 0.14 Published 2009 Journal Nephrology Dialysis Transplantation Section Body Doc Link PMC2698094 Disease Relevance 0.15 Pain Relevance 0.09

Another appealing option is represented by the administration of mobilizing/proliferating agents, such as G-CSF, that is able to both enhance the HSC mobilization into the peripheral blood and facilitate the endogenous LSC activation [5].

Localization (mobilization) of HSC in blood

11) Confidence 0.06 Published 2010 Journal Stem Cells International Section Body Doc Link PMC2963137 Disease Relevance 0.42 Pain Relevance 0

This study indicates a clinical applicable protocol for the use of HSC mobilization to ameliorate radiation-induced damage.

Localization (mobilization) of HSC

12) Confidence 0.04 Published 2010 Journal Stem Cell Res Ther Section Body Doc Link PMC2941114 Disease Relevance 0.34 Pain Relevance 0

Considering the localization of hOATs, it was suggested that the interactions of hOATs with NSAIDs are associated with the pharmacokinetics and the induction of adverse reactions of NSAIDs.

Localization (localization) of hOATs associated with adverse drug reaction and cinod

13) Confidence 0.00 Published 2002 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 12388633 Disease Relevance 0.23 Pain Relevance 1.17

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