INT194223

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Context Info
Confidence 0.21
First Reported 2006
Last Reported 2006
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 3
Disease Relevance 2.09
Pain Relevance 0

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

cell adhesion (Pvrl1) plasma membrane (Pvrl1)
Anatomy Link Frequency
lateral surfaces 3
Pvrl1 (Mus musculus)
Pain Link Frequency Relevance Heat
cytokine 126 25.64 Quite Low
Inflammation 75 25.24 Quite Low
Inflammatory response 6 5.00 Very Low Very Low Very Low
chemokine 3 5.00 Very Low Very Low Very Low
Pain 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Infection 60 100.00 Very High Very High Very High
Cold Sores 216 99.88 Very High Very High Very High
INFLAMMATION 81 25.24 Quite Low
Acquired Immune Deficiency Syndrome Or Hiv Infection 81 5.00 Very Low Very Low Very Low
Toxicity 66 5.00 Very Low Very Low Very Low
Chlamydia Infection 15 5.00 Very Low Very Low Very Low
Sperm Disorder 12 5.00 Very Low Very Low Very Low
Injury 6 5.00 Very Low Very Low Very Low
Ulcers 3 5.00 Very Low Very Low Very Low
Death 3 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
A possible mechanism for both the early and late phases of increased susceptibility that occur following epithelial exfoliation caused by detergents is suggested by the following findings regarding nectin-1, a major cell-surface entry receptor for HSV: 1) Mice are susceptible to HSV only during the stages of the estrous cycle when the vaginal epithelium expresses nectin-1, and the most susceptible stage can be maintained by treatment with Depo-Provera [45], 2) Incubating HSV with nectin-1 prior to vaginal inoculation blocked infection [45], 3) In the intact epithelium nectin-1 is primarily localized in the lateral surfaces between adjacent epithelial cells, a location where it is relatively inaccessible to HSV.
Localization (localized) of nectin-1 in lateral surfaces associated with cold sores and infection
1) Confidence 0.21 Published 2006 Journal BMC Infect Dis Section Body Doc Link PMC1523343 Disease Relevance 0.70 Pain Relevance 0
A possible mechanism for both the early and late phases of increased susceptibility that occur following epithelial exfoliation caused by detergents is suggested by the following findings regarding nectin-1, a major cell-surface entry receptor for HSV: 1) Mice are susceptible to HSV only during the stages of the estrous cycle when the vaginal epithelium expresses nectin-1, and the most susceptible stage can be maintained by treatment with Depo-Provera [45], 2) Incubating HSV with nectin-1 prior to vaginal inoculation blocked infection [45], 3) In the intact epithelium nectin-1 is primarily localized in the lateral surfaces between adjacent epithelial cells, a location where it is relatively inaccessible to HSV.
Localization (localized) of nectin-1 in lateral surfaces associated with cold sores and infection
2) Confidence 0.21 Published 2006 Journal BMC Infect Dis Section Body Doc Link PMC1523343 Disease Relevance 0.71 Pain Relevance 0
But upon epithelial disruption by low calcium, nectin-1 migrates from the lateral surfaces and becomes accessible to HSV on the apical surface, increasing viral entry by HSV [46].
Localization (migrates) of nectin-1 in lateral surfaces associated with cold sores
3) Confidence 0.20 Published 2006 Journal BMC Infect Dis Section Body Doc Link PMC1523343 Disease Relevance 0.69 Pain Relevance 0

General Comments

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