Evidence map›Paper›PMID 16759382›Full record

ReviewTheoretical biology & medical modelling2006

Free radical theory of autoimmunity.

Subburaj Kannan

Abstract readReview
In one paragraph

Review in Theoretical biology & medical modelling, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed.

  1. Article
  2. Article
  3. Observational
  4. Article
  5. Article
  6. Article
  7. Article
  8. Thiol/disulphide homeostasis in celiac disease.World journal of gastrointestinal pharmacology and therapeutics · 2017
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Subburaj KannanDNA Repair & Drug Resistance Group, Department of Microbiology, School of Medicine, University of Texas Medical Branch, Galveston, Texas 77555-0609, USA. skannan22@hotmail.com

Funding

OXIDATIVE STRESS, APOPTOSIS AND DRUG RESISTANCER01CA084461 · NCI · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI BOLDOGH, ISTVAN STEVEN · 2000 to 2003
$805k
NCI NIH HHS CA84461NCI NIH HHS R01 CA084461
6 · The paper itself

Abstract

backgroundDespite great advances in clinical oncology, the molecular mechanisms underlying the failure of chemotherapeutic intervention in treating lymphoproliferative and related disorders are not well understood. HYPOTHESIS: A hypothetical scheme to explain the damage induced by chemotherapy and associated chronic oxidative stress is proposed on the basis of published literature, experimental data and anecdotal observations. Brief accounts of multidrug resistance, lymphoid malignancy, the cellular and molecular basis of autoimmunity and chronic oxidative stress are assembled to form a basis for the hypothesis and to indicate the likelihood that it is valid in vivo.

conclusionThe argument set forward in this article suggests a possible mechanism for the development of autoimmunity. According to this view, the various sorts of damage induced by chemotherapy have a role in the pattern of drug resistance, which is associated with the initiation of autoimmunity.

Indexed as

AnimalsApoptosisAutoimmunityDrug Resistance, MultipleFree RadicalsHumansMolecular MimicryOxidative StressFree Radicals

Identifiers

PMID16759382
PMCPMC1508139

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.