ArticleConditioning medicine2018
The interferon response as a common final pathway for many preconditioning stimuli: unexpected crosstalk between hypoxic adaptation and antiviral defense.
Article in Conditioning medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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.
Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Phase II, Double-Blinded, Randomized, Placebo-Controlled Clinical Trial Investigating the Efficacy of Mebendazole in the Management of Symptomatic COVID-19 Patients.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Tilorone and Cridanimod Protect Mice and Show Antiviral Activity in Rats despite Absence of the Interferon-Inducing Effect in Rats.Pharmaceuticals (Basel, Switzerland) · 2022Article
- A STING agonist preconditions against ischaemic stroke via an adaptive antiviral Type 1 interferon response.Brain communications · 2022Article
- Neutrophils and Close Relatives in the Hypoxic Environment of the Tuberculous Granuloma: New Avenues for Host-Directed Therapies?Frontiers in immunology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Despite major advances in understanding how the brain goes awry in disease, identification of therapeutics for neuroprotection in stroke remains an unsolved challenge. A promising strategy to delineate endogenous mechanisms of neuroprotection is to understand adaptive homeostatic transcription induced by sublethal ischemia. Homeostatic adaptation is defined as the body's restorative responses to stress. Activating adaptive homeostatic pathways can lead to transcription of a panoply of genes involved in cell survival and repair, can suppress pro-death signaling, and can stimulate metabolic changes congruent with survival. All of these mechanisms have been shown to be operative in protection induced by sublethal stress. In this context, central mediators of cellular adaptation to hypoxic and viral stress have been implicated in preconditioning. Here we present data that suggest an unexpected convergence in the pathways triggering adaptation to hypoxia and viral infection leading to preconditioning neuroprotection in the CNS.
Identifiers
30198023PMC6126377W2990719051What OpenQuestion holds
Registered trials
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.