ArticleCurrent infectious disease reports2012
Immune aspects of sepsis and hope for new therapeutics.
Article in Current infectious disease reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Ginsenoside Rg3 attenuates sepsis-induced injury and mitochondrial dysfunction in liver via AMPK-mediated autophagy flux.Bioscience reports · 2017Article
- Prostaglandin E₂ constrains systemic inflammation through an innate lymphoid cell-IL-22 axis.Science (New York, N.Y.) · 2016Article
- Pleural innate response activator B cells protect against pneumonia via a GM-CSF-IgM axis.The Journal of experimental medicine · 2014Article
- Lipid mediators in immune dysfunction after severe inflammation.Trends in immunology · 2014Review
- Noncanonical Nuclear Factor Kappa B (NF-κB) Signaling and Potential for Therapeutics in Sepsis.Current infectious disease reports · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Marked alterations of the innate and adaptive immune response follow invasive infection and generalized inflammatory states. If left unchecked, this state of immune dysregulation contributes to a myriad of maladaptive cellular responses that culminate in multiple organ dysfunction, septic shock, and lethality. The molecular details of the cell-signaling networks that underlie the pathophysiology of systemic inflammation and sepsis are now increasingly well understood. While a vigorous and effective immune response to invasive pathogens is essential for microbial clearance and host survival, nonresolving, generalized inflammation can induce diffuse endovascular damage, increased capillary permeability, coagulopathy, and widespread tissue damage. Current evidence indicates that a state of relative immune suppression often accompanies sepsis and might provide novel therapeutic options in some patients. An expanding number of potential therapeutic options are now in clinical development to reestablish control and promote resolution over sepsis-induced systemic inflammation and organ dysfunction.
Identifiers
22851006What 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.