Evidence map›Paper›PMID 11176134›Full record

ArticleAnnals of surgery2001

Norepinephrine modulates myelopoiesis after experimental thermal injury with sepsis.

Y Tang, R Shankar, M Gamboa, S Desai, R L Gamelli, S B Jones

Open access · greenAbstract read
In one paragraph

Article in Annals of surgery, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 11% of its field
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

17 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Adrenergic Modulation of Hematopoiesis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020
    Review
  5. Article
  6. Review
  7. Article
  8. Neuroendocrine regulation of inflammation.Seminars in immunology · 2014
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Molecular pathways: beta-adrenergic signaling in cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2012
    Review
  14. Article
  15. Article
  16. Article
  17. Article
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

6 authors at 1 institution in 1 country.

Y TangDepartment of Physiology and the Burn and Shock Trauma Institute, Loyola University Medical Center, Maywood, Illinois 60153, USA.
R Shankar
M Gamboa
S Desai
R L Gamelli
S B Jones
Loyola University Medical Center · US

Funding

MYELOPOIETIC STIMULATION FOLLOWING BURN INJURYR01GM042577 · NIGMS · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI GAMELLI, RICHARD LOUIS · 1989 to 2007
$2.1M
MECHANISMS OF MYELOID MATURATION ARREST IN BURN SEPSISR01GM056424 · NIGMS · LOYOLA UNIVERSITY CHICAGO · PI SHANKAR, RAVI · 1998 to 2000
$198k
NIGMS NIH HHS GM42577NIGMS NIH HHS GM56424NIGMS NIH HHS R01 GM042577NIMH NIH HHS MH53562
6 · The paper itself

Abstract

objectiveTo determine whether thermal injury and sepsis cause an increase in bone marrow norepinephrine release and whether such a release influences bone marrow monocytopoiesis. SUMMARY BACKGROUND DATA: The authors previously demonstrated enhanced bone marrow monocytopoiesis after burn with sepsis. They also showed that physiologic stress and bacterial challenge without injury could lead to a dynamic release of norepinephrine from the bone marrow compartment. In this study, they sought to determine the potential cause-and-effect relationship of bone marrow norepinephrine release on increased monocytopoiesis after burn sepsis.

methodsNorepinephrine release from bone marrow was determined by traditional pulse-chase methods. Tissue and bone marrow norepinephrine content was ablated by chemical sympathectomy with 6-hydroxydopamine treatment. Clonogenic potential in response to colony-stimulating factors was determined in total nucleated bone marrow cells. Dual color flow cytometry was used to document the distribution pattern of monocyte progenitors.

resultsBurn sepsis induced increased norepinephrine release in bone marrow, spleen, and heart. Colony-forming assays demonstrated an increase in responsive colonies, which was significantly attenuated when norepinephrine content was reduced in animals before burn sepsis. Flow cytometric analysis of early and late monocyte progenitors showed a significantly altered distribution profile of monocyte progenitors in norepinephrine-depleted mice compared with norepinephrine-intact mice. Abrogation of bone marrow norepinephrine content resulted in a 62% survival rate in burn septic mice compared with no survivors in norepinephrine-intact mice.

conclusionsThese data suggest that enhanced bone marrow norepinephrine release after burn sepsis may play a role in bone marrow monocytopoiesis, thus contributing to the sustenance of inflammation.

Indexed as

LeukopoiesisAnimalsBurnsColony-Forming Units AssayDisease Models, AnimalFlow CytometryMaleMiceMice, Inbred StrainsNorepinephrineSepsisNorepinephrine

Identifiers

PMID11176134
PMCPMC1421210
OpenAlexW2070219770

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.