ArticleFrontiers in immunology2023
A 3-
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 16 citations in OpenAlex.
- Pathophysiology-guided biomarkers and therapeutics for precision trauma medicine in polytrauma with musculoskeletal injuries.Military Medical Research · 2026Review
- Pirinixic Acid Protects Against Hemorrhagic Shock by Regulating Neutrophil-Associated Key Genes.Shock (Augusta, Ga.) · 2026Article
- Plasma Regulates Homeostatic Pulmonary Endothelial Signaling to Mitigate Vascular Leak Following Polytrauma and Hemorrhagic Shock.Shock (Augusta, Ga.) · 2026Article
- From molecular networks to precision therapeutics: the evolving landscape of trauma-induced coagulopathy.World journal of emergency surgery : WJES · 2026Review
- A Developmental Roadmap Toward Abdominal Adhesions Prevention Technologies.Annals of surgery open : perspectives of surgical history, education, and clinical approaches · 2025Review
- 3-O Sulfated Heparan Sulfate (G2) Peptide Ligand Impairs the Infectivity ofBiomolecules · 2025Article
- Injury induced endotheliopathy: overview, diagnosis, and management.Current opinion in critical care · 2025Review
- THE INTERACTION BETWEEN ANTITHROMBIN AND ENDOTHELIAL HEPARAN SULFATE MITIGATES PULMONARY THROMBOINFLAMMATION AFTER TRAUMA AND HEMORRHAGIC SHOCK.Shock (Augusta, Ga.) · 2025Article
- Reducing the excessive inflammation after burn injury in aged mice by maintaining a healthier intestinal microbiome.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Transforming research to improve therapies for trauma in the twenty-first century.Critical care (London, England) · 2024Review
- Control of tissue homeostasis by the extracellular matrix: Synthetic heparan sulfate as a promising therapeutic for periodontal health and bone regeneration.Periodontology 2000 · 2024Review
- Trauma promotes heparan sulfate modifications and cleavage that disrupt homeostatic gene expression in microvascular endothelial cells.Frontiers in cell and developmental biology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Introduction: Dysregulated inflammation and coagulation are underlying mechanisms driving organ injury after trauma and hemorrhagic shock. Heparan sulfates, cell surface glycosaminoglycans abundantly expressed on the endothelial surface, regulate a variety of cellular processes. Endothelial heparan sulfate containing a rare 3- Methods: Male Sprague-Dawley rats were pre-treated subcutaneously with vehicle (saline) or dekaparin (2 mg/kg) and subjected to a trauma/hemorrhagic shock model through laparotomy, gut distention, and fixed-pressure hemorrhage. Vehicle and dekaparin-treated rats were resuscitated with Lactated Ringer's solution (LR) and compared to vehicle-treated fresh-frozen-plasma-(FFP)-resuscitated rats. Serial blood samples were collected at baseline, after induction of shock, and 3 hours after fluid resuscitation to measure hemodynamic and metabolic shock indicators, inflammatory mediators, and thrombin-antithrombin complex formation. Lungs and kidneys were processed for organ injury scoring and immunohistochemical analysis to quantify presence of neutrophils. Results: Induction of trauma and hemorrhagic shock resulted in significant increases in thrombin-antithrombin complex, inflammatory markers, and lung and kidney injury scores. Compared to vehicle, dekaparin treatment did not affect induction, severity, or recovery of shock as indicated by hemodynamics, metabolic indicators of shock (lactate and base excess), or metrics of bleeding, including overall blood loss, resuscitation volume, or hematocrit. While LR-vehicle-resuscitated rodents exhibited increased lung and kidney injury, administration of dekaparin significantly reduced organ injury scores and was similar to organ protection conferred by FFP resuscitation. This was associated with a significant reduction in neutrophil infiltration in lungs and kidneys and reduced lung fibrin deposition among dekaparin-treated rats compared to vehicle. No differences in organ injury, neutrophil infiltrates, or fibrin staining between dekaparin and FFP groups were observed. Finally, dekaparin treatment attenuated induction of thrombin-antithrombin complex and inflammatory mediators in plasma following trauma and hemorrhagic shock. Conclusion: Anti-thromboinflammatory properties of a synthetic 3-
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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.