Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

A protein C deficiency exacerbates inflammatory and hypotensive responses in mice during polymicrobial sepsis in a cecal ligation and puncture model.

The American journal of pathology - 1 Oct 2004

Ganopolsky Jorge G, Castellino Francis J

Abstract excerpt

During the systemic inflammatory state induced by sepsis, the potential for coagulopathy exists because of up-regulation of natural procoagulants and anti-fibrinolytics, and down-regulation of natural anti-coagulants, with protein C (PC) being a critical example of the latter case. PC functions a...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Blood Coagulation
Share to Blood Coagulation Factors
Share to Cecum

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hypotension

Share to Ligation

Share to Peritonitis

Share to Protein C Deficiency

Share to Sepsis

Source

Open in PubMed Open full text

Identifiers

PMID: 15466407
DOI: 10.1016/S0002-9440(10)63401-3
PMCID: PMC1618621

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-15466407-2026-09-04.1. Manifest publication-graph-cohort-2026-09-04.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A protein C deficiency exacerbates inflammatory and hypotensive responses in mice during polymicrobial sepsis in a cecal ligation and puncture model.PMID 15466407Read ↗

Acute inflammation is exacerbated in mice genetically predisposed to a severe protein C deficiency.Semantic proximity Read ↗

Cathelicidin-deficient mice exhibit increased survival and upregulation of key inflammatory response genes following cecal ligation and puncture.Semantic proximity Read ↗

Role of the complement in experimental sepsisSemantic proximity Read ↗

Absence of procarboxypeptidase R induces complement-mediated lethal inflammation in lipopolysaccharide-primed mice.Semantic proximity Read ↗

Pathogenesis of sepsis: new concepts and implications for future treatment.Semantic proximity Read ↗

Modulation of lipid and protein mediators of inflammation by cytosolic phospholipase A2alpha during experimental sepsis.Semantic proximity Read ↗

Thrombomodulin mutant mice with a strongly reduced capacity to generate activated protein C have an unaltered pulmonary immune response to respiratory pathogens and lipopolysaccharide.Semantic proximity Read ↗

Pathogenesis of Septic Shock: Implications for Prevention and TreatmentSemantic proximity Read ↗

The murine plasma protein response to polymicrobial intra-abdominal sepsis.Semantic proximity Read ↗

Optimization of a Fresh Fecal Intraperitoneal Injection Sepsis Model and Its Divergent Dynamics from Cecal Ligation and Puncture in MiceSemantic proximity Read ↗

Effect of protein C gene mutation on coagulation and inflammation in hemorrhagic shock.Semantic proximity Read ↗

Activated protein C mutant with minimal anticoagulant activity, normal cytoprotective activity, and preservation of thrombin activable fibrinolysis inhibitor-dependent cytoprotective functions.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.