The DOI matches its Crossref record; 42 of the 43 references it cites were found in a registry or an index; none of the 16 sources its claims cite is checked for support yet.
Role of tumor necrosis factor-alpha in the pathophysiologic alterations after hepatic ischemia/reperfusion injury in the rat.
Open accessAbstract
Cytokines are recognized as critical early mediators of organ injury. We attempted to determine whether or not severe hepatic ischemia/reperfusion injury results in tumor necrosis factor-alpha (TNF-alpha) release with subsequent local and systemic tissue injury. After 90 min of lobar hepatic ischemia, TNF was measurable during the reperfusion period in the plasma of all 14 experimental animals, with levels peaking between 9 and 352 pg/ml. Endotoxin was undetectable in the plasma of these animals. Pulmonary injury, as evidenced by a neutrophilic infiltrate, edema and intra-alveolar hemorrhage developed after hepatic reperfusion. The neutrophilic infiltrate was quantitated using a myeloperoxidase (MPO) assay; this demonstrated a significant increase in MPO after only 1 h of reperfusion. Anti-TNF antiserum pretreatment significantly reduced the pulmonary MPO after hepatic reperfusion. After a 12-h reperfusion period, there was histologic evidence of intra-alveolar hemorrhage and pulmonary edema. Morphometric assessment showed that pretreatment with anti-TNF antiserum was able to completely inhibit the development of pulmonary edema. Liver injury was quantitated by measuring serum glutamic pyruvic transaminase which showed peaks at 3 and 24 h. Anti-TNF antiserum pretreatment was able to significantly reduce both of these peak elevations. These data show that hepatic ischemia/reperfusion results in TNF production, and that this TNF is intimately associated with pulmonary and hepatic injury.
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Written from the paper’s full text.
TL;DR
In a rat model of 90-minute lobar hepatic ischemia/reperfusion, TNF became measurable in plasma in all 14 experimental animals and was associated with subsequent pulmonary and hepatic injury. Pretreatment with anti-TNF antiserum reduced pulmonary neutrophil sequestration, abolished pulmonary edema, and lowered serum SGPT elevations after reperfusion.
Key findings
- After hepatic ischemia/reperfusion, TNF was measurable in plasma of all 14 experimental animals, with a mean peak level of 69.4±30.3 pg/ml and a range of 9–352 pg/ml; TNF was undetectable in sham-operated controls, and endotoxin was undetectable (<5 pg/ml).
- Pulmonary neutrophil sequestration, measured by MPO, peaked after 1 h of reperfusion at 0.653±0.089 U versus 0.213±0.034 U in sham animals (P<0.005). Anti-TNF antiserum reduced MPO to 0.458±0.057 U compared with 0.701±0.040 U in control-serum animals (P<0.005), though it did not return values to sham baseline.
- After 12 h of reperfusion, control-serum animals had 20±4 flooded alveoli/high-power field, whereas anti-TNF antiserum-treated animals had 0±0 (P<0.05 by Wilcoxon rank-sum test).
- Serum SGPT peaked at 3 and 24 h after reperfusion; anti-TNF antiserum significantly reduced both peak elevations (P<0.05 at 3 h and P<0.005 at 24 h versus untreated and control-serum groups). Twenty-four-hour survival was 67% in untreated animals, 92% with anti-TNF antiserum, and 60% with control serum, but the differences were not statistically significant.
Methods
- Adult male pathogen-free Sprague-Dawley rats (200–300 g) underwent 90 min of lobar hepatic ischemia using a Heifitz clip, with sham-operated controls treated identically except for vascular occlusion.
- Plasma TNF activity was measured with a WEHI 164 subclone 13 bioassay; positive samples were confirmed by neutralization with polyclonal rabbit anti-murine TNF antiserum. Endotoxin was measured by a perchloric acid-modified chromogenic limulus assay.
- Organ injury was assessed by pulmonary MPO assay, blinded histologic morphometry of edema-filled alveoli, and serum SGPT. Anti-TNF effects were tested by pretreating rats with polyclonal rabbit anti-murine TNF antiserum versus control rabbit serum. Statistical comparisons used Student Newman-Keuls or Wilcoxon rank-sum tests when data were not normally distributed.
Limitations
- The paper states that 24-h survival differences were not statistically significant, most likely because of relatively small group sizes.
- The paper states that further studies are needed to document the degree to which the observed pulmonary pathology is neutrophil dependent.
- The paper states that the mechanism of TNF induction after hepatic ischemia/reperfusion is not completely clear; the text infers Kupffer cell production/leakage but does not directly establish the cellular source.
- Evident from the text: anti-TNF antiserum did not prevent the transient hypotension after revascularization, so the protective effects observed were not attributable to hemodynamic stabilization.
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“After 90 min of lobar hepatic ischemia, TNF was measurable during the reperfusion period in the plasma of all 14 experimental animals, with levels peaking between 9 and 352 pg/ml.”
- Also stated in: § Results · plain
“TNF was measurable in the plasma of all 14 experimental animals”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Abstract
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Endotoxin was undetectable in the plasma of these animals.”
- Also stated in: § Results · plain
“In addition, endotoxin was unde- tectable (< 5 pg/ml).”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Results · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“TNF was un- detectable at any time point in the three sham-operated con- trol animals”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The neutrophilic infiltrate was quantitated using a myeloperoxidase (MPO) assay; this demonstrated a significant increase in MPO after only 1 h of reperfusion.”
- Also stated in: § Results · plain
“1 h postrevascularization, mean pulmonary MPO was 0.653±0.089U as compared with 0.213±0.034U for sham-operated animals (P < 0.005; Fig. 3.).”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Results · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Pulmonary injury, as evidenced by a neutrophilic infiltrate, edema and intra-alveolar hemorrhage developed after hepatic reperfusion.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Abstract
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In the paper
“and that a picture of pulmonary neutrophil sequestration and hemorrhagic edema develops.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Discussion
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In the paper
“of 12 animals treated with anti-TNF antiserum before the induction of hepatic ischemia, 11 animals survived for 24 h, giving a 24-h survival of 92%.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > .)
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In the paper
“For animals undergoing hepatic ischemia and reperfusion alone, the mean minimum systolic blood was significantly different from sham-operated an- imals (P < 0.005).”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Results
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Of 24 animals undergoing 90 min of lobar hepatic ischemia and 24 h of reperfusion, eight animals ex- pired before 24 h, resulting in a 24-h survival of 67%.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > .)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This was not the result of protection from a hypotensive effect, since the anti-TNF and control serum groups showed the same degree of transient hypotension after clamp release.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Discussion
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- It may state two separate claims as one. 17
- The quote only partly states this claim. 3
- Probably not a substantial claim. 7
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The mean peak TNF level was 69.4±30.3pg/ml with a range of 9-352 pg/ml.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Results
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, anti-TNF treatment blunted the increase in pulmonary MPO but did not reduce the MPO level to that observed in sham-operated controls.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Results
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“MPO levels were maximal after 1 h of reperfusion and gradually decreased over the next 11 h.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Results
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In the paper
“24 h survival in animals treated with control serum was similar to that seen in the untreated experimental group with 6 of 10 animals surviving for 24 h.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > .)
Strength:plain· not yet calibratedn = 10Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the anti-TNF-treated rats illustrate essentially normal histology.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Discussion
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Anti-TNF antiserum pretreatment was able to significantly reduce both of these peak elevations.”
- Also stated in: § Results · plain
“SGPT levels were significantly decreased both 3 and 24 h postrevascularization in the animals treated with anti-TNF antiserum as compared to untreated experimental animals and animals treated with control serum (P < 0.05 after 3 h of reperfusion and”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Results · plain
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In the paper
“Statistical significance was not achieved between any of the groups, most likely due to the relatively small numbers in the groups.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > .)
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A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“After 3 h of hepatic reperfusion, there was a significant decrease in SGPT in animals pretreated with anti-TNF antiserum as compared with both the untreated ex- perimental animals and the control serum-treated animals.”
- Also stated in: § Discussion · hedged
“Animals treated with anti-TNF antiserum showed a significant reduction in a hepatocyte-specific enzyme (SGPT) after hepatic ischemia/reperfusion in comparison to controls treated with control serum”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Discussion
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- Also stated in: § Discussion · hedged
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Anti-TNF antiserum pretreatment significantly reduced the pulmonary MPO after hepatic reperfusion.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe quote only partly states this claim.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the operated rats show intra-alveolar hemorrhage and some edema fluid.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Discussion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Recent clinical data have shown that impaired hepatic function greatly influences severity and impedes reso- lution of ARDS (4).”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Introduction
What the sources say
- Not checked yetcites [4]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Since the pulmonary circulation represents the first vascu- lar bed into which these cytokines are delivered, the pulmonary parenchyma would be likely to manifest the toxic effects of these cytokines.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Introduction
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: The pulmonary circulation is the first vascular bed into which cytokines from injured liver are delivered.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The lower limit of endotoxin detection in this assay is 5 pg/ml.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Methods
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The TNF release also did not appear directly related to the hypotensive effect produced by the I/R process, since anti-TNF antiserum treatment blocked the observed pathology, but did not alter the hypotension following clamp release.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Discussion
Load-bearingStrength:hedged· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“primary nonfunction of the graft after liver transplantation is also associated with the rapid development ofpulmonary insufficiency (5).”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Introduction
What the sources say
- Not checked yetcites [5]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The pulmonary pathology appears to be a consequence of TNF, since pretreatment with neutralizing anti-TNF anti- serum blunted the neutrophilic infiltrate (as measured by MPO) and completely abolished both the diffuse edema and patchy hemorrhage.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Discussion
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What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Slides were examined in a blinded manner.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Myeloperoxidase (MPO) assay. Pulmonary neutrophil sequestra- tion was quantitated with the MPO assay (I14).
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Previous in vitro studies have docu- mented the ability of Kupffer cells to produce TNF (28).”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Discussion
What the sources say
- Not checked yetcites [28]
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“This antiserum neutralizes both natural and recombinant TNF, cross-reacts with rat TNF and has no cross-reactivity with interleukin 1.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Methods
What the sources say
- Not checked yetcites 1 1, 12
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Previous studies have documented a deleterious effect of TNF on the hepatocyte where infused rTNF results in focal hepatic necrosis, as does LPS infusion, and the latter finding could be blocked with anti-TNF antiserum (13).”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Discussion
What the sources say
- Not checked yetcites [13]
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“However, our model was specifically chosen to avoid such vascular con- gestion, involving only lobar vascular occlusion with unim- peded portal flow to the right lobe.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Discussion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The three caudal lobes retain an intact portal inflow and venous out- flow, preventing intestinal venous congestion and possible leakage of bacteria or bacterial products into the circulation.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Methods
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“These data confirm our earlier study which used an intravenous ra- dioactive tracer to document protein leakage into the lungs (9).”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Results
What the sources say
- Not checked yetcites [9]
Strength:plain· not yet calibratedn = 5Tests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“By utilizing a rat model of lobar, rather than total, hepatic ischemia, a severe ischemic insult was produced without in- ducing mesenteric venous hypertension (8).”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Methods
What the sources say
- Not checked yetcites [8]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“and that TNF has both local deleterious effects on the hepatocyte and extensive damaging effects on pulmonary integrity.”
§ Role of Tumor Necrosis Factor-a in the Pathophysiologic Alterations after Hepatic Ischemia/Reperfusion Injury in the Rat > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper relies on this without support.
TNF is produced primarily by cells of the monocyte/macrophage lineage.
“TNF is produced primarily by cells of the monocyte/macrophage lineage”
The paper relies on this without support.
The liver Kupffer cell mass is the largest fixed macrophage population in the body.
“the liver Kupffer cell mass is the largest fixed macrophage population in the body.”
The paper relies on this without support.
The pulmonary circulation is the first vascular bed into which cytokines from injured liver are delivered.
“the pulmonary circulation represents the first vascu- lar bed into which these cytokines are delivered”
The paper relies on this without support.
The anti-TNF antiserum used in these experiments neutralizes TNF in vivo and does not have other relevant biological activities that could account for the observed protection.
“pretreatment with neutralizing anti-TNF anti- serum blunted the neutrophilic infiltrate”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Reperfusion of ischemic tissues stimulates cytokine overproduction (e.g., TNF, IL-1, HMGB1), which contributes to the pathogenesis of resulting tissue damage (42)(43)(44).”
From Physiology and immunology of the cholinergic antiinflammatory pathway (2007) · cites this paper as [43]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Hepatocyte-injury claim cites the Limulus-assay reference
MinorThe discussion cites reference 13 for prior findings about TNF, LPS, and hepatic necrosis, but reference 13 describes a method for the Limulus test rather than those findings.
“Previous studies have documented a deleterious effect of TNF on the hepatocyte where infused rTNF results in focal hepatic necrosis, as does LPS infusion, and the latter finding could be blocked with anti-TNF antiserum (13).”
“13. Obayashi, T. 1984. Addition of perchloric acid to blood sam- ples for colorimetric limulus, test using chromogenic substrate: com- parison with conventional procedures and clinical applications. J. Lab. Clin. Med. 104:321-330.”
Allograft-rejection citation points to a parasitic-infection paper
MinorThe text cites reference 24 for TNF in renal allograft rejection, but reference 24 is titled as a study of parasitic infections. The renal allograft rejection paper appears as reference 25.
“renal allograft rejection (24)”
“24. Scuderi, P., K. E. Sterling, K. S. Lam, P. R. Finley, K. J. Ryan, C. G. Ray, E. Peterson, D. J. Slyman, and S. E. Salmon. 1986. Raised serum levels of tumor necrosis factor in parasitic infections. Lancet. 1:1364-1365.”
Citations
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Tumor Necrosis Factor and Disease Severity in Children with Falciparum Malaria
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Stimulation of neutrophils by tumor necrosis factor.
Klebanoff, S. J., Vadas, M. A., Harlan, J. M., Sparks, L., Gamble, J. R., Agosti, J. M., & Waltersdorph, A. M. (1986) · The Journal of Immunology · doi:10.4049/jimmunol.136.11.4220 · Cited by 832
Flagged first, then by citations
1 of the 43 references couldn’t be matched to a known paper.
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Cytokines and Extrahepatic Sequelae of Ischemia‐Reperfusion Injury to the Liver a
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Self-citationEFFECT OF PENTOXIFYLLINE ON ISCHEMIC ACUTE RENAL FAILURE IN RABBITS
Kim, Y. K., Yoo, J., Woo, J. S., et al. (2001) · Renal Failure · doi:10.1081/jdi-100108187 · Cited by 20
“tion in various cell types including the kidney in vivo (27,28) and in vitro (29).”
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Pretreatment of parecoxib attenuates hepatic ischemia/reperfusion injury in rats
Zhang, T., Ma, Y., Xu, K.-Q., & Huang, W. (2015) · BMC Anesthesiology · doi:10.1186/s12871-015-0147-0 · Cited by 20
Ferrigno, A., Berardo, C., Pasqua, L. G. D., et al. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19020314 · Cited by 19
“Ischemic stress enhances the expression and release of proinflammatory molecules, such as TNF-α and iNOS; in addition, TNF-α can directly trigger apoptosis [28] and, thanks to its central role in promoting an inflammatory response, suppressing the formation of TNF-α might well be effective in attenuating acute post-is…”
BackgroundPropofol Protects against Ischemia/Reperfusion Injury Associated with Reduced Apoptosis in Rat Liver
Abdel-Wahab, A. F., & Al-Harizy, W. M. (2013) · ISRN Anesthesiology · doi:10.1155/2013/517478 · Cited by 19
Protective effect of ischemic preconditioning on hepatic ischemia-reperfusion injury in mice
Tsuyama, H., Shimizu, K., Yoshimoto, K., et al. (2000) · Transplantation Proceedings · doi:10.1016/s0041-1345(00)01677-8 · Cited by 19
Mφller, L. N. O., Knudsen, A. R., Andersen, K. J., Nyengaard, J. R., Hamilton-Dutoit, S. J., Mφller, E. M. O., Svendsen, P., Møller, H. J., Moestrup, S. K., Graversen, J. H., et al. (2015) · Annals of Medicine and Surgery · doi:10.1016/j.amsu.2015.09.001 · Cited by 19
“Kupffer cells produce cytokines, important mediators of the inflammatory response [21,50,51].”
BackgroundTumor Necrosis Factor Alpha Alters the Cytotoxic Effect of Hydrogen Peroxide in Cultured Hepatocytes
Imanishi, H., Scales, W. E., & Campbell, D. A. (1997) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.1996.5901 · Cited by 19
Self-citationMulti-organ inflammation after hepatic cryoablation in BALB/c mice
Wudel, L. J., Allos, T. M., Washington, M. K., et al. (2003) · Journal of Surgical Research · doi:10.1016/s0022-4804(03)00088-x · Cited by 19
Pathophysiology of hepatic ischemia-reperfusion injury: The role of complement activation
Jaeschke, H. (1994) · Gastroenterology · doi:10.1016/0016-5085(94)90188-0 · Cited by 19
Ohsaka, Y., Ohgiya, S., Hoshino, T., et al. (2002) · Cellular Physiology and Biochemistry · doi:10.1159/000063787 · Cited by 19
Expression of Interleukin-6 in Association with Rat Lung Reimplantation and Allograft Rejection
Rolfe, M. W., Kunkel, S. L., DeMeester, S. R., et al. (1993) · American Review of Respiratory Disease · doi:10.1164/ajrccm/147.4.1010 · Cited by 19
Self-citationGlutathione and Ultrastructural Changes in Inflow Occlusion of Rat Liver
Armeni, T., Ghiselli, R., Balercia, G., et al. (2000) · Journal of Surgical Research · doi:10.1006/jsre.1999.5781 · Cited by 19
Messiha, B. A. S., & Abo‐Youssef, A. M. (2015) · Journal of Natural Science Biology and Medicine · doi:10.4103/0976-9668.160003 · Cited by 18
“The IR model was performed according to the method previously described[16] with a slight modification.”
MethodRegulatory Mechanisms of Injury and Repair after Hepatic Ischemia/Reperfusion
Lentsch, A. B. (2012) · Scientifica · doi:10.6064/2012/513192 · Cited by 18
Protective effect of carnosol on lung injury induced by intestinal ischemia/reperfusion
Tian, X., Yao, J.-H., Zhang, X., et al. (2010) · Surgery Today · doi:10.1007/s00595-009-4170-y · Cited by 18
INTESTINAL ISCHEMIA/REPERFUSION INDUCES BRONCHIAL HYPERREACTIVITY AND INCREASES SERUM TNF-α IN RATS
Arruda, M. J. C., Poggetti, R. S., Fontes, B., et al. (2006) · Clinics · doi:10.1590/s1807-59322006000100005 · Cited by 18
“Hemorrhagic shock, frequently associated with impaired mesenteric blood flow and tissue ischemia, is a common event in trauma patients.7 The successful management of shock with aggressive fluid replacement restores tissue reperfusion, but may be followed by the systemic inflammatory response syndrome (SIRS) and reperf…”
BackgroundMethodInfluentialAntioxidant Stress and Anti-Inflammation of PPARαon Warm Hepatic Ischemia-Reperfusion Injury
Gao, Z., & Li, Y. (2012) · PPAR Research · doi:10.1155/2012/738785 · Cited by 18
“[26] L.”
BackgroundProteasome inhibition attenuates lung injury induced by intestinal ischemia reperfusion in rats
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Yeh, C., Chen, T.-P., Lee, C.-H., Wu, Y., Lin, Y., & Lin, P. J. (2006) · Shock · doi:10.1097/01.shk.0000188709.04777.48 · Cited by 18
“Oxygen free radicals, neutrophils, cytokines, and adhesion molecules all contribute to cardiac ischemia/reperfusion injury during cardiopulmonary bypass (CPB) (3, 4).”
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“cals[1]. Even ischemia/reperfusion injury seems to be mediated by this cytokine [ 2 ].”
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Age-related differences in function and structure of rat livers subjected to ischemia/reperfusion
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Taurine Protects Against Ischemia-Reperfusion Injury in Rabbit Livers
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Modulation of the fibrinolytic system by major peripheral ischemia
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Effect of trolox on altered vasoregulatory gene expression in hepatic ischemia/reperfusion
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Circulating cytokine concentrations and outcome prediction in intensive care unit patients
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Effects of Tetrandrine on Ischemia/Reperfusion Injury in Mouse Liver
Cheng, F., Li, Y., Feng, L., et al. (2008) · Transplantation Proceedings · doi:10.1016/j.transproceed.2008.07.082 · Cited by 16
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“MPO is known as a parameter of polymorph nuclear leukocyte (PNL) infiltration and activation [27].”
BackgroundPentoxifylline Does Not Prevent Hypoxia/Reoxygenation-Induced Necrotizing Enterocolitis
Erdener, D., Bakirtas, F., Alkanat, M. B., et al. (2004) · Neonatology · doi:10.1159/000077290 · Cited by 16
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“These neutrophils seem to be recruited by the liver’s release of tumor necrosis factor (TNF)- in conjunction with vascular endothelial adhesion molecules (39,40).”
BackgroundGüler, C., Şamlı, M., Aksoy, Y., et al. (2004) · Journal of Endourology · doi:10.1089/089277904773582840 · Cited by 16
“22 In another study, performed by Colletti and associates, 23 pulmonary injury developed after hepatic I/R injury in the rat.”
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PECAM ‐1 modulates liver damage induced by synergistic effects of TNF ‐α and irradiation
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The Pro-Inflammatory Cytokine Cascade
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The pneumotoxicant paraquat potentiates IL-1 and TNF production by human mononuclear cells
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Splenic artery ligation ameliorates hepatic ischemia and reperfusion injury in rats
Ito, K., Ozasa, H., Noda, Y., & Horikawa, S. (2006) · Liver International · doi:10.1111/j.1478-3231.2005.01220.x · Cited by 15
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Protective effect of prednisolone on ischemia-induced liver injury in rats
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“In addition, inflammatory cytokines like interleukin-1β and tumor necrosis factor-α also play an important role in hepatic ischemia-reperfusion injury [ 17 ]”
BackgroundInfluentialProtection against lung damage in reduced-size liver transplantation*
Franco-Gou, R., Roselló‐Catafau, J., & Peralta, C. (2006) · Critical Care Medicine · doi:10.1097/01.ccm.0000215512.68930.a8 · Cited by 15
“Experimental data indicate that pulmonary damage associated with hepatic I/R is mediated by neutrophil infiltration and the release of inflammatory mediators including reactive oxygen species (40, 41).”
BackgroundConzelmann, L. O., Lehnert, M., Kremer, M., Zhong, Z., Wheeler, M. D., & Lemasters, J. J. (2006) · Transplantation · doi:10.1097/01.tp.0000239190.95190.5e · Cited by 15
“Tumor necrosis factor (TNF)- plays an important role in early graft injury (3, 4) and in hepatic regeneration (5).”
BackgroundChiang, C., Yu, C., Wu, C., Yan, H., & Perng, W. (2001) · Clinical Science · doi:10.1042/cs1010285 · Cited by 16
Altered macrophage function in tumor necrosis factor α- and endotoxin-induced tolerance
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Pringle maneuver during hepatic resection induces inflammatory cytokines
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“In an animal model, hepatic ischemia and reperfusion result in release of hepaticaily derived tumor necrosis factor-c~ (TNF-~) ( 5 ) and interleukin-8 (IL-8) (6), which mediates neutrophildependent microvascular injury.”
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“In rodents, TNF-a has been shown to both mediate hepatic ischemia-reperfusion injury and promote cellular regeneration [ ,”
BackgroundBrücken, A., Bleilevens, C., Berger, P., Nolte, K. W., Gaisa, N. T., Rossaint, R., Marx, G., Derwall, M., & Fries, M. (2018) · Scientific Reports · doi:10.1038/s41598-018-25213-1 · Cited by 14
Wang, Z. (2007) · World Journal of Gastroenterology · doi:10.3748/wjg.v13.i4.564 · Cited by 14
Role of NF-kappaB in liver ischemia reperfusion injury of rats
Xu, J., Yang, Z., & Jinhua, Z. (2003) · Current Medical Science · doi:10.1007/bf02859943 · Cited by 14
Combination effect of melatonin and dexamethasone on liver ischemia/reperfusion injury
Taghizadieh, M., Hajipour, B., Asl, N. A., et al. (2016) · Bratislavské lekárske listy/Bratislava medical journal · doi:10.4149/bll_2016_010 · Cited by 14
“Activation of Kupffer cells results in the production and release of proinfl ammatory cytokines, including tumor necrosis factor alpha (TNF-α) and interleukin 1b (IL-1b) (5).”
BackgroundMethodThe Role of IL-37 in Non-Cancerous Diseases
Ding, V. A., Zhu, Z., Mantz, A. A., et al. (2016) · Pathology & Oncology Research · doi:10.1007/s12253-016-0137-7 · Cited by 14
Improved Sensitivity of Colorimetric Compared to Chemiluminescence ELISAs for Cytokine Assays
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“These proteins have been implicated in the pathogenesis of several important disease states including asthma,([1]) transplant rejection,([2]) septic shock,([3]) and ischemia reperfusion injury.([4]) There is tremendous interest in accurate determination of the levels of cytokines in these disease states.”
BackgroundSelf-citationLee, C.-H., Kim, S., & Lee, S. (2008) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2008.07.064 · Cited by 14
“Typically, it was reported that ischemia and reperfusion injury occurs in a biphasic pattern, which consists of both acute and subacute responses (Colletti et al., 1990).”
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Hepatic Ischemia/Reperfusion Injury
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Adhesion Receptors and Cytokine Profiles in Controlled Tourniquet Ischaemia in the Upper Extremity
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Preservation-reperfusion injury, primary graft non-function and tumour necrosis factor
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Fisiopatología de la lesión hepática por isquemia-reperfusión
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“pathogenesis of remote organ injury after I/R injury [60,61].”
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Lead nitrate and gadolinium chloride administration modify hepatocyte cell surfaces
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“Liver apoptosis, although very rare in adult healthy liver, can be induced by a number of physiological and pathophysiological conditions and diseases, antitumoral chemicals, regeneration after partial hepatectomy, irradiation, and oxidative stress (Columbano et al. 1985; Coletti et al. 1990; Cohen 1993; Schulte-Herma…”
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“A pretreatment with TNF-antiserum was found to completely inhibit the development of pulmonary edema after hepatic I/R in rats (5).”
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“Inhibition of TNF-a signaling lessens hepatic reperfusion injury.(1,2) Downstream, the activation of JNK aggravates I/R injury, whereas the activation of NF-jB is”
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“Because it is widely accepted that suppression of TNF-alpha during the reperfusion period could contribute to reduce hepatic I/R injury [19], we evaluated the plasma TNF- alpha level in the present study.”
BackgroundThe role of TNF in diverse pathologic processes
Kunkel, S. L., Strieter, R. M., Chensue, S. W., et al. (1991) · Biotherapy · doi:10.1007/bf02172086 · Cited by 12
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“Tumor necrosis factor alpha (TNF-α), an inflammatory mediator, has been demonstrated to play an important role in several pathological and experimental conditions [ 1-5 ].”
BackgroundSubstantial Increases Occur in Serum Activins and Follistatin during Lung Transplantation
de Kretser, D. M., Bensley, J. G., Phillips, D. J., Levvey, B. J., Snell, G. I., Lin, E., Hedger, M. P., & O’Hehir, R. E. (2016) · PLoS ONE · doi:10.1371/journal.pone.0140948 · Cited by 11
“Paradoxically, transplant reperfusion initiates events culminating in graft inflammation by up-regulating agents that promote neutrophil adhesion, mononuclear cell organ infiltration and secretion of T-cell associated cytokines, all contributing to IRI [3–5, 9, 10].”
BackgroundThe effect of U-74389G on pancreas ischemia–reperfusion injury in a swine model
Chrysikos, D., Sergentanis, T. Ν., Zagouri, F., et al. (2013) · Journal of Surgical Research · doi:10.1016/j.jss.2013.11.1082 · Cited by 11
“[22] Colletti LM, Remick DG, Burtch GD, Kunkel SL, Strieter RM, Campbell DA Jr.”
BackgroundRodrı́guez-Reynoso, S., Leal-Cortés, C. Á., Buen, E. P., et al. (2018) · Archives of Medical Research · doi:10.1016/j.arcmed.2018.11.004 · Cited by 11
Metadata
- Authors
- Colletti, L. M., Remick, D. G., Burtch, G. D., Kunkel, S. L., Strieter, R. M., & Campbell, D. A.
- Affiliations
- University of Michigan (US)
- Venue
- Journal of Clinical Investigation
- Published
- 1990-06-01
- Volume
- 85
- Issue
- 6
- Pages
- 1936-1943
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC296661
- OpenAlex
- W2099883737
- Semantic Scholar
- ef00ab3fc75d2591f58ef3691dd24619b03cf25e
- Cited by
- 817
- References
- 43
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 2 · 2023: 5 · 2022: 10 · 2021: 8 · 2020: 5 · 2019: 6 · 2018: 16 · 2017: 12 · 2016: 6 · 2015: 15 · 2014: 12 · 2013: 20 · 2012: 24
- FWCI
- 40.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01hl031237-32)
- National Heart, Lung, and Blood Institute (HL-35276, HL31237, HL 31963, P01HL031963)
- Topics
- Health Sciences › Medicine › Surgery › Organ Transplantation Techniques and Outcomes
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
- Keywords
- TNF-α, hepatic ischemia-reperfusion injury, cytokines, pulmonary edema, intra-alveolar hemorrhage, neutrophil infiltration, myeloperoxidase, liver injury, systemic inflammatory response, endotoxin
- MeSH terms
- Alanine Transaminase, Animals, Hemodynamics, Ischemia, Liver, Liver Diseases, Lung, Peroxidase, Neutrophils, Time Factors, Tumor Necrosis Factor-alpha, Reperfusion Injury, Rats
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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