The DOI matches its Crossref record; 63 of the 63 references it cites were found in a registry or an index; none of the 64 sources its claims cite is checked for support yet.
A mechanism converting psychosocial stress into mononuclear cell activation
Open accessAbstract
Little is known about the mechanisms converting psychosocial stress into cellular dysfunction. Various genes, up-regulated in atherosclerosis but also by psychosocial stress, are controlled by the transcription factor nuclear factor κB (NF-κB). Therefore, NF-κB is a good candidate to convert psychosocial stress into cellular activation. Volunteers were subjected to a brief laboratory stress test and NF-κB activity was determined in peripheral blood mononuclear cells (PBMC), as a window into the body and because PBMC play a role in diseases such as atherosclerosis. In 17 of 19 volunteers, NF-κB was rapidly induced during stress exposure, in parallel with elevated levels of catecholamines and cortisol, and returned to basal levels within 60 min. To model this response, mice transgenic for a strictly NF-κB-controlled β-globin transgene were stressed by immobilization. Immobilization resulted in increased β-globin expression, which could be reduced in the presence of the α1-adrenergic inhibitor prazosin. To define the role of adrenergic stimulation in the up-regulation of NF-κB, THP-1 cells were induced with physiological amounts of catecholamines for 10 min. Only noradrenaline resulted in a dose- and time-dependent induction of NF-κB and NF-κB-dependent gene expression, which depended on pertussis-toxin-sensitive G protein-mediated phosphophatidylinositol 3-kinase, Ras/Raf, and mitogen-activated protein kinase activation. Induction was reduced by α 1 - and β-adrenergic inhibitors. Thus, noradrenaline-dependent adrenergic stimulation results in activation of NF-κB in vitro and in vivo . Activation of NF-κB represents a downstream effector for the neuroendocrine response to stressful psychosocial events and links changes in the activity of the neuroendocrine axis to the cellular response.
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“After mental stress induction (60 min), NF-B-binding activity had almost completely returned to baseline (166%; P ϭ 0.073) (Fig. 1b).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
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In the paper
“ACTH and cortisol plasma levels served as markers of the endocrine stress response, demonstrating the expected significant increases in ACTH and cortisol after stress (P Ͻ 0.0001; Fig. 1a Upper).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
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“Only weak signals for -globin mRNA could be detected in control mice (Fig. 2a Upper, lanes 1-3).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
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“The TSST further significantly increased AD and NA levels already 1 min after stress induction.(Fig. 1a Lower).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
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In the paper
“The TSST-mediated induction of NF-B-binding activity from 100% to 341% (P ϭ 0.0089) observed in PBMC 10 min after stress induction (Fig. 1b)”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
plaindirectn = 19 ·- Asserted: passes — The authors put it forward as true.
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“In none of the spectators, up-regulation of NF-B could be observed during the assay period (Fig. 1c).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
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“Two subjects, characterized by the absence of a stress-dependent increase in catecholamines, ACTH, and cortisol, did not induce NF-Bbinding activity,”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
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“No changes in OCT-1-binding activity were detected (Fig. 1d Right), as shown for one representative subject (Fig. 1d Left).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
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In the paper
“Although the intensity of NF-B-binding activity decreased in the recovery period, the composition of the NF-B subunits contributing to the NF-Bbinding activity did not change (data not shown).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“The  1 -antagonist metoprolol (100 nM) and the  2 -antagonist butoxamine (25 nM) also reduced the NA-dependent NF-B response (Fig. 4a, lanes 5 and 6).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
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- Probably not a substantial claim. 18
- It may state two separate claims as one. 28
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“NF-B-binding activity consisted of the NF-B heterodimer NF-Bp50͞p65 (data not shown).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
plain- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
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In the paper
“IL-6-mRNA, in part regulated by NF-B, was also induced in response to immobilization and reduced in the presence of prazosin (data not shown).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
plaindirect- Asserted: passes — The authors put it forward as true.
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It 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
“In 17 of 19 volunteers, NF-B was rapidly induced during stress exposure, in parallel with elevated levels of catecholamines and cortisol, and returned to basal levels within 60 min.”
- Also stated in: § Modulation of NF-B Activation. · plain
“Psychosocial stress induces the transcription factor NF-B in healthy volunteers undergoing the TSST.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Modulation of NF-B Activation.
plaincorrelationaln = 19- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Rests on an assumption: PBMC play a role in diseases such as atherosclerosis.
- Rests on an assumption: PBMC are a valid window into the body for assessing NF-κB activation.
- Also stated in: § Modulation of NF-B Activation. · 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
“Only noradrenaline resulted in a dose-and time-dependent induction of NF-B and NF-B-dependent gene expression, which depended on pertussis-toxin-sensitive G proteinmediated phosphophatidylinositol 3-kinase, Ras͞Raf, and mitogenactivated protein kinase activation.”
- Also stated in: § Modulation of NF-B Activation. · plain
“Physiological concentrations of NA induce functionally significant NF-B-binding activity in cultured THP-1 monocytic cells.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Modulation of NF-B Activation.
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Rests on an assumption: THP-1 monocytic cells model mononuclear cell activation in vivo.
- Also stated in: § Modulation of NF-B Activation. · 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
“Immobilization resulted in increased -globin expression, which could be reduced in the presence of the ␣1-adrenergic inhibitor prazosin.”
- Also stated in: § Modulation of NF-B Activation. · plain
“Immobilization stress induces NF-B-dependent gene expression in -globin transgenic mice.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Modulation of NF-B Activation.
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Rests on an assumption: The β-globin transgene in mice is strictly NF-κB-controlled.
- Rests on an assumption: Immobilization stress in mice models psychosocial stress.
- Also stated in: § Modulation of NF-B Activation. · plain
In the paper
“Constitutive expression of the -globin transgene is restricted to lymphoid tissues (36), whereas activation of the NF-B p50͞p65-heterodimer confers inducible transgene activation in all cells (36).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
What the sources say
- Not matchedcites [36] 36. Lernbecher, T., Muller, U. & Wirth, T. (1993) Nature 365, 767-770.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“T he cardiovascular system is a target of psychosocial stress associated with exercise-induced myocardial ischemia, increases in blood pressure, heart rate, and arrythmias, development of arteriosclerosis, and death (1)(2)(3)(4).”
What the sources say
- Not matchedcites (1)(2)(3)(4)
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In the paper
“was paralleled by the stress-dependent increase in ACTH, cortisol, and catecholamines, suggesting a rapid NF-B activation after a brief period (i.e., 10 min) of psychosocial stress.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
hedgedcorrelationaln = 19- Asserted: passes — The authors put it forward as true.
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In the paper
“Consistently, behavioral interventions, stress reduction, and stress management demonstrated benefits over and above usual medical care in hypertensive African Americans (13) and in cardiac patients with evidence of myocardial ischemia (14)(15)(16)(17)(18).”
What the sources say
- Not matchedcites [13] 13. Castillo-Richmond, A., Schneider, R. H., Alexander, C. N., Cook, R., Myers, H., Nidich, S., Haney, C., Rainforth, M. & Salerno, J. (2000) Stroke 31, 568-573.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites (14)(15)(16)(17)(18)
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boosteddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Increased NF-B activation also has been described in blood lymphocytes of women stressed by the experience of breast biopsy (31)”
What the sources say
- Not checked yetcites [31] 31. Nagabhushan, M., Mathews, H. L. & Witek-Janusek, L. (2001) Brain Behav. Immun. 15, 78-84.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Intervention studies in cynomolgus monkeys support this concept, showing not only activation of these processes by mental stress but also reduction of vascular dysfunction and disease by reducing psychosocial stress through -adrenergic blockade (8)(9)(10)(11)(12).”
What the sources say
- Not matchedcites (8)(9)(10)(11)(12)
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In the paper
“One observation pointing to a potential mechanism is the induction of inflammatory reactions and the simultaneous decrease of antiin-flammatory reactions leading to enhanced cytokine release and monocytic cell activation (19)(20)(21)(22)(23).”
What the sources say
- Not matchedcites (19)(20)(21)(22)(23)
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hedgeddirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“Potential toxic elements in the personality construct such as hostility, anger, cynicism, mistrust, and unhealthy lifestyle (1,5,6), as well as social isolation (5), lack of social support (6), and work-related stress (7), increase the risk for cardiovascular disease”
What the sources say
- Not matchedcites [1] 1. Rozanski, A., Blumenthal, J. A. & Kaplan, J. (2000) Circulation 99, 2192-2217.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [5] 5. Stansfeld, S. A., Fuhrer, R., Shipley, M. J. & Marmot, M. G. (2002) Int. J. Epidemiol. 31, 248-255.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked yetcites [6] 6. Berkman, L. F., Leo-Summers, L. & Horwitz, R. I. (1992) Ann. Intern. Med. 117, 1003-1009.
- Not matchedcites [7] 7. Bosma, H., Peter, R., Siegrist, J. & Marmot, M. (1998) Am. J. Public Health 88, 68-74.
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plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Thioctic acid (2 mM), known to inhibit reactive oxygen species-mediated NF-B activation (38)”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
What the sources say
- Not checked yetcites [38] 38. Packer, L. (1998) Drug Metab. Rev. 30, 245-275.
boosteddirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim.
In the paper
“NA-dependent activation of similar signal transduction cascades in various cell types implies that the cellular response to stress uses comparable pathways and suggests that monitoring stress-dependent cellular activation in PBMC might allow estimation of the effect of psychosocial stress on allostasis and its impact on the allostatic load (55).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Possible Role of NF-B Activation as a Pathway Leading to Atherosclerosis.
What the sources say
- Not matchedcites [55] 55. Karlamangla, A., Singer, B., McEwen, B. S., Rowe, J. & Seeman, T. (2002) J. Clin. Epidemiol. 55, 696-710.
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hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Procedures in this study were approved by the Animal Care and Use Committee at the Regierungspra ¨sidium Karlsruhe, Germany.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Transgenic Mouse Model.
plain- Asserted: passes — The authors put it forward as true.
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Probably 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
“Here we present an adrenergic signaling pathway that explains the rapid increase in activation of the transcription factor NF-B observed in PBMC shortly after exposure to psychosocial stress, thus linking psychosocial stress to mononuclear cell activation and subsequent changes in the immune system.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Discussion
plaindirect- Asserted: passes — The authors put it forward as true.
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- Rests on an assumption: Downstream signals converting psychosocial stress into cellular dysfunction and vascular disease are largely unknown.
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In the paper
“NF-B activation is supposed to contribute to the pathophysiology of lifestylerelated diseases such as diabetes mellitus, cardiovascular disease, and atherosclerosis (24-29, 38, 40, 57)”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Discussion
What the sources say
- Not matchedcites [24] 24. Hofmann, M., Schiekofer, S., Isermann, B., Kanitz, M., Henkels, M., Joswig, M., Treusch, A., Morcos, M., Weiss, T., Borcea, V., et al. (1999) Diabetologia 42, 222-232.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [25] 25. Bierhaus, A., Schiekofer, S., Schwaninger, M., Andrassy, M., Humpert, P. M., Chen, J., Hong, M., Luther, T., Henle, T., Kloting, I., et al. (2001) Diabetes 50, 2792-2808.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [26] 26. Ritchie, M. E. (1998) Circulation 98, 1707-1713.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [27] 27. Collins, T. & Cybulsky, M. I. (2001) J. Clin. Invest. 107, 255-264.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [28] 28. Breuss, J. M., Cejna, M., Bergmeister, H., Kadl, A., Baumgartl, G., Steurer, S., Xu, Z., Koshelnick, Y., Lipp, J., De Martin, R., et al. (2002) Circulation 105, 633-638.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [29] 29. Yoshimura, S., Morishita, R., Hayashi, K., Yamamoto, K., Nakagami, H., Kaneda, Y., Sakai, N. & Ogihara, T. (2001) Gene Ther. 8, 1635-1642.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked yetcites [38] 38. Packer, L. (1998) Drug Metab. Rev. 30, 245-275.
- Not matchedcites [40] 40. Evans, J. L., Goldfine, I. D., Maddux, B. A. & Grodsky, G. M. (2002) Endocr. Rev. 23, 599-622.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [57] 57. Schmidt, A. M. & Stern, D. (2000) Circ. Res. 87, 722-724.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
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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 consistent results obtained in healthy volunteers, animal studies, and studies in vitro provide strong evidence that the mechanism described is not only observed in a single model, but may be applicable to rather different situations with increased NA release as the common denominator.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Possible Role of NF-B Activation as a Pathway Leading to Atherosclerosis.
boostedconditional- Asserted: passes — The authors put it forward as true.
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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
“RT-PCR for -actin served as an internal control and confirmed the comparable RNA-input in each reaction (Fig. 2a Lower).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“The NAtriggered signaling cascades in mononuclear cells involve PI3kinase, Ras͞Raf, and members of the MAPK family and thus resemble the NA-induced-signaling pathways described in vascular cells (48)(49)(50)(51)(52)(53)(54), although NF-B activation has not yet been studied in these cells.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Possible Role of NF-B Activation as a Pathway Leading to Atherosclerosis.
What the sources say
- Not matchedcites (48)(49)(50)(51)(52)(53)(54)
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Consistent with a linkage of G protein activation to adrenergic signal transduction (39)”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
What the sources say
- Not matchedcites [39] 39. Williams, N. G., Zhong, H. & Minnemann, K. P. (1998) J. Biol. Chem. 273, 24624-24632.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
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None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“In addition, Ras is supposed to directly participate in p38-MAPK activation (45) and to represent a signaling target for free radicals and cellular redox stress (46).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > stress-dependent NF-B activation in the cumulative burden that finally leads to morbidity and mortality.
What the sources say
- Not matchedcites [45] 45. McDermott, E. P. & O'Neill, L. A. (2002) J. Biol. Chem. 277, 7808-7815.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [46] 46. Lander, H. M., Ogiste, J. S., Teng, K. K. & Novogrodsky, A. (1995) J. Biol. Chem. 270, 21195-21198.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
In the paper
“Subsequently, Raf can phosphorylate MEK1 and MEK2 (44), which in turn phosphorylate and activate ERK-1 and -2 (p44͞p42-MAPK) (44).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > stress-dependent NF-B activation in the cumulative burden that finally leads to morbidity and mortality.
What the sources say
- Not matchedcites [44] 44. Yoshizumi, M., Tsuchiya, K. & Tamaki, T. (2001) J. Med. Invest. 48, 11-24.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“pretreated with the ␣ 1 -antagonist prazosin (1 mg͞kg), known to reduce immobilization stress-mediated immediate early gene expression in the mouse brain (37).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
What the sources say
- Not matchedcites [37] 37. Stone, E. A. & Zhang, Y. (1995) Brain Res. 694, 279-286.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
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 observation that mental stress in humans and rodents results in nuclear translocation of NF-B and changes in transcriptional activity thus closes an important gap in understanding the cellular consequences of psychosocial stress.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Discussion
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: Downstream signals converting psychosocial stress into cellular dysfunction and vascular disease are largely unknown.
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
“Reactions lacking template RNA or AMV-reverse transcriptase served as internal controls.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > RT-PCR.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Because psychosocial stress has been described to increase the lymphocyte and monocyte population (21), PBMC had been adjusted to the same cell number before NF-B-binding activity was determined.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
What the sources say
- Not matchedcites [21] 21. Goebel, M. U., Mills, P. J., Irwin, M. R. & Ziegler, M. G. (2000) Psychosom. Med. 62, 591-598.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
- Not matched
In the paper
“Consistent with a recently reported linkage of G proteincoupled receptors to MAPK signaling through PI3-kinase ␥ (41)”
§ A mechanism converting psychosocial stress into mononuclear cell activation > stress-dependent NF-B activation in the cumulative burden that finally leads to morbidity and mortality.
What the sources say
- Not matchedcites [41] 41. Lopez-Ilsaca, M., Crespo, P., Pellici, P. G., Gutkind, J. S. & Wetzker, R. (1997) Science 275, 394-397.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
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 NAdependent adrenergic signal transduction is mediated by Ptxsensitive G proteins inducing PI3-kinase and Ras͞Raf signaling that results in MAPK activation and subsequent NF-B induction (Fig. 4).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Discussion
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“A cooperative action of catecholamines regulating receptor expression and other stress response modifiers might act in concert in controlling cell activation.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Modulation of NF-B Activation.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“indicates that the activation of NF-B might not only be terminating itself by a negative IB␣-dependent feed back loop (27), but that activation of NF-B by ␣-adrenergic receptors terminates itself by induction of  2 receptors able to antagonize the proinflammatory challenge (60).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Modulation of NF-B Activation.
What the sources say
- Not matchedcites [27] 27. Collins, T. & Cybulsky, M. I. (2001) J. Clin. Invest. 107, 255-264.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [60] 60. Farmer, P. & Pugin, J. (2000) Am. J. Physiol. 279, L675-L682.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
In the paper
“in accordance with a previous report demonstrating NA-dependent ERK-2-phosphorylation in human PBMC (47).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > stress-dependent NF-B activation in the cumulative burden that finally leads to morbidity and mortality.
What the sources say
- Not matchedcites [47] 47. Rouppe van der Voort, C., Kavelaars, A., van de Pol, M. & Heijnen, C. J. (2000) J. Neuroimmunol. 108, 82-91.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
None of the sources cited for this claim could be matched to a paper in Crossref, so there is nothing to check it against.
In the paper
“The relation of NF-B activation to cellular dysfunction and vascular disease has been directly established by using genetic approaches to overexpress the NF-Bspecific inhibitor IB␣ (28) and by indirect studies looking at the presence of cells with nuclear located NF-B in vascular disease (24)(25)(26)(27)29).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Modulation of NF-B Activation.
What the sources say
- Not matchedcites [28] 28. Breuss, J. M., Cejna, M., Bergmeister, H., Kadl, A., Baumgartl, G., Steurer, S., Xu, Z., Koshelnick, Y., Lipp, J., De Martin, R., et al. (2002) Circulation 105, 633-638.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [24] 24. Hofmann, M., Schiekofer, S., Isermann, B., Kanitz, M., Henkels, M., Joswig, M., Treusch, A., Morcos, M., Weiss, T., Borcea, V., et al. (1999) Diabetologia 42, 222-232.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [25] 25. Bierhaus, A., Schiekofer, S., Schwaninger, M., Andrassy, M., Humpert, P. M., Chen, J., Hong, M., Luther, T., Henle, T., Kloting, I., et al. (2001) Diabetes 50, 2792-2808.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Not matched
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
“Activation of NF-B represents a downstream effector for the neuroendocrine response to stressful psychosocial events and links changes in the activity of the neuroendocrine axis to the cellular response.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Modulation of NF-B Activation.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“The experiment was repeated two times with identical results and one representative experiment is shown.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Modulation of NF-B Activation.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. 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
“Psychosocial stress induces NA that binds to ␣1and -adrenergic receptors, which in turn recruit Ptx-sensitive G proteins.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Modulation of NF-B Activation.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“The experiments were repeated three (b and c) to five (a) times with identical results and confirmed by NF-Bp65-specific ELISA.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Modulation of NF-B Activation.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Clinical and experimental studies provide evidence that lowering psychosocial stress by -adrenergic inhibitors (9,11,12) and͞or stress management (13-16) lead to reduction of the intima media thickness (13) and the overall cardiovascular mortality (14,15).”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Possible Role of NF-B Activation as a Pathway Leading to Atherosclerosis.
What the sources say
- Not matchedcites [9] 9. Kaplan, J. R., Manuck, S. B., Adams, M. R., Weingand, K. W. & Clarkson, T. B. (1987) Circulation 76, 1365-1372.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [11] 11. Kaplan, J. R. & Manuck, S. B. (1994) Am. Heart J. 128, 1316-1328.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [12] 12. Skantze, H. B., Kaplan, J., Petterson, K., Manuck, S., Blomqvist, M., Kyes, R., Williams, K. & Bondjers, G. (1998) Atherosclerosis 136, 153-161.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [13] 13. Castillo-Richmond, A., Schneider, R. H., Alexander, C. N., Cook, R., Myers, H., Nidich, S., Haney, C., Rainforth, M. & Salerno, J. (2000) Stroke 31, 568-573.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [14] 14. Blumenthal, J. A., Babyak, M., Wei, J., O'Connor, C., Waugh, R., Eisenstein, E., Mark, D., Sherwood, A., Woodley, P. S., Irwin, R. J., et al. (2002) Am. J. Cardiol. 89, 164-168.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not matchedcites [15] 15. Denollet, J. & Brutsaert, D. L. (2001) Circulation 104, 2018-2023.
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked yetcites [16] 16. King, M. S., Carr, T. & D'Cruz, C. (2002) Aust. Fam. Physician 31, 164-168.
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
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
“Raf phosphorylates MEK-1 and -2, which activates p44͞p42-MAPK.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Modulation of NF-B Activation.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
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
“In addition, Ras, which is a target of cellular oxidative stress, can directly induce p38-MAPK activation.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Modulation of NF-B Activation.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
The paper relies on this without support.
Downstream signals converting psychosocial stress into cellular dysfunction and vascular disease are largely unknown.
“Further downstream signals converting psychosocial stress into cellular dysfunction and finally into vascular disease are still largely unknown.”
“much less is known about the molecular mechanisms converting psychosocial stress into cellular activation.”
The paper relies on this without support.
The neuroendocrine response to stress involves an interplay among the hypothalamus, pituitary gland, adrenal medulla, and sympathetic nerve terminals.
“Recent data have indicated an interplay among hypothalamus, pituitary gland, adrenal medulla, and sympathetic nerve terminals as the neuroendocrine response to stress.”
The paper relies on this without support.
Various genes up-regulated in atherosclerosis and by psychosocial stress are controlled by NF-κB.
“Various genes, up-regulated in atherosclerosis but also by psychosocial stress, are controlled by the transcription factor nuclear factor B (NF-B).”
The paper relies on this without support.
PBMC play a role in diseases such as atherosclerosis.
“because PBMC play a role in diseases such as atherosclerosis.”
The paper relies on this without support.
PBMC are a valid window into the body for assessing NF-κB activation.
“as a window into the body”
The paper relies on this without support.
The β-globin transgene in mice is strictly NF-κB-controlled.
“mice transgenic for a strictly NF-B-controlled -globin transgene”
The paper relies on this without support.
Immobilization stress in mice models psychosocial stress.
“To model this response, mice transgenic for a strictly NF-B-controlled -globin transgene were stressed by immobilization.”
The paper relies on this without support.
THP-1 monocytic cells model mononuclear cell activation in vivo.
“cultured THP-1 monocytic cells”
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?
The cited source doesn’t support the claim as written.
In the citing paper
“Under normal conditions, catecholamines and glucocorticoids regulate inflammation through the inhibition of proinflammatory cytokines, such as IL-6, IL-1β, and TNF-α, and the stimulation of anti-inflammatory cytokines, such as IL-4, IL-10, and IL-13 [38], by exerting action in the cytoplasm of immune cells.”
From The Role of Cortisol in Chronic Stress, Neurodegenerative Diseases, and Psychological Disorders (2023) · cites this paper as [38]
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Combining chronic HCC measurements with acute cortisol assessments provides a comprehensive understanding of the stress response and its relevance to psychiatric and stress-related disorders [37,38].”
From The Role of Cortisol in Chronic Stress, Neurodegenerative Diseases, and Psychological Disorders (2023) · cites this paper as [38]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Normal cortisol secretion acts inhibitory toward cells that produce peripheral cytokines, mitigating inflammation.”
From The Role of Cortisol in Chronic Stress, Neurodegenerative Diseases, and Psychological Disorders (2023) · cites this paper as [38]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The stressor activates key inflammatory pathways in peripheral blood mononuclear cells, including activation of the transcription factor nuclear factor–κB (NF-κB), and leads to marked increases in circulating levels of pro-inflammatory cytokines, such as interleukin-6 (IL-6)3,4.”
From The role of inflammation in depression: from evolutionary imperative to modern treatment target (2016) · cites this paper as [4]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In contrast, increased norepinephrine production following stressor exposure induces NFκB activity that activates the immune system and increases cytokine production (Bierhaus et al, 2003).”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Bierhaus et al, 2003
Experimental — accuracy not yet measured
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“For example, exposure to the laboratory Trier Social Stress Test activates the peripheral inflammatory response via increased NFκB transcriptional activity that results in increased circulating concentrations of IL-6 (Bierhaus et al, 2003).”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Bierhaus et al, 2003
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“This increased norepinephrine production in PTSD in response to stressful or threatening stimuli can induce cytokine release (Bierhaus et al, 2003).”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Bierhaus et al, 2003
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The subsequent immune response occurs via NFκBdependent and -independent mechanisms (Bierhaus et al, 2003;Tan et al, 2007).”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Bierhaus et al, 2003
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“More specifically, activation of adrenergic-β2 receptors stimulates IL-6 and IL-1β secretion from macrophages and monocytes via NFκB and ERK signaling pathways, respectively (Bierhaus et al, 2003;Tan et al, 2007).”
From Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017) · cites this paper as Bierhaus et al, 2003
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“the observation that exposure to a psychosocial laboratory stressor can activate an inflammatory response in humans was a major breakthrough in linking inflammation to depression3,4.”
From The role of inflammation in depression: from evolutionary imperative to modern treatment target (2016) · cites this paper as [4]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“The predictable growth rate of scalp hair, approximately 1 cm per month, makes the 1 cm hair segment a reflection of the prior month’s cortisol production.”
From The Role of Cortisol in Chronic Stress, Neurodegenerative Diseases, and Psychological Disorders (2023) · cites this paper as [38]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Hair cortisol concentration (HCC), measured from hair samples, offers a promising method for retrospectively assessing chronic stress over extended periods.”
From The Role of Cortisol in Chronic Stress, Neurodegenerative Diseases, and Psychological Disorders (2023) · cites this paper as [38]
Experimental — accuracy not yet measuredIn the citing paper
“NF-κB appears to be a prime bridge for stress-induced increases in proinflammatory cytokines and the genes that control their expression (5).”
From Stress, Food, and Inflammation: Psychoneuroimmunology and Nutrition at the Cutting Edge (2010) · cites this paper as [5]
In the citing paper
“Behavioral studies have demonstrated that stressful events and depression can also influence inflammation through these same processes.”
From Stress, Food, and Inflammation: Psychoneuroimmunology and Nutrition at the Cutting Edge (2010) · cites this paper as [5]
In the citing paper
“Experimental data indicate that acute psychosocial stress (e.g., public speaking, mental arithmetic) stimulates inflammatory signaling molecules194, and these responses are exaggerated in patients with depression190.”
From Psychobiological factors of resilience and depression in late life (2019) · cites this paper as [194]
In the citing paper
“Norepinephrine-dependent adrenergic stimulation activates transcription factor nuclear factor kappa B (NF-κB), an intracellular signaling molecule that activates gene expression of several inflammatory mediators”
From Close relationships, inflammation, and health (2010) · cites this paper as Bierhaus et al., 2003
In the citing paper
“Psychosocial stress can directly provoke proinflammatory cytokine production in the absence of infection or injury.”
From Close relationships, inflammation, and health (2010) · cites this paper as Bierhaus et al., 2003
In the citing paper
“repeated or severe stressor exposure, in the absence of pathogenic disease, increases affective dysregulation and inflammatory proteins in tissues and blood in humans (Bierhaus et al, 2003;Pace et al, 2006) and animals (Maslanik et al, 2012a, b).”
From Danger Signals and Inflammasomes: Stress-Evoked Sterile Inflammation in Mood Disorders (2017) · cites this paper as Bierhaus et al, 2003
In the citing paper
“Similarly, increased activity of the sympathetic nervous system increases pro-inflammatory cytokine production, whereas parasympathetic activity has the opposite effect.6,7”
From Sleep Deprivation and Circadian Disruption (2015) · cites this paper as [7]
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.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ A mechanism converting psychosocial stress into mononuclear cell activation > Results
“ACTH and cortisol plasma levels served as markers of the endocrine stress response”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Determination of Adrenocorticotropic Hormone (ACTH), Cortisol, and
“Salivary cortisol levels were determined by a timeresolved immunoassay with fluorometric detection as described (33).”
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ A mechanism converting psychosocial stress into mononuclear cell activation > Modulation of NF-B Activation.
“the farnesyl transferase inhibitor AFC (50 M; Fig. 3b, lane 8), which inhibits Ras activation.”
§ A mechanism converting psychosocial stress into mononuclear cell activation > Modulation of NF-B Activation.
“AFC (50 M, lane 8), and H7 (100 M, lane 9) (b)”
Citations
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Protective and Damaging Effects of Stress Mediators
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Oxidative Stress and Stress-Activated Signaling Pathways: A Unifying Hypothesis of Type 2 Diabetes
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Organization for physiological homeostasis
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Self-citationEmotional Support and Survival after Myocardial Infarction
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Two alternative job stress models and the risk of coronary heart disease.
Bosma, H., Peter, R., Siegrist, J., & Marmot, M. (1998) · American Journal of Public Health · doi:10.2105/ajph.88.1.68 · Cited by 831
Diabetes-Associated Sustained Activation of the Transcription Factor Nuclear Factor-κB
Bierhaus, A., Schiekofer, S., Schwaninger, M., Andrassy, M., Humpert, P. M., Chen, J., Hong, M., Luther, T., Henle, T., Klöting, I., et al. (2001) · Diabetes · doi:10.2337/diabetes.50.12.2792 · Cited by 826
Self-citation
Research works printed but not linked: 6
- M S King, T Carr, C D'Cruz Aust Fam Physician 31, 164–168 (2002).
- J Charvat, P Dell, B Folkow Cardiologia 44, 121–141 (1964).
- M Yoshizumi, K Tsuchiya, T Tamaki J Med Invest 48, 11–24 (2001).
- Z W Hu, X Y Shi, R Z Lin, J Chen, B B Hoffman J Pharmacol Exp Ther 290, 28–37 (1999).
- P Farmer, J Pugin Am J Physiol 279, L675–L682 (2000).
- M O Aksoy, W Bin, Y Yang, D Yun-You, S G Kelsen Am J Physiol 281, L1271–L1278 (2001).
Cited by
Sorted by citations
Reactive oxygen species (ROS) as pleiotropic physiological signalling agents
Sies, H., & Jones, D. P. (2020) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-020-0230-3 · Cited by 5,335
The Lifelong Effects of Early Childhood Adversity and Toxic Stress
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Metadata
- Authors
- Bierhaus, A., Wolf, J., Andrassy, M., Rohleder, N., Humpert, P. M., Petrov, D., Ferstl, R., von Eynatten, M., Wendt, T., Rudofsky, G., Joswig, M., Morcos, M., Schwaninger, M., McEwen, B., Kirschbaum, C., & Nawroth, P. P.
- Affiliations
- Heidelberg University (DE)
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2003-02-10
- Volume
- 100
- Issue
- 4
- Pages
- 1920-1925
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC149934
- OpenAlex
- W2151454086
- Cited by
- 927
- References
- 62
- Citations by year
- 2026: 16 · 2025: 37 · 2024: 33 · 2023: 46 · 2022: 46 · 2021: 39 · 2020: 49 · 2019: 53 · 2018: 39 · 2017: 40 · 2016: 47 · 2015: 56 · 2014: 51 · 2013: 36 · 2012: 58
- FWCI
- 8.03
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Stiftung VERUM
- Deutsche Forschungsgemeinschaft
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Stress, Anesthesia, and Immune Response
- Keywords
- psychosocial stress, NF-κB, mononuclear cells, atherosclerosis, catecholamines, cortisol, norepinephrine, adrenergic signaling, G protein-coupled receptor signaling, phosphatidylinositol 3-kinase, mitogen-activated protein kinase, neuroendocrine stress response, prazosin, THP-1 cells
- MeSH terms
- Adrenocorticotropic Hormone, Adult, Animals, Base Sequence, Cell Line, Epinephrine, Female, Humans, Hydrocortisone, Lymphocyte Activation, Male, Mice, Transgenic, Monocytes, Norepinephrine, Stress, Psychological, NF-kappa B, DNA Primers, Reverse Transcriptase Polymerase Chain Reaction, Electrophoretic Mobility Shift Assay, Mice
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 2026-10-25, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-25 (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.
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