| 1. |
- Goncalves, Isabel, et al.
(författare)
-
Activator protein-1 in carotid plaques is related to cerebrovascular symptoms and cholesteryl ester content
- 2011
-
Ingår i: Cardiovascular pathology. - : Elsevier. - 1054-8807 .- 1879-1336. ; 20:1, s. 36-43
-
Tidskriftsartikel (refereegranskat)abstract
- Transcription factor activator protein-1 regulates genes involved in inflammation and repair. The aim of this study was to determine whether transcription factor activator protein-1 activity in carotid plaques is related to symptoms, lipid accumulation, or extracellular matrix composition. Methods: Twenty-eight atherosclerotic carotid plaques were removed by endarterectomy and divided into two groups based on the presence or absence of ipsilateral symptoms (b1 month ago). Activator protein-1 DNA binding activity was assessed, and subunit (c-Jun, JunD, JunB, c-Fos, FosB, Fra-1, Fra-2) protein levels analyzed by immunoblotting. Distribution of c-Jun in plaques was analyzed by immunohistochemistry. Results: Plaques associated with symptoms had increased activator protein-1 activity and increased expression of c-Jun and JunD, as compared to asymptomatic plaques. Fra-1 and Fra-2 were present in equal amounts in both groups, whereas JunB, FosB, and c-Fos were undetectable. Activator protein-1 activity correlated with cholesteryl ester and elastin in plaques and decreased with age. Activator protein-1 activity did not correlate with collagen, calcified tissue, or proteoglycan content. Conclusions: Activator protein-1 is increased in plaques associated with symptoms. The correlation between activator protein-1 and cholesteryl esters suggests that high activator protein-1 is a marker of plaque vulnerability. Activator protein-1 expression can also reflect the activation of repair processes.
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
- Marabita, Francesco, et al.
(författare)
-
Multiomics and digital monitoring during lifestyle changes reveal independent dimensions of human biology and health
- 2022
-
Ingår i: Cell Systems. - : Cell Press. - 2405-4712 .- 2405-4720. ; 13:3, s. 241-255.e7
-
Tidskriftsartikel (refereegranskat)abstract
- We explored opportunities for personalized and predictive health care by collecting serial clinical measurements, health surveys, genomics, proteomics, autoantibodies, metabolomics, and gut microbiome data from 96 individuals who participated in a data-driven health coaching program over a 16-month period with continuous digital monitoring of activity and sleep. We generated a resource of >20,000 biological samples from this study and a compendium of >53 million primary data points for 558,032 distinct features. Multiomics factor analysis revealed distinct and independent molecular factors linked to obesity, diabetes, liver function, cardiovascular disease, inflammation, immunity, exercise, diet, and hormonal effects. For example, ethinyl estradiol, a common oral contraceptive, produced characteristic molecular and physiological effects, including increased levels of inflammation and impact on thyroid, cortisol levels, and pulse, that were distinct from other sources of variability observed in our study. In total, this work illustrates the value of combining deep molecular and digital monitoring of human health. A record of this paper's transparent peer review process is included in the supplemental information.
|
|
| 5. |
- Nilsson, Jan, et al.
(författare)
-
Inflammation and cholesterol
- 2002
-
Ingår i: European Heart Journal Supplements. - : Oxford University Press. - 1520-765X .- 1554-2815. ; 4:Suppl A, s. 18-25
-
Tidskriftsartikel (refereegranskat)abstract
- Atherosclerosis develops as a result of a chronic arterial inflammation and intimal Fibrosis. The disease represents in many respects a vascular repair process activated in response to injury caused by toxic breakdown products of aggregated and oxidized lipoproteins. The initial response of the artery involves expression of adhesion molecules and recruitment of leukocytes. Degenerated lipoproteins are removed front the extracellular space by macrophages. If lipoproteins continue to I process becomes chronic and accumulate. the inflammatory cytokines stimulate smooth muscle to migrate into the intima. These cells proliferate and form an atherosclerotic plaque. Plaque cell death and inflammation in response to oxidized lipids and other toxic factors May Cause plaques to rupture.
|
|
| 6. |
- Stollenwerk, Maria M, 1959-, et al.
(författare)
-
Very low-density lipoprotein induces interleukin-1beta expression in macrophages
- 2005
-
Ingår i: Biochemical and Biophysical Research Communications - BBRC. - : Elsevier. - 0006-291X .- 1090-2104. ; 335:2, s. 603-608
-
Tidskriftsartikel (refereegranskat)abstract
- Elevated plasma level of very low-density lipoprotein (VLDL) is a risk factor for coronary heart disease. We investigated the effect of VLDL on expression of the pro-inflammatory cytokine interleukin-1beta (IL-1beta) in human peripheral blood monocyte-derived macrophages. IL-1beta mRNA and protein expression was analysed by PCR and ELISA, respectively. Caspase activation was assessed by immunoblotting. Apart from potentiating lipopolysaccharide-induced secretion of IL-1beta, VLDL alone induced secretion of IL-1beta from human monocyte-derived macrophages. This effect was suppressed by an inhibitor of caspase-1, the protease which cleaves pro-IL-1beta. VLDL treatment activated caspase-1, as indicated by increased levels of the caspase-1 p20 subunit. Furthermore, VLDL increased IL-1beta mRNA expression, which was associated with activation of transcription factor AP-1. Inhibition of caspase-1 did not influence IL-1beta mRNA expression. In conclusion, VLDL induces IL-1beta mRNA expression, caspase-1 activation, and IL-1beta release from macrophages, suggesting that VLDL can promote inflammation in atherosclerotic lesions.
|
|
| 7. |
- van Leeuwen, Wessel M. A., et al.
(författare)
-
Physiological and autonomic stress responses after prolonged sleep restriction and subsequent recovery sleep in healthy young men
- 2018
-
Ingår i: Sleep and Biological Rhythms. - : Springer Science and Business Media LLC. - 1446-9235 .- 1479-8425. ; 16:1, s. 45-54
-
Tidskriftsartikel (refereegranskat)abstract
- PurposeSleep restriction is increasingly common and associated with the development of health problems. We investigated how the neuroendocrine stress systems respond to prolonged sleep restriction and subsequent recovery sleep in healthy young men.MethodsAfter two baseline (BL) nights of 8 h time in bed (TIB), TIB was restricted to 4 h per night for five nights (sleep restriction, SR, n = 15), followed by three recovery nights (REC) of 8 h TIB, representing a busy workweek and a recovery weekend. The control group (n = 8) had 8 h TIB throughout the experiment. A variety of autonomic cardiovascular parameters, together with salivary neuropeptide Y (NPY) and cortisol levels, were assessed.ResultsIn the control group, none of the parameters changed. In the experimental group, heart rate increased from 60 ± 1.8 beats per minute (bpm) at BL, to 63 ± 1.1 bpm after SR and further to 65 ± 1.8 bpm after REC. In addition, whole day low-frequency to-high frequency (LF/HF) power ratio of heart rate variability increased from 4.6 ± 0.4 at BL to 6.0 ± 0.6 after SR. Other parameters, including salivary NPY and cortisol levels, remained unaffected.ConclusionsIncreased heart rate and LF/HF power ratio are early signs of an increased sympathetic activity after prolonged sleep restriction. To reliably interpret the clinical significance of these early signs of physiological stress, a follow-up study would be needed to evaluate if the stress responses escalate and lead to more unfavourable reactions, such as elevated blood pressure and a subsequent elevated risk for cardiovascular health problems.
|
|
