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Biomedical subjects

Peter Riis Hansen

Publications and source records attributed to Peter Riis Hansen.

9 recordsLinked to original sources
PubMed2004

Spironolactone inhibits production of proinflammatory cytokines by human mononuclear cells.

BACKGROUND: The mineralocorticoid receptor antagonist spironolactone (SPIR) reduces the mortality and morbidity in patients with congestive heart failure (CHF). Overexpression of proinflammatory cytokines contribute to the development and progression of CHF. MATERIAL AND METHODS: We examined the effect of SPIR on in vitro cytokine production by human peripheral blood mononuclear cells (PBMC). PBMC were cultured with 10-1000 microM SPIR and stimulated with lipopolysaccharide or phytohaemagglutinin-P. Tumour necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, IL-1beta, and interferon (IFN)-gamma were measured in culture supernatants by enzyme-linked immunosorbent assay and mRNA expression of the cytokines was determined by real-time reverse transcriptase polymerase chain reaction (PCR). RESULTS: SPIR inhibited the stimulated production of TNF-alpha, IL-6, and IFN-gamma, whereas the release of IL-1beta was not significantly affected. The SPIR-induced cytokine inhibition occurred at the transcriptional level and was independent of antimineralocorticoid and antiandrogen activities. CONCLUSION: The findings suggest that inhibited production of proinflammatory cytokines may be an extrarenal mechanism that contributes to the beneficial effect of SPIR in patients with CHF.

Aldosterone↗
PubMed2003

[Thermography: a hot trail in the search for the vulnerable atherosclerotic plaque?].

Vulnerable atherosclerotic plaques are characterised by a large lipid core and a thin fibrous cap infiltrated with activated inflammatory cells. Heat is a cardinal sign of local inflammation, and atherosclerotic lesions display thermal heterogeneity, with increased temperature being correlated with inflammatory cell density, unstable clinical presentation, and unfavourable outcome after percutaneous interventions. Thermography is a promising new technique for assessment of atheroclerotic plaque composition.

Arteriosclerosis↗
PubMed2003

[Optical coherence tomography].

Optical coherence tomography (OCT) is a novel technique for two and three-dimensional imaging of tissues at a histological level. The technique is based on optical technology and commercially available fiber-optic components that may be adapted for use in conventional endoscopes or intravascular catheters. OCT is a non-invasive technique, which does not utilize ionizing radiation, and it may within a few seconds provide in vivo images ("optical biopsies") of tissues in cases where excisional biopsy is hazardous or impossible, or when repeated examinations are required. OCT has numerous potential clinical applications, and the technique is currently used in ophthalmology, where it may improve diagnosis and therapeutic control of various eye diseases. Detection and characterization of skin tumors and other dermatological diseases is another area where OCT has tremendous clinical potential. In the field of cardiology, intravascular OCT may be capable to contribute to early diagnosis of vulnerable atherosclerotic lesions. The OCT technique is also being developed in other clinical areas and is expected to become integrated in a range of clinical situations in the future.

Coronary Disease↗
PubMed2003

Thalidomide inhibits early atherogenesis in apoE-deficient mice.

Inflammation is present in all stages of atherosclerosis, from fatty streaks to rupture of mature plaques. Tumour necrosis factor (TNF)-alpha is expressed in atherosclerotic lesions but its role in atherogenesis has not been defined. To clarify the role of this cytokine, we administered thalidomide, a compound known to inhibit TNF-alpha production, to homozygous apolipoprotein E-deficient (apoE-/-) mice in order to examine the effect of thalidomide on the development of early atherosclerotic lesions. Twelve apoE-/- mice were randomized to receive either sustained-release thalidomide or placebo pellets implanted subcutaneously, and the amount of atherosclerosis was quantified six weeks later. Thalidomide was well tolerated and did not result in any changes in body weight. Mice treated with thalidomide had significantly smaller mean (7986 +/- 5189 vs 19607 +/- 10353 microns 2, p = 0.05) and maximum (15800 [12777-23675] vs 37169 [28000-41351] microns 2, p = 0.03) lesion sizes than those treated with placebo. Thus, thalidomide is capable of inhibiting the early development of atherosclerosis, presumably by inhibition of TNF-alpha secretion.

Animals↗