Biomedical subjects

Frank Michel

Publications and source records attributed to Frank Michel.

4 recordsLinked to original sources

PubMed2005

Peroxisome proliferator-activated receptor (PPAR) expression in cultured bovine endometrial cells and response to omega-3 fatty acid, growth hormone and agonist stimulation in relation to series 2 prostaglandin production.

The peroxisome proliferator-activated receptors (PPARs) are a family of nuclear transcription factors thought to act as receptors for polyunsaturated fatty acids and to reduce production of series 2 prostaglandins (PG). The objectives of the current study were to characterize PPAR expression and the prostaglandin synthetic activity of cultured bovine endometrial cells in response to known PPAR ligands, as well as to key stimulators and inhibitors of series 2 prostaglandin secretion. PPARalpha and PPARdelta, but not PPARgamma, mRNAs are expressed in the BEND cell line regardless of treatment. Under resting conditions, PPARalpha mRNA levels increase in response to growth hormone (P < 0.05). In cells stimulated with PdBu, growth hormone depresses PPARalpha mRNA levels, regardless of whether cells also are treated with IFNtau. In contrast, PPARdelta mRNA levels are increased by exposure to PdBu, eicosapentanoic acid and IFNtau, and these effects are additive. PPAR mRNA levels are not predictive of prostaglandin accumulation. Agonist activation of PPARalpha, PPARdelta or PPARgamma augments PdBu-induced increases in prostaglandin H synthase-2 mRNA and media accumulation of prostaglandins F2alpha and E2. Treatment with the PPARalpha/delta agonist carbaprostacyclin, but not the PPARalpha agonist Wy14643 or PPARgamma agonist ciglitazone, completely reverses the IFNtau suppression of prostaglandin synthesis. In conclusion, PPARalpha and PPARdelta function in the response of bovine endometrium to growth hormone and long chain omega-3 polyunsaturated fatty acids.

Animals↗

PubMed2004

Interferon-tau induces degradation of prostaglandin H synthase-2 messenger RNA in bovine endometrial cells through a transcription-dependent mechanism.

A series of experiments were undertaken to examine the effects of interferon (IFN)-tau on regulation of prostaglandin H synthase (PGHS)-2 mRNA in bovine endometrial (BEND) cells as a means to elucidate the actions of IFN-tau to maintain pregnancy. The objective was to determine if IFN-tau mediates posttranscriptional regulation of PGHS-2 mRNA. Cells were treated with phorbol 12,13-dibutyrate (PdBu) for 3 h to induce PGHS-2 mRNA expression. Actinomycin D (0 or 1 microg/ml) or the p38 mitogen-activated protein kinase (MAPK) inhibitor, SB203580 (1 microM), were added at 3 h, followed by addition of IFN-tau (0 or 50 ng/ml) at 3.5 h and extraction of RNA at 4.5 h. The concentrations of PGHS-2 mRNA were stable between 3 and 4.5 h regardless of actinomycin D. Simultaneous treatment of PdBu-treated cells with actinomycin D and SB203580 (1 microM) decreased PGHS-2 mRNA. Addition of IFN-tau (50 ng/ml) reduced PGHS-2 mRNA, which was not observed when actinomycin D was present. Concurrent treatments of cells with SB203580 and IFN-tau (5 ng/ml) decreased concentrations of PGHS-2 mRNA in an additive manner. Although IFN-tau reduced PGHS-2 mRNA concentrations, phosphorylation of p38 MAPK was induced by IFN-tau, PdBu, and PdBu combined with IFN-tau after 10 min of treatment. Both the p38 MAPK inhibitor and IFN-tau decreased prostaglandin F(2alpha) secretion, and decreases were additive when the two were given together. In summary, activation of p38 MAPK by PdBu is required for continued presence of PGHS-2 mRNA and secretion of prostaglandin F(2alpha) in BEND cells. Interferon-tau mediates a transcription-dependent mechanism, which induces degradation of PGHS-2 mRNA. However, the consequences of an IFN-tau-induced activation of p38 MAPK warrant further investigation, because inhibition of p38 MAPK caused a degradation of PGHS-2 mRNA.

Animals↗

PubMed2004

[Inhibition of arteriosclerotic plaque development by garlic].

OBJECTIVE: In an in vitro biosensor model (PCT/EP 97/05212), the interplay between different lipoproteins in arteriosclerotic nanoplaque formation, as well as aqueous garlic extract (0.2-5.0 g/l from LI 111 powder) as a possible candidate drug against arterio/atherosclerosis were tested within the frame of a high throughput screening. METHODS: The processes described below were studied by ellipsometric techniques quantifying the adsorbed amount (nanoplaque formation) and layer thickness (nanoplaque size). A thorough description of the experimental setup has been given previously. RESULTS: Proteoheparan sulfate (HS-PG) adsorption to hydrophobic silica was monoexponential and after approximately 30 min constant. The LDL plasma fraction (100 mg/dl) from a healthy probationer showed beginning arteriosclerotic nanoplaque formation already at a normal blood Ca2+ concentration, with a strong increase at higher Ca2+ concentrations. Aqueous garlic extract (GE), preferably in a concentration of 1 g/l, applied acutely in the experiment, markedly slowed down this process of ternary aggregational nanoplaque complexation at all Ca2+ concentrations used. In a normal blood Ca2+ concentration of 2.52 mmol/l, the garlic induced reduction of nanoplaque formation and molecular size amounted to 14.8 % and 3.9%, respectively, as compared to the controls. Furthermore, after ternary complex build-up, GE similar to HDL, was able to reduce nanoplaque formation and size. The incubation time for HDL and garlic was only 30 min each in these experiments. Nevertheless, after this short time the deposition of the ternary complex decreased by 6.2% resp. 16.5%, i.e. the complex aggregates were basically resolvable. CONCLUSIONS: These experiments clearly proved that garlic extract strongly inhibits Ca2+ binding to HS-PG. In consequence, the formation of the ternary HS-PG/LDL/Ca2+ complex, initially responsible for the 'nanoplaque' composition and ultimately for the arteriosclerotic plaque generation, is decisively blunted.

Adsorption↗

PubMedDate not supplied

Comparative visualization for wave-based and geometric acoustics.

We present a comparative visualization of the acoustic simulation results obtained by two different approaches that were combined into a single simulation algorithm. The first method solves the wave equation on a volume grid based on finite elements. The second method, phonon tracing, is a geometric approach that we have previously developed for interactive simulation, visualization and modeling of room acoustics. Geometric approaches of this kind are more efficient than FEM in the high and medium frequency range. For low frequencies they fail to represent diffraction, which on the other hand can be simulated properly by means of FEM. When combining both methods we need to calibrate them properly and estimate in which frequency range they provide comparable results. For this purpose we use an acoustic metric called gain and display the resulting error. Furthermore we visualize interference patterns, since these depend not only on diffraction, but also exhibit phase-dependent amplification and neutralization effects.

Journal Article↗