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D Janssens

Publications and source records attributed to D Janssens.

32 records · Page 2Linked to original sources
PubMed1996

Effect of aescine on hypoxia-induced activation of human endothelial cells.

Phlebotonic drugs are very often old drugs which improve symptoms in chronic venous insufficiency but their precise mechanism remains unclear. One reason for this lack of information is our poor understanding of the aetiology of the varicose vein. One hypothesis which is being more and more substantiated is that the origin of the disease lies in the activation of the endothelium during blood stasis, leading to a cascade of reactions which, in the long term, alter the structure of the vein wall. In this work, we tested aescine (Reparil i.v. form), a phlebotonic drug, in an in vitro model which mimics this situation, i.e. human endothelial cells exposed to hypoxic conditions. Aescine was shown to inhibit 2 important steps of the activation of endothelial cells incubated 120 min under hypoxia the decrease in ATP content, which is the starting point of the activation cascade, and the increase in the activity of phospholipase A2, an enzyme responsible for the release of precursors of inflammatory mediators. Hypoxia-activated endothelial cells also increase their adhesiveness for neutrophils. This process could also be prevented in a dose-dependent manner if endothelial cells were incubated in the presence of aescine. This inhibition was confirmed by morphological observations in scanning electron microscopy. All 3 effects were already evidenced at 100 ng/ml and were maximal at 750 ng/ml. These effects obtained at very low concentrations probably represent one of the main molecular and cellular mechanisms that underlie, among others, protection of the vessel wall. Objective criteria for our understanding of the preventive action of this phlebotonic drug are, thus, provided.

Adenosine Triphosphate↗
PubMed1996

Effects of hydroxyethylrutosides on hypoxia-induced activation of human endothelial cells in vitro.

1. A clinically available mixture of hydroxyethylrutosides (HR) was examined as inhibitors of endothelial cell activation by hypoxia in vitro. Thus, the effects of HR on ATP depletion, phospholipase A2 activation and neutrophil adherence were investigated in hypoxia-activated human umbilical vein endothelial cells in primary cell culture. 2. Our results show that HR inhibited two important steps of the activation of endothelial cells by hypoxia: the decrease in ATP content, which is the starting point of the process, and the activation of phospholipase A2 one enzyme responsible for the release of inflammatory mediators. This inhibition was dose-dependent with 70 to 90% inhibition at 500 micrograms ml-1 of HR. 3. In addition, hypoxia-activated endothelial cells increased their adhesiveness for neutrophils. This process could also be prevented in a dose-dependent manner if endothelial cells were incubated in the presence of HR. This inhibition was confirmed by a morphological study. 4. In conclusion, the results of this study suggest that a possible explanation for the improvement in venous insufficiency by HR observed clinically could be their ability to inhibit the activation of endothelial cells during blood stasis.

Adenosine Triphosphate↗
PubMed1996

Interactions between endothelial cells and smooth muscle cells after their activation by hypoxia. A possible etiology for venous disease.

Because of their localization at the interface between blood and tissue, endothelial cells are responsible for the maintenance of vascular homeostasis. They fulfil a series of various functions and constantly interact with circulating leukocytes and with the smooth muscle cells (SMC) present in the media. Any disturbance of their metabolism can thus lead to alterations of the blood vessel functions. We have shown that hypoxia, for example resulting from venous stasis, induces the activation of endothelial cells which then release inflammatory mediators able to activate neutrophils and to induce their infiltration as well as growth factors for SMC. We propose that these processes are the beginning of a cascade of events eventually leading to structural and functional modifications of the venous wall similar to the ones observed in varicose vein wall. The endothelium alterations resulting from venous stasis would thus be the origin of the development of the venous disease. Pharmacological and clinical evidence reinforce this hypothesis.

Cell Hypoxia↗
PubMed1995

Protection of hypoxia-induced ATP decrease in endothelial cells by ginkgo biloba extract and bilobalide.

Due to their localization at the interface between blood and tissue, endothelial cells are the first target of any change occurring within the blood, and alterations of their functions can seriously impair organs. During hypoxia, which mimics in vivo ischemia, a cascade of events occurs in the endothelial cells, starting with a decrease in ATP content and leading to their activation and release of inflammatory mediators. EGb 761 and one of its constituents, bilobalide, were shown to inhibit the hypoxia-induced decrease in ATP content in endothelial cells in vitro. Under these conditions, glycolysis was activated, as evidenced by increased glucose transport, as well as increased lactate production. Bilobalide was found to increase glucose transport under normoxic but not hypoxic conditions. In addition, EGb and bilobalide prevented the increase in total lactate production observed after 60 min of hypoxia. However, after 120 min of hypoxia, the total lactate production was similar under normoxic and hypoxic conditions, and both compounds increased this production. These results indicate that glycolysis slowed down between the 60th and 120th minute of hypoxia, while EGb and bilobalide delayed the onset of glycolysis activation. In another experimental model, both compounds were shown to increase the respiratory control ratio of mitochondria isolated from liver of rats treated orally. Since ischemia is known to uncouple mitochondria, the protection of ATP content and the delay in glycolysis activation observed during hypoxia in the presence of EGb 761 or bilobalide is best explained by a protection of mitochondrial respiratory activity, at least during the first 60 min of hypoxia incubation. Both products retain the ability to form ATP, thereby reducing the cell's need to induce glycolysis, probably by preserving ATP regeneration by mitochondria as long as oxygen is available.

Adenosine Triphosphate↗
PubMed1995

Hypoxia induces PMN adherence to umbilical vein endothelium.

OBJECTIVE: In vitro incubation of cultured endothelial cells under hypoxia leads to the activation of these cells and results in an increase of their adhesiveness for neutrophils (PMN). Because of the possible relevance of these observations for pathological situations, we investigated whether adherence of PMN also occurs in an entire vein after its incubation in hypoxic conditions. METHODS: Human umbilical veins in complete cords were incubated for 2 h in normoxic or hypoxic conditions and the adherence of unstimulated human 51Cr-labelled-PMN was measured under flow conditions. Experiments with human umbilical vein endothelial cells (HUVEC) were performed in parallel for comparison. Morphological studies in scanning electron microscopy were carried out in both in vitro and ex vivo situations. RESULTS: Hypoxia induced an increase in the adherence of PMN either to HUVEC or to the umbilical vein endothelium up to 5- to 6-fold when compared to normoxic conditions (P < 0.001). In both cases, this hypoxia-induced adherence was inhibited by anti-ICAM-1 antibodies or when the PAF (platelet-activating factor) synthesis was blocked during hypoxia by oleic acid. Furthermore, the adherence of PMN was inhibited when PMN were pre-incubated with WEB 2086 (a selective PAF receptor antagonist). These results indicate a crucial role of PAF in this process. Morphological studies confirmed that the number of PMN adherent to hypoxic HUVEC or to the hypoxic umbilical vein endothelium was much greater than the number of PMN on normoxic endothelial cells. Both in vitro and ex vivo, PMN adherent to the hypoxic endothelial cells to the contrary of the ones adherent to normoxic endothelial cells demonstrated membrane foldings typical of an activated state. CONCLUSION: These results show that in a complete vein, hypoxia induced an increased adhesiveness of endothelial cells for PMN by a similar mechanism to the one observed for cultured endothelial cells. They suggest an active role of endothelial cells in the initiation of the inflammatory response often described in ischemic-reperfused organs.

Antibodies, Monoclonal↗
PubMed1993

Effects of naftidrofuryl on hypoxia-induced activation and mortality of human endothelial cells.

The present study was designed to elucidate the possible beneficial effects of naftidrofuryl on ischemia-induced endothelium damage. For this purpose, an in vitro model was developed wherein human endothelial cells isolated from umbilical vein were submitted to hypoxia. Long-term hypoxia incubation (6 h) induced cell mortality, and naftidrofuryl strongly protected endothelial cells against this mortality in a dose-dependent manner and at concentrations as low as 10(-9) M. 66% protection was still observed after 16 h of hypoxia. Naftidrofuryl had to be present during the hypoxia incubation to exert its action; preincubation up to 24 h in the presence of naftidrofuryl could not protect endothelial cells incubated under hypoxia without naftidrofuryl. Short-term hypoxia, which does not induce mortality, strongly activates the endothelial cells with an increase in the cytosolic calcium concentration, in the phospholipase A2 activity, and in the synthesis of prostaglandin and of platelet-activating factor. It also enhances the adherence of polymorphonuclear neutrophils. Naftidrofuryl was able to markedly inhibit this whole cascade of events in a dose-dependent manner. We also demonstrated that naftidrofuryl could block the decrease in ATP concentration that results from the hypoxic conditions. These results indicate that by preserving the energetic level of the cells, naftidrofuryl prevents the activation of endothelial cells and the cell mortality induced by hypoxia. By maintaining an intact endothelium in vivo during ischemia, naftidrofuryl could prevent the further damage induced by leukocyte recruitment and activation.

Adenosine Triphosphate↗
PubMed1992

Rapid identification of bacteria of the Comamonadaceae with amplified ribosomal DNA-restriction analysis (ARDRA).

Ribosomal rRNA gene fragments (rDNA) encompassing the 16S rDNA, the 16S-23S rDNA spacer region and part of the 23S rDNA of 95 strains belonging to 13 well-described taxa of the eubacterial family Comamonadaceae (beta subclass of the Proteobacteria or rRNA superfamily III) were enzymatically amplified using conserved primers. The fragments of approximately 2400 base pairs were subjected to restriction analysis. Restriction fragment length patterns obtained with HinfI enabled us to distinguish 9 of the 13 taxa studied. Restriction with CfoI was necessary to differentiate Acidovorax delafieldii from A. temperans and Hydrogenophaga flava from H. pseudoflava. The results indicate that amplified rDNA restriction analysis is a simple and reliable tool for the identification of bacterial species.

Base Sequence↗
PubMed1988

Structuring strain data for storage and retrieval of information on fungi and yeasts in MINE, the Microbial Information Network Europe.

A distributed Microbial Information Network Europe (MINE) is being constructed by a number of major microbial culture collections in countries of the European Community, with the support of the Biotechnology Action Programme (BAP) of the Commission of the European Community. The representatives of the collections participating in MINE have agreed to adopt a general format for the computer storage and retrieval of strain data. This uniform format will facilitate the electronic combination and exchange of data from different collections in order to produce integrated catalogues and the use of identical commands to search the different databases. It is recommended to other collections who may wish to contribute data to the MINE network or between themselves. Three kinds of records can be linked to the leading 'species records': strain records, synonym records, and alternative morphonym records. A minimum data set of 30 fields (similar to the fields used for producing catalogues) is defined that facilitates the exchange of data between the national nodes and serves as a directory to strains available at other nodes. It is suggested that the full strain record comprise 99 fields, grouped in 12 blocks: internal administration--name--strain administration--status--environment and history--biological interactions--sexuality--properties (cytology, biomolecular data)--genotype and genetics--growth conditions--chemistry and enzymes--practical applications. Several fields are divided into subfields of different ranks. Delimiters are used either to separate a range of entries that have to be indexed or to divide an entry from the reference to its source or remarks that should not be indexed. The contents and structure of the fields proposed for filamentous fungi and yeasts are described and in some cases illustrated by examples. Uniformity of input is essential for indexed fields and desirable for non-indexed fields. Seven thesaurus files are envisaged to ensure consistency.

Data Collection↗
PubMed1988

Cardiovascular risk factors in a sample of a rural Belgian population: the Bellux MONICA Study.

A sample of 1949 subjects of the population of the Belgian province of Luxembourg was screened for levels of cardiovascular risk factors. Cigarette smoking was more prevalent among males (51%) than among females (17%). The relationship between smoking and socio-economic status was inverse in males (M) and direct in females (F). Blood pressure (BP) measurements showed definite high BP in 10% of this sample, and 60% of those with definite high BP were not taking any hypertensive drugs. The average total cholesterol value was 6.49 mmol/L in M and 6.45 mmol/L in F. F had lower values than M at a younger age, but higher values than M at an older age. The high-density lipoprotein cholesterol was higher in F (1.57 mmol/L) than in M (1.27 mmol/L). Diabetes was present in 4.2% of this sample. In nearly half of these participants, the disease had been discovered during the screening. Obesity was especially frequently among F in all three age groups. In conclusion, the main cardiovascular risk factors were found to be at a fairly high level in this population sample.

Adult↗
PubMed1983

Treatment of vaginal candidosis with oral ketoconazole.

Results with ketoconazole were studied in 281 non-pregnant patients with acute and chronic Candida-vaginitis. Several dose regimens were evaluated. The 5-day regimens (200 mg b.i.d. or 400 mg once daily) seem to be the most appropriate schedules in this infection. Side effects were minor. Relapse rates are not different from those, historically known, with topical antifungals.

Administration, Oral↗
PubMed1973

Vagitus uterinus.

Explore the source record for details and available documents.

Acid-Base Equilibrium↗
PubMedDate not supplied

Protection by bilobalide of the ischaemia-induced alterations of the mitochondrial respiratory activity.

Ischaemia is a common feature of most vascular diseases. There is evidence from experimental and clinical studies that Ginkgo biloba extract protects tissues from ischaemia/reperfusion damages. Bilobalide seems to be responsible, at least in part, for this activity. However, the mechanism of the protection afforded by bilobalide is not yet known. In this work, the effects of bilobalide on mitochondrial respiration were investigated during liver and brain ischaemia, since mitochondria alteration is an early event in ischaemia-induced damage. Bilobalide could prevent the decrease in respiratory activity induced by ischaemia in liver and in brain, both when glutamate/malate or succinate was used as substrate. Ischaemia decreased state 3 respiration rate and bilobalide prevented this decrease. While bilobalide was not able to prevent the decrease in adenine translocase activity, it protected complex I activity. Bilobalide allows mitochondria to maintain their respiratory activity in ischaemic conditions by protecting complex I and probably complex III activities. Hence, the energetic pool of tissues is preserved during the ischaemic period as well as its viability. This mechanism provides, a possible explanation for the anti-ischaemic properties of bilobalide and of Ginkgo biloba extract in therapeutic interventions.

Animals↗