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J Remacle

Publications and source records attributed to J Remacle.

162 records · Page 9Linked to original sources
PubMedDate not supplied

Alteration of enzymes in ageing human fibroblasts in culture. I. Conditions for the appearance of an alteration in glucose 6-phosphate dehydrogenase.

Glucose 6-phosphate dehydrogenase has been found to be altered in ageing human fibroblasts in culture. In this article, we have studied the effects of incubation conditions on glucose 6-phosphate dehydrogenase present in isolated cells or homogenates from young and old cells. We show that incubation at 4 degrees C and pH 7.4 induced the appearance of a heat-labile enzyme; this was not the case at pH 6.5. Also NADP+, when present, protects the enzyme from being modified. The kinetics of the modification indicates that the altered form of the enzyme is an intermediary stage between the active and inactive forms. We now have a model system in which the appearance of an altered enzyme can be induced in only a few hours; this model will be used in our next paper to study the mechanism of this alteration.

Cell Survival↗
PubMedDate not supplied

Alteration of enzymes in ageing human fibroblasts in culture. II. Conditions for the reversibility and the mechanism of the alteration of glucose 6-phosphate dehydrogenase.

The appearance of a heat-labile glucose 6-phosphate dehydrogenase fraction can be induced by incubation of human fibroblasts at 4 degrees C and pH 7.4. Using this system we first studied the effects of pH and NADP+ on the reversibility of the alteration. In young cells, the induced alteration of glucose 6-phosphate dehydrogenase disappeared if the pH of the medium was lowered to 6.5 or if NADP+ was added. In old cells, the disappearance of the natural heat-labile glucose 6-phosphate dehydrogenase was possible only if both pH 6.5 and NADP+ were present. Secondly, we studied the effects of the alteration and its reversibility on the equilibrium between the enzyme subunits; we showed that alteration and inactivation are linked to a dissociation of the enzyme subunits into inactive monomers. We also proposed a model where the heat-labile enzyme is a transient form between the active dimer and inactive monomer. Our results are in perfect agreement with the theories of post-translational modifications now proposed to explain the presence of the altered enzymes in old cells.

Cell Survival↗
PubMedDate not supplied

Cellular aging and the importance of energetic factors.

The in vitro aging of human fibroblasts has become a classical model for studying cellular aging. This model was lately redefined by showing that these cells represent a stem cell system in which they progressively pass through seven morphotypes. Experimental data showed that external conditions that can be considered as stresses for the cells, can modulate the genome expression by speeding up the passage of the cells from one morphotype to the other. In this article, we will interpret these observations from the point of view of the thermodynamics of far from equilibrium open systems, which shows the importance of the production and the use of energy, both responsible for the generation of a given amount of entropy production. In stable systems like these cell morphotypes, such a production is constant but external stresses can prematurely destabilize the steady state of entropy production and, in doing so, accelerate the process of aging. It is also predicted that cells submitted to a stress will use part of their energy in response to the stress. Some experimental data in favor of such an interpretation have been obtained and more will be presented here that show that both cell death and accelerated cell aging under stress are modulated by the level of energy metabolism. All theoretical and experimental arguments presented in this article will show that cellular aging is related to stress and also to energy production through a very elaborate system of regulatory processes necessary for the cell to survive and to perform specific functions according to its differentiated state. This regulatory system also permits the cell to adapt its response according to the intensity of external as well as internal challenges and one of these responses will influence the cellular aging rate.

Cell Death↗
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↗
PubMedDate not supplied

A low-density DNA microarray for analysis of markers in breast cancer.

Breast cancer remains a major cause of death in women from Western countries. In the near future, advances in both nucleic acids technology and tumor biology should be widely exploited to improve the diagnosis, prognosis, and outcome prediction of this disease. The DNA microarray, also called biochip, is a promising tool for performing massive, simultaneous, fast, and standardized analyses of multiple molecular markers in tumor samples. However, most currently available microarrays are expensive, which is mainly due to the amount (several thousands) of different DNA capture sequences that they carry. While these high-density microarrays are best suited for basic studies, their introduction into the clinical routine remains hypothetical. We describe here the principles of a low-density microarray, carrying only a few hundreds of capture sequences specific to markers whose importance in breast cancer is generally recognized or suggested by the current medical literature. We provide a list of about 250 of these markers. We also examine some potential difficulties (homologies between marker and/or variant sequences, size of sequences, etc.) associated with the production of such a low-cost microarray.

Breast Neoplasms↗
PubMedDate not supplied

[The relation between venous stasis and the occurrence of pain].

Venous stasis is a situation encountered commonly in varicose disorders. The potential implications of this decrease in oxygen levels in terms of the status of the cells of the vein were assessed. When endothelial cells are subjected to hypoxia, there is stimulation of the cells which shows itself as increased synthesis of prostaglandins and of PAF (Platelet Activating Factor). The synthesis of these typical mediators of inflammation results from activation by the calcium of phospholipase A2 which releases the arachidonic acid of phospholipids and this increase in intracellular calcium results itself from a fall in efficacy of calcium pumps due to the fall in ATP caused by hypoxia. Thus the fall in oxygen leads to the production of mediators of inflammation which activate leucocytes and result in local micro-inflammation which can be very rapidly eliminated if the circulation is restored but which can also cause irreversible damage to the vein by changes in venous tissue due to activated leucocytes which release proteases and free radicals after having penetrated the intima of the vein. These processes offer an explanation for the histological changes seen in varicose veins and the onset of localised pain during the development of such disease.

Humans↗
PubMedDate not supplied

[A comparative study of the protective effect of different phlebotonic agents on endothelial cells in hypoxia].

Numerous reported findings indicate that the etiology of venous diseases is multifactorial. One of the chief factors is certainly stasis of blood in the veins of the lower limbs during long periods spent standing up. This stasis causes tissue hypoxia which first affects the venous wall. Because of their location at the interface between blood and vein wall and because of their fragility, endothelial cells are the first to suffer from the lack of oxygen. With the aim of understanding these events, the authors have developed a model of endothelial cells in culture subjected to hypoxia in vitro which mimics the conditions encountered clinically. This model has enabled us to test various drugs commonly used in venous disease. These included GbE, the active ingredient of GINKOR FORT, diosmin and procyanidol oligomers. It was thus shown that only GbE was not toxic to endothelial cells. GbE was also found to be capable of effectively protecting cells exposed to hypoxia. Protection under the influence of diosmin was obtained only at concentrations very close to toxic doses. In contrast, procyanidol oligomers offered no protection. The protective effect of GbE is believed to be due to the action of terpenes on the energy metabolism of the cell.

Antihypertensive Agents↗
PubMedDate not supplied

[A comparative study of the protective effect of various phlebotonic agents on hypoxic endothelial cells].

Many findings indicate that the etiology of venous disease is multifactorial. One of the chief factors is certainly the stasis of blood in the lower limbs during long periods of standing. This stasis causes tissue hypoxia which first affects the venous wall. Because of their site at the blood/vein wall interface as well as their fragility, endothelial cells are the first to suffer from lack of oxygen. In order to understand these events, the authors have developed a model of endothelial cells in culture subjected to hypoxia in vitro which imitates conditions encountered clinically. This model was used to test different drugs commonly used in venous pathology. These included GbE, the active ingredient of GINKOR FORT, diosmine and procyanidolic oligomers. It was thus shown that only GbE was not toxic to endothelial cells. Furthermore, GbE was capable of effectively protecting cells subjected to hypoxia. Protection with diosmine was obtained only at concentrations very close to toxic doses. In contrast, procyanidolic oligomers afforded no protection. The protective effect of GbE is believed to be due to the action of terpenes on cellular energy metabolism.

Antihypertensive Agents↗
PubMedDate not supplied

[Behavior of human endothelial cells in hyperoxia and hypoxia: effect of Ginkor Fort].

Recent discoveries have shown that venous diseases have a multifactorial etiology. One of the factors which is definitely involved in this pathologic process is the change in the concentration of oxygen. An increase in the concentration of oxygen, hyperoxia, or reoxygenation following hypoxia, damages the tissues by stepping up the production of free radicals. In addition, a reduction in oxygen concentration, or hypoxia, is also damaging, probably through a reduction in ATP synthesis. From a therapeutic standpoint, the veins, and more particularly the endothelium, must be protected against the impact on the tissue of these changes in oxygen concentration. In this study, the effects of Ginkor Fort were tested on cultured endothelial cells subjected to varying oxygen pressures. The results show that Ginkor Fort can provide good protection of endothelial cells against hyperoxia and hypoxia-reoxygenation. These beneficial effects are probably due to the presence of flavonoids in the Ginko biloba extract; these flavonoids have an anti-oxidant effect. In addition, this substance also protects the cells against hypoxia, possibly by increasing the availability of oxygen for ATP synthesis. This dual protective effect, which is produced by two different mechanisms, may account for the wide spectrum of Ginkor Fort in its use in venous diseases.

Cell Survival↗
PubMedDate not supplied

[Recent maternity and manifestations of anxiety-depression. Epidemiological study of a population of non-consulting primiparas of the Liège region].

This study had for objective to detect the psychological morbidity of 176 non-consulting primiparas in the region of Liege using both the PSE and a sociological questionnaire. A high incidence of anxio-depressive manifestations was recorded in the month following birth (almost 27% of the cases) and their persistence at a lower rate in the 8th and 18th month. We were finally able to point out a certain number of risk factors: socioeconomic and familial conditions, somatic factors (difficult pregnancy and birth), recent psychological trauma or persistent conflict.

Adult↗