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Biomedical subjects

B Fouqueray

Publications and source records attributed to B Fouqueray.

51 records · Page 3Linked to original sources
PubMed1992

Up-regulation of tumour necrosis factor-alpha receptors on monocytes by desferrioxamine.

The effect of endogenously generated reactive oxygen metabolites on the interaction of human blood monocytes with tumour necrosis factor-alpha (TNF-alpha) was investigated. Pre-exposure of unactivated human blood monocytes to dimethylthiourea, a scavenger of hydroxyl radical (OH.), or to desferrioxamine (DFX), an iron chelator preventing the synthesis of OH., enhanced the specific binding of 125I-TNF-alpha to its receptors. Scavengers of superoxide anion or hydrogen peroxide were without effect. DFX-induced up-regulation of 125I-TNF-alpha binding depended on the concentration of the drug (1-5 mM) and on the duration of the treatment (1-18 h). It was not due to a reduction of receptor occupancy by endogenously generated TNF-alpha. Scatchard analysis of binding data revealed that DFX caused an approximately two-fold increase in the number of type II TNF-alpha receptors, with no change in their affinity. This up-regulation, that did not require synthesis of new proteins, was associated with a decrease in the internalization rate of TNF-alpha receptors, the half-life of which was doubled. Conversely, these findings suggest that OH. generation by monocytes may have a physiological role in reducing the activity of membrane-associated TNF-alpha receptors.

Binding, Competitive↗
PubMed1992

Reactive oxygen species as glomerular autacoids.

There is considerable evidence suggesting that reactive oxygen species (ROS; superoxide anion, hydrogen peroxide, hydroxyl radical, hypochlorous acid) are implicated in the pathogenesis of toxic, ischemic, and immunologically mediated glomerular injury. The capacity of glomerular cells, especially mesangial cells, to generate ROS in response to several stimuli suggests that these autacoids may play a role in models of glomerular injury that are independent of infiltrating polymorphonuclear leukocytes and monocytes. The mechanisms whereby ROS formation results in morphologic lesions and in modifications of glomerular permeability, blood flow, and filtration rate have been inferred from in vitro studies. They involve direct and indirect injury to resident cells (mesangiolysis) and glomerular basement membrane (in concert with metalloproteases) and alteration of both the release and binding of vasoactive substances, such as bioactive lipids (e.g., prostaglandin E2, prostacyclin, thromboxane), cytokines (e.g., tumor necrosis factor alpha), and possibly endothelium-derived relaxing factor. The importance of such processes appears to be modulated by the intrinsic antioxidant defenses of the glomeruli. Further studies are needed to address the role of ROS in human glomerular diseases.

Animals↗
PubMed1991

[Emphysematous pyelonephritis associated to urogenital tuberculosis].

Emphysematous pyelonephritis is a rare condition which in most cases occurs as a result of Escherichia coli infection of the urinary tract in patients known as being diabetic. The gas-filled abscesses carry a high mortality rate, especially when the antibiotic treatment is not combined with early surgery. We report a case where the failure of medical treatment led to curative nephrectomy. Unusually, diabetes was revealed by the pyelonephritis. Another particularity of this case was that the emphysematous pyelonephritis was associated with genitourinary tuberculosis. This association, of which no other example could be found in the literature, is discussed.

Adult↗
PubMed1991

Desferrioxamine regulates tumor necrosis factor release in mesangial cells.

Cultured rat mesangial cells have been demonstrated to express tumor necrosis factor alpha (TNF alpha) mRNA and to release TNF activity into the medium upon stimulation by bacterial lipopolysaccharide (LPS). The present study was undertaken to determine whether TNF was only secreted by mesangial cells or was also present as a cell-associated molecule. LPS-activated mesangial cells which had been fixed in paraformaldehyde lysed the TNF-sensitive L-929 fibroblasts, as assessed by 51Cr release. This cytotoxic activity was inhibited by anti-TNF alpha antiserum. Cell-associated TNF expression was demonstrable after less than one hour of exposure to LPS, peaked at two hours and decreased progressively thereafter, while TNF activity increased in the medium. Mesangial cell-associated TNF was localized at the cell surface, as shown by immunohistochemical demonstration and by the ability of plasma membranes purified from LPS-activated mesangial cells to lyse L-929 fibroblasts. Flow cytometry experiments revealed that two-thirds of LPS-activated mesangial cells were stained by anti-TNF alpha antiserum. The major part of these cell-associated TNF molecules persisted after low pH treatment, indicating that they were integral membrane proteins. As assessed by immunoprecipitation analysis, these proteins were 26 kDa molecules, whereas the released forms of TNF were 17 kDa molecules. Pretreatment of mesangial cells with desferrioxamine (DFX), an iron chelator preventing the synthesis of hydroxyl radicals (OH.), delayed the release of TNF from the membranes into the medium, and enhanced its cell surface expression. It also subsequently accelerated its decay in the medium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Hypercalcemia in blood diseases and cancers].

The clinical classification of malignant hypercalcaemias according to the presence or absence of bone lesions no longer corresponds to the physiopathology of these hypercalcaemias as it is known today. Both focal osteolysis and humoral hypercalcaemia involve a number of substances, such as prostaglandins, cytokines, growth factors, PTH-rp and calcitriol, the action of which is neither specific nor single. A knowledge of their role in the pathogenesis of hypercalcaemia should lead to the development of antagonists for therapeutic purpose and to a better understanding of their individual physiological effects, since some of these mediators are present in non-tumoral tissues. In humoral hypercalcaemia, PTH-rp seems to play a major role on kidneys and bones.

Humans↗
PubMed1988

Maximal PTH secretory rate and set point for calcium in normal subjects and patients with primary hyperparathyroidism. In vivo studies.

The characteristics of PTH secretion, which have been extensively studied in vitro with dispersed cells of normal and abnormal parathyroid glands, remain poorly studied in vivo. We performed ethylenediamine tetraacetate (EDTA) intravenous infusions in 12 normal subjects and 5 patients with hypercalcemia (serum ionized calcium between 2.72 and 2.89 mEq/l) and surgically proven primary hyperparathyroidism (PHPT) to establish the relationship between nephrogenous cyclic AMP (NcAMP) used as an index of PTH secretion and serum ionized calcium. We determined the maximal NcAMP taken as an index of maximal secretory rate for PTH, the set point and sensitivity of parathyroid cells for calcium. In normal subjects, mean values (+/- SD) were 4.04 +/- 0.47 nmol/dl glomerular filtrate (GF) for maximal NcAMP, 2.23 +/- 0.04 mEq/l for set point, and -250 +/- 58 for sensitivity when NcAMP was expressed in percent of maximal value and serum calcium in mEq/l. In patients with PHPT, the differences between maximal and basal values of NcAMP represented 50% or more of maximal NcAMP, indicating that PTH secretion was suppressible. Sensitivity values were within normal limits in all patients. Calculated set point values were abnormally elevated (between 2.64 and 2.83 mEq/l) in all patients. Maximal NcAMP values ranged from low to normal (2.77 nmol/dl GF) to abnormally high (6.64 nmol/dl GF), and a positive linear correlation was observed with parathyroid cell mass. Basal serum calcium concentrations were not correlated with either parathyroid cell mass or maximal NcAMP values, and were close to calculated set point values for each patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Validation of an self-measurement blood pressure device].

UNLABELLED: The aim of this study was to test the self-blood pressure (Self-BP) measurement device Copal UA-251 (Philips). This device uses auscultatory method for BP measurement. It was compared to reference methods: intraarterial and Hawksley Random Zero in 38 patients, selected in two groups: group RO (n = 18), compared Copal to Random Zero. 20 simultaneous measurements were recorded, with devices inversion at eleventh BP measurement, in 18 treated or untreated hypertensive patients. Group IA (n = 20) included 20 patients and compared Copal to intra-aortic measurement. Three simultaneous measurements were recorded, before a coronarography was performed, in 20 normo or hypertensive patients. RESULTS: (Table: see text). 1) A significant difference was recorded for SBP evaluated by Copal versus RO and for DBP measured by Copal versus IA. 2) A significant correlation was assessed between the different methods of measurement. 3) Differences between couples of RO-Copal values are not correlated to BP level, neither for SBP (r = 0.07), nor DBP (r = 0.05). Same results occur for IA-Copal values (SBP: r = 0.36, DBP: r = 0.30). 4) No order effect was found; no discrepancy between arms occurred in BP measurement. CONCLUSION: comparing intraaortic measure, Copal is efficient for SBP measurement, but overestimate DBP. Compared to R0, Copal overestimates SBP, but is efficient for DBP measurement. Regarding these results, a self-BP measurement is possible with this device.

Adolescent↗
PubMed1988

[Comparison of 3 methods of blood pressure measurement in obesity].

Arm girth and circumference often leads to difficulties in Blood Pressure (BP) measurement in obese patients. In order to assess the best method of BP measurement, we have compared in a triplicate study, Intra-arterial Pressure (INTRA) to indirect measurements: Mercury Sphygmomanometer (SPH) and oscillometric device Bard Sentron (SEN). SPH and SEN were successively connected to the same cuff (inflatable bladder 14 x 31 cm). Cuff was positioned on contralateral arm to arterial puncture. 19 subjects were studied (18 female); mean age was 51.3 +/- 9 years (extremes: 37-69), mean weight 104 +/- 19 kg (84-147), weight index 40 +/- 4.7 kg/m2 (34-49), and brachial circumference 39 +/- 4 cm (33-47). First out-patient mean blood pressure measurement was 182/104 mmHg (148-264/80-132). Mean SPH BP were 158 +/- 34/91 +/- 3 (98-230, 72-112) and mean INTRA: 171 +/- 37/85 +/- 5 (122-256/56-118). Mean systolic and diastolic differences (S, D, mmHg) were: (Table: see text). 1) SPH systolic BP underestimates HUM systolic BP. 2) Mean SEN measurements are very closed to HUM values. 3) A great intra-individual variability occurs since more than 50 per cent systolic SPH values show discrepancy of more than 10 mmHg for systolic and diastolic HUM BP; the same discrepancies occur for SEN vs HUM. 4) Differences between couples of values (HUM-SEN, HUM-SPH) are not correlated to BP level, neither for systolic nor for diastolic BP. 5) No significant correlation occurs when BP deltas are compared to weight index or arm circumference.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Interleukin 10: a logical candidate for suppressing glomerular inflammation?

Inflammatory processes within the glomerulus are switched off by the local generation of anti-inflammatory mediators. These mediators include eicosanoids (e.g., lipoxins), anti-inflammatory cytokines (interleukins 4 and 13), antagonists of proinflammatory cytokines (interleukin 1 receptor antagonist), neuropoietic cytokines (leukemia inhibitory factor and interleukin 6), as well as deactivators of inflammatory macrophages (transforming growth factor beta and interleukin 10). They limit the effects of proinflammatory mediators by inhibiting their production, stability, or function. Recent attempts to reduce inflammatory lesions in experimental glomerulonephritis have focused on upregulating the expression of these anti-inflammatory mediators by using protein or gene transfer. In particular administration of interleukin 4, interleukin 1 receptor antagonist, leukemia inhibitory factor, or interleukin 10 has been shown to be effective in the treatment of nephrotoxic nephritis. Of all the mediators already tested, interleukin 10 has the greatest potential because of its strong anti-inflammatory effects and weak adverse effects.

Animals↗
PubMedDate not supplied

Growth hormone and somatostatin in glomerular injury.

Among other neuropeptides and neurohormones, growth hormone (GH) and somatostatin (SRIF) have been shown to modulate the development of glomerular injury in various renal diseases. In particular, GH is implicated in the induction of glomerular hypertrophy and sclerosis in partial nephrectomy and diabetic nephropathy. While GH effects on glomerular hypertrophy are likely mediated by insulin-like growth factor I (IGF-I), GH effects on glomerular sclerosis are independent of IGF-I. Those effects rather require multiple signaling pathways functioning in series, e.g. angiotensin II binding preceding transforming growth factor beta (TGF-beta) release, or pro-inflammatory factor release preceding repair/scarring processes. In contrast with GH, SRIF administration prevents the development of glomerular lesions in experimental diabetes, partial nephrectomy and immune glomerulonephritis. Inhibitory effects of SRIF on glomerular hypotrophy may be through a decrease in GH secretion and/or IGF-I expression or through a direct blockade of glomerular cell proliferation. The mechanisms underlying the anti-inflammatory effects of SRIF are most likely a deactivation of inflammatory cells related in part to an upregulated response of these cells to glucocorticoids. Additional studies will be required to further define the role of GH and SRIF in the development of glomerular injury and, hence, to identify new targets for a therapeutic approach in glomerular diseases.

Diabetic Nephropathies↗